Opinion

Difficult economic times and the unpredictable consequences of health care reform are making an increasing number of solo practitioners and small private groups very nervous. Yet, many balk at the prospect of selling to private equity companies. I have received many inquiries about other protective options, such as merging two or more small practices into one larger entity.

Merging offers many benefits: Better overall management, centralized and efficient billing and collection, group purchasing discounts, and reduced overhead, among others; but careful planning, and a written agreement, are essential. If you are considering such an option, here are some things to think about.

You should begin with an evaluation and comparison of the separate groups’ respective finances. This should include a history of production, collections, overhead, and liabilities. Basically, you want to locate and identify all assets and liabilities that will be combined into the new group. One area of immediate importance is Medicare participation. Which members now currently participate and which do not? Since the new group will need to have a single position, all of the physicians must agree on that issue.

Who will be in charge? Not every physician is a qualified manager. The manager should be the physician who is willing to spend the time it takes to sign checks, interact with the administrator, and ensure that other matters such as filing tax returns and approving minor purchases arc carried out properly.

What is the compensation formula? Compensation arrangements should be based on each physician’s current financial data and the goals of the practice. Will everyone be paid only for what they do individually, or will revenue be shared equally? I favor a combination, so productivity is rewarded but your income doesn’t drop to zero when you take time off.

Which practices have a retirement plan and which do not? Will you keep your retirement plans separate, or combine them? If the latter, you will have to agree on the terms of the new plan, which can be the same or different from any of the existing plans. You’ll probably need some legal guidance to insure that assets from existing plans can be transferred into a new plan without tax issues. You may also have to address the problem of physicians who currently do not have a plan who, for whatever reason, may not want to be forced into making retirement plan contributions.

The often-problematic issue of employees and their salaries needs to be addressed, to decide which employees will be needed in the new group, and to determine a salary structure. Each practice’s policies related to vacation, sick leave, and other such issues should be reviewed, and an overall policy for the new group developed.

Other common sticking points are issues related to facilities. If the practices intend to consolidate into one location, the physicians must decide which of the specific assets of each practice will be contributed to the new entity. Ideally, each party brings an equal amount of assets to the table, but in the real world that is hardly ever the case. Physicians whose assets are to be used generally want to be compensated, and those who have to dispose of or store assets are in a quandary. The solution to this predicament will vary depending on the circumstances of each merger. One alternative is to agree that any inequalities will be compensated at the other end, in the form of buyout value; that is, physicians contributing more assets will receive larger buyouts when they leave or retire than those contributing less.

Buyouts should be addressed in advance as well. You must decide when a buyout would occur – usually in the event of retirement, death, disability, or withdrawal (voluntary or involuntary) – how the buyout amount will be calculated, and how it will be paid. Then, you must agree on how a buyout amount will be valued. Remember that any buyout calculated at “appraised value” is a problem, because the buyout amount remains a mystery until an appraisal is performed. If the appraised value ends up being too high, the remaining owners may refuse to pay it. I suggest having an actuary create a formula, so that the buyout figure can be calculated at any time. This area, especially, is where you need experienced, competent legal advice.

Noncompete provisions are always a difficult issue, mostly because they are so hard (and expensive) to enforce. An increasingly popular alternative is, once again, to deal with it at the other end, with a buyout penalty. An unhappy partner can leave, and compete, but at the cost of a substantially reduced buyout. This permits competition, but discourages it; and it compensates the remaining partners.

These are only some of the pivotal business and legal issues that must be settled in advance. A little planning and negotiation can prevent a lot of grief, regret, and legal expenses in the future. I’ll discuss some other, more complicated merger options in my next column.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Difficult economic times and the unpredictable consequences of health care reform are making an increasing number of solo practitioners and small private groups very nervous. Yet, many balk at the prospect of selling to private equity companies. I have received many inquiries about other protective options, such as merging two or more small practices into one larger entity.

Merging offers many benefits: Better overall management, centralized and efficient billing and collection, group purchasing discounts, and reduced overhead, among others; but careful planning, and a written agreement, are essential. If you are considering such an option, here are some things to think about.

You should begin with an evaluation and comparison of the separate groups’ respective finances. This should include a history of production, collections, overhead, and liabilities. Basically, you want to locate and identify all assets and liabilities that will be combined into the new group. One area of immediate importance is Medicare participation. Which members now currently participate and which do not? Since the new group will need to have a single position, all of the physicians must agree on that issue.

Who will be in charge? Not every physician is a qualified manager. The manager should be the physician who is willing to spend the time it takes to sign checks, interact with the administrator, and ensure that other matters such as filing tax returns and approving minor purchases arc carried out properly.

What is the compensation formula? Compensation arrangements should be based on each physician’s current financial data and the goals of the practice. Will everyone be paid only for what they do individually, or will revenue be shared equally? I favor a combination, so productivity is rewarded but your income doesn’t drop to zero when you take time off.

Which practices have a retirement plan and which do not? Will you keep your retirement plans separate, or combine them? If the latter, you will have to agree on the terms of the new plan, which can be the same or different from any of the existing plans. You’ll probably need some legal guidance to insure that assets from existing plans can be transferred into a new plan without tax issues. You may also have to address the problem of physicians who currently do not have a plan who, for whatever reason, may not want to be forced into making retirement plan contributions.

The often-problematic issue of employees and their salaries needs to be addressed, to decide which employees will be needed in the new group, and to determine a salary structure. Each practice’s policies related to vacation, sick leave, and other such issues should be reviewed, and an overall policy for the new group developed.

Other common sticking points are issues related to facilities. If the practices intend to consolidate into one location, the physicians must decide which of the specific assets of each practice will be contributed to the new entity. Ideally, each party brings an equal amount of assets to the table, but in the real world that is hardly ever the case. Physicians whose assets are to be used generally want to be compensated, and those who have to dispose of or store assets are in a quandary. The solution to this predicament will vary depending on the circumstances of each merger. One alternative is to agree that any inequalities will be compensated at the other end, in the form of buyout value; that is, physicians contributing more assets will receive larger buyouts when they leave or retire than those contributing less.

Buyouts should be addressed in advance as well. You must decide when a buyout would occur – usually in the event of retirement, death, disability, or withdrawal (voluntary or involuntary) – how the buyout amount will be calculated, and how it will be paid. Then, you must agree on how a buyout amount will be valued. Remember that any buyout calculated at “appraised value” is a problem, because the buyout amount remains a mystery until an appraisal is performed. If the appraised value ends up being too high, the remaining owners may refuse to pay it. I suggest having an actuary create a formula, so that the buyout figure can be calculated at any time. This area, especially, is where you need experienced, competent legal advice.

Noncompete provisions are always a difficult issue, mostly because they are so hard (and expensive) to enforce. An increasingly popular alternative is, once again, to deal with it at the other end, with a buyout penalty. An unhappy partner can leave, and compete, but at the cost of a substantially reduced buyout. This permits competition, but discourages it; and it compensates the remaining partners.

These are only some of the pivotal business and legal issues that must be settled in advance. A little planning and negotiation can prevent a lot of grief, regret, and legal expenses in the future. I’ll discuss some other, more complicated merger options in my next column.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Difficult economic times and the unpredictable consequences of health care reform are making an increasing number of solo practitioners and small private groups very nervous. Yet, many balk at the prospect of selling to private equity companies. I have received many inquiries about other protective options, such as merging two or more small practices into one larger entity.

Merging offers many benefits: Better overall management, centralized and efficient billing and collection, group purchasing discounts, and reduced overhead, among others; but careful planning, and a written agreement, are essential. If you are considering such an option, here are some things to think about.

You should begin with an evaluation and comparison of the separate groups’ respective finances. This should include a history of production, collections, overhead, and liabilities. Basically, you want to locate and identify all assets and liabilities that will be combined into the new group. One area of immediate importance is Medicare participation. Which members now currently participate and which do not? Since the new group will need to have a single position, all of the physicians must agree on that issue.

Who will be in charge? Not every physician is a qualified manager. The manager should be the physician who is willing to spend the time it takes to sign checks, interact with the administrator, and ensure that other matters such as filing tax returns and approving minor purchases arc carried out properly.

What is the compensation formula? Compensation arrangements should be based on each physician’s current financial data and the goals of the practice. Will everyone be paid only for what they do individually, or will revenue be shared equally? I favor a combination, so productivity is rewarded but your income doesn’t drop to zero when you take time off.

Which practices have a retirement plan and which do not? Will you keep your retirement plans separate, or combine them? If the latter, you will have to agree on the terms of the new plan, which can be the same or different from any of the existing plans. You’ll probably need some legal guidance to insure that assets from existing plans can be transferred into a new plan without tax issues. You may also have to address the problem of physicians who currently do not have a plan who, for whatever reason, may not want to be forced into making retirement plan contributions.

The often-problematic issue of employees and their salaries needs to be addressed, to decide which employees will be needed in the new group, and to determine a salary structure. Each practice’s policies related to vacation, sick leave, and other such issues should be reviewed, and an overall policy for the new group developed.

Other common sticking points are issues related to facilities. If the practices intend to consolidate into one location, the physicians must decide which of the specific assets of each practice will be contributed to the new entity. Ideally, each party brings an equal amount of assets to the table, but in the real world that is hardly ever the case. Physicians whose assets are to be used generally want to be compensated, and those who have to dispose of or store assets are in a quandary. The solution to this predicament will vary depending on the circumstances of each merger. One alternative is to agree that any inequalities will be compensated at the other end, in the form of buyout value; that is, physicians contributing more assets will receive larger buyouts when they leave or retire than those contributing less.

Buyouts should be addressed in advance as well. You must decide when a buyout would occur – usually in the event of retirement, death, disability, or withdrawal (voluntary or involuntary) – how the buyout amount will be calculated, and how it will be paid. Then, you must agree on how a buyout amount will be valued. Remember that any buyout calculated at “appraised value” is a problem, because the buyout amount remains a mystery until an appraisal is performed. If the appraised value ends up being too high, the remaining owners may refuse to pay it. I suggest having an actuary create a formula, so that the buyout figure can be calculated at any time. This area, especially, is where you need experienced, competent legal advice.

Noncompete provisions are always a difficult issue, mostly because they are so hard (and expensive) to enforce. An increasingly popular alternative is, once again, to deal with it at the other end, with a buyout penalty. An unhappy partner can leave, and compete, but at the cost of a substantially reduced buyout. This permits competition, but discourages it; and it compensates the remaining partners.

These are only some of the pivotal business and legal issues that must be settled in advance. A little planning and negotiation can prevent a lot of grief, regret, and legal expenses in the future. I’ll discuss some other, more complicated merger options in my next column.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

My inspiration to write about cupping this month stems from the perception that everyone seems to be talking about it, from a facialist who suggested it for me to a coworker who swears by cupping to treat her allergies. Cupping is by no means a novel procedure. Its use as a health therapy dates back thousands of years to ancient Egypt (1500 BCE), ancient Greece (described by Hippocrates), ancient Rome (described by the Greek physician Galen), China (during the Han dynasty, 206 BCE to 220 CE) and traditional Islamic culture.¹ Over the past decade, the popularity of this ancient procedure has been increasing in the United States.¹ Cupping has been applied as a remedy for various dermatologic and medical conditions, including herpes zoster, headaches, diminished appetite, maldigestion, abscess evacuation, narcolepsy, pain, fever, dysmenorrhea, and gout.^1,2

Theories on the mechanism(s) of action

The practice of cupping is differentiated into dry and wet cupping.^1,2 Traditionally, with dry cupping, a flame is applied to heat the air inside a thick glass cup (rather than the cup itself).¹ The cup is placed on the skin surface, and negative pressure suctions the skin into the cup. Wet cupping differs mainly from dry cupping in that it involves blood-letting. Cups made of either silicone or glass of varying size and shapes are used. Modern adaptations to cupping include needle, herbal, and pulsatile cupping, as well as a “moving cupping” technique (vs. traditionally stationary cups).¹

Thinkstock

There are several theories, many of which are derived from the nondermatologic literature (that is, pain management), as to how cupping may deliver a clinical benefit. Some theories are based in scientific and medical principles, whereas other theories are more whimsical – specifically, that cupping draws out evil spirits.² Studies of dry cupping have suggested that the procedure results in increased oxygenation of muscles via a local increase in oxygenated hemoglobin, which may help improve muscular activity and reduce pain.¹ As theorized by Lowe in 2017, negative pressure exerted by dry cupping leads to stretching and dilation of capillaries, which increases blood flow.³ Wet cupping has been shown to increase heat shock protein 70 (HSP70) and beta-endorphin expression in rat models, which is thought to facilitate pain management.1 Removal of oxidants and reduction of reactive oxygen species in the blood is believed to be among the benefits of wet cupping.¹
 

Cupping in general dermatology

While cupping has been used to treat a wide array of medical conditions, the ancient practice has been utilized in dermatology as a therapy mainly for herpes zoster and associated postherpetic neuralgia, as well as various inflammatory conditions.

Herpes zoster

In 2010, Cao et al. reported on their systematic review of wet cupping after completing searches of multiple databases (that is, PubMed, the Cochrane Library [Issue 3, 2008], China Network Knowledge Infrastructure, Chinese Scientific Journal Database, and Wan Fang Database). They identified eight randomized controlled trials involving 651 patients, with meta-analyses revealing that wet cupping performed better than medications in terms of the number of “cured” patients, number of patients with improved symptoms, and a lower incidence of postherpetic neuralgia. Wet cupping, in addition to medication, was also found to be superior to medication alone in multiple patients. The researchers concluded that wet cupping appears to effectively treat herpes zoster.⁴ However, the study failed to identify which medications were used to treat herpes zoster. In the United States, common medications for herpes zoster include acyclovir, valacyclovir, steroids, gabapentin, and other neuromodulators. Without knowing which medications were used, it is difficult to compare cupping to medication in terms of efficacy in treating herpes zoster.

Urticaria

Urticaria (hives) is an inflammatory skin condition that can be very uncomfortable for patients but often resolves without intervention within several months after onset. In 2001, Li and Ding reported on the treatment with cupping of 40 patients with urticaria. The cure rate among the treatment group was cited as 55%, compared with 30% in the control group, who were treated with a traditional Chinese remedy and an unidentified first-generation antihistamine.^1,5 In 2020, Xiao et al. conducted a systematic review and meta-analysis of cupping therapy for patients with chronic urticaria. They identified 13 comparisons from 12 randomized controlled trials involving 842 subjects. The investigators found no significant differences between wet cupping and medication usage. They also found that cupping combined with antihistamine treatment was superior to antihistamines alone, and cupping therapy with acupuncture was more effective than acupuncture alone. The investigators did call for caution, citing the poor quality of the studies reviewed.⁶

It is important to note that it is difficult to attribute resolution of urticaria to the use of cupping given the self-resolution often associated with this condition. Antihistamines are the mainstay of therapy for urticaria, but in my personal experience, patients are not entirely satisfied with the level of symptom control with antihistamines alone and often search for alternative therapies to control the pesky hives and associated itch. In 2014, omalizumab (Xolair) was approved for treating chronic idiopathic urticaria, which has helped patients control symptoms of chronic idiopathic urticaria without needing to take antihistamines. There was no indication that the studies reviewed by Xiao et al. compared cupping against this new effective treatment. Therefore, these studies comparing cupping to medical management are outdated.

Acne, eczema, and psoriasis

Soliman’s 2018 review of cupping in dermatology included a few studies on these common cutaneous conditions. For instance, a 2013 single-blind prospective study by Xu et al. reported on the results of patients with moderate acne who received wet cupping (in the form of prickling bloodletting) twice weekly for 6 weeks.⁷ They reported that patients demonstrated improvement in the global acne grading system (GAGS) score by the end of the trial.^1,7 Unfortunately, cupping was not compared with standard acne treatments (that is, benzoyl peroxide, topical and oral antibiotics, isotretinoin, topical retinoids, spironolactone).

In evaluating cupping for acute eczema, wet cupping was compared with oral loratadine and topical ointments in a 2007 study by Yao and Li. They divided 88 cases into treatment and control groups, with the former group (n = 46) receiving bloodletting puncturing and cupping and the control group (n = 42) receiving oral loratadine and topical Pairuisong (an herbal ointment used in Chinese medicine). The investigators observed no significant difference in total effective rates but a superior difference in the rates of responses that were considered “cured” and “markedly effective” in favor of the cupping treatment.^1,8 However, a case report by Hon et al. has indicated that cupping therapy may be associated with more harm than benefit when used as an eczema treatment.^1,9

In addition, it is important to note that the past 5 years have been gamechanging in the management of chronic eczema in terms of the array of novel and effective therapies (e.g., dupilumab and JAK inhibitors) and chronic moderate-to-severe eczema has become very treatable. Similarly, acute eczema is often successfully managed with topical steroids, calcineurin inhibitors, and emollients. As such, there is no compelling reason to consider an unproven treatment such as cupping.

In 2020, Xing et al. reviewed 16 randomized controlled trials assessing the use of “moving cupping” for plaque psoriasis, with 1,164 patients meeting inclusion criteria. Moving cupping was found to be significantly more effective than “no-moving” cupping therapy, and moving cupping, combined with medications, performed better than medications alone.¹⁰ None of the trials evaluated in this study included randomized controlled trials that compared patients using any of the more modern psoriasis medications, specifically biologics. And, again, the studies evaluated were not of the highest quality.

The data that support cupping, as summarized above, are based mostly on case reports, and strong double-blind prospective studies are lacking. Additionally, most of the studies cited gauged the efficacy of cupping using qualitative endpoints, rather than standardized quantitative endpoints and scales. Moreover, spontaneous remission of various dermatoses can occur, or they can improve over time, including acute eczema, psoriasis, and, especially, urticaria.
 

Adverse effects of cupping

Often alternative therapies are seen as “benign” and without adverse effects. However, complications can result from cupping. Trauma can be induced from the cupping itself by damaging superficial blood vessels and causing bruising.^1,11 Blistering can also occur secondary to the suction effect, and the epidermal and dermal layers of the skin can be separated.^1,11 Further, burns and discoloration have also been noted secondary to heat, trauma, and post inflammatory pigmentary changes.^1,11 Another risk of cupping is the Koebner phenomenon, which occurs with psoriasis, with new lesions appearing in traumatized skin.¹² Other adverse outcomes that have been reported with cupping include reactivation of herpes simplex virus secondary to skin trauma, iron deficiency anemia (secondary to blood loss), panniculitis, infections, and residual marks mistaken for signs of child abuse.^1,11

Cupping in aesthetic dermatology

Facial cupping, a distinct practice from body cupping used to treat general dermatology conditions described previously, is also increasing in popularity. This practice is usually conducted in association with a facial or facial acupuncture by an aesthetician or other licensed professional. It can also be performed using at-home kits. The marketing claims for facial cupping cite improved tightening and contouring of facial skin, increased facial microcirculation and collagen synthesis, and enhanced lymphatic flow to aid with facial puffiness or swelling. One supposed mechanism for these benefits is that cupping increases blood flow. Interestingly, there was a 2020 animal study in which photoacoustic imaging of a mouse ear revealed increased temporary blood flow in the cupping microenvironment.¹³ Currently, however, there is no evidence in the English scientific literature that supports facial cupping. The benefits attributed to facial cupping for aesthetic purposes have emerged only in personal anecdotes. The temporary increase in blood flow may induce inflammation and swelling that adds volume to the face and temporarily diminishes wrinkles. However, this temporary plumpness may be associated with adverse effects, such as local trauma, irritation, bruising, postinflammatory pigmentary alteration, or even herpes reactivation. In my opinion, the possible adverse effects of cupping outweigh any potential benefit, especially given the insufficient evidence supporting the utility of cupping for cosmetic enhancement.

Summary

There is increasing interest among patients to incorporate complementary and alternative medicine – including the ancient tradition of cupping – in managing medical dermatologic conditions. However, current evidence supporting cupping as an effective therapeutic strategy is not strong, with most studies to date appearing to be of poor quality or not sufficiently convincing to displace standard therapies. Our medical strategies for managing chronic dermatologic conditions, particularly inflammatory disorders, continue to improve from both a safety and a proven efficacy standpoint. Therefore, I would not forgo medical management in favor of cupping. While cupping can be used as an adjunct therapy, I would caution patients about possible adverse side effects. In the aesthetic world, cupping is also gaining popularity, but this trend is also not supported by current evidence or studies, at least in the Western literature.

Dr. Goldman is a dermatologist in private practice in Miami and specializes in cosmetic and general dermatology. She practices at Baumann Cosmetic & Research Institute and is also opening a general dermatology practice. Write to her at [email protected] or message her on Instragram @DrChloeGoldman. Dr. Goldman receives compensation to create social media content for Replenix, a skin care company. She has no other disclosures.

References

1. Soliman Y et al. Acta Dermatovenerol Alp Pannonica Adriat. 2018 Jun;27(2):103-7.

2. França K and Lotti T. Advances in Integrative Dermatology. John Wiley & Sons, 2019.

3. Lowe DT. Complement Ther Clin Pract. 2017 Nov;29:162-8.

4.Cao H et al. Altern Ther Health Med. 2010 Nov-Dec;16(6):48-54.

5. Li L and Ding J. J Tradit Chin Med. 2001 Mar;21(1):37-8.

6. Xiao XJ et al. J Integr Med. 2020 Jul;18(4):303-12.

7. Xu J et al. J Tradit Chin Med. 2013 Dec;33(6):752-6.

8. Yao J et al. Zhongguo Zhen Jiu. 2007; Jun;27(6):424-6.

9. Hon KL et al. Case Rep Pediatr. 2013;2013:605829.

10. Xing M et al. Medicine (Baltimore). 2020 Oct 9;99(41):e22539.

11. Kim TH et al. Eur J Integr Med. 2014 Aug 1;6(4):434-40.

12. Vender R and Vender R. J Cutan Med Surg. 2015 May-Jun;19(3):320-2.

13. Zhou Y et al. Biomed Opt Express. 2020 Apr 6;11(5):2394-401.

This article was updated 4/25/22.

My inspiration to write about cupping this month stems from the perception that everyone seems to be talking about it, from a facialist who suggested it for me to a coworker who swears by cupping to treat her allergies. Cupping is by no means a novel procedure. Its use as a health therapy dates back thousands of years to ancient Egypt (1500 BCE), ancient Greece (described by Hippocrates), ancient Rome (described by the Greek physician Galen), China (during the Han dynasty, 206 BCE to 220 CE) and traditional Islamic culture.¹ Over the past decade, the popularity of this ancient procedure has been increasing in the United States.¹ Cupping has been applied as a remedy for various dermatologic and medical conditions, including herpes zoster, headaches, diminished appetite, maldigestion, abscess evacuation, narcolepsy, pain, fever, dysmenorrhea, and gout.^1,2

Theories on the mechanism(s) of action

The practice of cupping is differentiated into dry and wet cupping.^1,2 Traditionally, with dry cupping, a flame is applied to heat the air inside a thick glass cup (rather than the cup itself).¹ The cup is placed on the skin surface, and negative pressure suctions the skin into the cup. Wet cupping differs mainly from dry cupping in that it involves blood-letting. Cups made of either silicone or glass of varying size and shapes are used. Modern adaptations to cupping include needle, herbal, and pulsatile cupping, as well as a “moving cupping” technique (vs. traditionally stationary cups).¹

Thinkstock

There are several theories, many of which are derived from the nondermatologic literature (that is, pain management), as to how cupping may deliver a clinical benefit. Some theories are based in scientific and medical principles, whereas other theories are more whimsical – specifically, that cupping draws out evil spirits.² Studies of dry cupping have suggested that the procedure results in increased oxygenation of muscles via a local increase in oxygenated hemoglobin, which may help improve muscular activity and reduce pain.¹ As theorized by Lowe in 2017, negative pressure exerted by dry cupping leads to stretching and dilation of capillaries, which increases blood flow.³ Wet cupping has been shown to increase heat shock protein 70 (HSP70) and beta-endorphin expression in rat models, which is thought to facilitate pain management.1 Removal of oxidants and reduction of reactive oxygen species in the blood is believed to be among the benefits of wet cupping.¹
 

Cupping in general dermatology

While cupping has been used to treat a wide array of medical conditions, the ancient practice has been utilized in dermatology as a therapy mainly for herpes zoster and associated postherpetic neuralgia, as well as various inflammatory conditions.

Herpes zoster

In 2010, Cao et al. reported on their systematic review of wet cupping after completing searches of multiple databases (that is, PubMed, the Cochrane Library [Issue 3, 2008], China Network Knowledge Infrastructure, Chinese Scientific Journal Database, and Wan Fang Database). They identified eight randomized controlled trials involving 651 patients, with meta-analyses revealing that wet cupping performed better than medications in terms of the number of “cured” patients, number of patients with improved symptoms, and a lower incidence of postherpetic neuralgia. Wet cupping, in addition to medication, was also found to be superior to medication alone in multiple patients. The researchers concluded that wet cupping appears to effectively treat herpes zoster.⁴ However, the study failed to identify which medications were used to treat herpes zoster. In the United States, common medications for herpes zoster include acyclovir, valacyclovir, steroids, gabapentin, and other neuromodulators. Without knowing which medications were used, it is difficult to compare cupping to medication in terms of efficacy in treating herpes zoster.

Urticaria

Urticaria (hives) is an inflammatory skin condition that can be very uncomfortable for patients but often resolves without intervention within several months after onset. In 2001, Li and Ding reported on the treatment with cupping of 40 patients with urticaria. The cure rate among the treatment group was cited as 55%, compared with 30% in the control group, who were treated with a traditional Chinese remedy and an unidentified first-generation antihistamine.^1,5 In 2020, Xiao et al. conducted a systematic review and meta-analysis of cupping therapy for patients with chronic urticaria. They identified 13 comparisons from 12 randomized controlled trials involving 842 subjects. The investigators found no significant differences between wet cupping and medication usage. They also found that cupping combined with antihistamine treatment was superior to antihistamines alone, and cupping therapy with acupuncture was more effective than acupuncture alone. The investigators did call for caution, citing the poor quality of the studies reviewed.⁶

It is important to note that it is difficult to attribute resolution of urticaria to the use of cupping given the self-resolution often associated with this condition. Antihistamines are the mainstay of therapy for urticaria, but in my personal experience, patients are not entirely satisfied with the level of symptom control with antihistamines alone and often search for alternative therapies to control the pesky hives and associated itch. In 2014, omalizumab (Xolair) was approved for treating chronic idiopathic urticaria, which has helped patients control symptoms of chronic idiopathic urticaria without needing to take antihistamines. There was no indication that the studies reviewed by Xiao et al. compared cupping against this new effective treatment. Therefore, these studies comparing cupping to medical management are outdated.

Acne, eczema, and psoriasis

Soliman’s 2018 review of cupping in dermatology included a few studies on these common cutaneous conditions. For instance, a 2013 single-blind prospective study by Xu et al. reported on the results of patients with moderate acne who received wet cupping (in the form of prickling bloodletting) twice weekly for 6 weeks.⁷ They reported that patients demonstrated improvement in the global acne grading system (GAGS) score by the end of the trial.^1,7 Unfortunately, cupping was not compared with standard acne treatments (that is, benzoyl peroxide, topical and oral antibiotics, isotretinoin, topical retinoids, spironolactone).

In evaluating cupping for acute eczema, wet cupping was compared with oral loratadine and topical ointments in a 2007 study by Yao and Li. They divided 88 cases into treatment and control groups, with the former group (n = 46) receiving bloodletting puncturing and cupping and the control group (n = 42) receiving oral loratadine and topical Pairuisong (an herbal ointment used in Chinese medicine). The investigators observed no significant difference in total effective rates but a superior difference in the rates of responses that were considered “cured” and “markedly effective” in favor of the cupping treatment.^1,8 However, a case report by Hon et al. has indicated that cupping therapy may be associated with more harm than benefit when used as an eczema treatment.^1,9

In addition, it is important to note that the past 5 years have been gamechanging in the management of chronic eczema in terms of the array of novel and effective therapies (e.g., dupilumab and JAK inhibitors) and chronic moderate-to-severe eczema has become very treatable. Similarly, acute eczema is often successfully managed with topical steroids, calcineurin inhibitors, and emollients. As such, there is no compelling reason to consider an unproven treatment such as cupping.

In 2020, Xing et al. reviewed 16 randomized controlled trials assessing the use of “moving cupping” for plaque psoriasis, with 1,164 patients meeting inclusion criteria. Moving cupping was found to be significantly more effective than “no-moving” cupping therapy, and moving cupping, combined with medications, performed better than medications alone.¹⁰ None of the trials evaluated in this study included randomized controlled trials that compared patients using any of the more modern psoriasis medications, specifically biologics. And, again, the studies evaluated were not of the highest quality.

The data that support cupping, as summarized above, are based mostly on case reports, and strong double-blind prospective studies are lacking. Additionally, most of the studies cited gauged the efficacy of cupping using qualitative endpoints, rather than standardized quantitative endpoints and scales. Moreover, spontaneous remission of various dermatoses can occur, or they can improve over time, including acute eczema, psoriasis, and, especially, urticaria.
 

Adverse effects of cupping

Often alternative therapies are seen as “benign” and without adverse effects. However, complications can result from cupping. Trauma can be induced from the cupping itself by damaging superficial blood vessels and causing bruising.^1,11 Blistering can also occur secondary to the suction effect, and the epidermal and dermal layers of the skin can be separated.^1,11 Further, burns and discoloration have also been noted secondary to heat, trauma, and post inflammatory pigmentary changes.^1,11 Another risk of cupping is the Koebner phenomenon, which occurs with psoriasis, with new lesions appearing in traumatized skin.¹² Other adverse outcomes that have been reported with cupping include reactivation of herpes simplex virus secondary to skin trauma, iron deficiency anemia (secondary to blood loss), panniculitis, infections, and residual marks mistaken for signs of child abuse.^1,11

Cupping in aesthetic dermatology

Facial cupping, a distinct practice from body cupping used to treat general dermatology conditions described previously, is also increasing in popularity. This practice is usually conducted in association with a facial or facial acupuncture by an aesthetician or other licensed professional. It can also be performed using at-home kits. The marketing claims for facial cupping cite improved tightening and contouring of facial skin, increased facial microcirculation and collagen synthesis, and enhanced lymphatic flow to aid with facial puffiness or swelling. One supposed mechanism for these benefits is that cupping increases blood flow. Interestingly, there was a 2020 animal study in which photoacoustic imaging of a mouse ear revealed increased temporary blood flow in the cupping microenvironment.¹³ Currently, however, there is no evidence in the English scientific literature that supports facial cupping. The benefits attributed to facial cupping for aesthetic purposes have emerged only in personal anecdotes. The temporary increase in blood flow may induce inflammation and swelling that adds volume to the face and temporarily diminishes wrinkles. However, this temporary plumpness may be associated with adverse effects, such as local trauma, irritation, bruising, postinflammatory pigmentary alteration, or even herpes reactivation. In my opinion, the possible adverse effects of cupping outweigh any potential benefit, especially given the insufficient evidence supporting the utility of cupping for cosmetic enhancement.

Summary

There is increasing interest among patients to incorporate complementary and alternative medicine – including the ancient tradition of cupping – in managing medical dermatologic conditions. However, current evidence supporting cupping as an effective therapeutic strategy is not strong, with most studies to date appearing to be of poor quality or not sufficiently convincing to displace standard therapies. Our medical strategies for managing chronic dermatologic conditions, particularly inflammatory disorders, continue to improve from both a safety and a proven efficacy standpoint. Therefore, I would not forgo medical management in favor of cupping. While cupping can be used as an adjunct therapy, I would caution patients about possible adverse side effects. In the aesthetic world, cupping is also gaining popularity, but this trend is also not supported by current evidence or studies, at least in the Western literature.

Dr. Goldman is a dermatologist in private practice in Miami and specializes in cosmetic and general dermatology. She practices at Baumann Cosmetic & Research Institute and is also opening a general dermatology practice. Write to her at [email protected] or message her on Instragram @DrChloeGoldman. Dr. Goldman receives compensation to create social media content for Replenix, a skin care company. She has no other disclosures.

References

1. Soliman Y et al. Acta Dermatovenerol Alp Pannonica Adriat. 2018 Jun;27(2):103-7.

2. França K and Lotti T. Advances in Integrative Dermatology. John Wiley & Sons, 2019.

3. Lowe DT. Complement Ther Clin Pract. 2017 Nov;29:162-8.

4.Cao H et al. Altern Ther Health Med. 2010 Nov-Dec;16(6):48-54.

5. Li L and Ding J. J Tradit Chin Med. 2001 Mar;21(1):37-8.

6. Xiao XJ et al. J Integr Med. 2020 Jul;18(4):303-12.

7. Xu J et al. J Tradit Chin Med. 2013 Dec;33(6):752-6.

8. Yao J et al. Zhongguo Zhen Jiu. 2007; Jun;27(6):424-6.

9. Hon KL et al. Case Rep Pediatr. 2013;2013:605829.

10. Xing M et al. Medicine (Baltimore). 2020 Oct 9;99(41):e22539.

11. Kim TH et al. Eur J Integr Med. 2014 Aug 1;6(4):434-40.

12. Vender R and Vender R. J Cutan Med Surg. 2015 May-Jun;19(3):320-2.

13. Zhou Y et al. Biomed Opt Express. 2020 Apr 6;11(5):2394-401.

This article was updated 4/25/22.

My inspiration to write about cupping this month stems from the perception that everyone seems to be talking about it, from a facialist who suggested it for me to a coworker who swears by cupping to treat her allergies. Cupping is by no means a novel procedure. Its use as a health therapy dates back thousands of years to ancient Egypt (1500 BCE), ancient Greece (described by Hippocrates), ancient Rome (described by the Greek physician Galen), China (during the Han dynasty, 206 BCE to 220 CE) and traditional Islamic culture.¹ Over the past decade, the popularity of this ancient procedure has been increasing in the United States.¹ Cupping has been applied as a remedy for various dermatologic and medical conditions, including herpes zoster, headaches, diminished appetite, maldigestion, abscess evacuation, narcolepsy, pain, fever, dysmenorrhea, and gout.^1,2

Theories on the mechanism(s) of action

The practice of cupping is differentiated into dry and wet cupping.^1,2 Traditionally, with dry cupping, a flame is applied to heat the air inside a thick glass cup (rather than the cup itself).¹ The cup is placed on the skin surface, and negative pressure suctions the skin into the cup. Wet cupping differs mainly from dry cupping in that it involves blood-letting. Cups made of either silicone or glass of varying size and shapes are used. Modern adaptations to cupping include needle, herbal, and pulsatile cupping, as well as a “moving cupping” technique (vs. traditionally stationary cups).¹

Thinkstock

There are several theories, many of which are derived from the nondermatologic literature (that is, pain management), as to how cupping may deliver a clinical benefit. Some theories are based in scientific and medical principles, whereas other theories are more whimsical – specifically, that cupping draws out evil spirits.² Studies of dry cupping have suggested that the procedure results in increased oxygenation of muscles via a local increase in oxygenated hemoglobin, which may help improve muscular activity and reduce pain.¹ As theorized by Lowe in 2017, negative pressure exerted by dry cupping leads to stretching and dilation of capillaries, which increases blood flow.³ Wet cupping has been shown to increase heat shock protein 70 (HSP70) and beta-endorphin expression in rat models, which is thought to facilitate pain management.1 Removal of oxidants and reduction of reactive oxygen species in the blood is believed to be among the benefits of wet cupping.¹
 

Cupping in general dermatology

While cupping has been used to treat a wide array of medical conditions, the ancient practice has been utilized in dermatology as a therapy mainly for herpes zoster and associated postherpetic neuralgia, as well as various inflammatory conditions.

Herpes zoster

In 2010, Cao et al. reported on their systematic review of wet cupping after completing searches of multiple databases (that is, PubMed, the Cochrane Library [Issue 3, 2008], China Network Knowledge Infrastructure, Chinese Scientific Journal Database, and Wan Fang Database). They identified eight randomized controlled trials involving 651 patients, with meta-analyses revealing that wet cupping performed better than medications in terms of the number of “cured” patients, number of patients with improved symptoms, and a lower incidence of postherpetic neuralgia. Wet cupping, in addition to medication, was also found to be superior to medication alone in multiple patients. The researchers concluded that wet cupping appears to effectively treat herpes zoster.⁴ However, the study failed to identify which medications were used to treat herpes zoster. In the United States, common medications for herpes zoster include acyclovir, valacyclovir, steroids, gabapentin, and other neuromodulators. Without knowing which medications were used, it is difficult to compare cupping to medication in terms of efficacy in treating herpes zoster.

Urticaria

Urticaria (hives) is an inflammatory skin condition that can be very uncomfortable for patients but often resolves without intervention within several months after onset. In 2001, Li and Ding reported on the treatment with cupping of 40 patients with urticaria. The cure rate among the treatment group was cited as 55%, compared with 30% in the control group, who were treated with a traditional Chinese remedy and an unidentified first-generation antihistamine.^1,5 In 2020, Xiao et al. conducted a systematic review and meta-analysis of cupping therapy for patients with chronic urticaria. They identified 13 comparisons from 12 randomized controlled trials involving 842 subjects. The investigators found no significant differences between wet cupping and medication usage. They also found that cupping combined with antihistamine treatment was superior to antihistamines alone, and cupping therapy with acupuncture was more effective than acupuncture alone. The investigators did call for caution, citing the poor quality of the studies reviewed.⁶

It is important to note that it is difficult to attribute resolution of urticaria to the use of cupping given the self-resolution often associated with this condition. Antihistamines are the mainstay of therapy for urticaria, but in my personal experience, patients are not entirely satisfied with the level of symptom control with antihistamines alone and often search for alternative therapies to control the pesky hives and associated itch. In 2014, omalizumab (Xolair) was approved for treating chronic idiopathic urticaria, which has helped patients control symptoms of chronic idiopathic urticaria without needing to take antihistamines. There was no indication that the studies reviewed by Xiao et al. compared cupping against this new effective treatment. Therefore, these studies comparing cupping to medical management are outdated.

Acne, eczema, and psoriasis

Soliman’s 2018 review of cupping in dermatology included a few studies on these common cutaneous conditions. For instance, a 2013 single-blind prospective study by Xu et al. reported on the results of patients with moderate acne who received wet cupping (in the form of prickling bloodletting) twice weekly for 6 weeks.⁷ They reported that patients demonstrated improvement in the global acne grading system (GAGS) score by the end of the trial.^1,7 Unfortunately, cupping was not compared with standard acne treatments (that is, benzoyl peroxide, topical and oral antibiotics, isotretinoin, topical retinoids, spironolactone).

In evaluating cupping for acute eczema, wet cupping was compared with oral loratadine and topical ointments in a 2007 study by Yao and Li. They divided 88 cases into treatment and control groups, with the former group (n = 46) receiving bloodletting puncturing and cupping and the control group (n = 42) receiving oral loratadine and topical Pairuisong (an herbal ointment used in Chinese medicine). The investigators observed no significant difference in total effective rates but a superior difference in the rates of responses that were considered “cured” and “markedly effective” in favor of the cupping treatment.^1,8 However, a case report by Hon et al. has indicated that cupping therapy may be associated with more harm than benefit when used as an eczema treatment.^1,9

In addition, it is important to note that the past 5 years have been gamechanging in the management of chronic eczema in terms of the array of novel and effective therapies (e.g., dupilumab and JAK inhibitors) and chronic moderate-to-severe eczema has become very treatable. Similarly, acute eczema is often successfully managed with topical steroids, calcineurin inhibitors, and emollients. As such, there is no compelling reason to consider an unproven treatment such as cupping.

In 2020, Xing et al. reviewed 16 randomized controlled trials assessing the use of “moving cupping” for plaque psoriasis, with 1,164 patients meeting inclusion criteria. Moving cupping was found to be significantly more effective than “no-moving” cupping therapy, and moving cupping, combined with medications, performed better than medications alone.¹⁰ None of the trials evaluated in this study included randomized controlled trials that compared patients using any of the more modern psoriasis medications, specifically biologics. And, again, the studies evaluated were not of the highest quality.

The data that support cupping, as summarized above, are based mostly on case reports, and strong double-blind prospective studies are lacking. Additionally, most of the studies cited gauged the efficacy of cupping using qualitative endpoints, rather than standardized quantitative endpoints and scales. Moreover, spontaneous remission of various dermatoses can occur, or they can improve over time, including acute eczema, psoriasis, and, especially, urticaria.
 

Adverse effects of cupping

Often alternative therapies are seen as “benign” and without adverse effects. However, complications can result from cupping. Trauma can be induced from the cupping itself by damaging superficial blood vessels and causing bruising.^1,11 Blistering can also occur secondary to the suction effect, and the epidermal and dermal layers of the skin can be separated.^1,11 Further, burns and discoloration have also been noted secondary to heat, trauma, and post inflammatory pigmentary changes.^1,11 Another risk of cupping is the Koebner phenomenon, which occurs with psoriasis, with new lesions appearing in traumatized skin.¹² Other adverse outcomes that have been reported with cupping include reactivation of herpes simplex virus secondary to skin trauma, iron deficiency anemia (secondary to blood loss), panniculitis, infections, and residual marks mistaken for signs of child abuse.^1,11

Cupping in aesthetic dermatology

Facial cupping, a distinct practice from body cupping used to treat general dermatology conditions described previously, is also increasing in popularity. This practice is usually conducted in association with a facial or facial acupuncture by an aesthetician or other licensed professional. It can also be performed using at-home kits. The marketing claims for facial cupping cite improved tightening and contouring of facial skin, increased facial microcirculation and collagen synthesis, and enhanced lymphatic flow to aid with facial puffiness or swelling. One supposed mechanism for these benefits is that cupping increases blood flow. Interestingly, there was a 2020 animal study in which photoacoustic imaging of a mouse ear revealed increased temporary blood flow in the cupping microenvironment.¹³ Currently, however, there is no evidence in the English scientific literature that supports facial cupping. The benefits attributed to facial cupping for aesthetic purposes have emerged only in personal anecdotes. The temporary increase in blood flow may induce inflammation and swelling that adds volume to the face and temporarily diminishes wrinkles. However, this temporary plumpness may be associated with adverse effects, such as local trauma, irritation, bruising, postinflammatory pigmentary alteration, or even herpes reactivation. In my opinion, the possible adverse effects of cupping outweigh any potential benefit, especially given the insufficient evidence supporting the utility of cupping for cosmetic enhancement.

Summary

There is increasing interest among patients to incorporate complementary and alternative medicine – including the ancient tradition of cupping – in managing medical dermatologic conditions. However, current evidence supporting cupping as an effective therapeutic strategy is not strong, with most studies to date appearing to be of poor quality or not sufficiently convincing to displace standard therapies. Our medical strategies for managing chronic dermatologic conditions, particularly inflammatory disorders, continue to improve from both a safety and a proven efficacy standpoint. Therefore, I would not forgo medical management in favor of cupping. While cupping can be used as an adjunct therapy, I would caution patients about possible adverse side effects. In the aesthetic world, cupping is also gaining popularity, but this trend is also not supported by current evidence or studies, at least in the Western literature.

Dr. Goldman is a dermatologist in private practice in Miami and specializes in cosmetic and general dermatology. She practices at Baumann Cosmetic & Research Institute and is also opening a general dermatology practice. Write to her at [email protected] or message her on Instragram @DrChloeGoldman. Dr. Goldman receives compensation to create social media content for Replenix, a skin care company. She has no other disclosures.

References

1. Soliman Y et al. Acta Dermatovenerol Alp Pannonica Adriat. 2018 Jun;27(2):103-7.

2. França K and Lotti T. Advances in Integrative Dermatology. John Wiley & Sons, 2019.

3. Lowe DT. Complement Ther Clin Pract. 2017 Nov;29:162-8.

4.Cao H et al. Altern Ther Health Med. 2010 Nov-Dec;16(6):48-54.

5. Li L and Ding J. J Tradit Chin Med. 2001 Mar;21(1):37-8.

6. Xiao XJ et al. J Integr Med. 2020 Jul;18(4):303-12.

7. Xu J et al. J Tradit Chin Med. 2013 Dec;33(6):752-6.

8. Yao J et al. Zhongguo Zhen Jiu. 2007; Jun;27(6):424-6.

9. Hon KL et al. Case Rep Pediatr. 2013;2013:605829.

10. Xing M et al. Medicine (Baltimore). 2020 Oct 9;99(41):e22539.

11. Kim TH et al. Eur J Integr Med. 2014 Aug 1;6(4):434-40.

12. Vender R and Vender R. J Cutan Med Surg. 2015 May-Jun;19(3):320-2.

13. Zhou Y et al. Biomed Opt Express. 2020 Apr 6;11(5):2394-401.

This article was updated 4/25/22.

Across the country, taxes unite us. Not that we all share the same, rather that we all have to do them. It was recently tax weekend in our house: The Saturday and Sunday that cap off weeks of hunting and gathering faded receipts and sorting through reams of credit card bills to find all the dollars we spent on work. The task is more tedious than all the Wednesdays of taking out trash bins combined, and equally as exciting. But wait, that’s not all.

This weekend I’ve been chatting with bots from a solar company trying to solve our drop in energy production and sat on terminal hold with apparently one person who answers the phone for Amazon. There’s also an homeowner’s association meeting to prepare for and research to be done on ceiling fans.

“Life admin” is a crisp phrase coined by Elizabeth Emens, JD, PhD, that captures the never-ending to-do list that comes with running a household. An accomplished law professor at Columbia University, New York, Dr. Emens noticed the negative impact this life admin has on our quality of life. Reading her book, “Life Admin: How I Learned to Do Less, Do Better, and Live More” (New York: HarperOne, 2019), your eyes widen as she magically makes salient all this hidden work that is stealing our time. Life admin, kidmin, mom and dadmin, just rattling them off feels like donning x-ray glasses allowing us to see how much work we do outside of our work. As doctors, I would add “family house calls,” as a contributing factor: Random family and friends who want to talk for a minute about their knee replacement or what drug the ICU should give Uncle Larry who is fighting COVID. (I only know ivermectin, but it would only help if he just had scabies).

By all accounts, the amount of life admin is growing insidiously, worsened by the great pandemic. There are events to plan and reply to, more DIY customer service to fix your own problems, more work to find a VRBO for a weekend getaway at the beach. (There are none on the entire coast of California this summer, so I just saved you time there. You’re welcome.)

There is no good time to do this work and combined with the heavy burden of our responsibilities as physicians, it can feel like fuel feeding the burnout fire.

Dr. Emens has some top tips to help. First up, know your admin type. Are you a super doer, reluctant doer, admin denier, or admin avoider? I’m mostly in the avoider quadrant, dropping into reluctant doer when consequences loom. Next, choose strategies that fit you. Instead of avoiding, there are some things I might deflect. For example, When your aunt in Peoria asks where she can get a COVID test, you can use LMGTFY.com to generate a link that will show them how to use Google to help with their question. Dr. Emens is joking, but the point rang true. We can lighten the load a bit if we delegate or push back the excessive or undue requests. For some tasks, we’d be better off paying someone to take it over. Last tip here, try doing life admin with a partner, be it spouse, friend, or colleague. This is particularly useful when your partner is a super doer, as mine is. Not only can they make the work lighter, but also less dreary.

We physicians are focused on fixing physician burnout. Maybe we should also be looking at what happens in the “second shift” at home. Tax season is over, but will be back soon.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected]

Across the country, taxes unite us. Not that we all share the same, rather that we all have to do them. It was recently tax weekend in our house: The Saturday and Sunday that cap off weeks of hunting and gathering faded receipts and sorting through reams of credit card bills to find all the dollars we spent on work. The task is more tedious than all the Wednesdays of taking out trash bins combined, and equally as exciting. But wait, that’s not all.

This weekend I’ve been chatting with bots from a solar company trying to solve our drop in energy production and sat on terminal hold with apparently one person who answers the phone for Amazon. There’s also an homeowner’s association meeting to prepare for and research to be done on ceiling fans.

“Life admin” is a crisp phrase coined by Elizabeth Emens, JD, PhD, that captures the never-ending to-do list that comes with running a household. An accomplished law professor at Columbia University, New York, Dr. Emens noticed the negative impact this life admin has on our quality of life. Reading her book, “Life Admin: How I Learned to Do Less, Do Better, and Live More” (New York: HarperOne, 2019), your eyes widen as she magically makes salient all this hidden work that is stealing our time. Life admin, kidmin, mom and dadmin, just rattling them off feels like donning x-ray glasses allowing us to see how much work we do outside of our work. As doctors, I would add “family house calls,” as a contributing factor: Random family and friends who want to talk for a minute about their knee replacement or what drug the ICU should give Uncle Larry who is fighting COVID. (I only know ivermectin, but it would only help if he just had scabies).

By all accounts, the amount of life admin is growing insidiously, worsened by the great pandemic. There are events to plan and reply to, more DIY customer service to fix your own problems, more work to find a VRBO for a weekend getaway at the beach. (There are none on the entire coast of California this summer, so I just saved you time there. You’re welcome.)

There is no good time to do this work and combined with the heavy burden of our responsibilities as physicians, it can feel like fuel feeding the burnout fire.

Dr. Emens has some top tips to help. First up, know your admin type. Are you a super doer, reluctant doer, admin denier, or admin avoider? I’m mostly in the avoider quadrant, dropping into reluctant doer when consequences loom. Next, choose strategies that fit you. Instead of avoiding, there are some things I might deflect. For example, When your aunt in Peoria asks where she can get a COVID test, you can use LMGTFY.com to generate a link that will show them how to use Google to help with their question. Dr. Emens is joking, but the point rang true. We can lighten the load a bit if we delegate or push back the excessive or undue requests. For some tasks, we’d be better off paying someone to take it over. Last tip here, try doing life admin with a partner, be it spouse, friend, or colleague. This is particularly useful when your partner is a super doer, as mine is. Not only can they make the work lighter, but also less dreary.

We physicians are focused on fixing physician burnout. Maybe we should also be looking at what happens in the “second shift” at home. Tax season is over, but will be back soon.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected]

Across the country, taxes unite us. Not that we all share the same, rather that we all have to do them. It was recently tax weekend in our house: The Saturday and Sunday that cap off weeks of hunting and gathering faded receipts and sorting through reams of credit card bills to find all the dollars we spent on work. The task is more tedious than all the Wednesdays of taking out trash bins combined, and equally as exciting. But wait, that’s not all.

This weekend I’ve been chatting with bots from a solar company trying to solve our drop in energy production and sat on terminal hold with apparently one person who answers the phone for Amazon. There’s also an homeowner’s association meeting to prepare for and research to be done on ceiling fans.

“Life admin” is a crisp phrase coined by Elizabeth Emens, JD, PhD, that captures the never-ending to-do list that comes with running a household. An accomplished law professor at Columbia University, New York, Dr. Emens noticed the negative impact this life admin has on our quality of life. Reading her book, “Life Admin: How I Learned to Do Less, Do Better, and Live More” (New York: HarperOne, 2019), your eyes widen as she magically makes salient all this hidden work that is stealing our time. Life admin, kidmin, mom and dadmin, just rattling them off feels like donning x-ray glasses allowing us to see how much work we do outside of our work. As doctors, I would add “family house calls,” as a contributing factor: Random family and friends who want to talk for a minute about their knee replacement or what drug the ICU should give Uncle Larry who is fighting COVID. (I only know ivermectin, but it would only help if he just had scabies).

By all accounts, the amount of life admin is growing insidiously, worsened by the great pandemic. There are events to plan and reply to, more DIY customer service to fix your own problems, more work to find a VRBO for a weekend getaway at the beach. (There are none on the entire coast of California this summer, so I just saved you time there. You’re welcome.)

There is no good time to do this work and combined with the heavy burden of our responsibilities as physicians, it can feel like fuel feeding the burnout fire.

Dr. Emens has some top tips to help. First up, know your admin type. Are you a super doer, reluctant doer, admin denier, or admin avoider? I’m mostly in the avoider quadrant, dropping into reluctant doer when consequences loom. Next, choose strategies that fit you. Instead of avoiding, there are some things I might deflect. For example, When your aunt in Peoria asks where she can get a COVID test, you can use LMGTFY.com to generate a link that will show them how to use Google to help with their question. Dr. Emens is joking, but the point rang true. We can lighten the load a bit if we delegate or push back the excessive or undue requests. For some tasks, we’d be better off paying someone to take it over. Last tip here, try doing life admin with a partner, be it spouse, friend, or colleague. This is particularly useful when your partner is a super doer, as mine is. Not only can they make the work lighter, but also less dreary.

We physicians are focused on fixing physician burnout. Maybe we should also be looking at what happens in the “second shift” at home. Tax season is over, but will be back soon.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected]

Mrs. Smith came in for neck pain.

This isn’t a new issue, her last flare was 4 or 5 years ago. I’d done an MRI back then, which just showed reassuringly typical arthritic changes, and she did great with a few sessions of physical therapy.

She’d woke one morning a few months ago with a stiff and aching neck, similar to how this started last time. A couple weeks of rest and NSAIDs hadn’t helped. There were no radiating symptoms and her exam was the same as it’s been since I met her back in 2010.

I wrote her an order for physical therapy and found the address and phone number of the place she’d gone to for it a few years ago. She looked at my order, then set it on my desk and said “Doctor, I’d really like an MRI.”

I went back to her chart and reread my note for her last flare of neck pain. Identical symptoms, identical exam. I pulled up the previous MRI report and went over it. Then I explained to her that there really was no indication for an MRI at this point. I suggested we go ahead with physical therapy, and if that didn’t help I would then re-check the study.

She wasn’t going to budge. A friend of hers had recently needed urgent surgery for a cervical myelopathy and was in rehab. Mrs. Smith’s husband’s health was getting worse, and if her neck had something seriously wrong she wouldn’t be able to take care of him if it went unchecked.

So I backed down and ordered a cervical spine MRI, which was pretty much unchanged from the previous MRI. After it came back she was willing to do therapy.

I’m sure some out there will accuse me, the doctor, of letting the patient call the shots. To some degree you’re correct. But it’s not like the request was insanely unreasonable. Obviously, there were other factors going on, too. She was scared and needed reassurance that there wasn’t anything therapy wouldn’t help and that she would be able to keep caring for her ailing husband during his cancer treatments.

There are doctors out there with a more paternalistic view of patient care than mine. They’re probably thinking I should have taken a hardball approach of “you don’t need an MRI. You can do therapy, or you can find another doctor.” But that’s not me. I can’t do that to a nice older lady, especially one who’s been coming to me for various ailments over the last 12 years.

Not only that, but such an approach seemed doomed to fail in this case. It might have gotten her to go to therapy, but I suspect she wouldn’t have gotten better. Her fears about a serious neck issue would increase over time, until she (or the therapist) finally called, said she wasn’t getting better, and could I order an MRI now?

In that way, maybe the MRI helped guarantee that she’d have a good response to therapy.

Medicine is never easy. We learn a lot of rules and guidelines in the name of providing good, economically viable, patient care, but still have to recognize that there isn’t a one-size-fits-all approach.

I can’t say that what I did was the right thing. But it was right for Mrs. Smith.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Mrs. Smith came in for neck pain.

This isn’t a new issue, her last flare was 4 or 5 years ago. I’d done an MRI back then, which just showed reassuringly typical arthritic changes, and she did great with a few sessions of physical therapy.

She’d woke one morning a few months ago with a stiff and aching neck, similar to how this started last time. A couple weeks of rest and NSAIDs hadn’t helped. There were no radiating symptoms and her exam was the same as it’s been since I met her back in 2010.

I wrote her an order for physical therapy and found the address and phone number of the place she’d gone to for it a few years ago. She looked at my order, then set it on my desk and said “Doctor, I’d really like an MRI.”

I went back to her chart and reread my note for her last flare of neck pain. Identical symptoms, identical exam. I pulled up the previous MRI report and went over it. Then I explained to her that there really was no indication for an MRI at this point. I suggested we go ahead with physical therapy, and if that didn’t help I would then re-check the study.

She wasn’t going to budge. A friend of hers had recently needed urgent surgery for a cervical myelopathy and was in rehab. Mrs. Smith’s husband’s health was getting worse, and if her neck had something seriously wrong she wouldn’t be able to take care of him if it went unchecked.

So I backed down and ordered a cervical spine MRI, which was pretty much unchanged from the previous MRI. After it came back she was willing to do therapy.

I’m sure some out there will accuse me, the doctor, of letting the patient call the shots. To some degree you’re correct. But it’s not like the request was insanely unreasonable. Obviously, there were other factors going on, too. She was scared and needed reassurance that there wasn’t anything therapy wouldn’t help and that she would be able to keep caring for her ailing husband during his cancer treatments.

There are doctors out there with a more paternalistic view of patient care than mine. They’re probably thinking I should have taken a hardball approach of “you don’t need an MRI. You can do therapy, or you can find another doctor.” But that’s not me. I can’t do that to a nice older lady, especially one who’s been coming to me for various ailments over the last 12 years.

Not only that, but such an approach seemed doomed to fail in this case. It might have gotten her to go to therapy, but I suspect she wouldn’t have gotten better. Her fears about a serious neck issue would increase over time, until she (or the therapist) finally called, said she wasn’t getting better, and could I order an MRI now?

In that way, maybe the MRI helped guarantee that she’d have a good response to therapy.

Medicine is never easy. We learn a lot of rules and guidelines in the name of providing good, economically viable, patient care, but still have to recognize that there isn’t a one-size-fits-all approach.

I can’t say that what I did was the right thing. But it was right for Mrs. Smith.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Mrs. Smith came in for neck pain.

This isn’t a new issue, her last flare was 4 or 5 years ago. I’d done an MRI back then, which just showed reassuringly typical arthritic changes, and she did great with a few sessions of physical therapy.

She’d woke one morning a few months ago with a stiff and aching neck, similar to how this started last time. A couple weeks of rest and NSAIDs hadn’t helped. There were no radiating symptoms and her exam was the same as it’s been since I met her back in 2010.

I wrote her an order for physical therapy and found the address and phone number of the place she’d gone to for it a few years ago. She looked at my order, then set it on my desk and said “Doctor, I’d really like an MRI.”

I went back to her chart and reread my note for her last flare of neck pain. Identical symptoms, identical exam. I pulled up the previous MRI report and went over it. Then I explained to her that there really was no indication for an MRI at this point. I suggested we go ahead with physical therapy, and if that didn’t help I would then re-check the study.

She wasn’t going to budge. A friend of hers had recently needed urgent surgery for a cervical myelopathy and was in rehab. Mrs. Smith’s husband’s health was getting worse, and if her neck had something seriously wrong she wouldn’t be able to take care of him if it went unchecked.

So I backed down and ordered a cervical spine MRI, which was pretty much unchanged from the previous MRI. After it came back she was willing to do therapy.

I’m sure some out there will accuse me, the doctor, of letting the patient call the shots. To some degree you’re correct. But it’s not like the request was insanely unreasonable. Obviously, there were other factors going on, too. She was scared and needed reassurance that there wasn’t anything therapy wouldn’t help and that she would be able to keep caring for her ailing husband during his cancer treatments.

There are doctors out there with a more paternalistic view of patient care than mine. They’re probably thinking I should have taken a hardball approach of “you don’t need an MRI. You can do therapy, or you can find another doctor.” But that’s not me. I can’t do that to a nice older lady, especially one who’s been coming to me for various ailments over the last 12 years.

Not only that, but such an approach seemed doomed to fail in this case. It might have gotten her to go to therapy, but I suspect she wouldn’t have gotten better. Her fears about a serious neck issue would increase over time, until she (or the therapist) finally called, said she wasn’t getting better, and could I order an MRI now?

In that way, maybe the MRI helped guarantee that she’d have a good response to therapy.

Medicine is never easy. We learn a lot of rules and guidelines in the name of providing good, economically viable, patient care, but still have to recognize that there isn’t a one-size-fits-all approach.

I can’t say that what I did was the right thing. But it was right for Mrs. Smith.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Purpura annularis telangiectodes of Majocchi (PATM) or Majocchi’s disease, is an uncommon subtype of pigmented purpuric dermatosis (PPD) or capillaritis, typically characterized by symmetrical, nonblanching, purpuric, telangiectatic, and atrophic patches with a predilection for the lower extremities and buttocks.

Courtesy Lynette Xu and Dr. Brooke Resh Sateesh

Plaques are usually 1-3 cm in diameter and annular with punctate telangiectasias and cayenne pepper petechiae in the border. The annular patches may form concentric rings. It is most commonly seen in children and young females.

The etiology of Majocchi’s disease is largely unknown and idiopathic.

Courtesy Lynette Xu and Dr. Brooke Resh Sateesh

Triggers are not always detected but may be associated with viral infections, chronic comorbidities, and medications. Levofloxacin and isotretinoin have been described in as reports as causing PATM. Other medications reported to cause PPD include sedatives, stimulants, antibiotics, NSAIDS, and cardiovascular drugs.

Diagnosis of PATM is clinical and histopathologic. Direct immunofluorescence (DIF) may show fibrinogen, IgM, and/or C3 deposition in superficial dermal vessels. Histopathologic findings show lymphocytic infiltrate involving the superficial small vessels, extravasated red blood cells, and hemosiderin-laden macrophages.

There is no consensus regarding treatment with variable responses to proposed treatment based on reports and case studies. The first line of treatment is topical corticosteroids and compression hose. Additional treatments, including narrowband UVB phototherapy (NBUVB), griseofulvin, pentoxifylline, cyclosporine, colchicine, rutoside with ascorbic acid, and methotrexate, have been used with varying success.

In this patient, a punch biopsy was performed, which revealed lymphocytes and extravasated erythrocytes and siderophages in the dermis. She was treated with topical steroids with improvement. She started NBUVB, a short course of griseofulvin, and vitamin C supplements.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

References

1. Garcez A et al. An Bras Dermatol. Sep-Oct 2020;95(5):664-6. doi: 10.1016/j.abd.2020.02.007.

2. Asadbeigi S, Momtahen S. Pigmented purpuric dermatosis. PathologyOutlines.com website.

3. Martínez P et al. Actas Dermosifiliogr (Engl Ed). 2020 Apr;111(3):196-204. doi: 10.1016/j.ad.2019.02.013.

4. Hoesly FJ et al. Int J Dermatol. 2009 Oct;48(10):1129-33. doi: 10.1111/j.1365-4632.2009.04160.x.

Purpura annularis telangiectodes of Majocchi (PATM) or Majocchi’s disease, is an uncommon subtype of pigmented purpuric dermatosis (PPD) or capillaritis, typically characterized by symmetrical, nonblanching, purpuric, telangiectatic, and atrophic patches with a predilection for the lower extremities and buttocks.

Courtesy Lynette Xu and Dr. Brooke Resh Sateesh

Plaques are usually 1-3 cm in diameter and annular with punctate telangiectasias and cayenne pepper petechiae in the border. The annular patches may form concentric rings. It is most commonly seen in children and young females.

The etiology of Majocchi’s disease is largely unknown and idiopathic.

Courtesy Lynette Xu and Dr. Brooke Resh Sateesh

Triggers are not always detected but may be associated with viral infections, chronic comorbidities, and medications. Levofloxacin and isotretinoin have been described in as reports as causing PATM. Other medications reported to cause PPD include sedatives, stimulants, antibiotics, NSAIDS, and cardiovascular drugs.

Diagnosis of PATM is clinical and histopathologic. Direct immunofluorescence (DIF) may show fibrinogen, IgM, and/or C3 deposition in superficial dermal vessels. Histopathologic findings show lymphocytic infiltrate involving the superficial small vessels, extravasated red blood cells, and hemosiderin-laden macrophages.

There is no consensus regarding treatment with variable responses to proposed treatment based on reports and case studies. The first line of treatment is topical corticosteroids and compression hose. Additional treatments, including narrowband UVB phototherapy (NBUVB), griseofulvin, pentoxifylline, cyclosporine, colchicine, rutoside with ascorbic acid, and methotrexate, have been used with varying success.

In this patient, a punch biopsy was performed, which revealed lymphocytes and extravasated erythrocytes and siderophages in the dermis. She was treated with topical steroids with improvement. She started NBUVB, a short course of griseofulvin, and vitamin C supplements.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

References

1. Garcez A et al. An Bras Dermatol. Sep-Oct 2020;95(5):664-6. doi: 10.1016/j.abd.2020.02.007.

2. Asadbeigi S, Momtahen S. Pigmented purpuric dermatosis. PathologyOutlines.com website.

3. Martínez P et al. Actas Dermosifiliogr (Engl Ed). 2020 Apr;111(3):196-204. doi: 10.1016/j.ad.2019.02.013.

4. Hoesly FJ et al. Int J Dermatol. 2009 Oct;48(10):1129-33. doi: 10.1111/j.1365-4632.2009.04160.x.

Purpura annularis telangiectodes of Majocchi (PATM) or Majocchi’s disease, is an uncommon subtype of pigmented purpuric dermatosis (PPD) or capillaritis, typically characterized by symmetrical, nonblanching, purpuric, telangiectatic, and atrophic patches with a predilection for the lower extremities and buttocks.

Courtesy Lynette Xu and Dr. Brooke Resh Sateesh

Plaques are usually 1-3 cm in diameter and annular with punctate telangiectasias and cayenne pepper petechiae in the border. The annular patches may form concentric rings. It is most commonly seen in children and young females.

The etiology of Majocchi’s disease is largely unknown and idiopathic.

Courtesy Lynette Xu and Dr. Brooke Resh Sateesh

Triggers are not always detected but may be associated with viral infections, chronic comorbidities, and medications. Levofloxacin and isotretinoin have been described in as reports as causing PATM. Other medications reported to cause PPD include sedatives, stimulants, antibiotics, NSAIDS, and cardiovascular drugs.

Diagnosis of PATM is clinical and histopathologic. Direct immunofluorescence (DIF) may show fibrinogen, IgM, and/or C3 deposition in superficial dermal vessels. Histopathologic findings show lymphocytic infiltrate involving the superficial small vessels, extravasated red blood cells, and hemosiderin-laden macrophages.

There is no consensus regarding treatment with variable responses to proposed treatment based on reports and case studies. The first line of treatment is topical corticosteroids and compression hose. Additional treatments, including narrowband UVB phototherapy (NBUVB), griseofulvin, pentoxifylline, cyclosporine, colchicine, rutoside with ascorbic acid, and methotrexate, have been used with varying success.

In this patient, a punch biopsy was performed, which revealed lymphocytes and extravasated erythrocytes and siderophages in the dermis. She was treated with topical steroids with improvement. She started NBUVB, a short course of griseofulvin, and vitamin C supplements.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

References

1. Garcez A et al. An Bras Dermatol. Sep-Oct 2020;95(5):664-6. doi: 10.1016/j.abd.2020.02.007.

2. Asadbeigi S, Momtahen S. Pigmented purpuric dermatosis. PathologyOutlines.com website.

3. Martínez P et al. Actas Dermosifiliogr (Engl Ed). 2020 Apr;111(3):196-204. doi: 10.1016/j.ad.2019.02.013.

4. Hoesly FJ et al. Int J Dermatol. 2009 Oct;48(10):1129-33. doi: 10.1111/j.1365-4632.2009.04160.x.

Photosensitivity due to doxycycline

As the patient’s rash presented in sun-exposed areas with both skin and nail changes, our patient was diagnosed with a phototoxic reaction to doxycycline, the oral antibiotic used to treat his acne.

Photosensitive cutaneous drug eruptions are reactions that occur after exposure to a medication and subsequent exposure to UV radiation or visible light. Reactions can be classified into two ways based on their mechanism of action: phototoxic or photoallergic.¹ Phototoxic reactions are more common and are a result of direct keratinocyte damage and cellular necrosis. Many classes of medications may cause this adverse effect, but the tetracycline class of antibiotics is a common culprit.² Photoallergic reactions are less common and are a result of a type IV immune reaction to the offending agent.¹

Courtesy Dr. Catalina Matiz

Phototoxic reactions generally present shortly after sun or UV exposure with a photo-distributed eruption pattern.³ Commonly involved areas include the face, the neck, and the extensor surfaces of extremities, with sparing of relatively protected skin such as the upper eyelids and the skin folds.² Erythema may initially develop in the exposed skin areas, followed by appearance of edema, vesicles, or bullae.^1-3 The eruption may be painful and itchy, with some patients reporting severe pain.³

Courtesy Dr. Catalina Matiz

Doxycycline phototoxicity may also cause onycholysis of the nails.² The reaction is dose dependent, with higher doses of medication leading to a higher likelihood of symptoms.^1,2 It is also more prevalent in patients with Fitzpatrick skin type I and II. The usual UVA wavelength required to induce this reaction appears to be in the 320-400 nm range of the UV spectrum.⁴ By contrast, photoallergic reactions are dose independent, and require a sensitization period prior to the eruption.¹ An eczematous eruption is most commonly seen with photoallergic reactions.³

Treatment of drug-induced photosensitivity reactions requires proper identification of the diagnosis and the offending agent, followed by cessation of the medication. If cessation is not possible, then lowering the dose can help to minimize worsening of the condition. However, for photoallergic reactions, the reaction is dose independent so switching to another tolerated agent is likely required. For persistent symptoms following medication withdrawal, topical or systemic steroids and oral antihistamine can help with symptom management.¹ For patients with photo-onycholysis, treatment involves stopping the medication and waiting for the intact nail plate to grow.

Courtesy Dr. Catalina Matiz

Dermatomyositis

Dermatomyositis is an autoimmune condition that presents with skin lesions as well as systemic findings such as myositis. The cutaneous findings are variable, but pathognomonic findings include Gottron papules of the hands, Gottron’s sign on the elbows, knees, and ankles, and the heliotrope rash of the face. Eighty percent of patients have myopathy presenting as muscle weakness, and commonly have elevated creatine kinase, aspartate transaminase, and alanine transaminase values.⁵ Diagnosis may be confirmed through skin or muscle biopsy, though antibody studies can also play a helpful role in diagnosis. Treatment is generally with oral corticosteroids or other immunosuppressants as well as sun protection.⁶ The rash seen in our patient could have been seen in patients with dermatomyositis, though it was not in the typical location on the knuckles (Gottron papules) as it also affected the lateral sides of the fingers.

Systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune condition characterized by systemic and cutaneous manifestations. Systemic symptoms may include weight loss, fever, fatigue, arthralgia, or arthritis; patients are at risk of renal, cardiovascular, pulmonary, and neurologic complications of SLE.⁷ The most common cutaneous finding is malar rash, though there are myriad dermatologic manifestations that can occur associated with photosensitivity. Diagnosis is made based on history, physical, and laboratory testing. Treatment options include NSAIDs, oral glucocorticoids, antimalarial drugs, and immunosuppressants.⁷ Though our patient exhibited photosensitivity, he had none of the systemic findings associated with SLE, making this diagnosis unlikely.

Allergic contact dermatitis

Allergic contact dermatitis (ACD) is a type IV hypersensitivity reaction, and may present as acute, subacute, or chronic dermatitis. The clinical findings vary based on chronicity. Acute ACD presents as pruritic erythematous papules and vesicles or bullae, similar to how it occurred in our patient, though our patient’s lesions were more tender than pruritic. Chronic ACD presents with erythematous lesions with pruritis, lichenification, scaling, and/or fissuring. Observing shapes or sharp demarcation of lesions may help with diagnosis. Patch testing is also useful in the diagnosis of ACD.

Treatment generally involves avoiding the offending agent with topical corticosteroids for symptom management.⁸

Polymorphous light eruption

Polymorphous light eruption (PLE) is a delayed, type IV hypersensitivity reaction to UV-induced antigens, though these antigens are unknown. PLE presents hours to days following solar or UV exposure and presents only in sun-exposed areas. Itching and burning are always present, but lesion morphology varies from erythema and papules to vesico-papules and blisters. Notably, PLE must be distinguished from drug photosensitivity through history. Treatment generally involves symptom management with topical steroids and sun protective measures for prevention.⁹ While PLE may present similarly to drug photosensitivity reactions, our patient’s use of a known phototoxic agent makes PLE a less likely diagnosis.

Ms. Appiah is a pediatric dermatology research associate and medical student at the University of California, San Diego, and Rady Children’s Hospital, San Diego. Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Neither Dr. Matiz nor Ms. Appiah has any relevant financial disclosures.

References

1. Montgomery S et al. Clin Dermatol. 2022;40(1):57-63.

2. Blakely KM et al. Drug Saf. 2019;42(7):827-47.

3. Goetze S et al. Skin Pharmacol Physiol. 2017;30(2):76-80.

4. Odorici G et al. Dermatol Ther. 2021;34(4):e14978.

5. DeWane ME et al. J Am Acad Dermatol. 2020;82(2):267-81.

6. Waldman R et al. J Am Acad Dermatol. 2020;82(2):283-96.

7. Kiriakidou M et al. Ann Intern Med. 2020;172(11):ITC81-ITC96.

8. Nassau S et al. Med Clin North Am. 2020;104(1):61-76.

9. Guarrera M. Adv Exp Med Biol. 2017;996:61-70.

Photosensitivity due to doxycycline

As the patient’s rash presented in sun-exposed areas with both skin and nail changes, our patient was diagnosed with a phototoxic reaction to doxycycline, the oral antibiotic used to treat his acne.

Photosensitive cutaneous drug eruptions are reactions that occur after exposure to a medication and subsequent exposure to UV radiation or visible light. Reactions can be classified into two ways based on their mechanism of action: phototoxic or photoallergic.¹ Phototoxic reactions are more common and are a result of direct keratinocyte damage and cellular necrosis. Many classes of medications may cause this adverse effect, but the tetracycline class of antibiotics is a common culprit.² Photoallergic reactions are less common and are a result of a type IV immune reaction to the offending agent.¹

Courtesy Dr. Catalina Matiz

Phototoxic reactions generally present shortly after sun or UV exposure with a photo-distributed eruption pattern.³ Commonly involved areas include the face, the neck, and the extensor surfaces of extremities, with sparing of relatively protected skin such as the upper eyelids and the skin folds.² Erythema may initially develop in the exposed skin areas, followed by appearance of edema, vesicles, or bullae.^1-3 The eruption may be painful and itchy, with some patients reporting severe pain.³

Courtesy Dr. Catalina Matiz

Doxycycline phototoxicity may also cause onycholysis of the nails.² The reaction is dose dependent, with higher doses of medication leading to a higher likelihood of symptoms.^1,2 It is also more prevalent in patients with Fitzpatrick skin type I and II. The usual UVA wavelength required to induce this reaction appears to be in the 320-400 nm range of the UV spectrum.⁴ By contrast, photoallergic reactions are dose independent, and require a sensitization period prior to the eruption.¹ An eczematous eruption is most commonly seen with photoallergic reactions.³

Treatment of drug-induced photosensitivity reactions requires proper identification of the diagnosis and the offending agent, followed by cessation of the medication. If cessation is not possible, then lowering the dose can help to minimize worsening of the condition. However, for photoallergic reactions, the reaction is dose independent so switching to another tolerated agent is likely required. For persistent symptoms following medication withdrawal, topical or systemic steroids and oral antihistamine can help with symptom management.¹ For patients with photo-onycholysis, treatment involves stopping the medication and waiting for the intact nail plate to grow.

Courtesy Dr. Catalina Matiz

Dermatomyositis

Dermatomyositis is an autoimmune condition that presents with skin lesions as well as systemic findings such as myositis. The cutaneous findings are variable, but pathognomonic findings include Gottron papules of the hands, Gottron’s sign on the elbows, knees, and ankles, and the heliotrope rash of the face. Eighty percent of patients have myopathy presenting as muscle weakness, and commonly have elevated creatine kinase, aspartate transaminase, and alanine transaminase values.⁵ Diagnosis may be confirmed through skin or muscle biopsy, though antibody studies can also play a helpful role in diagnosis. Treatment is generally with oral corticosteroids or other immunosuppressants as well as sun protection.⁶ The rash seen in our patient could have been seen in patients with dermatomyositis, though it was not in the typical location on the knuckles (Gottron papules) as it also affected the lateral sides of the fingers.

Systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune condition characterized by systemic and cutaneous manifestations. Systemic symptoms may include weight loss, fever, fatigue, arthralgia, or arthritis; patients are at risk of renal, cardiovascular, pulmonary, and neurologic complications of SLE.⁷ The most common cutaneous finding is malar rash, though there are myriad dermatologic manifestations that can occur associated with photosensitivity. Diagnosis is made based on history, physical, and laboratory testing. Treatment options include NSAIDs, oral glucocorticoids, antimalarial drugs, and immunosuppressants.⁷ Though our patient exhibited photosensitivity, he had none of the systemic findings associated with SLE, making this diagnosis unlikely.

Allergic contact dermatitis

Allergic contact dermatitis (ACD) is a type IV hypersensitivity reaction, and may present as acute, subacute, or chronic dermatitis. The clinical findings vary based on chronicity. Acute ACD presents as pruritic erythematous papules and vesicles or bullae, similar to how it occurred in our patient, though our patient’s lesions were more tender than pruritic. Chronic ACD presents with erythematous lesions with pruritis, lichenification, scaling, and/or fissuring. Observing shapes or sharp demarcation of lesions may help with diagnosis. Patch testing is also useful in the diagnosis of ACD.

Treatment generally involves avoiding the offending agent with topical corticosteroids for symptom management.⁸

Polymorphous light eruption

Polymorphous light eruption (PLE) is a delayed, type IV hypersensitivity reaction to UV-induced antigens, though these antigens are unknown. PLE presents hours to days following solar or UV exposure and presents only in sun-exposed areas. Itching and burning are always present, but lesion morphology varies from erythema and papules to vesico-papules and blisters. Notably, PLE must be distinguished from drug photosensitivity through history. Treatment generally involves symptom management with topical steroids and sun protective measures for prevention.⁹ While PLE may present similarly to drug photosensitivity reactions, our patient’s use of a known phototoxic agent makes PLE a less likely diagnosis.

Ms. Appiah is a pediatric dermatology research associate and medical student at the University of California, San Diego, and Rady Children’s Hospital, San Diego. Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Neither Dr. Matiz nor Ms. Appiah has any relevant financial disclosures.

References

1. Montgomery S et al. Clin Dermatol. 2022;40(1):57-63.

2. Blakely KM et al. Drug Saf. 2019;42(7):827-47.

3. Goetze S et al. Skin Pharmacol Physiol. 2017;30(2):76-80.

4. Odorici G et al. Dermatol Ther. 2021;34(4):e14978.

5. DeWane ME et al. J Am Acad Dermatol. 2020;82(2):267-81.

6. Waldman R et al. J Am Acad Dermatol. 2020;82(2):283-96.

7. Kiriakidou M et al. Ann Intern Med. 2020;172(11):ITC81-ITC96.

8. Nassau S et al. Med Clin North Am. 2020;104(1):61-76.

9. Guarrera M. Adv Exp Med Biol. 2017;996:61-70.

Photosensitivity due to doxycycline

As the patient’s rash presented in sun-exposed areas with both skin and nail changes, our patient was diagnosed with a phototoxic reaction to doxycycline, the oral antibiotic used to treat his acne.

Photosensitive cutaneous drug eruptions are reactions that occur after exposure to a medication and subsequent exposure to UV radiation or visible light. Reactions can be classified into two ways based on their mechanism of action: phototoxic or photoallergic.¹ Phototoxic reactions are more common and are a result of direct keratinocyte damage and cellular necrosis. Many classes of medications may cause this adverse effect, but the tetracycline class of antibiotics is a common culprit.² Photoallergic reactions are less common and are a result of a type IV immune reaction to the offending agent.¹

Courtesy Dr. Catalina Matiz

Phototoxic reactions generally present shortly after sun or UV exposure with a photo-distributed eruption pattern.³ Commonly involved areas include the face, the neck, and the extensor surfaces of extremities, with sparing of relatively protected skin such as the upper eyelids and the skin folds.² Erythema may initially develop in the exposed skin areas, followed by appearance of edema, vesicles, or bullae.^1-3 The eruption may be painful and itchy, with some patients reporting severe pain.³

Courtesy Dr. Catalina Matiz

Doxycycline phototoxicity may also cause onycholysis of the nails.² The reaction is dose dependent, with higher doses of medication leading to a higher likelihood of symptoms.^1,2 It is also more prevalent in patients with Fitzpatrick skin type I and II. The usual UVA wavelength required to induce this reaction appears to be in the 320-400 nm range of the UV spectrum.⁴ By contrast, photoallergic reactions are dose independent, and require a sensitization period prior to the eruption.¹ An eczematous eruption is most commonly seen with photoallergic reactions.³

Treatment of drug-induced photosensitivity reactions requires proper identification of the diagnosis and the offending agent, followed by cessation of the medication. If cessation is not possible, then lowering the dose can help to minimize worsening of the condition. However, for photoallergic reactions, the reaction is dose independent so switching to another tolerated agent is likely required. For persistent symptoms following medication withdrawal, topical or systemic steroids and oral antihistamine can help with symptom management.¹ For patients with photo-onycholysis, treatment involves stopping the medication and waiting for the intact nail plate to grow.

Courtesy Dr. Catalina Matiz

Dermatomyositis

Dermatomyositis is an autoimmune condition that presents with skin lesions as well as systemic findings such as myositis. The cutaneous findings are variable, but pathognomonic findings include Gottron papules of the hands, Gottron’s sign on the elbows, knees, and ankles, and the heliotrope rash of the face. Eighty percent of patients have myopathy presenting as muscle weakness, and commonly have elevated creatine kinase, aspartate transaminase, and alanine transaminase values.⁵ Diagnosis may be confirmed through skin or muscle biopsy, though antibody studies can also play a helpful role in diagnosis. Treatment is generally with oral corticosteroids or other immunosuppressants as well as sun protection.⁶ The rash seen in our patient could have been seen in patients with dermatomyositis, though it was not in the typical location on the knuckles (Gottron papules) as it also affected the lateral sides of the fingers.

Systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune condition characterized by systemic and cutaneous manifestations. Systemic symptoms may include weight loss, fever, fatigue, arthralgia, or arthritis; patients are at risk of renal, cardiovascular, pulmonary, and neurologic complications of SLE.⁷ The most common cutaneous finding is malar rash, though there are myriad dermatologic manifestations that can occur associated with photosensitivity. Diagnosis is made based on history, physical, and laboratory testing. Treatment options include NSAIDs, oral glucocorticoids, antimalarial drugs, and immunosuppressants.⁷ Though our patient exhibited photosensitivity, he had none of the systemic findings associated with SLE, making this diagnosis unlikely.

Allergic contact dermatitis

Allergic contact dermatitis (ACD) is a type IV hypersensitivity reaction, and may present as acute, subacute, or chronic dermatitis. The clinical findings vary based on chronicity. Acute ACD presents as pruritic erythematous papules and vesicles or bullae, similar to how it occurred in our patient, though our patient’s lesions were more tender than pruritic. Chronic ACD presents with erythematous lesions with pruritis, lichenification, scaling, and/or fissuring. Observing shapes or sharp demarcation of lesions may help with diagnosis. Patch testing is also useful in the diagnosis of ACD.

Treatment generally involves avoiding the offending agent with topical corticosteroids for symptom management.⁸

Polymorphous light eruption

Polymorphous light eruption (PLE) is a delayed, type IV hypersensitivity reaction to UV-induced antigens, though these antigens are unknown. PLE presents hours to days following solar or UV exposure and presents only in sun-exposed areas. Itching and burning are always present, but lesion morphology varies from erythema and papules to vesico-papules and blisters. Notably, PLE must be distinguished from drug photosensitivity through history. Treatment generally involves symptom management with topical steroids and sun protective measures for prevention.⁹ While PLE may present similarly to drug photosensitivity reactions, our patient’s use of a known phototoxic agent makes PLE a less likely diagnosis.

Ms. Appiah is a pediatric dermatology research associate and medical student at the University of California, San Diego, and Rady Children’s Hospital, San Diego. Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Neither Dr. Matiz nor Ms. Appiah has any relevant financial disclosures.

References

1. Montgomery S et al. Clin Dermatol. 2022;40(1):57-63.

2. Blakely KM et al. Drug Saf. 2019;42(7):827-47.

3. Goetze S et al. Skin Pharmacol Physiol. 2017;30(2):76-80.

4. Odorici G et al. Dermatol Ther. 2021;34(4):e14978.

5. DeWane ME et al. J Am Acad Dermatol. 2020;82(2):267-81.

6. Waldman R et al. J Am Acad Dermatol. 2020;82(2):283-96.

7. Kiriakidou M et al. Ann Intern Med. 2020;172(11):ITC81-ITC96.

8. Nassau S et al. Med Clin North Am. 2020;104(1):61-76.

9. Guarrera M. Adv Exp Med Biol. 2017;996:61-70.

The war in Ukraine is resulting in a devastating loss of life, catastrophic injuries, and physical destruction. But the war also will take an enormous mental health toll on millions of people, resulting in what I think will lead to an epidemic of posttraumatic stress disorder.

Think about the horrors that Ukrainians are experiencing. Millions of Ukrainians have been displaced to locations inside and outside of the country. People are being forced to leave behind family members, neighbors, and their pets and homes. In one recent news report, a Ukrainian woman who left Kyiv for Belgium reported having dreams in which she heard explosions. Smells, sounds, and even colors can trigger intrusive memories and a host of other problems. The mind can barely comprehend the scope of this human crisis.

Ukrainian soldiers are witnessing horrors that are unspeakable. Doctors, emergency service workers, and other medical professionals in Ukraine are being exposed to the catastrophe on a large scale. Children and youth are among the most affected victims, and it is difficult to predict the impact all of this upheaval is having on them.

The most important question for those of us who treat mental illness is “how will we help devastated people suffering from extreme trauma tied to death, dying, severe injuries, and torture by the invading soldiers?”

I have been treating patients with PTSD for many years. In my lifetime, the devastation in Ukraine will translate into what I expect will be the first overwhelming mass epidemic of PTSD – at least that I can recall. Yes, surely PTSD occurred during and after the Holocaust in the World War II era, but at that time, the mental health profession was not equipped to recognize it – even though the disorder most certainly existed. Even in ancient times, an Assyrian text from Mesopotamia (currently Iraq) described what we would define as PTSD symptoms in soldiers, such as sleep disturbances, flashbacks, and “low mood,” according to a 2014 article in the journal Early Science and Medicine.

The DSM-5 describes numerous criteria for PTSD mainly centering on trauma exposing a person to actual or threatened death, serious injury, or a variety of assaults, including direct exposure or witnessing the event. However, in my clinical experience, I’ve seen lesser events leading to PTSD. Much depends on how each individual processes what is occurring or has occurred.

What appears to be clear is that some key aspects of PTSD according to the DSM-5 – such as trauma-related thoughts or feelings, or trauma-related reminders, as well as nightmares and flashbacks – are likely occurring among Ukrainians. In addition, hypervigilance and exaggerated startle response seem to be key components of PTSD whether or not the cause is a major event or what one would perceive as less traumatic or dramatic.

I’ve certainly seen PTSD secondary to a hospitalization, especially in care involving ICUs or cardiac care units. In addition, I’ve had the occasion to note PTSD signs and symptoms after financial loss or divorce, situations in which some clinicians would never believe PTSD would occur, and would often diagnose as anxiety or depression. For me, again from a clinical point of view, it’s always been critical to assess how individuals process the event or events around them.

We know that there is already a shortage of mental health clinicians across the globe. This means that, in light of the hundreds of thousands – possibly millions – of Ukrainians affected by PTSD, a one-to-one approach will not do. For those Ukrainians who are able to find safe havens, I believe that organized medicine, including the various psychiatric/psychological associations in Europe as well as the American Psychiatric Association and the American Psychological Association, need to establish group care using telemedicine to reach large numbers of people. PTSD symptoms can be debilitating, and the mental health community needs to begin putting supports in place now to address this trauma.

Specifically, proven cognitive-behavioral therapy (CBT) and guided imagery should be used to begin helping some of these people recover from the unbelievable trauma of war. For some, medication management might be helpful in those experiencing nightmares combined with anxiety and depression. But the main approach and first line of care should be CBT and guided imagery.

PTSD symptoms can make people feel like they are losing control, and prevent them from rebuilding their lives. We must do all we can in the mental health community to destigmatize care and develop support services to get ahead of this crisis. Only through medical, psychiatric, and health care organizations banding together using modern technology can the large number of people psychologically affected by this ongoing crisis be helped and saved.
 

Dr. London is a practicing psychiatrist who has been a newspaper columnist for 35 years, specializing in writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019). He has no conflicts of interest.

The war in Ukraine is resulting in a devastating loss of life, catastrophic injuries, and physical destruction. But the war also will take an enormous mental health toll on millions of people, resulting in what I think will lead to an epidemic of posttraumatic stress disorder.

Think about the horrors that Ukrainians are experiencing. Millions of Ukrainians have been displaced to locations inside and outside of the country. People are being forced to leave behind family members, neighbors, and their pets and homes. In one recent news report, a Ukrainian woman who left Kyiv for Belgium reported having dreams in which she heard explosions. Smells, sounds, and even colors can trigger intrusive memories and a host of other problems. The mind can barely comprehend the scope of this human crisis.

Ukrainian soldiers are witnessing horrors that are unspeakable. Doctors, emergency service workers, and other medical professionals in Ukraine are being exposed to the catastrophe on a large scale. Children and youth are among the most affected victims, and it is difficult to predict the impact all of this upheaval is having on them.

The most important question for those of us who treat mental illness is “how will we help devastated people suffering from extreme trauma tied to death, dying, severe injuries, and torture by the invading soldiers?”

I have been treating patients with PTSD for many years. In my lifetime, the devastation in Ukraine will translate into what I expect will be the first overwhelming mass epidemic of PTSD – at least that I can recall. Yes, surely PTSD occurred during and after the Holocaust in the World War II era, but at that time, the mental health profession was not equipped to recognize it – even though the disorder most certainly existed. Even in ancient times, an Assyrian text from Mesopotamia (currently Iraq) described what we would define as PTSD symptoms in soldiers, such as sleep disturbances, flashbacks, and “low mood,” according to a 2014 article in the journal Early Science and Medicine.

The DSM-5 describes numerous criteria for PTSD mainly centering on trauma exposing a person to actual or threatened death, serious injury, or a variety of assaults, including direct exposure or witnessing the event. However, in my clinical experience, I’ve seen lesser events leading to PTSD. Much depends on how each individual processes what is occurring or has occurred.

What appears to be clear is that some key aspects of PTSD according to the DSM-5 – such as trauma-related thoughts or feelings, or trauma-related reminders, as well as nightmares and flashbacks – are likely occurring among Ukrainians. In addition, hypervigilance and exaggerated startle response seem to be key components of PTSD whether or not the cause is a major event or what one would perceive as less traumatic or dramatic.

I’ve certainly seen PTSD secondary to a hospitalization, especially in care involving ICUs or cardiac care units. In addition, I’ve had the occasion to note PTSD signs and symptoms after financial loss or divorce, situations in which some clinicians would never believe PTSD would occur, and would often diagnose as anxiety or depression. For me, again from a clinical point of view, it’s always been critical to assess how individuals process the event or events around them.

We know that there is already a shortage of mental health clinicians across the globe. This means that, in light of the hundreds of thousands – possibly millions – of Ukrainians affected by PTSD, a one-to-one approach will not do. For those Ukrainians who are able to find safe havens, I believe that organized medicine, including the various psychiatric/psychological associations in Europe as well as the American Psychiatric Association and the American Psychological Association, need to establish group care using telemedicine to reach large numbers of people. PTSD symptoms can be debilitating, and the mental health community needs to begin putting supports in place now to address this trauma.

Specifically, proven cognitive-behavioral therapy (CBT) and guided imagery should be used to begin helping some of these people recover from the unbelievable trauma of war. For some, medication management might be helpful in those experiencing nightmares combined with anxiety and depression. But the main approach and first line of care should be CBT and guided imagery.

PTSD symptoms can make people feel like they are losing control, and prevent them from rebuilding their lives. We must do all we can in the mental health community to destigmatize care and develop support services to get ahead of this crisis. Only through medical, psychiatric, and health care organizations banding together using modern technology can the large number of people psychologically affected by this ongoing crisis be helped and saved.
 

Dr. London is a practicing psychiatrist who has been a newspaper columnist for 35 years, specializing in writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019). He has no conflicts of interest.

The war in Ukraine is resulting in a devastating loss of life, catastrophic injuries, and physical destruction. But the war also will take an enormous mental health toll on millions of people, resulting in what I think will lead to an epidemic of posttraumatic stress disorder.

Think about the horrors that Ukrainians are experiencing. Millions of Ukrainians have been displaced to locations inside and outside of the country. People are being forced to leave behind family members, neighbors, and their pets and homes. In one recent news report, a Ukrainian woman who left Kyiv for Belgium reported having dreams in which she heard explosions. Smells, sounds, and even colors can trigger intrusive memories and a host of other problems. The mind can barely comprehend the scope of this human crisis.

Ukrainian soldiers are witnessing horrors that are unspeakable. Doctors, emergency service workers, and other medical professionals in Ukraine are being exposed to the catastrophe on a large scale. Children and youth are among the most affected victims, and it is difficult to predict the impact all of this upheaval is having on them.

The most important question for those of us who treat mental illness is “how will we help devastated people suffering from extreme trauma tied to death, dying, severe injuries, and torture by the invading soldiers?”

I have been treating patients with PTSD for many years. In my lifetime, the devastation in Ukraine will translate into what I expect will be the first overwhelming mass epidemic of PTSD – at least that I can recall. Yes, surely PTSD occurred during and after the Holocaust in the World War II era, but at that time, the mental health profession was not equipped to recognize it – even though the disorder most certainly existed. Even in ancient times, an Assyrian text from Mesopotamia (currently Iraq) described what we would define as PTSD symptoms in soldiers, such as sleep disturbances, flashbacks, and “low mood,” according to a 2014 article in the journal Early Science and Medicine.

The DSM-5 describes numerous criteria for PTSD mainly centering on trauma exposing a person to actual or threatened death, serious injury, or a variety of assaults, including direct exposure or witnessing the event. However, in my clinical experience, I’ve seen lesser events leading to PTSD. Much depends on how each individual processes what is occurring or has occurred.

What appears to be clear is that some key aspects of PTSD according to the DSM-5 – such as trauma-related thoughts or feelings, or trauma-related reminders, as well as nightmares and flashbacks – are likely occurring among Ukrainians. In addition, hypervigilance and exaggerated startle response seem to be key components of PTSD whether or not the cause is a major event or what one would perceive as less traumatic or dramatic.

I’ve certainly seen PTSD secondary to a hospitalization, especially in care involving ICUs or cardiac care units. In addition, I’ve had the occasion to note PTSD signs and symptoms after financial loss or divorce, situations in which some clinicians would never believe PTSD would occur, and would often diagnose as anxiety or depression. For me, again from a clinical point of view, it’s always been critical to assess how individuals process the event or events around them.

We know that there is already a shortage of mental health clinicians across the globe. This means that, in light of the hundreds of thousands – possibly millions – of Ukrainians affected by PTSD, a one-to-one approach will not do. For those Ukrainians who are able to find safe havens, I believe that organized medicine, including the various psychiatric/psychological associations in Europe as well as the American Psychiatric Association and the American Psychological Association, need to establish group care using telemedicine to reach large numbers of people. PTSD symptoms can be debilitating, and the mental health community needs to begin putting supports in place now to address this trauma.

Specifically, proven cognitive-behavioral therapy (CBT) and guided imagery should be used to begin helping some of these people recover from the unbelievable trauma of war. For some, medication management might be helpful in those experiencing nightmares combined with anxiety and depression. But the main approach and first line of care should be CBT and guided imagery.

PTSD symptoms can make people feel like they are losing control, and prevent them from rebuilding their lives. We must do all we can in the mental health community to destigmatize care and develop support services to get ahead of this crisis. Only through medical, psychiatric, and health care organizations banding together using modern technology can the large number of people psychologically affected by this ongoing crisis be helped and saved.
 

Dr. London is a practicing psychiatrist who has been a newspaper columnist for 35 years, specializing in writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019). He has no conflicts of interest.

In the presentation of secondary amenorrhea, pregnancy is the No. 1 differential diagnosis. Once this has been excluded, an algorithm is initiated to determine the etiology, including an assessment of the hypothalamic-pituitary-ovarian axis. While the early onset of ovarian failure can be physically and psychologically disrupting, the effect on fertility is an especially devastating event. Previously identified by terms including premature ovarian failure and premature menopause, “primary ovarian insufficiency” (POI) is now the preferred designation. This month’s article will address the diagnosis, evaluation, and management of POI.

The definition of POI is the development of primary hypogonadism before the age of 40 years. Spontaneous POI occurs in approximately 1 in 250 women by age 35 years and 1 in 100 by age 40 years. After excluding pregnancy, the clinician should determine signs and symptoms that can lead to expedited and cost-efficient testing.

Consequences

POI is an important risk factor for bone loss and osteoporosis, especially in young women who develop ovarian dysfunction before they achieve peak adult bone mass. At the time of diagnosis of POI, a bone density test (dual-energy x-ray absorptiometry) should be obtained. Women with POI may also develop depression and anxiety as well as experience an increased risk for cardiovascular morbidity and mortality, possibly related to endothelial dysfunction.

Young women with spontaneous POI are at increased risk of developing autoimmune adrenal insufficiency (AAI), a potentially fatal disorder. Consequently, to diagnose AAI, serum adrenal cortical and 21-hydroxylase antibodies should be measured in all women who have a karyotype of 46,XX and experience spontaneous POI. Women with AAI have a 50% risk of developing adrenal insufficiency. Despite initial normal adrenal function, women with positive adrenal cortical antibodies should be followed annually.
 

Causes (see table for a more complete list)

Iatrogenic

Known causes of POI include chemotherapy/radiation often in the setting of cancer treatment. The three most commonly used drugs, cyclophosphamide, cisplatin, and doxorubicin, cause POI by inducing death and/or accelerated activation of primordial follicles and increased atresia of growing follicles. The most damaging agents are alkylating drugs. A cyclophosphamide equivalent dose calculator has been established for ovarian failure risk stratification from chemotherapy based on the cumulative dose of alkylating agents received.

One study estimated the radiosensitivity of the oocyte to be less than 2 Gy. Based upon this estimate, the authors calculated the dose of radiotherapy that would result in immediate and permanent ovarian failure in 97.5% of patients as follows:

• 20.3 Gy at birth
• 18.4 Gy at age 10 years
• 16.5 Gy at age 20 years
• 14.3 Gy at age 30 years

Genetic

Approximately 10% of cases are familial. A family history of POI raises concern for a fragile X premutation. Fragile X syndrome is an X-linked form of intellectual disability that is one of the most common causes of mental retardation worldwide. There is a strong relationship between age at menopause, including POI, and premutations for fragile X syndrome. The American College of Obstetricians and Gynecologists recommends that women with POI or an elevated follicle-stimulating hormone (FSH) level before age 40 years without known cause be screened for FMR1 premutations. Approximately 6% of cases of POI are associated with premutations in the FMR1 gene.

Turner syndrome is one of the most common causes of POI and results from the lack of a second X chromosome. The most common chromosomal defect in humans, TS occurs in up to 1.5% of conceptions, 10% of spontaneous abortions, and 1 of 2,500 live births.

Serum antiadrenal and/or anti–21-hydroxylase antibodies and antithyroid antiperoxidase antibodies, can aid in the diagnosis of adrenal gland, ovary, and thyroid autoimmune causes, which is found in 4% of women with spontaneous POI. Testing for the presence of 21-hydroxylase autoantibodies or adrenal autoantibodies is sufficient to make the diagnosis of autoimmune oophoritis in women with proven spontaneous POI.

The etiology of POI remains unknown in approximately 75%-90% of cases. However, studies using whole exome or whole genome sequencing have identified genetic variants in approximately 30%-35% of these patients.
 

Risk factors

Factors that are thought to play a role in determining the age of menopause, include genetics (e.g., FMR1 premutation and mosaic Turner syndrome), ethnicity (earlier among Hispanic women and later in Japanese American women when compared with White women), and smoking (reduced by approximately 2 years ).

Regarding ovarian aging, the holy grail of the reproductive life span is to predict menopause. While the definitive age eludes us, anti-Müllerian hormone levels appear to show promise. An ultrasensitive anti-Müllerian hormone assay (< 0.01 ng/mL) predicted a 79% probability of menopause within 12 months for women aged 51 and above; the probability was 51% for women below age 48.
 

Diagnosis

The three P’s of secondary amenorrhea are physiological, pharmacological, or pathological and can guide the clinician to a targeted evaluation. Physiological causes are pregnancy, the first 6 months of continuous breastfeeding (from elevated prolactin), and natural menopause. Pharmacological etiologies, excluding hormonal treatment that suppresses ovulation (combined oral contraceptives, gonadotropin-releasing hormone agonist/antagonist, or danazol), include agents that inhibit dopamine thereby increasing serum prolactin, such as metoclopramide; phenothiazine antipsychotics, such as haloperidol; and tardive dystonia dopamine-depleting medications, such as reserpine. Pathological causes include pituitary adenomas, thyroid disease, functional hypothalamic amenorrhea from changes in weight, exercise regimen, and stress.

Management

About 50%-75% of women with 46,XX spontaneous POI experience intermittent ovarian function and 5%-10% of women remain able to conceive. Anecdotally, a 32-year-old woman presented to me with primary infertility, secondary amenorrhea, and suspected POI based on vasomotor symptoms and elevated FSH levels. Pelvic ultrasound showed a hemorrhagic cyst, suspicious for a corpus luteum. Two weeks thereafter she reported a positive home urine human chorionic gonadotropin test and ultimately delivered twins. Her diagnosis of POI with amenorrhea remained postpartum.

Unless there is an absolute contraindication, estrogen therapy should be prescribed to women with POI to reduce the risk of osteoporosis, cardiovascular disease, and urogenital atrophy as well as to maintain sexual health and quality of life. For those with an intact uterus, women should receive progesterone because of the risk of endometrial hyperplasia from unopposed estrogen. Rather than oral estrogen, the use of transdermal or vaginal delivery of estrogen is a more physiological approach and provides lower risks of venous thromboembolism and gallbladder disease. Of note, standard postmenopausal hormone therapy, which has a much lower dose of estrogen than combined estrogen-progestin contraceptives, does not provide effective contraception. Per ACOG, systemic hormone treatment should be prescribed until age 50-51 years to all women with POI.

For fertility, women with spontaneous POI can be offered oocyte or embryo donation. The uterus does not age reproductively, unlike oocytes, therefore women can achieve reasonable pregnancy success rates through egg donation despite experiencing menopause.
 

Future potential options

Female germline stem cells have been isolated from neonatal mice and transplanted into sterile adult mice, who then were able to produce offspring. In a second study, oogonial stem cells were isolated from neonatal and adult mouse ovaries; pups were subsequently born from the oocytes. Further experiments are needed before the implications for humans can be determined.

Emotionally traumatic for most women, POI disrupts life plans, hopes, and dreams of raising a family. The approach to the patient with POI involves the above evidence-based testing along with empathy from the health care provider.

Dr. Trolice is director of The IVF Center in Winter Park, Fla., and professor of obstetrics and gynecology at the University of Central Florida, Orlando.

In the presentation of secondary amenorrhea, pregnancy is the No. 1 differential diagnosis. Once this has been excluded, an algorithm is initiated to determine the etiology, including an assessment of the hypothalamic-pituitary-ovarian axis. While the early onset of ovarian failure can be physically and psychologically disrupting, the effect on fertility is an especially devastating event. Previously identified by terms including premature ovarian failure and premature menopause, “primary ovarian insufficiency” (POI) is now the preferred designation. This month’s article will address the diagnosis, evaluation, and management of POI.

The definition of POI is the development of primary hypogonadism before the age of 40 years. Spontaneous POI occurs in approximately 1 in 250 women by age 35 years and 1 in 100 by age 40 years. After excluding pregnancy, the clinician should determine signs and symptoms that can lead to expedited and cost-efficient testing.

Consequences

POI is an important risk factor for bone loss and osteoporosis, especially in young women who develop ovarian dysfunction before they achieve peak adult bone mass. At the time of diagnosis of POI, a bone density test (dual-energy x-ray absorptiometry) should be obtained. Women with POI may also develop depression and anxiety as well as experience an increased risk for cardiovascular morbidity and mortality, possibly related to endothelial dysfunction.

Young women with spontaneous POI are at increased risk of developing autoimmune adrenal insufficiency (AAI), a potentially fatal disorder. Consequently, to diagnose AAI, serum adrenal cortical and 21-hydroxylase antibodies should be measured in all women who have a karyotype of 46,XX and experience spontaneous POI. Women with AAI have a 50% risk of developing adrenal insufficiency. Despite initial normal adrenal function, women with positive adrenal cortical antibodies should be followed annually.
 

Causes (see table for a more complete list)

Iatrogenic

Known causes of POI include chemotherapy/radiation often in the setting of cancer treatment. The three most commonly used drugs, cyclophosphamide, cisplatin, and doxorubicin, cause POI by inducing death and/or accelerated activation of primordial follicles and increased atresia of growing follicles. The most damaging agents are alkylating drugs. A cyclophosphamide equivalent dose calculator has been established for ovarian failure risk stratification from chemotherapy based on the cumulative dose of alkylating agents received.

One study estimated the radiosensitivity of the oocyte to be less than 2 Gy. Based upon this estimate, the authors calculated the dose of radiotherapy that would result in immediate and permanent ovarian failure in 97.5% of patients as follows:

• 20.3 Gy at birth
• 18.4 Gy at age 10 years
• 16.5 Gy at age 20 years
• 14.3 Gy at age 30 years

Genetic

Approximately 10% of cases are familial. A family history of POI raises concern for a fragile X premutation. Fragile X syndrome is an X-linked form of intellectual disability that is one of the most common causes of mental retardation worldwide. There is a strong relationship between age at menopause, including POI, and premutations for fragile X syndrome. The American College of Obstetricians and Gynecologists recommends that women with POI or an elevated follicle-stimulating hormone (FSH) level before age 40 years without known cause be screened for FMR1 premutations. Approximately 6% of cases of POI are associated with premutations in the FMR1 gene.

Turner syndrome is one of the most common causes of POI and results from the lack of a second X chromosome. The most common chromosomal defect in humans, TS occurs in up to 1.5% of conceptions, 10% of spontaneous abortions, and 1 of 2,500 live births.

Serum antiadrenal and/or anti–21-hydroxylase antibodies and antithyroid antiperoxidase antibodies, can aid in the diagnosis of adrenal gland, ovary, and thyroid autoimmune causes, which is found in 4% of women with spontaneous POI. Testing for the presence of 21-hydroxylase autoantibodies or adrenal autoantibodies is sufficient to make the diagnosis of autoimmune oophoritis in women with proven spontaneous POI.

The etiology of POI remains unknown in approximately 75%-90% of cases. However, studies using whole exome or whole genome sequencing have identified genetic variants in approximately 30%-35% of these patients.
 

Risk factors

Factors that are thought to play a role in determining the age of menopause, include genetics (e.g., FMR1 premutation and mosaic Turner syndrome), ethnicity (earlier among Hispanic women and later in Japanese American women when compared with White women), and smoking (reduced by approximately 2 years ).

Regarding ovarian aging, the holy grail of the reproductive life span is to predict menopause. While the definitive age eludes us, anti-Müllerian hormone levels appear to show promise. An ultrasensitive anti-Müllerian hormone assay (< 0.01 ng/mL) predicted a 79% probability of menopause within 12 months for women aged 51 and above; the probability was 51% for women below age 48.
 

Diagnosis

The three P’s of secondary amenorrhea are physiological, pharmacological, or pathological and can guide the clinician to a targeted evaluation. Physiological causes are pregnancy, the first 6 months of continuous breastfeeding (from elevated prolactin), and natural menopause. Pharmacological etiologies, excluding hormonal treatment that suppresses ovulation (combined oral contraceptives, gonadotropin-releasing hormone agonist/antagonist, or danazol), include agents that inhibit dopamine thereby increasing serum prolactin, such as metoclopramide; phenothiazine antipsychotics, such as haloperidol; and tardive dystonia dopamine-depleting medications, such as reserpine. Pathological causes include pituitary adenomas, thyroid disease, functional hypothalamic amenorrhea from changes in weight, exercise regimen, and stress.

Management

About 50%-75% of women with 46,XX spontaneous POI experience intermittent ovarian function and 5%-10% of women remain able to conceive. Anecdotally, a 32-year-old woman presented to me with primary infertility, secondary amenorrhea, and suspected POI based on vasomotor symptoms and elevated FSH levels. Pelvic ultrasound showed a hemorrhagic cyst, suspicious for a corpus luteum. Two weeks thereafter she reported a positive home urine human chorionic gonadotropin test and ultimately delivered twins. Her diagnosis of POI with amenorrhea remained postpartum.

Unless there is an absolute contraindication, estrogen therapy should be prescribed to women with POI to reduce the risk of osteoporosis, cardiovascular disease, and urogenital atrophy as well as to maintain sexual health and quality of life. For those with an intact uterus, women should receive progesterone because of the risk of endometrial hyperplasia from unopposed estrogen. Rather than oral estrogen, the use of transdermal or vaginal delivery of estrogen is a more physiological approach and provides lower risks of venous thromboembolism and gallbladder disease. Of note, standard postmenopausal hormone therapy, which has a much lower dose of estrogen than combined estrogen-progestin contraceptives, does not provide effective contraception. Per ACOG, systemic hormone treatment should be prescribed until age 50-51 years to all women with POI.

For fertility, women with spontaneous POI can be offered oocyte or embryo donation. The uterus does not age reproductively, unlike oocytes, therefore women can achieve reasonable pregnancy success rates through egg donation despite experiencing menopause.
 

Future potential options

Female germline stem cells have been isolated from neonatal mice and transplanted into sterile adult mice, who then were able to produce offspring. In a second study, oogonial stem cells were isolated from neonatal and adult mouse ovaries; pups were subsequently born from the oocytes. Further experiments are needed before the implications for humans can be determined.

Emotionally traumatic for most women, POI disrupts life plans, hopes, and dreams of raising a family. The approach to the patient with POI involves the above evidence-based testing along with empathy from the health care provider.

Dr. Trolice is director of The IVF Center in Winter Park, Fla., and professor of obstetrics and gynecology at the University of Central Florida, Orlando.

In the presentation of secondary amenorrhea, pregnancy is the No. 1 differential diagnosis. Once this has been excluded, an algorithm is initiated to determine the etiology, including an assessment of the hypothalamic-pituitary-ovarian axis. While the early onset of ovarian failure can be physically and psychologically disrupting, the effect on fertility is an especially devastating event. Previously identified by terms including premature ovarian failure and premature menopause, “primary ovarian insufficiency” (POI) is now the preferred designation. This month’s article will address the diagnosis, evaluation, and management of POI.

The definition of POI is the development of primary hypogonadism before the age of 40 years. Spontaneous POI occurs in approximately 1 in 250 women by age 35 years and 1 in 100 by age 40 years. After excluding pregnancy, the clinician should determine signs and symptoms that can lead to expedited and cost-efficient testing.

Consequences

POI is an important risk factor for bone loss and osteoporosis, especially in young women who develop ovarian dysfunction before they achieve peak adult bone mass. At the time of diagnosis of POI, a bone density test (dual-energy x-ray absorptiometry) should be obtained. Women with POI may also develop depression and anxiety as well as experience an increased risk for cardiovascular morbidity and mortality, possibly related to endothelial dysfunction.

Young women with spontaneous POI are at increased risk of developing autoimmune adrenal insufficiency (AAI), a potentially fatal disorder. Consequently, to diagnose AAI, serum adrenal cortical and 21-hydroxylase antibodies should be measured in all women who have a karyotype of 46,XX and experience spontaneous POI. Women with AAI have a 50% risk of developing adrenal insufficiency. Despite initial normal adrenal function, women with positive adrenal cortical antibodies should be followed annually.
 

Causes (see table for a more complete list)

Iatrogenic

Known causes of POI include chemotherapy/radiation often in the setting of cancer treatment. The three most commonly used drugs, cyclophosphamide, cisplatin, and doxorubicin, cause POI by inducing death and/or accelerated activation of primordial follicles and increased atresia of growing follicles. The most damaging agents are alkylating drugs. A cyclophosphamide equivalent dose calculator has been established for ovarian failure risk stratification from chemotherapy based on the cumulative dose of alkylating agents received.

One study estimated the radiosensitivity of the oocyte to be less than 2 Gy. Based upon this estimate, the authors calculated the dose of radiotherapy that would result in immediate and permanent ovarian failure in 97.5% of patients as follows:

• 20.3 Gy at birth
• 18.4 Gy at age 10 years
• 16.5 Gy at age 20 years
• 14.3 Gy at age 30 years

Genetic

Approximately 10% of cases are familial. A family history of POI raises concern for a fragile X premutation. Fragile X syndrome is an X-linked form of intellectual disability that is one of the most common causes of mental retardation worldwide. There is a strong relationship between age at menopause, including POI, and premutations for fragile X syndrome. The American College of Obstetricians and Gynecologists recommends that women with POI or an elevated follicle-stimulating hormone (FSH) level before age 40 years without known cause be screened for FMR1 premutations. Approximately 6% of cases of POI are associated with premutations in the FMR1 gene.

Turner syndrome is one of the most common causes of POI and results from the lack of a second X chromosome. The most common chromosomal defect in humans, TS occurs in up to 1.5% of conceptions, 10% of spontaneous abortions, and 1 of 2,500 live births.

Serum antiadrenal and/or anti–21-hydroxylase antibodies and antithyroid antiperoxidase antibodies, can aid in the diagnosis of adrenal gland, ovary, and thyroid autoimmune causes, which is found in 4% of women with spontaneous POI. Testing for the presence of 21-hydroxylase autoantibodies or adrenal autoantibodies is sufficient to make the diagnosis of autoimmune oophoritis in women with proven spontaneous POI.

The etiology of POI remains unknown in approximately 75%-90% of cases. However, studies using whole exome or whole genome sequencing have identified genetic variants in approximately 30%-35% of these patients.
 

Risk factors

Factors that are thought to play a role in determining the age of menopause, include genetics (e.g., FMR1 premutation and mosaic Turner syndrome), ethnicity (earlier among Hispanic women and later in Japanese American women when compared with White women), and smoking (reduced by approximately 2 years ).

Regarding ovarian aging, the holy grail of the reproductive life span is to predict menopause. While the definitive age eludes us, anti-Müllerian hormone levels appear to show promise. An ultrasensitive anti-Müllerian hormone assay (< 0.01 ng/mL) predicted a 79% probability of menopause within 12 months for women aged 51 and above; the probability was 51% for women below age 48.
 

Diagnosis

The three P’s of secondary amenorrhea are physiological, pharmacological, or pathological and can guide the clinician to a targeted evaluation. Physiological causes are pregnancy, the first 6 months of continuous breastfeeding (from elevated prolactin), and natural menopause. Pharmacological etiologies, excluding hormonal treatment that suppresses ovulation (combined oral contraceptives, gonadotropin-releasing hormone agonist/antagonist, or danazol), include agents that inhibit dopamine thereby increasing serum prolactin, such as metoclopramide; phenothiazine antipsychotics, such as haloperidol; and tardive dystonia dopamine-depleting medications, such as reserpine. Pathological causes include pituitary adenomas, thyroid disease, functional hypothalamic amenorrhea from changes in weight, exercise regimen, and stress.

Management

About 50%-75% of women with 46,XX spontaneous POI experience intermittent ovarian function and 5%-10% of women remain able to conceive. Anecdotally, a 32-year-old woman presented to me with primary infertility, secondary amenorrhea, and suspected POI based on vasomotor symptoms and elevated FSH levels. Pelvic ultrasound showed a hemorrhagic cyst, suspicious for a corpus luteum. Two weeks thereafter she reported a positive home urine human chorionic gonadotropin test and ultimately delivered twins. Her diagnosis of POI with amenorrhea remained postpartum.

Unless there is an absolute contraindication, estrogen therapy should be prescribed to women with POI to reduce the risk of osteoporosis, cardiovascular disease, and urogenital atrophy as well as to maintain sexual health and quality of life. For those with an intact uterus, women should receive progesterone because of the risk of endometrial hyperplasia from unopposed estrogen. Rather than oral estrogen, the use of transdermal or vaginal delivery of estrogen is a more physiological approach and provides lower risks of venous thromboembolism and gallbladder disease. Of note, standard postmenopausal hormone therapy, which has a much lower dose of estrogen than combined estrogen-progestin contraceptives, does not provide effective contraception. Per ACOG, systemic hormone treatment should be prescribed until age 50-51 years to all women with POI.

For fertility, women with spontaneous POI can be offered oocyte or embryo donation. The uterus does not age reproductively, unlike oocytes, therefore women can achieve reasonable pregnancy success rates through egg donation despite experiencing menopause.
 

Future potential options

Female germline stem cells have been isolated from neonatal mice and transplanted into sterile adult mice, who then were able to produce offspring. In a second study, oogonial stem cells were isolated from neonatal and adult mouse ovaries; pups were subsequently born from the oocytes. Further experiments are needed before the implications for humans can be determined.

Emotionally traumatic for most women, POI disrupts life plans, hopes, and dreams of raising a family. The approach to the patient with POI involves the above evidence-based testing along with empathy from the health care provider.

Dr. Trolice is director of The IVF Center in Winter Park, Fla., and professor of obstetrics and gynecology at the University of Central Florida, Orlando.

In a recent article published in JAMA Psychiatry, Joshua E. J. Buckman and coauthors described the results of a large research study which concludes that depression is harder to treat in those who are homeless or unemployed.

It is always good to get more data and this article adds to the literature about the social determinants of depression. A frustrating aspect is that this is no surprise at all, not least for anyone in the mental health field. We have known that intuitively for decades.

Again, data is always good to bolster intuition with science. But what are the actionable items to take from the paper?

Homelessness and unemployment are things very hard to fix and the millions of homeless in one of the richest countries of the world illustrate the many complexities. However, there are a few policy and clinical points I would like to make, reflecting some of the chapters in a recently published book – edited by me and my colleague Maria D. Llorente – “Clinical Management of the Homeless Patient: Social Medical and Psychiatric Issues” (New York: Springer, May 2021).

The first is, if you really tackle homelessness, with a combination of federal, state, and local resources, you can make a difference. The Department of Veterans Affairs, under the leadership of former VA Secretary Eric Shinseki and others, has been markedly successful. Note, for instance, the Health Care for Homeless Veterans program , which conducts outreach to vulnerable veterans not currently receiving services and engages them in treatment and rehabilitative programs.

Secondly, there is a marked absence of shelters that can care for the homeless with medical problems. This leads to extended and extensive hospital stays. This is especially frustrating during the COVID era, when hospital beds are in such short supply. Having a safe place to discharge patients who still need wound or diabetes care would save money for the overall health care system and be best for the patient.

Third, it may be best to modify discharge regimens for those patients who are unhoused. For example, metformin, taken by mouth once a day, is more practical for unhoused patients with diabetes than insulin, which needs to be refrigerated and injected multiple times a day. While one can argue whether care for the homeless should differ from those who are housed, in practical terms, simplifying regimens is more likely to promote compliance.

My last take-home point is check the Feet. So many of our homeless patients who end up on hospital wards have been wearing ill-fitting or no shoes while they are out on the street. Their toenails may be long and thick. They may have cellulitis or ulcers. Or gangrene. Unfortunately, these medical issues can also cause surgical amputations of the lower extremities.

Back to the article by Buckman and colleagues. The data they provide is good to have. But we need more action to provide appropriate and compassionate care for those who are unhoused and ill – care that is good for them, good for the nation’s finances, and good for our moral standing in the world.

Dr. Ritchie is chair of psychiatry at Medstar Washington (D.C.) Hospital Center. She is a member of the Clinical Psychiatry News editorial advisory board, and has no conflicts of interest.

In a recent article published in JAMA Psychiatry, Joshua E. J. Buckman and coauthors described the results of a large research study which concludes that depression is harder to treat in those who are homeless or unemployed.

It is always good to get more data and this article adds to the literature about the social determinants of depression. A frustrating aspect is that this is no surprise at all, not least for anyone in the mental health field. We have known that intuitively for decades.

Again, data is always good to bolster intuition with science. But what are the actionable items to take from the paper?

Homelessness and unemployment are things very hard to fix and the millions of homeless in one of the richest countries of the world illustrate the many complexities. However, there are a few policy and clinical points I would like to make, reflecting some of the chapters in a recently published book – edited by me and my colleague Maria D. Llorente – “Clinical Management of the Homeless Patient: Social Medical and Psychiatric Issues” (New York: Springer, May 2021).

The first is, if you really tackle homelessness, with a combination of federal, state, and local resources, you can make a difference. The Department of Veterans Affairs, under the leadership of former VA Secretary Eric Shinseki and others, has been markedly successful. Note, for instance, the Health Care for Homeless Veterans program , which conducts outreach to vulnerable veterans not currently receiving services and engages them in treatment and rehabilitative programs.

Secondly, there is a marked absence of shelters that can care for the homeless with medical problems. This leads to extended and extensive hospital stays. This is especially frustrating during the COVID era, when hospital beds are in such short supply. Having a safe place to discharge patients who still need wound or diabetes care would save money for the overall health care system and be best for the patient.

Third, it may be best to modify discharge regimens for those patients who are unhoused. For example, metformin, taken by mouth once a day, is more practical for unhoused patients with diabetes than insulin, which needs to be refrigerated and injected multiple times a day. While one can argue whether care for the homeless should differ from those who are housed, in practical terms, simplifying regimens is more likely to promote compliance.

My last take-home point is check the Feet. So many of our homeless patients who end up on hospital wards have been wearing ill-fitting or no shoes while they are out on the street. Their toenails may be long and thick. They may have cellulitis or ulcers. Or gangrene. Unfortunately, these medical issues can also cause surgical amputations of the lower extremities.

Back to the article by Buckman and colleagues. The data they provide is good to have. But we need more action to provide appropriate and compassionate care for those who are unhoused and ill – care that is good for them, good for the nation’s finances, and good for our moral standing in the world.

Dr. Ritchie is chair of psychiatry at Medstar Washington (D.C.) Hospital Center. She is a member of the Clinical Psychiatry News editorial advisory board, and has no conflicts of interest.

In a recent article published in JAMA Psychiatry, Joshua E. J. Buckman and coauthors described the results of a large research study which concludes that depression is harder to treat in those who are homeless or unemployed.

It is always good to get more data and this article adds to the literature about the social determinants of depression. A frustrating aspect is that this is no surprise at all, not least for anyone in the mental health field. We have known that intuitively for decades.

Again, data is always good to bolster intuition with science. But what are the actionable items to take from the paper?

Homelessness and unemployment are things very hard to fix and the millions of homeless in one of the richest countries of the world illustrate the many complexities. However, there are a few policy and clinical points I would like to make, reflecting some of the chapters in a recently published book – edited by me and my colleague Maria D. Llorente – “Clinical Management of the Homeless Patient: Social Medical and Psychiatric Issues” (New York: Springer, May 2021).

The first is, if you really tackle homelessness, with a combination of federal, state, and local resources, you can make a difference. The Department of Veterans Affairs, under the leadership of former VA Secretary Eric Shinseki and others, has been markedly successful. Note, for instance, the Health Care for Homeless Veterans program , which conducts outreach to vulnerable veterans not currently receiving services and engages them in treatment and rehabilitative programs.

Secondly, there is a marked absence of shelters that can care for the homeless with medical problems. This leads to extended and extensive hospital stays. This is especially frustrating during the COVID era, when hospital beds are in such short supply. Having a safe place to discharge patients who still need wound or diabetes care would save money for the overall health care system and be best for the patient.

Third, it may be best to modify discharge regimens for those patients who are unhoused. For example, metformin, taken by mouth once a day, is more practical for unhoused patients with diabetes than insulin, which needs to be refrigerated and injected multiple times a day. While one can argue whether care for the homeless should differ from those who are housed, in practical terms, simplifying regimens is more likely to promote compliance.

My last take-home point is check the Feet. So many of our homeless patients who end up on hospital wards have been wearing ill-fitting or no shoes while they are out on the street. Their toenails may be long and thick. They may have cellulitis or ulcers. Or gangrene. Unfortunately, these medical issues can also cause surgical amputations of the lower extremities.

Back to the article by Buckman and colleagues. The data they provide is good to have. But we need more action to provide appropriate and compassionate care for those who are unhoused and ill – care that is good for them, good for the nation’s finances, and good for our moral standing in the world.

Dr. Ritchie is chair of psychiatry at Medstar Washington (D.C.) Hospital Center. She is a member of the Clinical Psychiatry News editorial advisory board, and has no conflicts of interest.

Reports of long waiting times at mental health clinics and anecdotal observations by health care providers suggest the pandemic has generated a dramatic increase in the incidence of eating disorders among the pediatric population. Of course this should come as no surprise to pediatricians.

Eating disorders come in many different forms and a triggering event is sometimes difficult to define. Often the adolescent or preadolescent is searching for some sense of stability in a life tossed on a stormy sea roiled by hormonal and physical change. Wresting control of their bodies during a period of uncertainty may result in a downward spiral into dangerously unhealthy weight loss. If nothing else, the pandemic has been a period of dramatic uncertainty unlike what most children and few adults in this country have ever experienced.

With the unprecedented increase in eating disorder cases, providers in several disciplines are searching for novel strategies to ease the burden on their patients and their practices. I recently learned of a pediatric practice in California that is considering blinding all patients aged 12 and older to the body mass measurements obtained at their health maintenance visits.

Blind weight checks for children with eating disorders, particularly those who seem to be nearing recovery, has been a common and often helpful practice. However, I am unaware of any practice that has made it a universal office policy. I’m unsure of the rationale behind this practice’s policy, but on several fronts, suppressing body mass measurements in the age group most vulnerable to eating disorders makes some sense.

Universal blind weight checks could minimize the risk of in-office shaming. However, careful training of support staff and thoughtful placement of the scales could serve the same purpose. This new policy acknowledges not only the ubiquity of the problem but also that many, maybe even most, children with eating disorders appear normal. And of course, there is the unfortunate fact that body mass is a poor screening test for eating disorders.

As I thought more about this novel approach I came to see its educational value for patients, parents, and even physicians. I can envision how a 13-year-old’s first health maintenance visit would go after the roll-out of the new policy. “Dr. Smith, aren’t you going to tell us how much I (or my daughter Jenny) weigh(s)?” This could, or more likely, should launch a discussion about weight and body image. It might continue with questions like, “How much do you think you weigh?” Or, “Do you think you are too heavy or too thin?”

Or, the conversation could include the provider’s observations that weight is just one measure of health and in fact not a very good one. Other ingredients in a healthy life style, such as sleep and physical activity, are not as easy to measure as weight but in many cases are more important.

As my mind struggled to restructure a health maintenance schedule that included blind weight checks, I wondered why we should wait until age 12. Of course, it is unreasonable to expect parents to stick with a pediatric practice that seems to ignore their infant’s weight. I’m sure that, like me, you have always discouraged new parents from having a baby scale at home because in the first few months too-frequent weighings can usually cause more angst than good.

It might make sense to remove a within-earshot discussion of a child’s weight from the health maintenance visit as soon as the child can absorb and digest the discussion; say, around age 3 years. In a perfect world, the provider should have already elicited a history that suggested a young child’s vulnerability to obesity before the scale and the growth chart told the unfortunate story. But, neither you nor I are perfect providers and so we will always need the scale to document our concerns. However, when and how we report that one vital sign to the patient and his or her parents is a topic ripe for discussion and improvement.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Reports of long waiting times at mental health clinics and anecdotal observations by health care providers suggest the pandemic has generated a dramatic increase in the incidence of eating disorders among the pediatric population. Of course this should come as no surprise to pediatricians.

Eating disorders come in many different forms and a triggering event is sometimes difficult to define. Often the adolescent or preadolescent is searching for some sense of stability in a life tossed on a stormy sea roiled by hormonal and physical change. Wresting control of their bodies during a period of uncertainty may result in a downward spiral into dangerously unhealthy weight loss. If nothing else, the pandemic has been a period of dramatic uncertainty unlike what most children and few adults in this country have ever experienced.

With the unprecedented increase in eating disorder cases, providers in several disciplines are searching for novel strategies to ease the burden on their patients and their practices. I recently learned of a pediatric practice in California that is considering blinding all patients aged 12 and older to the body mass measurements obtained at their health maintenance visits.

Blind weight checks for children with eating disorders, particularly those who seem to be nearing recovery, has been a common and often helpful practice. However, I am unaware of any practice that has made it a universal office policy. I’m unsure of the rationale behind this practice’s policy, but on several fronts, suppressing body mass measurements in the age group most vulnerable to eating disorders makes some sense.

Universal blind weight checks could minimize the risk of in-office shaming. However, careful training of support staff and thoughtful placement of the scales could serve the same purpose. This new policy acknowledges not only the ubiquity of the problem but also that many, maybe even most, children with eating disorders appear normal. And of course, there is the unfortunate fact that body mass is a poor screening test for eating disorders.

As I thought more about this novel approach I came to see its educational value for patients, parents, and even physicians. I can envision how a 13-year-old’s first health maintenance visit would go after the roll-out of the new policy. “Dr. Smith, aren’t you going to tell us how much I (or my daughter Jenny) weigh(s)?” This could, or more likely, should launch a discussion about weight and body image. It might continue with questions like, “How much do you think you weigh?” Or, “Do you think you are too heavy or too thin?”

Or, the conversation could include the provider’s observations that weight is just one measure of health and in fact not a very good one. Other ingredients in a healthy life style, such as sleep and physical activity, are not as easy to measure as weight but in many cases are more important.

As my mind struggled to restructure a health maintenance schedule that included blind weight checks, I wondered why we should wait until age 12. Of course, it is unreasonable to expect parents to stick with a pediatric practice that seems to ignore their infant’s weight. I’m sure that, like me, you have always discouraged new parents from having a baby scale at home because in the first few months too-frequent weighings can usually cause more angst than good.

It might make sense to remove a within-earshot discussion of a child’s weight from the health maintenance visit as soon as the child can absorb and digest the discussion; say, around age 3 years. In a perfect world, the provider should have already elicited a history that suggested a young child’s vulnerability to obesity before the scale and the growth chart told the unfortunate story. But, neither you nor I are perfect providers and so we will always need the scale to document our concerns. However, when and how we report that one vital sign to the patient and his or her parents is a topic ripe for discussion and improvement.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Reports of long waiting times at mental health clinics and anecdotal observations by health care providers suggest the pandemic has generated a dramatic increase in the incidence of eating disorders among the pediatric population. Of course this should come as no surprise to pediatricians.

Eating disorders come in many different forms and a triggering event is sometimes difficult to define. Often the adolescent or preadolescent is searching for some sense of stability in a life tossed on a stormy sea roiled by hormonal and physical change. Wresting control of their bodies during a period of uncertainty may result in a downward spiral into dangerously unhealthy weight loss. If nothing else, the pandemic has been a period of dramatic uncertainty unlike what most children and few adults in this country have ever experienced.

With the unprecedented increase in eating disorder cases, providers in several disciplines are searching for novel strategies to ease the burden on their patients and their practices. I recently learned of a pediatric practice in California that is considering blinding all patients aged 12 and older to the body mass measurements obtained at their health maintenance visits.

Blind weight checks for children with eating disorders, particularly those who seem to be nearing recovery, has been a common and often helpful practice. However, I am unaware of any practice that has made it a universal office policy. I’m unsure of the rationale behind this practice’s policy, but on several fronts, suppressing body mass measurements in the age group most vulnerable to eating disorders makes some sense.

Universal blind weight checks could minimize the risk of in-office shaming. However, careful training of support staff and thoughtful placement of the scales could serve the same purpose. This new policy acknowledges not only the ubiquity of the problem but also that many, maybe even most, children with eating disorders appear normal. And of course, there is the unfortunate fact that body mass is a poor screening test for eating disorders.

As I thought more about this novel approach I came to see its educational value for patients, parents, and even physicians. I can envision how a 13-year-old’s first health maintenance visit would go after the roll-out of the new policy. “Dr. Smith, aren’t you going to tell us how much I (or my daughter Jenny) weigh(s)?” This could, or more likely, should launch a discussion about weight and body image. It might continue with questions like, “How much do you think you weigh?” Or, “Do you think you are too heavy or too thin?”

Or, the conversation could include the provider’s observations that weight is just one measure of health and in fact not a very good one. Other ingredients in a healthy life style, such as sleep and physical activity, are not as easy to measure as weight but in many cases are more important.

As my mind struggled to restructure a health maintenance schedule that included blind weight checks, I wondered why we should wait until age 12. Of course, it is unreasonable to expect parents to stick with a pediatric practice that seems to ignore their infant’s weight. I’m sure that, like me, you have always discouraged new parents from having a baby scale at home because in the first few months too-frequent weighings can usually cause more angst than good.

It might make sense to remove a within-earshot discussion of a child’s weight from the health maintenance visit as soon as the child can absorb and digest the discussion; say, around age 3 years. In a perfect world, the provider should have already elicited a history that suggested a young child’s vulnerability to obesity before the scale and the growth chart told the unfortunate story. But, neither you nor I are perfect providers and so we will always need the scale to document our concerns. However, when and how we report that one vital sign to the patient and his or her parents is a topic ripe for discussion and improvement.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].