Article

Migraine pathophysiology has been shown to be associated with vascular and inflammatory processes. Diet and lifestyle can have an effect on an individual's inflammatory process, and research regarding the steps between these factors and inflammation is vague and nonspecific. The Dietary Inflammation Score (DIS), which is calculated on the basis of a questionnaire, is used to score the inflammatory potential of an individual's diet. The Dietary and Lifestyle Inflammation Score (DLIS) includes the DIS questions, and also incorporates body mass index (BMI), physical activity, smoking, and alcohol consumption. A recent study, based on a secondary analysis of previous data, examined the correlation between migraine and DIS and DLIS among 285 women, 40% of whom had a chronic migraine diagnosis. Results published in Scientific Reports in July 2024 noted that participants with chronic migraine had a significantly higher DIS and DLIS than those who were not diagnosed with chronic migraine. It is important to note that migraine-associated inflammation can also result from genetic factors. A previous study, published in 2023 in Nature Genetics, described a correlation between genetic markers of inflammatory disorders, such as endometriosis, asthma, and migraine.¹ These results, consistent with our current understanding of the genetic contribution to migraine risk, emphasize that lifestyle modifications alone are not usually adequate for complete management of migraines.

Patients who experience chronic migraine may be inclined to reduce their time spent exercising and engaging in physical activity, as these activities can exacerbate migraine symptoms. Additionally, after recovering from a migraine, patients often need to catch up on tasks and responsibilities, which can squeeze out time for physical activity and exercise (often considered luxuries that can be done during leisure time). Results of a small cross-sectional retrospective study published in Scientific Reports in 2024 suggested a correlation between daily walking steps and response to calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb). According to the study, which included 22 patients who were diagnosed with migraine and treated with CGRP mAb, patients who experienced an improvement of their migraine symptoms also increased their average daily steps by almost 1000 steps per day. The authors suggested that steps can be used as a marker of treatment response in migraine.

Screen time is often blamed as a cause for a number of different ailments, including obesity, anxiety, depression, insomnia, and migraine. An article published in June 2024 in European Journal of Pain described results of a meta-analysis examining the association between sedentary lifestyle and migraine. The authors noted that time spent watching television could be causally associated with an increased risk for migraine.²Another study, with results published in July 2024 in The Journal of Headache and Pain, examined the relationship between migraine and leisure screen time. The researchers used data from 661,399 European individuals from 53 studies to look at genetically predicted leisure screen time, rather than actual leisure screen time. They reported that genetically predicted leisure screen time was associated with a 27.7% increase in migraine risk. While the results are consistent with what is already widely accepted about screen time and migraine, the inclusion of genetic predisposition to screen time is interesting in suggesting that some underlying drive could be contributing to increased screen time among patients who have migraine.

The results of these studies reemphasize the importance of the link between lifestyle factors and migraine but warn against oversimplifying the correlation. There is a bidirectional relationship between migraine and inflammation. We know that inflammation is mediated by diet as well as physical activity. During a migraine, patients may turn to foods that have a high inflammatory potential. Furthermore, migraine can influence a person's inclination to participate in physical activity, as the pain and discomfort can make it difficult engage in exercise. During a migraine, patients may prefer sedentary activities. Screen time can be appealing or relaxing while recovering from a migraine. Genetic predisposition is an interesting additional contributor to this link. Acknowledging genetic predisposition to inflammation or sedentary activity can be a step in helping patients recognize that it could be challenging to overcome these genetically inherent drives or conditions, while providing encouragement regarding the potential benefits of doing so.

Additional References

1. Rahmioglu N, Mortlock S, Ghiasi M, et al. The genetic basis of endometriosis and comorbidity with other pain and inflammatory conditions. Nat Genet. 2023;55(3):423-436. Doi: 10.1038/s41588-023-01323-z Source

2. Li P, Li J, Zhu H, et al. Causal effects of sedentary behaviours on the risk of migraine: A univariable and multivariable Mendelian randomization study. Eur J Pain. 2024 (Jun 4). Doi: 10.1002/ejp.2296  Source

Migraine pathophysiology has been shown to be associated with vascular and inflammatory processes. Diet and lifestyle can have an effect on an individual's inflammatory process, and research regarding the steps between these factors and inflammation is vague and nonspecific. The Dietary Inflammation Score (DIS), which is calculated on the basis of a questionnaire, is used to score the inflammatory potential of an individual's diet. The Dietary and Lifestyle Inflammation Score (DLIS) includes the DIS questions, and also incorporates body mass index (BMI), physical activity, smoking, and alcohol consumption. A recent study, based on a secondary analysis of previous data, examined the correlation between migraine and DIS and DLIS among 285 women, 40% of whom had a chronic migraine diagnosis. Results published in Scientific Reports in July 2024 noted that participants with chronic migraine had a significantly higher DIS and DLIS than those who were not diagnosed with chronic migraine. It is important to note that migraine-associated inflammation can also result from genetic factors. A previous study, published in 2023 in Nature Genetics, described a correlation between genetic markers of inflammatory disorders, such as endometriosis, asthma, and migraine.¹ These results, consistent with our current understanding of the genetic contribution to migraine risk, emphasize that lifestyle modifications alone are not usually adequate for complete management of migraines.

Patients who experience chronic migraine may be inclined to reduce their time spent exercising and engaging in physical activity, as these activities can exacerbate migraine symptoms. Additionally, after recovering from a migraine, patients often need to catch up on tasks and responsibilities, which can squeeze out time for physical activity and exercise (often considered luxuries that can be done during leisure time). Results of a small cross-sectional retrospective study published in Scientific Reports in 2024 suggested a correlation between daily walking steps and response to calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb). According to the study, which included 22 patients who were diagnosed with migraine and treated with CGRP mAb, patients who experienced an improvement of their migraine symptoms also increased their average daily steps by almost 1000 steps per day. The authors suggested that steps can be used as a marker of treatment response in migraine.

Screen time is often blamed as a cause for a number of different ailments, including obesity, anxiety, depression, insomnia, and migraine. An article published in June 2024 in European Journal of Pain described results of a meta-analysis examining the association between sedentary lifestyle and migraine. The authors noted that time spent watching television could be causally associated with an increased risk for migraine.²Another study, with results published in July 2024 in The Journal of Headache and Pain, examined the relationship between migraine and leisure screen time. The researchers used data from 661,399 European individuals from 53 studies to look at genetically predicted leisure screen time, rather than actual leisure screen time. They reported that genetically predicted leisure screen time was associated with a 27.7% increase in migraine risk. While the results are consistent with what is already widely accepted about screen time and migraine, the inclusion of genetic predisposition to screen time is interesting in suggesting that some underlying drive could be contributing to increased screen time among patients who have migraine.

The results of these studies reemphasize the importance of the link between lifestyle factors and migraine but warn against oversimplifying the correlation. There is a bidirectional relationship between migraine and inflammation. We know that inflammation is mediated by diet as well as physical activity. During a migraine, patients may turn to foods that have a high inflammatory potential. Furthermore, migraine can influence a person's inclination to participate in physical activity, as the pain and discomfort can make it difficult engage in exercise. During a migraine, patients may prefer sedentary activities. Screen time can be appealing or relaxing while recovering from a migraine. Genetic predisposition is an interesting additional contributor to this link. Acknowledging genetic predisposition to inflammation or sedentary activity can be a step in helping patients recognize that it could be challenging to overcome these genetically inherent drives or conditions, while providing encouragement regarding the potential benefits of doing so.

Additional References

1. Rahmioglu N, Mortlock S, Ghiasi M, et al. The genetic basis of endometriosis and comorbidity with other pain and inflammatory conditions. Nat Genet. 2023;55(3):423-436. Doi: 10.1038/s41588-023-01323-z Source

2. Li P, Li J, Zhu H, et al. Causal effects of sedentary behaviours on the risk of migraine: A univariable and multivariable Mendelian randomization study. Eur J Pain. 2024 (Jun 4). Doi: 10.1002/ejp.2296  Source

Migraine pathophysiology has been shown to be associated with vascular and inflammatory processes. Diet and lifestyle can have an effect on an individual's inflammatory process, and research regarding the steps between these factors and inflammation is vague and nonspecific. The Dietary Inflammation Score (DIS), which is calculated on the basis of a questionnaire, is used to score the inflammatory potential of an individual's diet. The Dietary and Lifestyle Inflammation Score (DLIS) includes the DIS questions, and also incorporates body mass index (BMI), physical activity, smoking, and alcohol consumption. A recent study, based on a secondary analysis of previous data, examined the correlation between migraine and DIS and DLIS among 285 women, 40% of whom had a chronic migraine diagnosis. Results published in Scientific Reports in July 2024 noted that participants with chronic migraine had a significantly higher DIS and DLIS than those who were not diagnosed with chronic migraine. It is important to note that migraine-associated inflammation can also result from genetic factors. A previous study, published in 2023 in Nature Genetics, described a correlation between genetic markers of inflammatory disorders, such as endometriosis, asthma, and migraine.¹ These results, consistent with our current understanding of the genetic contribution to migraine risk, emphasize that lifestyle modifications alone are not usually adequate for complete management of migraines.

Patients who experience chronic migraine may be inclined to reduce their time spent exercising and engaging in physical activity, as these activities can exacerbate migraine symptoms. Additionally, after recovering from a migraine, patients often need to catch up on tasks and responsibilities, which can squeeze out time for physical activity and exercise (often considered luxuries that can be done during leisure time). Results of a small cross-sectional retrospective study published in Scientific Reports in 2024 suggested a correlation between daily walking steps and response to calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb). According to the study, which included 22 patients who were diagnosed with migraine and treated with CGRP mAb, patients who experienced an improvement of their migraine symptoms also increased their average daily steps by almost 1000 steps per day. The authors suggested that steps can be used as a marker of treatment response in migraine.

Screen time is often blamed as a cause for a number of different ailments, including obesity, anxiety, depression, insomnia, and migraine. An article published in June 2024 in European Journal of Pain described results of a meta-analysis examining the association between sedentary lifestyle and migraine. The authors noted that time spent watching television could be causally associated with an increased risk for migraine.²Another study, with results published in July 2024 in The Journal of Headache and Pain, examined the relationship between migraine and leisure screen time. The researchers used data from 661,399 European individuals from 53 studies to look at genetically predicted leisure screen time, rather than actual leisure screen time. They reported that genetically predicted leisure screen time was associated with a 27.7% increase in migraine risk. While the results are consistent with what is already widely accepted about screen time and migraine, the inclusion of genetic predisposition to screen time is interesting in suggesting that some underlying drive could be contributing to increased screen time among patients who have migraine.

The results of these studies reemphasize the importance of the link between lifestyle factors and migraine but warn against oversimplifying the correlation. There is a bidirectional relationship between migraine and inflammation. We know that inflammation is mediated by diet as well as physical activity. During a migraine, patients may turn to foods that have a high inflammatory potential. Furthermore, migraine can influence a person's inclination to participate in physical activity, as the pain and discomfort can make it difficult engage in exercise. During a migraine, patients may prefer sedentary activities. Screen time can be appealing or relaxing while recovering from a migraine. Genetic predisposition is an interesting additional contributor to this link. Acknowledging genetic predisposition to inflammation or sedentary activity can be a step in helping patients recognize that it could be challenging to overcome these genetically inherent drives or conditions, while providing encouragement regarding the potential benefits of doing so.

Additional References

1. Rahmioglu N, Mortlock S, Ghiasi M, et al. The genetic basis of endometriosis and comorbidity with other pain and inflammatory conditions. Nat Genet. 2023;55(3):423-436. Doi: 10.1038/s41588-023-01323-z Source

2. Li P, Li J, Zhu H, et al. Causal effects of sedentary behaviours on the risk of migraine: A univariable and multivariable Mendelian randomization study. Eur J Pain. 2024 (Jun 4). Doi: 10.1002/ejp.2296  Source

The number of patients treated with anticoagulants has significantly increased over the past decade, largely owing to the introduction of direct oral anticoagulants (DOACs). Currently, more than 6 million people nationwide are taking anticoagulants; these include patients receiving care through the Veterans Health Administration.

However, the growing use of oral anticoagulants has been accompanied by a rise in anticoagulant-related bleeding incidents. Dr Geoffrey Barnes from the University of Michigan discusses strategies to assess and manage bleeding events, and he reviews the most current recommendations on the appropriate selection and use of anticoagulation reversal agents.

Dr Barnes also underscores the importance of monitoring for thromboembolic complications in patients treated for life-threatening bleeding to prevent post-bleed thromboembolic events.

--

Associate Professor, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, Michigan

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Pfizer; Bristol-Myers Squibb; Janssen; Bayer; AstraZeneca; Sanofi; Anthos; Abbott Vascular; Boston Scientific

Received research grant from: Boston Scientific

The number of patients treated with anticoagulants has significantly increased over the past decade, largely owing to the introduction of direct oral anticoagulants (DOACs). Currently, more than 6 million people nationwide are taking anticoagulants; these include patients receiving care through the Veterans Health Administration.

However, the growing use of oral anticoagulants has been accompanied by a rise in anticoagulant-related bleeding incidents. Dr Geoffrey Barnes from the University of Michigan discusses strategies to assess and manage bleeding events, and he reviews the most current recommendations on the appropriate selection and use of anticoagulation reversal agents.

Dr Barnes also underscores the importance of monitoring for thromboembolic complications in patients treated for life-threatening bleeding to prevent post-bleed thromboembolic events.

--

Associate Professor, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, Michigan

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Pfizer; Bristol-Myers Squibb; Janssen; Bayer; AstraZeneca; Sanofi; Anthos; Abbott Vascular; Boston Scientific

Received research grant from: Boston Scientific

The number of patients treated with anticoagulants has significantly increased over the past decade, largely owing to the introduction of direct oral anticoagulants (DOACs). Currently, more than 6 million people nationwide are taking anticoagulants; these include patients receiving care through the Veterans Health Administration.

However, the growing use of oral anticoagulants has been accompanied by a rise in anticoagulant-related bleeding incidents. Dr Geoffrey Barnes from the University of Michigan discusses strategies to assess and manage bleeding events, and he reviews the most current recommendations on the appropriate selection and use of anticoagulation reversal agents.

Dr Barnes also underscores the importance of monitoring for thromboembolic complications in patients treated for life-threatening bleeding to prevent post-bleed thromboembolic events.

--

Associate Professor, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, Michigan

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Pfizer; Bristol-Myers Squibb; Janssen; Bayer; AstraZeneca; Sanofi; Anthos; Abbott Vascular; Boston Scientific

Received research grant from: Boston Scientific

The Cutis Editorial Board is now accepting applications for the 2025 Resident Corner column. The Editorial Board will select 2 to 3 residents to serve as the Resident Corner columnists for 1 year. Articles are posted online only at www.mdedge.com/dermatology but will be referenced in Index Medicus. All applicants must be current residents and will be in residency throughout 2025.

For consideration, send your curriculum vitae along with a brief (not to exceed 500 words) statement of why you enjoy Cutis and what you can offer your fellow residents in contributing a monthly column.

A signed letter of recommendation from the Director of the dermatology residency program also should be supplied.

All materials should be submitted via email to Alicia Sonners ([email protected]) by November 1. The residents who are selected to write the column for the upcoming year will be notified by November 15.

We look forward to continuing to educate dermatology residents on topics that are most important to them!

The Cutis Editorial Board is now accepting applications for the 2025 Resident Corner column. The Editorial Board will select 2 to 3 residents to serve as the Resident Corner columnists for 1 year. Articles are posted online only at www.mdedge.com/dermatology but will be referenced in Index Medicus. All applicants must be current residents and will be in residency throughout 2025.

For consideration, send your curriculum vitae along with a brief (not to exceed 500 words) statement of why you enjoy Cutis and what you can offer your fellow residents in contributing a monthly column.

A signed letter of recommendation from the Director of the dermatology residency program also should be supplied.

All materials should be submitted via email to Alicia Sonners ([email protected]) by November 1. The residents who are selected to write the column for the upcoming year will be notified by November 15.

We look forward to continuing to educate dermatology residents on topics that are most important to them!

The Cutis Editorial Board is now accepting applications for the 2025 Resident Corner column. The Editorial Board will select 2 to 3 residents to serve as the Resident Corner columnists for 1 year. Articles are posted online only at www.mdedge.com/dermatology but will be referenced in Index Medicus. All applicants must be current residents and will be in residency throughout 2025.

For consideration, send your curriculum vitae along with a brief (not to exceed 500 words) statement of why you enjoy Cutis and what you can offer your fellow residents in contributing a monthly column.

A signed letter of recommendation from the Director of the dermatology residency program also should be supplied.

All materials should be submitted via email to Alicia Sonners ([email protected]) by November 1. The residents who are selected to write the column for the upcoming year will be notified by November 15.

We look forward to continuing to educate dermatology residents on topics that are most important to them!

To the Editor:
Crusted scabies (formerly known as Norwegian scabies) is a rare and highly contagious variant of scabies, in which the skin is infested with thousands to millions of Sarcoptes scabiei var hominis mites. We present a case of skin changes that were misdiagnosed as atopic dermatitis, seborrhea, xerosis, and drug eruption on initial presentation, which prompted treatment with a corticosteroid that inadvertently caused progression to crusted scabies.

A 79-year-old woman who uses a wheelchair presented to the clinic with skin changes that consisted of diffuse, severely pruritic, erythematous plaques on the head, neck, trunk, face, and extremities of 2 years’ duration. She had a medical history of hyperlipidemia, hypertension, and hyperglycemia, as well as a stroke that required hospitalization 2 years prior to the onset of the skin changes. She had no history of allergies.

Prior clinical diagnoses by primary care and dermatology included xerosis, atopic dermatitis, seborrhea, and drug eruption. She was treated with a mid-potency topical corticosteroid (triamcinolone acetonide cream 0.1%) twice daily and prednisone 40 mg once daily for 2- to 4-week courses over an 8-month period without reduction in symptoms.

Physical examination at the current presentation revealed golden, crusted, fine, powdery but slightly sticky flakes that spread diffusely across the entire body and came off in crumbles with a simple touch. These widespread crusts were easily visible on clothing. There was underlying diffuse erythema beneath the flaking skin on the trunk and proximal extremities. The scale and shedding skin laid in piles on the patient’s lap and resembled brown sugar (Figure 1). The patient also reported decreased hand function and dexterity due to the yellowbrown, thick, crusty plaques that had developed on both the palmar and dorsal sides of the hands (Figure 2). Erythematous plaques on the scalp, forehead, and inner ears resembled seborrhea (Figure 3). Pruritus severity was rated by the patient as 10 of 10, and she scratched her skin the entire time she was in the clinic. The patient was emotional and stated that she had not been able to sleep due to the discomfort. We suspected scabies, and the patient was reassured to learn that it could be confirmed with a simple skin scrape test.

The crusted lesions on the patient's hands were scraped with a #15-blade scalpel, and a routine potassium hydroxide mount was performed. The skin scrapings were placed on a slide with a drop of 10% potassium hydroxide and observed under low-power (×10) and high-power (×40) microscopy, which revealed thousands of mites and eggs (along with previously hatched eggs) (Figure 4) and quickly confirmed a diagnosis of crusted scabies.an extremely contagious form of scabies seen in older patients with compromised immune systems, malnutrition, or disabilities. The patient was prescribed oral ivermectin (3 mg dosed at 200 μg/kg of body weight) and topical permethrin 5%, neither of which she took, as she died of a COVID-19 infection complication 3 days after this diagnostic clinic visit.

Classic and crusted scabies are both caused by infestation of the Sarcoptes scabiei var hominis mite. Classic scabies is a result of an infestation of a small number of mites (commonly 5–15 mites), while crusted scabies is due to hyperinfestation by as many as millions of mites, the latter often requiring more aggressive treatment. The mites are first transmitted to humans by either skin-toskin contact or fomites on bedding and clothing. The scabies mite undergoes 4 life cycle stages: egg, larvae, nymph, and adult. Once female mites are transmitted, they burrow under the skin and lay 2 to 3 eggs per day. The eggs hatch within 3 to 4 days, after which the larvae migrate to the skin surface. The larval stage lasts for 3 to 4 days, during which the larvae burrow into the stratum corneum to create molting pouches, until they molt into slightly larger nymphs. Nymphs can be found in hair follicles or molting pouches until they further molt within 3 to 4 days into adults, which are round, saclike mites. The adult male and female mites then mate, leaving the female fertile for the rest of her 1- to 2-month lifespan. Impregnated female mites traverse the skin surface in search of a burrow site, using the pulvilli on the anterior aspect of 2 legs to hold onto the skin. Once burrowed, the female mite continues to lay eggs for the rest of her life, with approximately 10% of her eggs resulting in adult mites. Male mites feed in shallow pits of the skin until they find a female burrow site for mating.¹ This continuous life cycle of the scabies mite gives rise to highly transmissible, pruritic skin excoriations, as demonstrated in our patient.

The skin has a relatively late inflammatory and adaptive immune response to scabies, typically occurring 4 to 6 weeks after the initial infestation.² This delayed inflammatory response and onset of symptoms may be due to the scabies mite’s ability to alter aspects of the host’s immune response, which differs in classic vs crusted scabies. In classic scabies, there is a predominance of CD4+ T cells in the dermis and minimal CD8+ T cells. The opposite is true in crusted scabies— there is an overwhelming infiltration of CD8+ T cells and minimal CD4+ T cells.³ The CD8+ T-cell predominance in crusted scabies is hypothesized to be the cause of keratinocyte apoptosis, resulting in epidermal hyperproliferation. Keratinocyte apoptosis also secretes cytokines, which may lead to the immunologic targeting of healthy skin cells. The damage of healthy dermal cells contributes to the inability of the skin’s immune system to mount an effective response, allowing the parasite to grow uncontrollably in patients with crusted scabies.⁴

This ineffective immune response is further exacerbated by corticosteroids, which are commonly prescribed for pruritus experienced by patients with scabies infestations. The mechanism of action of corticosteroids is the production of anti-inflammatory, antimitotic, and immunosuppressive effects.⁵ Because the integumentary immune system is imbalanced during crusted scabies infestation, the immunosuppressive mechanism of oral and topical corticosteroids further reduces the cellular immune response to scabies. The flourishing of the scabies mites along with keratinocyte apoptosis⁴ results in the development of hyperkeratotic skin crusting, most frequently on the palms, soles, arms, and legs. Risk factors for crusted scabies include immunosuppression, hospitalization, crowded living conditions, and poor hygiene, though no known risk factors were documented in up to 42% (33/78) of patients with crusted scabies in one study.⁶

Patients with crusted scabies typically present with generalized, poorly defined, erythematous, fissured plaques covered by scaling and crusts. Plaques on bony prominences such as finger articulations and elbows may have a thick verrucous aspect.¹ Skin flaking that resembles brown sugar—a mixture of white sugar and molasses—is a clue to the diagnosis of crusted scabies. Brown sugar has a slightly sandy and sticky texture that ranges in color from very light brown to very dark brown. When present, flakes always appears slightly lighter than the patient’s skin tone. Although skin burrows are pathognomonic and clinically recognizable features of scabies, these burrows can be disguised by lesions, such as the hyperkeratotic plaques seen in our patient. The lesions may or may not be associated with pruritus, which may occur only at night, and bacterial superinfection has been reported in severe cases of crusted scabies,⁷ as scratching can cause sores, which may lead to infection. In severe cases, the constant scratching could lead to sepsis if the infection enters the bloodstream.⁸ Another symptom of scabies is a rash that causes small bumps that tend to form in a line, resembling small bites, hives, or pimples, and scaly plaques can lead to misdiagnosis as atopic dermatitis.

Treatment often is delayed due to misdiagnosis, as seen in our patient. Common misdiagnoses include atopic dermatitis, pityriasis rosea, systemic lupus erythematosus, bullous pemphigoid, lichen planus, pediculosis corporis, seborrheic scalp dermatitis, and adverse drug reactions.⁹ Patients with extensive infestations of crusted scabies should be treated with a 4-week course of permethrin cream 5% daily for 1 week, then twice per week until resolved, and oral ivermectin 200 μg/kg dosed 1 week apart for up to 4 weeks, if needed.¹ Topical permethrin works by producing a selective neurotoxic effect on invertebrates such as scabies mites, which disrupts the function of voltage-gated sodium channels, thereby paralyzing the adult mites to halt the spread of infestation. However, treatment with topical medications can be difficult due to the thick crusts that have formed, which make it more challenging for the skin to properly absorb the treatment. Additionally, surgical debridement as an adjunct procedure has been done to improve the effectiveness of topical medications by removing all the mites in skin.¹⁰ On the other hand, the mechanism in which ivermectin treats scabies infestations is poorly understood. Current research suggests that ivermectin works by causing persistent opening of pH-gated chloride channels in scabies mites.¹¹ There is emerging concern for drug resistance to these scabicides,¹² revealing a need for further research of treatment options.

Patients with crusted scabies can have an extremely large number of mites (up to 2 million), making them more infectious than patients with classic scabies.¹³ As a result, it is imperative to reduce environmental transmission and risk for reinfection with mites during treatment. Because crusted scabies is transmitted by prolonged skinto- skin contact or by contact with personal items of an infected person (eg, bedding, clothing), treatment guidelines require all clothing, bedding, and towels of a patient with scabies to be machine-washed and dried with hot water and hot dryer cycles. If an item cannot be washed, it should be stored in a sealed plastic bag for 1 week, as scabies mites cannot survive more than 2 to 3 days away from their host of human skin.¹³ Treatment of close contacts of patients with scabies is recommended, as well as for those in endemic areas or closed communities, such as nursing homes or jails.

To the Editor:
Crusted scabies (formerly known as Norwegian scabies) is a rare and highly contagious variant of scabies, in which the skin is infested with thousands to millions of Sarcoptes scabiei var hominis mites. We present a case of skin changes that were misdiagnosed as atopic dermatitis, seborrhea, xerosis, and drug eruption on initial presentation, which prompted treatment with a corticosteroid that inadvertently caused progression to crusted scabies.

A 79-year-old woman who uses a wheelchair presented to the clinic with skin changes that consisted of diffuse, severely pruritic, erythematous plaques on the head, neck, trunk, face, and extremities of 2 years’ duration. She had a medical history of hyperlipidemia, hypertension, and hyperglycemia, as well as a stroke that required hospitalization 2 years prior to the onset of the skin changes. She had no history of allergies.

Prior clinical diagnoses by primary care and dermatology included xerosis, atopic dermatitis, seborrhea, and drug eruption. She was treated with a mid-potency topical corticosteroid (triamcinolone acetonide cream 0.1%) twice daily and prednisone 40 mg once daily for 2- to 4-week courses over an 8-month period without reduction in symptoms.

Physical examination at the current presentation revealed golden, crusted, fine, powdery but slightly sticky flakes that spread diffusely across the entire body and came off in crumbles with a simple touch. These widespread crusts were easily visible on clothing. There was underlying diffuse erythema beneath the flaking skin on the trunk and proximal extremities. The scale and shedding skin laid in piles on the patient’s lap and resembled brown sugar (Figure 1). The patient also reported decreased hand function and dexterity due to the yellowbrown, thick, crusty plaques that had developed on both the palmar and dorsal sides of the hands (Figure 2). Erythematous plaques on the scalp, forehead, and inner ears resembled seborrhea (Figure 3). Pruritus severity was rated by the patient as 10 of 10, and she scratched her skin the entire time she was in the clinic. The patient was emotional and stated that she had not been able to sleep due to the discomfort. We suspected scabies, and the patient was reassured to learn that it could be confirmed with a simple skin scrape test.

The crusted lesions on the patient's hands were scraped with a #15-blade scalpel, and a routine potassium hydroxide mount was performed. The skin scrapings were placed on a slide with a drop of 10% potassium hydroxide and observed under low-power (×10) and high-power (×40) microscopy, which revealed thousands of mites and eggs (along with previously hatched eggs) (Figure 4) and quickly confirmed a diagnosis of crusted scabies.an extremely contagious form of scabies seen in older patients with compromised immune systems, malnutrition, or disabilities. The patient was prescribed oral ivermectin (3 mg dosed at 200 μg/kg of body weight) and topical permethrin 5%, neither of which she took, as she died of a COVID-19 infection complication 3 days after this diagnostic clinic visit.

Classic and crusted scabies are both caused by infestation of the Sarcoptes scabiei var hominis mite. Classic scabies is a result of an infestation of a small number of mites (commonly 5–15 mites), while crusted scabies is due to hyperinfestation by as many as millions of mites, the latter often requiring more aggressive treatment. The mites are first transmitted to humans by either skin-toskin contact or fomites on bedding and clothing. The scabies mite undergoes 4 life cycle stages: egg, larvae, nymph, and adult. Once female mites are transmitted, they burrow under the skin and lay 2 to 3 eggs per day. The eggs hatch within 3 to 4 days, after which the larvae migrate to the skin surface. The larval stage lasts for 3 to 4 days, during which the larvae burrow into the stratum corneum to create molting pouches, until they molt into slightly larger nymphs. Nymphs can be found in hair follicles or molting pouches until they further molt within 3 to 4 days into adults, which are round, saclike mites. The adult male and female mites then mate, leaving the female fertile for the rest of her 1- to 2-month lifespan. Impregnated female mites traverse the skin surface in search of a burrow site, using the pulvilli on the anterior aspect of 2 legs to hold onto the skin. Once burrowed, the female mite continues to lay eggs for the rest of her life, with approximately 10% of her eggs resulting in adult mites. Male mites feed in shallow pits of the skin until they find a female burrow site for mating.¹ This continuous life cycle of the scabies mite gives rise to highly transmissible, pruritic skin excoriations, as demonstrated in our patient.

The skin has a relatively late inflammatory and adaptive immune response to scabies, typically occurring 4 to 6 weeks after the initial infestation.² This delayed inflammatory response and onset of symptoms may be due to the scabies mite’s ability to alter aspects of the host’s immune response, which differs in classic vs crusted scabies. In classic scabies, there is a predominance of CD4+ T cells in the dermis and minimal CD8+ T cells. The opposite is true in crusted scabies— there is an overwhelming infiltration of CD8+ T cells and minimal CD4+ T cells.³ The CD8+ T-cell predominance in crusted scabies is hypothesized to be the cause of keratinocyte apoptosis, resulting in epidermal hyperproliferation. Keratinocyte apoptosis also secretes cytokines, which may lead to the immunologic targeting of healthy skin cells. The damage of healthy dermal cells contributes to the inability of the skin’s immune system to mount an effective response, allowing the parasite to grow uncontrollably in patients with crusted scabies.⁴

This ineffective immune response is further exacerbated by corticosteroids, which are commonly prescribed for pruritus experienced by patients with scabies infestations. The mechanism of action of corticosteroids is the production of anti-inflammatory, antimitotic, and immunosuppressive effects.⁵ Because the integumentary immune system is imbalanced during crusted scabies infestation, the immunosuppressive mechanism of oral and topical corticosteroids further reduces the cellular immune response to scabies. The flourishing of the scabies mites along with keratinocyte apoptosis⁴ results in the development of hyperkeratotic skin crusting, most frequently on the palms, soles, arms, and legs. Risk factors for crusted scabies include immunosuppression, hospitalization, crowded living conditions, and poor hygiene, though no known risk factors were documented in up to 42% (33/78) of patients with crusted scabies in one study.⁶

Patients with crusted scabies typically present with generalized, poorly defined, erythematous, fissured plaques covered by scaling and crusts. Plaques on bony prominences such as finger articulations and elbows may have a thick verrucous aspect.¹ Skin flaking that resembles brown sugar—a mixture of white sugar and molasses—is a clue to the diagnosis of crusted scabies. Brown sugar has a slightly sandy and sticky texture that ranges in color from very light brown to very dark brown. When present, flakes always appears slightly lighter than the patient’s skin tone. Although skin burrows are pathognomonic and clinically recognizable features of scabies, these burrows can be disguised by lesions, such as the hyperkeratotic plaques seen in our patient. The lesions may or may not be associated with pruritus, which may occur only at night, and bacterial superinfection has been reported in severe cases of crusted scabies,⁷ as scratching can cause sores, which may lead to infection. In severe cases, the constant scratching could lead to sepsis if the infection enters the bloodstream.⁸ Another symptom of scabies is a rash that causes small bumps that tend to form in a line, resembling small bites, hives, or pimples, and scaly plaques can lead to misdiagnosis as atopic dermatitis.

Treatment often is delayed due to misdiagnosis, as seen in our patient. Common misdiagnoses include atopic dermatitis, pityriasis rosea, systemic lupus erythematosus, bullous pemphigoid, lichen planus, pediculosis corporis, seborrheic scalp dermatitis, and adverse drug reactions.⁹ Patients with extensive infestations of crusted scabies should be treated with a 4-week course of permethrin cream 5% daily for 1 week, then twice per week until resolved, and oral ivermectin 200 μg/kg dosed 1 week apart for up to 4 weeks, if needed.¹ Topical permethrin works by producing a selective neurotoxic effect on invertebrates such as scabies mites, which disrupts the function of voltage-gated sodium channels, thereby paralyzing the adult mites to halt the spread of infestation. However, treatment with topical medications can be difficult due to the thick crusts that have formed, which make it more challenging for the skin to properly absorb the treatment. Additionally, surgical debridement as an adjunct procedure has been done to improve the effectiveness of topical medications by removing all the mites in skin.¹⁰ On the other hand, the mechanism in which ivermectin treats scabies infestations is poorly understood. Current research suggests that ivermectin works by causing persistent opening of pH-gated chloride channels in scabies mites.¹¹ There is emerging concern for drug resistance to these scabicides,¹² revealing a need for further research of treatment options.

Patients with crusted scabies can have an extremely large number of mites (up to 2 million), making them more infectious than patients with classic scabies.¹³ As a result, it is imperative to reduce environmental transmission and risk for reinfection with mites during treatment. Because crusted scabies is transmitted by prolonged skinto- skin contact or by contact with personal items of an infected person (eg, bedding, clothing), treatment guidelines require all clothing, bedding, and towels of a patient with scabies to be machine-washed and dried with hot water and hot dryer cycles. If an item cannot be washed, it should be stored in a sealed plastic bag for 1 week, as scabies mites cannot survive more than 2 to 3 days away from their host of human skin.¹³ Treatment of close contacts of patients with scabies is recommended, as well as for those in endemic areas or closed communities, such as nursing homes or jails.

To the Editor:
Crusted scabies (formerly known as Norwegian scabies) is a rare and highly contagious variant of scabies, in which the skin is infested with thousands to millions of Sarcoptes scabiei var hominis mites. We present a case of skin changes that were misdiagnosed as atopic dermatitis, seborrhea, xerosis, and drug eruption on initial presentation, which prompted treatment with a corticosteroid that inadvertently caused progression to crusted scabies.

A 79-year-old woman who uses a wheelchair presented to the clinic with skin changes that consisted of diffuse, severely pruritic, erythematous plaques on the head, neck, trunk, face, and extremities of 2 years’ duration. She had a medical history of hyperlipidemia, hypertension, and hyperglycemia, as well as a stroke that required hospitalization 2 years prior to the onset of the skin changes. She had no history of allergies.

Prior clinical diagnoses by primary care and dermatology included xerosis, atopic dermatitis, seborrhea, and drug eruption. She was treated with a mid-potency topical corticosteroid (triamcinolone acetonide cream 0.1%) twice daily and prednisone 40 mg once daily for 2- to 4-week courses over an 8-month period without reduction in symptoms.

Physical examination at the current presentation revealed golden, crusted, fine, powdery but slightly sticky flakes that spread diffusely across the entire body and came off in crumbles with a simple touch. These widespread crusts were easily visible on clothing. There was underlying diffuse erythema beneath the flaking skin on the trunk and proximal extremities. The scale and shedding skin laid in piles on the patient’s lap and resembled brown sugar (Figure 1). The patient also reported decreased hand function and dexterity due to the yellowbrown, thick, crusty plaques that had developed on both the palmar and dorsal sides of the hands (Figure 2). Erythematous plaques on the scalp, forehead, and inner ears resembled seborrhea (Figure 3). Pruritus severity was rated by the patient as 10 of 10, and she scratched her skin the entire time she was in the clinic. The patient was emotional and stated that she had not been able to sleep due to the discomfort. We suspected scabies, and the patient was reassured to learn that it could be confirmed with a simple skin scrape test.

The crusted lesions on the patient's hands were scraped with a #15-blade scalpel, and a routine potassium hydroxide mount was performed. The skin scrapings were placed on a slide with a drop of 10% potassium hydroxide and observed under low-power (×10) and high-power (×40) microscopy, which revealed thousands of mites and eggs (along with previously hatched eggs) (Figure 4) and quickly confirmed a diagnosis of crusted scabies.an extremely contagious form of scabies seen in older patients with compromised immune systems, malnutrition, or disabilities. The patient was prescribed oral ivermectin (3 mg dosed at 200 μg/kg of body weight) and topical permethrin 5%, neither of which she took, as she died of a COVID-19 infection complication 3 days after this diagnostic clinic visit.

Classic and crusted scabies are both caused by infestation of the Sarcoptes scabiei var hominis mite. Classic scabies is a result of an infestation of a small number of mites (commonly 5–15 mites), while crusted scabies is due to hyperinfestation by as many as millions of mites, the latter often requiring more aggressive treatment. The mites are first transmitted to humans by either skin-toskin contact or fomites on bedding and clothing. The scabies mite undergoes 4 life cycle stages: egg, larvae, nymph, and adult. Once female mites are transmitted, they burrow under the skin and lay 2 to 3 eggs per day. The eggs hatch within 3 to 4 days, after which the larvae migrate to the skin surface. The larval stage lasts for 3 to 4 days, during which the larvae burrow into the stratum corneum to create molting pouches, until they molt into slightly larger nymphs. Nymphs can be found in hair follicles or molting pouches until they further molt within 3 to 4 days into adults, which are round, saclike mites. The adult male and female mites then mate, leaving the female fertile for the rest of her 1- to 2-month lifespan. Impregnated female mites traverse the skin surface in search of a burrow site, using the pulvilli on the anterior aspect of 2 legs to hold onto the skin. Once burrowed, the female mite continues to lay eggs for the rest of her life, with approximately 10% of her eggs resulting in adult mites. Male mites feed in shallow pits of the skin until they find a female burrow site for mating.¹ This continuous life cycle of the scabies mite gives rise to highly transmissible, pruritic skin excoriations, as demonstrated in our patient.

The skin has a relatively late inflammatory and adaptive immune response to scabies, typically occurring 4 to 6 weeks after the initial infestation.² This delayed inflammatory response and onset of symptoms may be due to the scabies mite’s ability to alter aspects of the host’s immune response, which differs in classic vs crusted scabies. In classic scabies, there is a predominance of CD4+ T cells in the dermis and minimal CD8+ T cells. The opposite is true in crusted scabies— there is an overwhelming infiltration of CD8+ T cells and minimal CD4+ T cells.³ The CD8+ T-cell predominance in crusted scabies is hypothesized to be the cause of keratinocyte apoptosis, resulting in epidermal hyperproliferation. Keratinocyte apoptosis also secretes cytokines, which may lead to the immunologic targeting of healthy skin cells. The damage of healthy dermal cells contributes to the inability of the skin’s immune system to mount an effective response, allowing the parasite to grow uncontrollably in patients with crusted scabies.⁴

This ineffective immune response is further exacerbated by corticosteroids, which are commonly prescribed for pruritus experienced by patients with scabies infestations. The mechanism of action of corticosteroids is the production of anti-inflammatory, antimitotic, and immunosuppressive effects.⁵ Because the integumentary immune system is imbalanced during crusted scabies infestation, the immunosuppressive mechanism of oral and topical corticosteroids further reduces the cellular immune response to scabies. The flourishing of the scabies mites along with keratinocyte apoptosis⁴ results in the development of hyperkeratotic skin crusting, most frequently on the palms, soles, arms, and legs. Risk factors for crusted scabies include immunosuppression, hospitalization, crowded living conditions, and poor hygiene, though no known risk factors were documented in up to 42% (33/78) of patients with crusted scabies in one study.⁶

Patients with crusted scabies typically present with generalized, poorly defined, erythematous, fissured plaques covered by scaling and crusts. Plaques on bony prominences such as finger articulations and elbows may have a thick verrucous aspect.¹ Skin flaking that resembles brown sugar—a mixture of white sugar and molasses—is a clue to the diagnosis of crusted scabies. Brown sugar has a slightly sandy and sticky texture that ranges in color from very light brown to very dark brown. When present, flakes always appears slightly lighter than the patient’s skin tone. Although skin burrows are pathognomonic and clinically recognizable features of scabies, these burrows can be disguised by lesions, such as the hyperkeratotic plaques seen in our patient. The lesions may or may not be associated with pruritus, which may occur only at night, and bacterial superinfection has been reported in severe cases of crusted scabies,⁷ as scratching can cause sores, which may lead to infection. In severe cases, the constant scratching could lead to sepsis if the infection enters the bloodstream.⁸ Another symptom of scabies is a rash that causes small bumps that tend to form in a line, resembling small bites, hives, or pimples, and scaly plaques can lead to misdiagnosis as atopic dermatitis.

Treatment often is delayed due to misdiagnosis, as seen in our patient. Common misdiagnoses include atopic dermatitis, pityriasis rosea, systemic lupus erythematosus, bullous pemphigoid, lichen planus, pediculosis corporis, seborrheic scalp dermatitis, and adverse drug reactions.⁹ Patients with extensive infestations of crusted scabies should be treated with a 4-week course of permethrin cream 5% daily for 1 week, then twice per week until resolved, and oral ivermectin 200 μg/kg dosed 1 week apart for up to 4 weeks, if needed.¹ Topical permethrin works by producing a selective neurotoxic effect on invertebrates such as scabies mites, which disrupts the function of voltage-gated sodium channels, thereby paralyzing the adult mites to halt the spread of infestation. However, treatment with topical medications can be difficult due to the thick crusts that have formed, which make it more challenging for the skin to properly absorb the treatment. Additionally, surgical debridement as an adjunct procedure has been done to improve the effectiveness of topical medications by removing all the mites in skin.¹⁰ On the other hand, the mechanism in which ivermectin treats scabies infestations is poorly understood. Current research suggests that ivermectin works by causing persistent opening of pH-gated chloride channels in scabies mites.¹¹ There is emerging concern for drug resistance to these scabicides,¹² revealing a need for further research of treatment options.

Patients with crusted scabies can have an extremely large number of mites (up to 2 million), making them more infectious than patients with classic scabies.¹³ As a result, it is imperative to reduce environmental transmission and risk for reinfection with mites during treatment. Because crusted scabies is transmitted by prolonged skinto- skin contact or by contact with personal items of an infected person (eg, bedding, clothing), treatment guidelines require all clothing, bedding, and towels of a patient with scabies to be machine-washed and dried with hot water and hot dryer cycles. If an item cannot be washed, it should be stored in a sealed plastic bag for 1 week, as scabies mites cannot survive more than 2 to 3 days away from their host of human skin.¹³ Treatment of close contacts of patients with scabies is recommended, as well as for those in endemic areas or closed communities, such as nursing homes or jails.

Key clinical point: A Mendelian randomization analysis revealed that psoriatic arthritis (PsA) was a significant risk factor for ulcerative colitis (UC) and vice versa.

Major finding: UC was associated with a 45.8% increased risk for PsA (odds ratio [OR] 1.458; P = .0013); conversely, PsA was associated with a 32.9% increased risk for UC (OR 1.329; P < .001).

Study details: This Mendelian randomization study evaluated the causal association between PsA, UC, and psoriasis using 123 single nucleotide polymorphisms from genome-wide association studies as genetic instrumental variables.

Disclosures: This study did not receive any specific funding. The authors declared no conflicts of interest.

Source: Pan J, Lv Y, Wang L, et al. Mendelian randomization analysis of psoriasis and psoriatic arthritis associated with risks of ulcerative colitis. Skin Res Technol. 2024;30:e13795 (Jul 12). Doi: 10.3390/jcm13154567 Source

Key clinical point: A Mendelian randomization analysis revealed that psoriatic arthritis (PsA) was a significant risk factor for ulcerative colitis (UC) and vice versa.

Major finding: UC was associated with a 45.8% increased risk for PsA (odds ratio [OR] 1.458; P = .0013); conversely, PsA was associated with a 32.9% increased risk for UC (OR 1.329; P < .001).

Study details: This Mendelian randomization study evaluated the causal association between PsA, UC, and psoriasis using 123 single nucleotide polymorphisms from genome-wide association studies as genetic instrumental variables.

Disclosures: This study did not receive any specific funding. The authors declared no conflicts of interest.

Source: Pan J, Lv Y, Wang L, et al. Mendelian randomization analysis of psoriasis and psoriatic arthritis associated with risks of ulcerative colitis. Skin Res Technol. 2024;30:e13795 (Jul 12). Doi: 10.3390/jcm13154567 Source

Key clinical point: A Mendelian randomization analysis revealed that psoriatic arthritis (PsA) was a significant risk factor for ulcerative colitis (UC) and vice versa.

Major finding: UC was associated with a 45.8% increased risk for PsA (odds ratio [OR] 1.458; P = .0013); conversely, PsA was associated with a 32.9% increased risk for UC (OR 1.329; P < .001).

Study details: This Mendelian randomization study evaluated the causal association between PsA, UC, and psoriasis using 123 single nucleotide polymorphisms from genome-wide association studies as genetic instrumental variables.

Disclosures: This study did not receive any specific funding. The authors declared no conflicts of interest.

Source: Pan J, Lv Y, Wang L, et al. Mendelian randomization analysis of psoriasis and psoriatic arthritis associated with risks of ulcerative colitis. Skin Res Technol. 2024;30:e13795 (Jul 12). Doi: 10.3390/jcm13154567 Source

Key clinical point: Ultrasound detected active enthesitis and synovitis in a non-negligible proportion of patients with psoriatic arthritis (PsA) who achieved remission or low disease activity with biological or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARD).

Major finding: Despite achieving the Disease Activity Index for Psoriatic Arthritis (DAPSA) treatment target, 21.6% patients had at least one painful enthesis on clinical examination. Ultrasound showed evidence of active enthesitis in 19.6% and active synovitis in 15.7% patients.

Study details: This cross-sectional study included 51 patients with PsA who met the DAPSA treatment target after at least 6 months of therapy with b/tsDMARD and underwent bilateral ultrasound and clinical examination of entheses and joints.

Disclosures: This study did not receive any external funding. The authors declared no conflicts of interests.

Source: Agache M, Popescu CC, Enache L, et al. Additional value of ultrasound in patients with psoriatic arthritis within treatment target. J Clin Med. 2024;13(5):4567 (Aug 5). Doi: 10.3390/jcm13154567 Source

Key clinical point: Ultrasound detected active enthesitis and synovitis in a non-negligible proportion of patients with psoriatic arthritis (PsA) who achieved remission or low disease activity with biological or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARD).

Major finding: Despite achieving the Disease Activity Index for Psoriatic Arthritis (DAPSA) treatment target, 21.6% patients had at least one painful enthesis on clinical examination. Ultrasound showed evidence of active enthesitis in 19.6% and active synovitis in 15.7% patients.

Study details: This cross-sectional study included 51 patients with PsA who met the DAPSA treatment target after at least 6 months of therapy with b/tsDMARD and underwent bilateral ultrasound and clinical examination of entheses and joints.

Disclosures: This study did not receive any external funding. The authors declared no conflicts of interests.

Source: Agache M, Popescu CC, Enache L, et al. Additional value of ultrasound in patients with psoriatic arthritis within treatment target. J Clin Med. 2024;13(5):4567 (Aug 5). Doi: 10.3390/jcm13154567 Source

Key clinical point: Ultrasound detected active enthesitis and synovitis in a non-negligible proportion of patients with psoriatic arthritis (PsA) who achieved remission or low disease activity with biological or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARD).

Major finding: Despite achieving the Disease Activity Index for Psoriatic Arthritis (DAPSA) treatment target, 21.6% patients had at least one painful enthesis on clinical examination. Ultrasound showed evidence of active enthesitis in 19.6% and active synovitis in 15.7% patients.

Study details: This cross-sectional study included 51 patients with PsA who met the DAPSA treatment target after at least 6 months of therapy with b/tsDMARD and underwent bilateral ultrasound and clinical examination of entheses and joints.

Disclosures: This study did not receive any external funding. The authors declared no conflicts of interests.

Source: Agache M, Popescu CC, Enache L, et al. Additional value of ultrasound in patients with psoriatic arthritis within treatment target. J Clin Med. 2024;13(5):4567 (Aug 5). Doi: 10.3390/jcm13154567 Source

Key clinical point: Exercise and a Mediterranean diet improved disease activity outcomes pertaining to skin and joints in patients with psoriatic arthritis (PsA), indicating that combining lifestyle changes with conventional medical treatment can benefit patients with PsA.

Major finding: High vs low levels of exercise were associated with lower median values of Disease Activity in PsA Score (10.6 vs 28.5; P = .004), erythrocyte sedimentation rate (9 vs 16; P = .001), and fewer tender (1.5 vs 10; P = .003) and swollen (1.5 vs 9; P = .016) joints. Similarly, high vs low adherence to the Mediterranean diet was associated with a lower Psoriasis Area and Severity Index (0.9 vs 1.5; P = .001) and body surface area (1 vs 2; P = .009).

Study details: This cross-sectional study enrolled 355 patients with psoriatic disease (age > 18 years), including 279 patients with PsA and 76 patients with psoriasis.

Disclosures: No funding sources were declared for this study. The authors did not declare any conflicts of interest.

Source: Katsimbri P, Grivas A, Papadavid E, et al. Mediterranean diet and exercise are associated with better disease control in psoriatic arthritis. Clin Rheumatol. 2024 (Jul 25). Doi: 10.1007/s10067-024-07080-6 Source

Key clinical point: Exercise and a Mediterranean diet improved disease activity outcomes pertaining to skin and joints in patients with psoriatic arthritis (PsA), indicating that combining lifestyle changes with conventional medical treatment can benefit patients with PsA.

Major finding: High vs low levels of exercise were associated with lower median values of Disease Activity in PsA Score (10.6 vs 28.5; P = .004), erythrocyte sedimentation rate (9 vs 16; P = .001), and fewer tender (1.5 vs 10; P = .003) and swollen (1.5 vs 9; P = .016) joints. Similarly, high vs low adherence to the Mediterranean diet was associated with a lower Psoriasis Area and Severity Index (0.9 vs 1.5; P = .001) and body surface area (1 vs 2; P = .009).

Study details: This cross-sectional study enrolled 355 patients with psoriatic disease (age > 18 years), including 279 patients with PsA and 76 patients with psoriasis.

Disclosures: No funding sources were declared for this study. The authors did not declare any conflicts of interest.

Source: Katsimbri P, Grivas A, Papadavid E, et al. Mediterranean diet and exercise are associated with better disease control in psoriatic arthritis. Clin Rheumatol. 2024 (Jul 25). Doi: 10.1007/s10067-024-07080-6 Source

Key clinical point: Exercise and a Mediterranean diet improved disease activity outcomes pertaining to skin and joints in patients with psoriatic arthritis (PsA), indicating that combining lifestyle changes with conventional medical treatment can benefit patients with PsA.

Major finding: High vs low levels of exercise were associated with lower median values of Disease Activity in PsA Score (10.6 vs 28.5; P = .004), erythrocyte sedimentation rate (9 vs 16; P = .001), and fewer tender (1.5 vs 10; P = .003) and swollen (1.5 vs 9; P = .016) joints. Similarly, high vs low adherence to the Mediterranean diet was associated with a lower Psoriasis Area and Severity Index (0.9 vs 1.5; P = .001) and body surface area (1 vs 2; P = .009).

Study details: This cross-sectional study enrolled 355 patients with psoriatic disease (age > 18 years), including 279 patients with PsA and 76 patients with psoriasis.

Disclosures: No funding sources were declared for this study. The authors did not declare any conflicts of interest.

Source: Katsimbri P, Grivas A, Papadavid E, et al. Mediterranean diet and exercise are associated with better disease control in psoriatic arthritis. Clin Rheumatol. 2024 (Jul 25). Doi: 10.1007/s10067-024-07080-6 Source

Key clinical point: Patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), and certain other autoimmune diseases (AID) may have an increased risk of developing psoriatic arthritis (PsA).

Major finding: The risk factors for PsA included RA (inverse variance weighting odds ratio [OR_IVW] 1.11; P = .0205), SLE (OR_IVW 1.04; P = .0107), AS (OR_IVW 2.18; P = .000155), Crohn's disease (CD; OR_IVW 1.07; P = .01), Hashimoto's thyroiditis (HT; OR_IVW 1.23; P = .00143), and vitiligo (OR_IVW 1.27; P = .0000267). However, PsA did not increase the risk for these AID.

Study details: This bidirectional two-sample Mendelian randomization study used genome-wide association data for PsA (3186 cases and 240,862 control individuals and  an additional 5065 cases and 21,286 control individuals), psoriasis, and AID.

Disclosures: This study was supported by two research projects from China. The authors declared no conflicts of interest.

Source: Duan K, Wang J, Chen S, et al. Causal associations between both psoriasis and psoriatic arthritis and multiple autoimmune diseases: A bidirectional two-sample Mendelian randomization study. Front. Immunol. 2024;15:1422626 (Jul 24). Doi: 10.3389/fimmu.2024.1422626 Source

Key clinical point: Patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), and certain other autoimmune diseases (AID) may have an increased risk of developing psoriatic arthritis (PsA).

Major finding: The risk factors for PsA included RA (inverse variance weighting odds ratio [OR_IVW] 1.11; P = .0205), SLE (OR_IVW 1.04; P = .0107), AS (OR_IVW 2.18; P = .000155), Crohn's disease (CD; OR_IVW 1.07; P = .01), Hashimoto's thyroiditis (HT; OR_IVW 1.23; P = .00143), and vitiligo (OR_IVW 1.27; P = .0000267). However, PsA did not increase the risk for these AID.

Study details: This bidirectional two-sample Mendelian randomization study used genome-wide association data for PsA (3186 cases and 240,862 control individuals and  an additional 5065 cases and 21,286 control individuals), psoriasis, and AID.

Disclosures: This study was supported by two research projects from China. The authors declared no conflicts of interest.

Source: Duan K, Wang J, Chen S, et al. Causal associations between both psoriasis and psoriatic arthritis and multiple autoimmune diseases: A bidirectional two-sample Mendelian randomization study. Front. Immunol. 2024;15:1422626 (Jul 24). Doi: 10.3389/fimmu.2024.1422626 Source

Key clinical point: Patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), and certain other autoimmune diseases (AID) may have an increased risk of developing psoriatic arthritis (PsA).

Major finding: The risk factors for PsA included RA (inverse variance weighting odds ratio [OR_IVW] 1.11; P = .0205), SLE (OR_IVW 1.04; P = .0107), AS (OR_IVW 2.18; P = .000155), Crohn's disease (CD; OR_IVW 1.07; P = .01), Hashimoto's thyroiditis (HT; OR_IVW 1.23; P = .00143), and vitiligo (OR_IVW 1.27; P = .0000267). However, PsA did not increase the risk for these AID.

Study details: This bidirectional two-sample Mendelian randomization study used genome-wide association data for PsA (3186 cases and 240,862 control individuals and  an additional 5065 cases and 21,286 control individuals), psoriasis, and AID.

Disclosures: This study was supported by two research projects from China. The authors declared no conflicts of interest.

Source: Duan K, Wang J, Chen S, et al. Causal associations between both psoriasis and psoriatic arthritis and multiple autoimmune diseases: A bidirectional two-sample Mendelian randomization study. Front. Immunol. 2024;15:1422626 (Jul 24). Doi: 10.3389/fimmu.2024.1422626 Source

Key clinical point: The second proximal interphalangeal (PIP) joint of the right hand and the right knee joint were the most affected in patients with psoriatic arthritis (PsA), particularly in those with older age and an earlier onset of PsA.

Major finding: The second PIP joint of the right hand had the greatest prevalence of swelling (18.9%), and the right knee joint had the highest prevalence of tenderness (24.2%). Older age was a risk factor, whereas an earlier onset of PsA was a protective factor for both swelling of the second PIP joint of the right hand and tenderness of right knee joint (P < .05 for all).

Study details: This cross-sectional study included 264 patients with PsA.

Disclosures: This study was funded by the National Key Research and Development Program of China and the National Natural Science Foundation of China. The authors did not declare any conflicts of interest.

Source: Li J, Xiao J, Xie X, et al. Individual joints involvement pattern in psoriatic arthritis: A cross-sectional study in China. J Dermatol. 2024 (Jul 12). Doi: 10.1111/1346-8138.17369 Source

Key clinical point: The second proximal interphalangeal (PIP) joint of the right hand and the right knee joint were the most affected in patients with psoriatic arthritis (PsA), particularly in those with older age and an earlier onset of PsA.

Major finding: The second PIP joint of the right hand had the greatest prevalence of swelling (18.9%), and the right knee joint had the highest prevalence of tenderness (24.2%). Older age was a risk factor, whereas an earlier onset of PsA was a protective factor for both swelling of the second PIP joint of the right hand and tenderness of right knee joint (P < .05 for all).

Study details: This cross-sectional study included 264 patients with PsA.

Disclosures: This study was funded by the National Key Research and Development Program of China and the National Natural Science Foundation of China. The authors did not declare any conflicts of interest.

Source: Li J, Xiao J, Xie X, et al. Individual joints involvement pattern in psoriatic arthritis: A cross-sectional study in China. J Dermatol. 2024 (Jul 12). Doi: 10.1111/1346-8138.17369 Source

Key clinical point: The second proximal interphalangeal (PIP) joint of the right hand and the right knee joint were the most affected in patients with psoriatic arthritis (PsA), particularly in those with older age and an earlier onset of PsA.

Major finding: The second PIP joint of the right hand had the greatest prevalence of swelling (18.9%), and the right knee joint had the highest prevalence of tenderness (24.2%). Older age was a risk factor, whereas an earlier onset of PsA was a protective factor for both swelling of the second PIP joint of the right hand and tenderness of right knee joint (P < .05 for all).

Study details: This cross-sectional study included 264 patients with PsA.

Disclosures: This study was funded by the National Key Research and Development Program of China and the National Natural Science Foundation of China. The authors did not declare any conflicts of interest.

Source: Li J, Xiao J, Xie X, et al. Individual joints involvement pattern in psoriatic arthritis: A cross-sectional study in China. J Dermatol. 2024 (Jul 12). Doi: 10.1111/1346-8138.17369 Source

Key clinical point: A dose of 160 mg bimekizumab every 4 weeks demonstrated greater long-term efficacy than 45 or 90 mg ustekinumab every 12 weeks in patients with psoriatic arthritis (PsA) who were biologic-naïve or showed inadequate response to tumor necrosis factor inhibitors (TNFi-IR).

Major finding: At week 52, both biologic-naive (adjusted odds ratio [aOR] 3.33; P < .001) and TNFi-IR (aOR 9.85; P < .001) patients receiving bimekizumab vs 45 mg ustekinumab were more likely to achieve ≥70% improvement in the American College of Rheumatology response, with similar effect observed for bimekizumab vs 90 mg ustekinumab.

Study details: This was matching-adjusted indirect comparison of data from several phase 3 trials of bimekizumab (BE OPTIMAL, BE COMPLETE, and BE VITAL) and ustekinumab (PSUMMIT1 and PSUMMIT2). The trials involved patients with PsA who received bimekizumab (n = 698) or ustekinumab (45 mg: n = 265; 90 mg: n = 262).

Disclosures: This study was sponsored by UCB Pharma and supported by the NIHR Manchester Biomedical Research Centre, UK. Three authors declared being employees and shareholders of UCB Pharma. Several authors declared having ties with various sources, including UCB Pharma.

Source: Mease PJ, Warren RB, Nash P, et al. Comparative effectiveness of bimekizumab and ustekinumab in patients with psoriatic arthritis at 52 weeks assessed using a matching-adjusted indirect comparison. Rheumatol Ther. 2024 (Aug 9). Doi: 10.1007/s40744-024-00705-x Source

Key clinical point: A dose of 160 mg bimekizumab every 4 weeks demonstrated greater long-term efficacy than 45 or 90 mg ustekinumab every 12 weeks in patients with psoriatic arthritis (PsA) who were biologic-naïve or showed inadequate response to tumor necrosis factor inhibitors (TNFi-IR).

Major finding: At week 52, both biologic-naive (adjusted odds ratio [aOR] 3.33; P < .001) and TNFi-IR (aOR 9.85; P < .001) patients receiving bimekizumab vs 45 mg ustekinumab were more likely to achieve ≥70% improvement in the American College of Rheumatology response, with similar effect observed for bimekizumab vs 90 mg ustekinumab.

Study details: This was matching-adjusted indirect comparison of data from several phase 3 trials of bimekizumab (BE OPTIMAL, BE COMPLETE, and BE VITAL) and ustekinumab (PSUMMIT1 and PSUMMIT2). The trials involved patients with PsA who received bimekizumab (n = 698) or ustekinumab (45 mg: n = 265; 90 mg: n = 262).

Disclosures: This study was sponsored by UCB Pharma and supported by the NIHR Manchester Biomedical Research Centre, UK. Three authors declared being employees and shareholders of UCB Pharma. Several authors declared having ties with various sources, including UCB Pharma.

Source: Mease PJ, Warren RB, Nash P, et al. Comparative effectiveness of bimekizumab and ustekinumab in patients with psoriatic arthritis at 52 weeks assessed using a matching-adjusted indirect comparison. Rheumatol Ther. 2024 (Aug 9). Doi: 10.1007/s40744-024-00705-x Source

Key clinical point: A dose of 160 mg bimekizumab every 4 weeks demonstrated greater long-term efficacy than 45 or 90 mg ustekinumab every 12 weeks in patients with psoriatic arthritis (PsA) who were biologic-naïve or showed inadequate response to tumor necrosis factor inhibitors (TNFi-IR).

Major finding: At week 52, both biologic-naive (adjusted odds ratio [aOR] 3.33; P < .001) and TNFi-IR (aOR 9.85; P < .001) patients receiving bimekizumab vs 45 mg ustekinumab were more likely to achieve ≥70% improvement in the American College of Rheumatology response, with similar effect observed for bimekizumab vs 90 mg ustekinumab.

Study details: This was matching-adjusted indirect comparison of data from several phase 3 trials of bimekizumab (BE OPTIMAL, BE COMPLETE, and BE VITAL) and ustekinumab (PSUMMIT1 and PSUMMIT2). The trials involved patients with PsA who received bimekizumab (n = 698) or ustekinumab (45 mg: n = 265; 90 mg: n = 262).

Disclosures: This study was sponsored by UCB Pharma and supported by the NIHR Manchester Biomedical Research Centre, UK. Three authors declared being employees and shareholders of UCB Pharma. Several authors declared having ties with various sources, including UCB Pharma.

Source: Mease PJ, Warren RB, Nash P, et al. Comparative effectiveness of bimekizumab and ustekinumab in patients with psoriatic arthritis at 52 weeks assessed using a matching-adjusted indirect comparison. Rheumatol Ther. 2024 (Aug 9). Doi: 10.1007/s40744-024-00705-x Source