Article

Key clinical point: Dupilumab provides rapid improvement in atopic dermatitis (AD) signs and symptoms and is well tolerated in patients with moderate-to-severe AD in a real-world setting.

Major finding: At week 12, the percentages of patients who achieved ≥75% improvement in the Eczema Area and Severity Index, an Investigator’s Global Assessment score of 0/1 with a ≥2-point reduction from baseline, and a ≥4-point decrease in itch-numerical rating scale score were 59.4%, 33.0%, and 57.0%, respectively. Adverse event rates were lower than those reported in previous phase 3 trials.

Study details: Findings are from a 12-week analysis of the multicenter prospective real-life study PROLEAD including 828 dupilumab-naive adult patients with moderate-to-severe AD who received dupilumab.

Disclosures: This study was funded by Sanofi. Some authors reported ties with various organizations, including Sanofi. Three authors declared being employees of or holding stock or stock options in Sanofi.

Source: Augustin M et al. Dupilumab demonstrates rapid onset of action in improving signs, symptoms and quality of life in adults with atopic dermatitis. Dermatol Ther (Heidelb). 2023 (Feb 4). Doi: 10.1007/s13555-023-00894-3

Key clinical point: Dupilumab provides rapid improvement in atopic dermatitis (AD) signs and symptoms and is well tolerated in patients with moderate-to-severe AD in a real-world setting.

Major finding: At week 12, the percentages of patients who achieved ≥75% improvement in the Eczema Area and Severity Index, an Investigator’s Global Assessment score of 0/1 with a ≥2-point reduction from baseline, and a ≥4-point decrease in itch-numerical rating scale score were 59.4%, 33.0%, and 57.0%, respectively. Adverse event rates were lower than those reported in previous phase 3 trials.

Study details: Findings are from a 12-week analysis of the multicenter prospective real-life study PROLEAD including 828 dupilumab-naive adult patients with moderate-to-severe AD who received dupilumab.

Disclosures: This study was funded by Sanofi. Some authors reported ties with various organizations, including Sanofi. Three authors declared being employees of or holding stock or stock options in Sanofi.

Source: Augustin M et al. Dupilumab demonstrates rapid onset of action in improving signs, symptoms and quality of life in adults with atopic dermatitis. Dermatol Ther (Heidelb). 2023 (Feb 4). Doi: 10.1007/s13555-023-00894-3

Key clinical point: Dupilumab provides rapid improvement in atopic dermatitis (AD) signs and symptoms and is well tolerated in patients with moderate-to-severe AD in a real-world setting.

Major finding: At week 12, the percentages of patients who achieved ≥75% improvement in the Eczema Area and Severity Index, an Investigator’s Global Assessment score of 0/1 with a ≥2-point reduction from baseline, and a ≥4-point decrease in itch-numerical rating scale score were 59.4%, 33.0%, and 57.0%, respectively. Adverse event rates were lower than those reported in previous phase 3 trials.

Study details: Findings are from a 12-week analysis of the multicenter prospective real-life study PROLEAD including 828 dupilumab-naive adult patients with moderate-to-severe AD who received dupilumab.

Disclosures: This study was funded by Sanofi. Some authors reported ties with various organizations, including Sanofi. Three authors declared being employees of or holding stock or stock options in Sanofi.

Source: Augustin M et al. Dupilumab demonstrates rapid onset of action in improving signs, symptoms and quality of life in adults with atopic dermatitis. Dermatol Ther (Heidelb). 2023 (Feb 4). Doi: 10.1007/s13555-023-00894-3

Key clinical point: Tralokinumab was effective and safe in a real-world cohort of patients with moderate-to-severe atopic dermatitis (AD) who had failed prior systemic therapy.

Major finding: At last review (24 weeks of maximum follow-up), 59% of patients were still on tralokinumab therapy and showed a decrease in the median Numeric Rating Scale Peak Pruritus Score over the past 7 days (from 5 at baseline to 2) but without any change in the median Investigator Global Assessment score. Treatment-related adverse events were mostly mild in severity.

Study details: Findings are from an observational, prospective cohort study including 37 patients aged ≥15 years with moderate-to-severe AD who had failed prior therapy with immunosuppressants, biologics, or a Janus kinase inhibitor and received subcutaneous tralokinumab.

Disclosures: This study did not receive any funding. DJ Hijnen declared serving as an investigator for and receiving consulting fees from various sources.

Source: Schlösser AR et al. Tralokinumab for moderate-to-severe atopic dermatitis patients: First daily practice results. Clin Exp Dermatol. 2023 (Jan 26). Doi: 10.1093/ced/llad038

Key clinical point: Tralokinumab was effective and safe in a real-world cohort of patients with moderate-to-severe atopic dermatitis (AD) who had failed prior systemic therapy.

Major finding: At last review (24 weeks of maximum follow-up), 59% of patients were still on tralokinumab therapy and showed a decrease in the median Numeric Rating Scale Peak Pruritus Score over the past 7 days (from 5 at baseline to 2) but without any change in the median Investigator Global Assessment score. Treatment-related adverse events were mostly mild in severity.

Study details: Findings are from an observational, prospective cohort study including 37 patients aged ≥15 years with moderate-to-severe AD who had failed prior therapy with immunosuppressants, biologics, or a Janus kinase inhibitor and received subcutaneous tralokinumab.

Disclosures: This study did not receive any funding. DJ Hijnen declared serving as an investigator for and receiving consulting fees from various sources.

Source: Schlösser AR et al. Tralokinumab for moderate-to-severe atopic dermatitis patients: First daily practice results. Clin Exp Dermatol. 2023 (Jan 26). Doi: 10.1093/ced/llad038

Key clinical point: Tralokinumab was effective and safe in a real-world cohort of patients with moderate-to-severe atopic dermatitis (AD) who had failed prior systemic therapy.

Major finding: At last review (24 weeks of maximum follow-up), 59% of patients were still on tralokinumab therapy and showed a decrease in the median Numeric Rating Scale Peak Pruritus Score over the past 7 days (from 5 at baseline to 2) but without any change in the median Investigator Global Assessment score. Treatment-related adverse events were mostly mild in severity.

Study details: Findings are from an observational, prospective cohort study including 37 patients aged ≥15 years with moderate-to-severe AD who had failed prior therapy with immunosuppressants, biologics, or a Janus kinase inhibitor and received subcutaneous tralokinumab.

Disclosures: This study did not receive any funding. DJ Hijnen declared serving as an investigator for and receiving consulting fees from various sources.

Source: Schlösser AR et al. Tralokinumab for moderate-to-severe atopic dermatitis patients: First daily practice results. Clin Exp Dermatol. 2023 (Jan 26). Doi: 10.1093/ced/llad038

Key clinical point: Tralokinumab was effective and safe in a real-world cohort of patients with moderate-to-severe atopic dermatitis (AD) who had failed prior systemic therapy.

Major finding: At last review (24 weeks of maximum follow-up), 59% of patients were still on tralokinumab therapy and showed a decrease in the median Numeric Rating Scale Peak Pruritus Score over the past 7 days (from 5 at baseline to 2) but without any change in the median Investigator Global Assessment score. Treatment-related adverse events were mostly mild in severity.

Study details: Findings are from an observational, prospective cohort study including 37 patients aged ≥15 years with moderate-to-severe AD who had failed prior therapy with immunosuppressants, biologics, or a Janus kinase inhibitor and received subcutaneous tralokinumab.

Disclosures: This study did not receive any funding. DJ Hijnen declared serving as an investigator for and receiving consulting fees from various sources.

Source: Schlösser AR et al. Tralokinumab for moderate-to-severe atopic dermatitis patients: First daily practice results. Clin Exp Dermatol. 2023 (Jan 26). Doi: 10.1093/ced/llad038

Key clinical point: Tralokinumab was effective and safe in a real-world cohort of patients with moderate-to-severe atopic dermatitis (AD) who had failed prior systemic therapy.

Major finding: At last review (24 weeks of maximum follow-up), 59% of patients were still on tralokinumab therapy and showed a decrease in the median Numeric Rating Scale Peak Pruritus Score over the past 7 days (from 5 at baseline to 2) but without any change in the median Investigator Global Assessment score. Treatment-related adverse events were mostly mild in severity.

Study details: Findings are from an observational, prospective cohort study including 37 patients aged ≥15 years with moderate-to-severe AD who had failed prior therapy with immunosuppressants, biologics, or a Janus kinase inhibitor and received subcutaneous tralokinumab.

Disclosures: This study did not receive any funding. DJ Hijnen declared serving as an investigator for and receiving consulting fees from various sources.

Source: Schlösser AR et al. Tralokinumab for moderate-to-severe atopic dermatitis patients: First daily practice results. Clin Exp Dermatol. 2023 (Jan 26). Doi: 10.1093/ced/llad038

Key clinical point: Tralokinumab was effective and safe in a real-world cohort of patients with moderate-to-severe atopic dermatitis (AD) who had failed prior systemic therapy.

Major finding: At last review (24 weeks of maximum follow-up), 59% of patients were still on tralokinumab therapy and showed a decrease in the median Numeric Rating Scale Peak Pruritus Score over the past 7 days (from 5 at baseline to 2) but without any change in the median Investigator Global Assessment score. Treatment-related adverse events were mostly mild in severity.

Study details: Findings are from an observational, prospective cohort study including 37 patients aged ≥15 years with moderate-to-severe AD who had failed prior therapy with immunosuppressants, biologics, or a Janus kinase inhibitor and received subcutaneous tralokinumab.

Disclosures: This study did not receive any funding. DJ Hijnen declared serving as an investigator for and receiving consulting fees from various sources.

Source: Schlösser AR et al. Tralokinumab for moderate-to-severe atopic dermatitis patients: First daily practice results. Clin Exp Dermatol. 2023 (Jan 26). Doi: 10.1093/ced/llad038

Key clinical point: Children born by cesarean section or instrumental vaginal delivery are at a greater risk of developing atopic dermatitis (AD) compared with those born by uncomplicated vaginal delivery.

Major finding: Children aged <1 year born by instrumental vaginal delivery (adjusted hazard ratio [aHR] 1.10; 95% CI 1.07-1.13), emergency cesarean section (aHR 1.12; 95% CI 1.10-1.15), and elective caesarean section (aHR 1.13; 95% CI 1.10-1.16) were at a higher risk for AD compared with those born by uncomplicated vaginal delivery, with the risk being similar in children aged ≥1 year.

Study details: This prospective population-based study included 1,399,406 children aged ≤5 years with available information on the mode of delivery and mother's identity.

Disclosures: This study was supported by the Swedish Research Council, Swedish Heart-Lung Foundation, and Stiftelsen Frimurare Barnhuset i Stockholm. The authors declared no conflicts of interest.

Source: Mubanga M et al. Mode of delivery and offspring atopic dermatitis in a Swedish nationwide study. Pediatr Allergy Immunol. 2023;34(1):e13904 (Jan 11). Doi: 10.1111/pai.13904

Key clinical point: Children born by cesarean section or instrumental vaginal delivery are at a greater risk of developing atopic dermatitis (AD) compared with those born by uncomplicated vaginal delivery.

Major finding: Children aged <1 year born by instrumental vaginal delivery (adjusted hazard ratio [aHR] 1.10; 95% CI 1.07-1.13), emergency cesarean section (aHR 1.12; 95% CI 1.10-1.15), and elective caesarean section (aHR 1.13; 95% CI 1.10-1.16) were at a higher risk for AD compared with those born by uncomplicated vaginal delivery, with the risk being similar in children aged ≥1 year.

Study details: This prospective population-based study included 1,399,406 children aged ≤5 years with available information on the mode of delivery and mother's identity.

Disclosures: This study was supported by the Swedish Research Council, Swedish Heart-Lung Foundation, and Stiftelsen Frimurare Barnhuset i Stockholm. The authors declared no conflicts of interest.

Source: Mubanga M et al. Mode of delivery and offspring atopic dermatitis in a Swedish nationwide study. Pediatr Allergy Immunol. 2023;34(1):e13904 (Jan 11). Doi: 10.1111/pai.13904

Key clinical point: Children born by cesarean section or instrumental vaginal delivery are at a greater risk of developing atopic dermatitis (AD) compared with those born by uncomplicated vaginal delivery.

Major finding: Children aged <1 year born by instrumental vaginal delivery (adjusted hazard ratio [aHR] 1.10; 95% CI 1.07-1.13), emergency cesarean section (aHR 1.12; 95% CI 1.10-1.15), and elective caesarean section (aHR 1.13; 95% CI 1.10-1.16) were at a higher risk for AD compared with those born by uncomplicated vaginal delivery, with the risk being similar in children aged ≥1 year.

Study details: This prospective population-based study included 1,399,406 children aged ≤5 years with available information on the mode of delivery and mother's identity.

Disclosures: This study was supported by the Swedish Research Council, Swedish Heart-Lung Foundation, and Stiftelsen Frimurare Barnhuset i Stockholm. The authors declared no conflicts of interest.

Source: Mubanga M et al. Mode of delivery and offspring atopic dermatitis in a Swedish nationwide study. Pediatr Allergy Immunol. 2023;34(1):e13904 (Jan 11). Doi: 10.1111/pai.13904

Key clinical point: Dupilumab with or without concomitant topical corticosteroids (TCS) was safe and provided rapid and sustained improvements in atopic dermatitis (AD) signs and symptoms in patients with erythrodermic AD.

Major finding: At week 16, dupilumab without and with concomitant TCS vs placebo provided significant improvements in the percentage of AD-affected body surface area (P = .02 and P < .001, respectively), Eczema Area and Severity Index score (P = .002 and P < .001, respectively), and Peak Pruritus Numerical Rating Scale score (P < .001 and P = .002, respectively), with improvements observed from week 1. Most treatment-emergent adverse events were mild or moderate in severity.

Study details: This post hoc analysis of six multicenter randomized trials included 209 patients with erythrodermic AD who were randomly assigned to receive dupilumab or placebo (both with or without concomitant TCS).

Disclosures: This study was funded by Sanofi-Regeneron Pharmaceuticals Inc. Some authors reported ties with various organizations, including Sanofi/Regeneron. Four authors declared being employees of or holding stock or stock options in Sanofi/Regeneron.

Source: Paller AS et al. Efficacy and safety of dupilumab in patients with erythrodermic atopic dermatitis: A post hoc analysis of 6 randomized clinical trials. JAMA Dermatol. 2023 (Feb 1). Doi: 10.1001/jamadermatol.2022.6192

Key clinical point: Dupilumab with or without concomitant topical corticosteroids (TCS) was safe and provided rapid and sustained improvements in atopic dermatitis (AD) signs and symptoms in patients with erythrodermic AD.

Major finding: At week 16, dupilumab without and with concomitant TCS vs placebo provided significant improvements in the percentage of AD-affected body surface area (P = .02 and P < .001, respectively), Eczema Area and Severity Index score (P = .002 and P < .001, respectively), and Peak Pruritus Numerical Rating Scale score (P < .001 and P = .002, respectively), with improvements observed from week 1. Most treatment-emergent adverse events were mild or moderate in severity.

Study details: This post hoc analysis of six multicenter randomized trials included 209 patients with erythrodermic AD who were randomly assigned to receive dupilumab or placebo (both with or without concomitant TCS).

Disclosures: This study was funded by Sanofi-Regeneron Pharmaceuticals Inc. Some authors reported ties with various organizations, including Sanofi/Regeneron. Four authors declared being employees of or holding stock or stock options in Sanofi/Regeneron.

Source: Paller AS et al. Efficacy and safety of dupilumab in patients with erythrodermic atopic dermatitis: A post hoc analysis of 6 randomized clinical trials. JAMA Dermatol. 2023 (Feb 1). Doi: 10.1001/jamadermatol.2022.6192

Key clinical point: Dupilumab with or without concomitant topical corticosteroids (TCS) was safe and provided rapid and sustained improvements in atopic dermatitis (AD) signs and symptoms in patients with erythrodermic AD.

Major finding: At week 16, dupilumab without and with concomitant TCS vs placebo provided significant improvements in the percentage of AD-affected body surface area (P = .02 and P < .001, respectively), Eczema Area and Severity Index score (P = .002 and P < .001, respectively), and Peak Pruritus Numerical Rating Scale score (P < .001 and P = .002, respectively), with improvements observed from week 1. Most treatment-emergent adverse events were mild or moderate in severity.

Study details: This post hoc analysis of six multicenter randomized trials included 209 patients with erythrodermic AD who were randomly assigned to receive dupilumab or placebo (both with or without concomitant TCS).

Disclosures: This study was funded by Sanofi-Regeneron Pharmaceuticals Inc. Some authors reported ties with various organizations, including Sanofi/Regeneron. Four authors declared being employees of or holding stock or stock options in Sanofi/Regeneron.

Source: Paller AS et al. Efficacy and safety of dupilumab in patients with erythrodermic atopic dermatitis: A post hoc analysis of 6 randomized clinical trials. JAMA Dermatol. 2023 (Feb 1). Doi: 10.1001/jamadermatol.2022.6192

To the Editor:

One of the more common tick-borne infections seen in travelers returning from sub-Saharan Africa is caused by Rickettsia africae, which is the etiologic agent of African tick-bite fever (ATBF), the most common tick-borne bacterial zoonosis.¹ There are 2 known tick vectors of disease: Amblyomma variegatum, found in sub-Saharan Africa and the West Indies, and Amblyomma hebraeum, found specifically in southern Africa.^2,3

Unlike other disease-carrying ticks that passively wait on vegetation to be picked up by a host, A hebraeum uniquely attract other nearby ticks to the host. Studies have shown that male ticks feeding on a nonhuman host (usually cattle) can emit an aggression-attachment pheromone that attracts other ticks to the host. The presence of the pheromone allows unfed ticks to actively discriminate between hosts on which these parasites have fed successfully (ie, suitable hosts) and those on which they have not.⁴

The aggressive hunting nature of A hebraeum explains the clinical presentation of multiple eschars and why large groups of exposed travelers—such as soldiers, leisure safari tourists, game hunters, and foreign-aid workers—are affected.²

Another southern African spotted fever group, Rickettsia conorii is the causative agent of Mediterranean spotted fever (MSF). Ticks carrying R conorii exhibit a much less aggressive hunting stylethan A hebraeum; consequently, infected patients present with a single eschar site.⁵

Rickettsia africae is estimated to have very high prevalence (95.2%) in Amblyomma ticks and a fairly high prevalence (approximately 4.0% to 8.6%) in travelers coming from rural southern Africa,^6,7 with an incubation period of 5 to 10 days after inoculation by an infected tick.⁸ Signs include fever, a generalized maculopapular or papulovesicular rash, and regional lymphadenopathy; symptoms include fatigue, headache, and myalgia.

The inoculation eschar—single or multiple—commonly presents on the legs and is accompanied by tender lymphadenopathy of draining nodes^1,8 More severe findings, such as myocarditis and subacute neuropathy, have been reported in elderly patients.⁹

A 77-year-old man presented with a pruritic maculopapular and papulovesicular rash distributed over the upper and lower extremities of 3 weeks’ duration. The patient reported having been on a 12-day mission trip to Limpopo, South Africa, where he was constructing and installing safe toilets to replace dangerous toilet pits. He believed he had been bitten by 2 ticks, after which he noted a dark purple and black patch on the left lower leg by the third day of the trip. He developed a sudden persistent pruritic rash, first on the lower extremities and then spreading to the upper extremities. The patient was seen by an American physician in South Africa who gave him a 7-day course of oral doxycycline monohydrate 100 mg twice daily. He then returned to the United States.

Sixteen days after being bitten by the ticks, the patient was examined in our dermatology office. Physical examination revealed an erythematous plaque with a central eschar over the medial aspect of the left leg (Figure 1) and multiple 3- to 6-mm, erythematous, dome-shaped papules scattered over the dorsal aspects of the feet and ankles (Figure 2). The examination was otherwise normal. Blood was drawn the same day for laboratory analysis; no abnormalities of platelets, red blood cells, or white blood cells were found. Results of a chemistry panel and liver enzyme tests were within reference range.

Skin biopsies were taken to elucidate the underlying pathology. Although an arthropod assault was suspected, there also was concern for deep vessel vasculitis because of the presence of considerable petechiae and purpura (Figure 3). Histologically, leukocytoclasia was seen in deep dermal blood vessels. A mild eosinophilic spongiosis with a mixed dermal infiltrate was identified—strengthening our suspicion of an arthropod assault. Bacterial cultures for aerobes and anaerobes using material taken from the right shin showed no growth.

Ten days after the initial biopsies, serum specimens were drawn and swabs of eschar were collected and sent to the Centers for Disease Control and Prevention for further testing. Serum was tested by immunofluorescence assay (IFA) for spotted fever group IgG to detect Rocky Mountain spotted fever and ATBF antibodies; both tests were negative. Swab material from eschar was tested again by IFA for spotted fever group IgG (Rocky Mountain spotted fever) and antibodies to ATBF and with bacterial culture isolation and nucleic acid amplification; the culture and amplification came back positive for R africae.

Because the specialized tests confirmed infection with R africae, the patient was given triamcinolone cream 0.1% to apply twice daily to the pruritic lesions for as long as 4 weeks; an additional 14-day course of oral doxycycline monohydrate (100 mg twice daily) was given. At follow-up, the lesions had fully resolved without evident scarring.

Various diagnostic techniques can detect R africae. Bacterial culture and the polymerase chain reaction are specific and therefore diagnostic. In addition, the diagnosis of rickettsiosis can be made with serology testing, in which disease-specific antibodies are detected by indirect IFA using disease-specific antigens.

Antigens from R rickettsii (the agent of Rocky Mountain spotted fever), R conorii (Mediterranean spotted fever), and R africae (ATBF) are commercially available for making the diagnosis of rickettsiosis. However, antigens from R conorii exhibit cross-reactivity with R africae, which can confound the diagnosis.^1,10 Serologic IFA tests have been shown to be less sensitive, especially when performed after antibacterial treatment has started.

In a study, 17 of 65 (26%) ATBF-confirmed patients were seronegative (acute and convalescent-phase sera) against R africae; 14 had received doxycycline during the first week of clinical signs. The current hypothesis is that R africae is highly sensitive to doxycycline and that early exposure to the drug prevented development of detectable titers of reactive antibodies, thus producing a negative serology test.¹¹

Furthermore, it has been shown that seroconversion of IgG and IgM antibodies in R africae–infected sera is delayed compared to what is observed with R conorii–infected sera. Typically, seroconversion of R conorii–infected sera can be detected within 2 weeks; seroconversion in R africae–infected sera can take 4 weeks or longer.¹¹

Our patient had a confirmed case of ATBF secondary to R africae infection, which was evident from tissue culture isolation and polymerase chain reaction analysis of swab material obtained from eschar sites, both of which yielded a positive result for R africae. The traveler’s negative serologic status might be due to his early exposure to doxycycline or to the 4-week delay in R africae seroconversion; his serum was collected only 3 weeks after the tick bites.

Clinical signs also aid in making the diagnosis of ATBF and distinguishing R conorii from R africae infection. Because of the aggressive hunting nature of the tick carrying R africae, they are associated with multiple eschars and tend to affect groups of multiple people, especially in rural areas.^4,5 In contrast, ticks carrying R conorii yield a single eschar due to their passive style of infecting a host and because they favor a single host within urban areas.⁵ Both infections exhibit a maculopapular or papulovesicular rash and are accompanied by fatigue, headache, and myalgia, though ATBF tends to present with a milder rash than MSF.

Infection with either R conorii or R africae responds to tetracyclines, quinolones, and macrolides.^10,12

African tick-bite fever is becoming more common, which should encourage clinicians to become familiar with the disease. Less than 2 decades ago, ATBF virtually was unknown outside of Zimbabwe, Botswana, Tanzania, Zambia, and Kenya, where it is endemic. However, after the abolition of apartheid in the 1990s, international tourism in southern Africa increased 6-fold.¹³ African tick-bite fever is now one of the most common rickettsial infections in Africa.⁷ In addition to diagnosing ATBF and managing infected patients, clinicians can help prevent ATBF in individuals who travel to endemic areas by recommending commercial topical insect repellents containing at least 19.5% N,N-diethyl-meta-toluamide (DEET).¹⁴

To the Editor:

One of the more common tick-borne infections seen in travelers returning from sub-Saharan Africa is caused by Rickettsia africae, which is the etiologic agent of African tick-bite fever (ATBF), the most common tick-borne bacterial zoonosis.¹ There are 2 known tick vectors of disease: Amblyomma variegatum, found in sub-Saharan Africa and the West Indies, and Amblyomma hebraeum, found specifically in southern Africa.^2,3

Unlike other disease-carrying ticks that passively wait on vegetation to be picked up by a host, A hebraeum uniquely attract other nearby ticks to the host. Studies have shown that male ticks feeding on a nonhuman host (usually cattle) can emit an aggression-attachment pheromone that attracts other ticks to the host. The presence of the pheromone allows unfed ticks to actively discriminate between hosts on which these parasites have fed successfully (ie, suitable hosts) and those on which they have not.⁴

The aggressive hunting nature of A hebraeum explains the clinical presentation of multiple eschars and why large groups of exposed travelers—such as soldiers, leisure safari tourists, game hunters, and foreign-aid workers—are affected.²

Another southern African spotted fever group, Rickettsia conorii is the causative agent of Mediterranean spotted fever (MSF). Ticks carrying R conorii exhibit a much less aggressive hunting stylethan A hebraeum; consequently, infected patients present with a single eschar site.⁵

Rickettsia africae is estimated to have very high prevalence (95.2%) in Amblyomma ticks and a fairly high prevalence (approximately 4.0% to 8.6%) in travelers coming from rural southern Africa,^6,7 with an incubation period of 5 to 10 days after inoculation by an infected tick.⁸ Signs include fever, a generalized maculopapular or papulovesicular rash, and regional lymphadenopathy; symptoms include fatigue, headache, and myalgia.

The inoculation eschar—single or multiple—commonly presents on the legs and is accompanied by tender lymphadenopathy of draining nodes^1,8 More severe findings, such as myocarditis and subacute neuropathy, have been reported in elderly patients.⁹

A 77-year-old man presented with a pruritic maculopapular and papulovesicular rash distributed over the upper and lower extremities of 3 weeks’ duration. The patient reported having been on a 12-day mission trip to Limpopo, South Africa, where he was constructing and installing safe toilets to replace dangerous toilet pits. He believed he had been bitten by 2 ticks, after which he noted a dark purple and black patch on the left lower leg by the third day of the trip. He developed a sudden persistent pruritic rash, first on the lower extremities and then spreading to the upper extremities. The patient was seen by an American physician in South Africa who gave him a 7-day course of oral doxycycline monohydrate 100 mg twice daily. He then returned to the United States.

Sixteen days after being bitten by the ticks, the patient was examined in our dermatology office. Physical examination revealed an erythematous plaque with a central eschar over the medial aspect of the left leg (Figure 1) and multiple 3- to 6-mm, erythematous, dome-shaped papules scattered over the dorsal aspects of the feet and ankles (Figure 2). The examination was otherwise normal. Blood was drawn the same day for laboratory analysis; no abnormalities of platelets, red blood cells, or white blood cells were found. Results of a chemistry panel and liver enzyme tests were within reference range.

Skin biopsies were taken to elucidate the underlying pathology. Although an arthropod assault was suspected, there also was concern for deep vessel vasculitis because of the presence of considerable petechiae and purpura (Figure 3). Histologically, leukocytoclasia was seen in deep dermal blood vessels. A mild eosinophilic spongiosis with a mixed dermal infiltrate was identified—strengthening our suspicion of an arthropod assault. Bacterial cultures for aerobes and anaerobes using material taken from the right shin showed no growth.

Ten days after the initial biopsies, serum specimens were drawn and swabs of eschar were collected and sent to the Centers for Disease Control and Prevention for further testing. Serum was tested by immunofluorescence assay (IFA) for spotted fever group IgG to detect Rocky Mountain spotted fever and ATBF antibodies; both tests were negative. Swab material from eschar was tested again by IFA for spotted fever group IgG (Rocky Mountain spotted fever) and antibodies to ATBF and with bacterial culture isolation and nucleic acid amplification; the culture and amplification came back positive for R africae.

Because the specialized tests confirmed infection with R africae, the patient was given triamcinolone cream 0.1% to apply twice daily to the pruritic lesions for as long as 4 weeks; an additional 14-day course of oral doxycycline monohydrate (100 mg twice daily) was given. At follow-up, the lesions had fully resolved without evident scarring.

Various diagnostic techniques can detect R africae. Bacterial culture and the polymerase chain reaction are specific and therefore diagnostic. In addition, the diagnosis of rickettsiosis can be made with serology testing, in which disease-specific antibodies are detected by indirect IFA using disease-specific antigens.

Antigens from R rickettsii (the agent of Rocky Mountain spotted fever), R conorii (Mediterranean spotted fever), and R africae (ATBF) are commercially available for making the diagnosis of rickettsiosis. However, antigens from R conorii exhibit cross-reactivity with R africae, which can confound the diagnosis.^1,10 Serologic IFA tests have been shown to be less sensitive, especially when performed after antibacterial treatment has started.

In a study, 17 of 65 (26%) ATBF-confirmed patients were seronegative (acute and convalescent-phase sera) against R africae; 14 had received doxycycline during the first week of clinical signs. The current hypothesis is that R africae is highly sensitive to doxycycline and that early exposure to the drug prevented development of detectable titers of reactive antibodies, thus producing a negative serology test.¹¹

Furthermore, it has been shown that seroconversion of IgG and IgM antibodies in R africae–infected sera is delayed compared to what is observed with R conorii–infected sera. Typically, seroconversion of R conorii–infected sera can be detected within 2 weeks; seroconversion in R africae–infected sera can take 4 weeks or longer.¹¹

Our patient had a confirmed case of ATBF secondary to R africae infection, which was evident from tissue culture isolation and polymerase chain reaction analysis of swab material obtained from eschar sites, both of which yielded a positive result for R africae. The traveler’s negative serologic status might be due to his early exposure to doxycycline or to the 4-week delay in R africae seroconversion; his serum was collected only 3 weeks after the tick bites.

Clinical signs also aid in making the diagnosis of ATBF and distinguishing R conorii from R africae infection. Because of the aggressive hunting nature of the tick carrying R africae, they are associated with multiple eschars and tend to affect groups of multiple people, especially in rural areas.^4,5 In contrast, ticks carrying R conorii yield a single eschar due to their passive style of infecting a host and because they favor a single host within urban areas.⁵ Both infections exhibit a maculopapular or papulovesicular rash and are accompanied by fatigue, headache, and myalgia, though ATBF tends to present with a milder rash than MSF.

Infection with either R conorii or R africae responds to tetracyclines, quinolones, and macrolides.^10,12

African tick-bite fever is becoming more common, which should encourage clinicians to become familiar with the disease. Less than 2 decades ago, ATBF virtually was unknown outside of Zimbabwe, Botswana, Tanzania, Zambia, and Kenya, where it is endemic. However, after the abolition of apartheid in the 1990s, international tourism in southern Africa increased 6-fold.¹³ African tick-bite fever is now one of the most common rickettsial infections in Africa.⁷ In addition to diagnosing ATBF and managing infected patients, clinicians can help prevent ATBF in individuals who travel to endemic areas by recommending commercial topical insect repellents containing at least 19.5% N,N-diethyl-meta-toluamide (DEET).¹⁴

To the Editor:

One of the more common tick-borne infections seen in travelers returning from sub-Saharan Africa is caused by Rickettsia africae, which is the etiologic agent of African tick-bite fever (ATBF), the most common tick-borne bacterial zoonosis.¹ There are 2 known tick vectors of disease: Amblyomma variegatum, found in sub-Saharan Africa and the West Indies, and Amblyomma hebraeum, found specifically in southern Africa.^2,3

Unlike other disease-carrying ticks that passively wait on vegetation to be picked up by a host, A hebraeum uniquely attract other nearby ticks to the host. Studies have shown that male ticks feeding on a nonhuman host (usually cattle) can emit an aggression-attachment pheromone that attracts other ticks to the host. The presence of the pheromone allows unfed ticks to actively discriminate between hosts on which these parasites have fed successfully (ie, suitable hosts) and those on which they have not.⁴

The aggressive hunting nature of A hebraeum explains the clinical presentation of multiple eschars and why large groups of exposed travelers—such as soldiers, leisure safari tourists, game hunters, and foreign-aid workers—are affected.²

Another southern African spotted fever group, Rickettsia conorii is the causative agent of Mediterranean spotted fever (MSF). Ticks carrying R conorii exhibit a much less aggressive hunting stylethan A hebraeum; consequently, infected patients present with a single eschar site.⁵

Rickettsia africae is estimated to have very high prevalence (95.2%) in Amblyomma ticks and a fairly high prevalence (approximately 4.0% to 8.6%) in travelers coming from rural southern Africa,^6,7 with an incubation period of 5 to 10 days after inoculation by an infected tick.⁸ Signs include fever, a generalized maculopapular or papulovesicular rash, and regional lymphadenopathy; symptoms include fatigue, headache, and myalgia.

The inoculation eschar—single or multiple—commonly presents on the legs and is accompanied by tender lymphadenopathy of draining nodes^1,8 More severe findings, such as myocarditis and subacute neuropathy, have been reported in elderly patients.⁹

A 77-year-old man presented with a pruritic maculopapular and papulovesicular rash distributed over the upper and lower extremities of 3 weeks’ duration. The patient reported having been on a 12-day mission trip to Limpopo, South Africa, where he was constructing and installing safe toilets to replace dangerous toilet pits. He believed he had been bitten by 2 ticks, after which he noted a dark purple and black patch on the left lower leg by the third day of the trip. He developed a sudden persistent pruritic rash, first on the lower extremities and then spreading to the upper extremities. The patient was seen by an American physician in South Africa who gave him a 7-day course of oral doxycycline monohydrate 100 mg twice daily. He then returned to the United States.

Sixteen days after being bitten by the ticks, the patient was examined in our dermatology office. Physical examination revealed an erythematous plaque with a central eschar over the medial aspect of the left leg (Figure 1) and multiple 3- to 6-mm, erythematous, dome-shaped papules scattered over the dorsal aspects of the feet and ankles (Figure 2). The examination was otherwise normal. Blood was drawn the same day for laboratory analysis; no abnormalities of platelets, red blood cells, or white blood cells were found. Results of a chemistry panel and liver enzyme tests were within reference range.

Skin biopsies were taken to elucidate the underlying pathology. Although an arthropod assault was suspected, there also was concern for deep vessel vasculitis because of the presence of considerable petechiae and purpura (Figure 3). Histologically, leukocytoclasia was seen in deep dermal blood vessels. A mild eosinophilic spongiosis with a mixed dermal infiltrate was identified—strengthening our suspicion of an arthropod assault. Bacterial cultures for aerobes and anaerobes using material taken from the right shin showed no growth.

Ten days after the initial biopsies, serum specimens were drawn and swabs of eschar were collected and sent to the Centers for Disease Control and Prevention for further testing. Serum was tested by immunofluorescence assay (IFA) for spotted fever group IgG to detect Rocky Mountain spotted fever and ATBF antibodies; both tests were negative. Swab material from eschar was tested again by IFA for spotted fever group IgG (Rocky Mountain spotted fever) and antibodies to ATBF and with bacterial culture isolation and nucleic acid amplification; the culture and amplification came back positive for R africae.

Because the specialized tests confirmed infection with R africae, the patient was given triamcinolone cream 0.1% to apply twice daily to the pruritic lesions for as long as 4 weeks; an additional 14-day course of oral doxycycline monohydrate (100 mg twice daily) was given. At follow-up, the lesions had fully resolved without evident scarring.

Various diagnostic techniques can detect R africae. Bacterial culture and the polymerase chain reaction are specific and therefore diagnostic. In addition, the diagnosis of rickettsiosis can be made with serology testing, in which disease-specific antibodies are detected by indirect IFA using disease-specific antigens.

Antigens from R rickettsii (the agent of Rocky Mountain spotted fever), R conorii (Mediterranean spotted fever), and R africae (ATBF) are commercially available for making the diagnosis of rickettsiosis. However, antigens from R conorii exhibit cross-reactivity with R africae, which can confound the diagnosis.^1,10 Serologic IFA tests have been shown to be less sensitive, especially when performed after antibacterial treatment has started.

In a study, 17 of 65 (26%) ATBF-confirmed patients were seronegative (acute and convalescent-phase sera) against R africae; 14 had received doxycycline during the first week of clinical signs. The current hypothesis is that R africae is highly sensitive to doxycycline and that early exposure to the drug prevented development of detectable titers of reactive antibodies, thus producing a negative serology test.¹¹

Furthermore, it has been shown that seroconversion of IgG and IgM antibodies in R africae–infected sera is delayed compared to what is observed with R conorii–infected sera. Typically, seroconversion of R conorii–infected sera can be detected within 2 weeks; seroconversion in R africae–infected sera can take 4 weeks or longer.¹¹

Our patient had a confirmed case of ATBF secondary to R africae infection, which was evident from tissue culture isolation and polymerase chain reaction analysis of swab material obtained from eschar sites, both of which yielded a positive result for R africae. The traveler’s negative serologic status might be due to his early exposure to doxycycline or to the 4-week delay in R africae seroconversion; his serum was collected only 3 weeks after the tick bites.

Clinical signs also aid in making the diagnosis of ATBF and distinguishing R conorii from R africae infection. Because of the aggressive hunting nature of the tick carrying R africae, they are associated with multiple eschars and tend to affect groups of multiple people, especially in rural areas.^4,5 In contrast, ticks carrying R conorii yield a single eschar due to their passive style of infecting a host and because they favor a single host within urban areas.⁵ Both infections exhibit a maculopapular or papulovesicular rash and are accompanied by fatigue, headache, and myalgia, though ATBF tends to present with a milder rash than MSF.

Infection with either R conorii or R africae responds to tetracyclines, quinolones, and macrolides.^10,12

African tick-bite fever is becoming more common, which should encourage clinicians to become familiar with the disease. Less than 2 decades ago, ATBF virtually was unknown outside of Zimbabwe, Botswana, Tanzania, Zambia, and Kenya, where it is endemic. However, after the abolition of apartheid in the 1990s, international tourism in southern Africa increased 6-fold.¹³ African tick-bite fever is now one of the most common rickettsial infections in Africa.⁷ In addition to diagnosing ATBF and managing infected patients, clinicians can help prevent ATBF in individuals who travel to endemic areas by recommending commercial topical insect repellents containing at least 19.5% N,N-diethyl-meta-toluamide (DEET).¹⁴

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease that typically presents as inflamed nodules, abscesses, and sinus tracts in the apocrine gland–bearing regions.  

Chronic pain, fatigue, and social isolation put patients with HS at risk for psychiatric comorbidities, with the prevalence of depression estimated to be as high as 43%. Work productivity and sexual relationships may also be affected.  

Early treatment of the condition, as well as screening for depression, may help alleviate the psychosocial burden of HS.  

In this ReCAP, Dr Jennifer Hsiao from Keck School of Medicine, University of Southern California, Los Angeles, outlines mental health screening tools that dermatologists can use to help recognize at-risk patients and potentially refer them to mental health experts.  

--

Jennifer Hsiao, MD, Associate Professor, Department of Dermatology, Keck School of Medicine, University of Southern California, Los Angeles, California  

Jennifer Hsiao, MD, has disclosed the following relevant financial relationships: 

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Boehringer Ingelheim; Novartis; UCB 

Serve(d) as a speaker or a member of a speakers bureau for: AbbVie 

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease that typically presents as inflamed nodules, abscesses, and sinus tracts in the apocrine gland–bearing regions.  

Chronic pain, fatigue, and social isolation put patients with HS at risk for psychiatric comorbidities, with the prevalence of depression estimated to be as high as 43%. Work productivity and sexual relationships may also be affected.  

Early treatment of the condition, as well as screening for depression, may help alleviate the psychosocial burden of HS.  

In this ReCAP, Dr Jennifer Hsiao from Keck School of Medicine, University of Southern California, Los Angeles, outlines mental health screening tools that dermatologists can use to help recognize at-risk patients and potentially refer them to mental health experts.  

--

Jennifer Hsiao, MD, Associate Professor, Department of Dermatology, Keck School of Medicine, University of Southern California, Los Angeles, California  

Jennifer Hsiao, MD, has disclosed the following relevant financial relationships: 

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Boehringer Ingelheim; Novartis; UCB 

Serve(d) as a speaker or a member of a speakers bureau for: AbbVie 

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease that typically presents as inflamed nodules, abscesses, and sinus tracts in the apocrine gland–bearing regions.  

Chronic pain, fatigue, and social isolation put patients with HS at risk for psychiatric comorbidities, with the prevalence of depression estimated to be as high as 43%. Work productivity and sexual relationships may also be affected.  

Early treatment of the condition, as well as screening for depression, may help alleviate the psychosocial burden of HS.  

In this ReCAP, Dr Jennifer Hsiao from Keck School of Medicine, University of Southern California, Los Angeles, outlines mental health screening tools that dermatologists can use to help recognize at-risk patients and potentially refer them to mental health experts.  

--

Jennifer Hsiao, MD, Associate Professor, Department of Dermatology, Keck School of Medicine, University of Southern California, Los Angeles, California  

Jennifer Hsiao, MD, has disclosed the following relevant financial relationships: 

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Boehringer Ingelheim; Novartis; UCB 

Serve(d) as a speaker or a member of a speakers bureau for: AbbVie 

Rives-Lange C, Poghosyan T, Phan A, et al. Risk-benefit balance associated with obstetric, neonatal, and child outcomes after metabolic and bariatric surgery. JAMA Surg. 2023;158:36-44. doi:10.1001/jamasurg.2022.5450.

EXPERT COMMENTARY

Prepregnancy obesity continues to rise, with approximately 40% of reproductive-aged patients having a body mass index greater than 30 kg/m².¹ Several adverse perinatal outcomes are more common in pregnant patients with obesity.² In addition, their infants have a higher risk of obesity, insulin resistance, hypertension, and neurodevelopmental disorders in the long term.^3,4

Bariatric surgery is an effective procedure for weight loss and has been shown to lower adverse pregnancy outcomes, such as hypertensive disorders of pregnancy and gestational diabetes.^5,6 Benefits to newborns, however, have been debated.⁵ In addition, long-term benefits to infants were unknown until a recent study evaluated neonatal and child outcomes up to 2 years after pregnancy among patients who had undergone bariatric surgery.

Details of the study

Using the French nationwide database, Rives-Lange and colleagues performed a population-based study that included patients who had at least 1 pregnancy before and 1 pregnancy after bariatric surgery. Their objective was to compare pregnancy, neonatal, and child outcomes between pregnancies pre- and post-bariatric surgery.

Results. Among 3,686 patients who had at least 1 pregnancy before and after bariatric surgery, the authors found that pregnancies after bariatric surgery had lower rates of several adverse pregnancy outcomes, including preeclampsia (OR, 0.19), gestational hypertension (OR, 0.16), and gestational diabetes (OR, 0.39), compared with pregnancies before bariatric surgery. Regarding neonatal and child outcomes up to 2 years after pregnancy, there were lower rates of birth injuries (OR, 0.27), convulsions (OR, 0.43), newborn carbohydrate metabolism disorders (OR, 0.54),and viral intestinal infections (OR, 0.56) in pregnancies after bariatric surgery compared with those before surgery.

Notably, respiratory failure rates associated with bronchiolitis increased in pregnancies after bariatric surgery (OR, 2.42). This finding remained associated after adjusting for prematurity and small for gestational age as well as including 2 successive pregnancies before bariatric surgery (OR, 1.37).

Study strengths and limitations

A limitation of this study is the use of an administrative database, which may be biased and missing relevant variables. However, the study’s major strength was the large sample of patients serving as their own control to compare outcomes from pre-bariatric surgery with those of post-bariatric surgery. In addition, to account for confounders such as age and parity, the authors also evaluated for associations between 2 consecutive pregnancies among patients before bariatric surgery. They did not consider diagnoses found to be associated with bariatric surgery if they were also significant in the analysis between 2 consecutive pregnancies before bariatric surgery.

The finding of increased risk of respiratory failure from bronchiolitis after bariatric surgery is surprising given that obesity is a risk factor for the severity of bronchiolitis.⁷ Although this risk remained significant after including the analysis that used 2 consecutive pregnancies pre-bariatric surgery, the risk was lower (from an OR of 2.42 to an OR of 1.37). Thus, more data are required to confirm this potential risk. Despite this concerning finding, the overwhelming pregnancy, neonatal, and child benefits found and confirmed in this large, well-designed study support the continued practice of counseling on the benefits of bariatric surgery to our obese patients. ●

Rives-Lange C, Poghosyan T, Phan A, et al. Risk-benefit balance associated with obstetric, neonatal, and child outcomes after metabolic and bariatric surgery. JAMA Surg. 2023;158:36-44. doi:10.1001/jamasurg.2022.5450.

EXPERT COMMENTARY

Prepregnancy obesity continues to rise, with approximately 40% of reproductive-aged patients having a body mass index greater than 30 kg/m².¹ Several adverse perinatal outcomes are more common in pregnant patients with obesity.² In addition, their infants have a higher risk of obesity, insulin resistance, hypertension, and neurodevelopmental disorders in the long term.^3,4

Bariatric surgery is an effective procedure for weight loss and has been shown to lower adverse pregnancy outcomes, such as hypertensive disorders of pregnancy and gestational diabetes.^5,6 Benefits to newborns, however, have been debated.⁵ In addition, long-term benefits to infants were unknown until a recent study evaluated neonatal and child outcomes up to 2 years after pregnancy among patients who had undergone bariatric surgery.

Details of the study

Using the French nationwide database, Rives-Lange and colleagues performed a population-based study that included patients who had at least 1 pregnancy before and 1 pregnancy after bariatric surgery. Their objective was to compare pregnancy, neonatal, and child outcomes between pregnancies pre- and post-bariatric surgery.

Results. Among 3,686 patients who had at least 1 pregnancy before and after bariatric surgery, the authors found that pregnancies after bariatric surgery had lower rates of several adverse pregnancy outcomes, including preeclampsia (OR, 0.19), gestational hypertension (OR, 0.16), and gestational diabetes (OR, 0.39), compared with pregnancies before bariatric surgery. Regarding neonatal and child outcomes up to 2 years after pregnancy, there were lower rates of birth injuries (OR, 0.27), convulsions (OR, 0.43), newborn carbohydrate metabolism disorders (OR, 0.54),and viral intestinal infections (OR, 0.56) in pregnancies after bariatric surgery compared with those before surgery.

Notably, respiratory failure rates associated with bronchiolitis increased in pregnancies after bariatric surgery (OR, 2.42). This finding remained associated after adjusting for prematurity and small for gestational age as well as including 2 successive pregnancies before bariatric surgery (OR, 1.37).

Study strengths and limitations

A limitation of this study is the use of an administrative database, which may be biased and missing relevant variables. However, the study’s major strength was the large sample of patients serving as their own control to compare outcomes from pre-bariatric surgery with those of post-bariatric surgery. In addition, to account for confounders such as age and parity, the authors also evaluated for associations between 2 consecutive pregnancies among patients before bariatric surgery. They did not consider diagnoses found to be associated with bariatric surgery if they were also significant in the analysis between 2 consecutive pregnancies before bariatric surgery.

The finding of increased risk of respiratory failure from bronchiolitis after bariatric surgery is surprising given that obesity is a risk factor for the severity of bronchiolitis.⁷ Although this risk remained significant after including the analysis that used 2 consecutive pregnancies pre-bariatric surgery, the risk was lower (from an OR of 2.42 to an OR of 1.37). Thus, more data are required to confirm this potential risk. Despite this concerning finding, the overwhelming pregnancy, neonatal, and child benefits found and confirmed in this large, well-designed study support the continued practice of counseling on the benefits of bariatric surgery to our obese patients. ●

Rives-Lange C, Poghosyan T, Phan A, et al. Risk-benefit balance associated with obstetric, neonatal, and child outcomes after metabolic and bariatric surgery. JAMA Surg. 2023;158:36-44. doi:10.1001/jamasurg.2022.5450.

EXPERT COMMENTARY

Prepregnancy obesity continues to rise, with approximately 40% of reproductive-aged patients having a body mass index greater than 30 kg/m².¹ Several adverse perinatal outcomes are more common in pregnant patients with obesity.² In addition, their infants have a higher risk of obesity, insulin resistance, hypertension, and neurodevelopmental disorders in the long term.^3,4

Bariatric surgery is an effective procedure for weight loss and has been shown to lower adverse pregnancy outcomes, such as hypertensive disorders of pregnancy and gestational diabetes.^5,6 Benefits to newborns, however, have been debated.⁵ In addition, long-term benefits to infants were unknown until a recent study evaluated neonatal and child outcomes up to 2 years after pregnancy among patients who had undergone bariatric surgery.

Details of the study

Using the French nationwide database, Rives-Lange and colleagues performed a population-based study that included patients who had at least 1 pregnancy before and 1 pregnancy after bariatric surgery. Their objective was to compare pregnancy, neonatal, and child outcomes between pregnancies pre- and post-bariatric surgery.

Results. Among 3,686 patients who had at least 1 pregnancy before and after bariatric surgery, the authors found that pregnancies after bariatric surgery had lower rates of several adverse pregnancy outcomes, including preeclampsia (OR, 0.19), gestational hypertension (OR, 0.16), and gestational diabetes (OR, 0.39), compared with pregnancies before bariatric surgery. Regarding neonatal and child outcomes up to 2 years after pregnancy, there were lower rates of birth injuries (OR, 0.27), convulsions (OR, 0.43), newborn carbohydrate metabolism disorders (OR, 0.54),and viral intestinal infections (OR, 0.56) in pregnancies after bariatric surgery compared with those before surgery.

Notably, respiratory failure rates associated with bronchiolitis increased in pregnancies after bariatric surgery (OR, 2.42). This finding remained associated after adjusting for prematurity and small for gestational age as well as including 2 successive pregnancies before bariatric surgery (OR, 1.37).

Study strengths and limitations

A limitation of this study is the use of an administrative database, which may be biased and missing relevant variables. However, the study’s major strength was the large sample of patients serving as their own control to compare outcomes from pre-bariatric surgery with those of post-bariatric surgery. In addition, to account for confounders such as age and parity, the authors also evaluated for associations between 2 consecutive pregnancies among patients before bariatric surgery. They did not consider diagnoses found to be associated with bariatric surgery if they were also significant in the analysis between 2 consecutive pregnancies before bariatric surgery.

The finding of increased risk of respiratory failure from bronchiolitis after bariatric surgery is surprising given that obesity is a risk factor for the severity of bronchiolitis.⁷ Although this risk remained significant after including the analysis that used 2 consecutive pregnancies pre-bariatric surgery, the risk was lower (from an OR of 2.42 to an OR of 1.37). Thus, more data are required to confirm this potential risk. Despite this concerning finding, the overwhelming pregnancy, neonatal, and child benefits found and confirmed in this large, well-designed study support the continued practice of counseling on the benefits of bariatric surgery to our obese patients. ●

The Diagnosis: Discoid Lupus Erythematosus

The biopsies demonstrated vacuolar interface changes with superficial and deep perivascular and periadnexal inflammation as well as increased background mucin deposition. The clinical morphology and distributions of the plaques limited to the photoexposed areas of the head suggested a diagnosis of discoid lupus erythematosus (DLE). The interface changes on histopathology supported this clinical impression. Our patient was treated with limited application of triamcinolone ointment 0.1% twice daily around the ears and neck, tacrolimus ointment 0.1% twice daily on the face, and hydroxychloroquine, as well as sun protection instructions. Smoking cessation was strongly advised.

Discoid lupus erythematosus is a disorder with chronic, erythematous, scaly, coin-shaped (discoid) plaques and is the most common form of chronic cutaneous lupus erythematosus.¹ Lesions usually present on sun-exposed areas of the face, scalp, neck, ears, lips, or upper torso. They expand slowly with an active peripheral margin and a central scar that can result in induration, pigmentation changes, telangiectases, pruritus, or tenderness. Hair-bearing areas may be involved, causing hair loss due to follicular plugging; irreversible scarring alopecia can result. Facial DLE often spares the nasolabial folds. Ear involvement characteristically includes the conchal bowl and the outer external auditory canal. Discoid lupus erythematosus is considered localized if most of the head and neck region is involved or generalized if lesions also are present below the neck. Risk factors for DLE include genetic and environmental factors such as UV exposure, hormones, or exposure to toxins such as cigarette smoke.¹ The disorder most commonly affects females and has a higher prevalence in patients of African descent than in Asian and White patients. Disease can occur at any age but usually occurs between 20 and 40 years of age.² Discoid lupus erythematosus and other forms of chronic cutaneous lupus can occur independently or in conjunction with systemic lupus erythematosus (SLE), and approximately 15% to 30% of SLE patients develop DLE.¹

Discoid lupus erythematosus is clinically diagnosed by the presentation of plaques in the characteristic distribution with confirmation via skin biopsy.¹ Elman et al³ created a system for DLE classification that was only clinical and did not involve histopathology. Histologically, DLE often includes basement membrane thickening, follicular keratin plugs, mucin deposition, and vacuolar change with an interface, and a perivascular and periadnexal lymphocytic infiltrate.^3,4 Antibodies such as antinuclear antibodies, rheumatoid factor, anti–double-stranded DNA, anti-Smith, and Sjögren syndrome A and B antibodies may be present (albeit with low positive frequency) in cutaneous lupus erythematosus.4 Characteristics of SLE also may be present, helping to confirm the diagnosis. Because there is an association of DLE with SLE, various laboratory tests should be ordered, including complete blood cell count, renal function panel, inflammatory markers, antibodies, and urinalysis for proteinuria.^2,4

Treatment of DLE consists of preventative measures, such as sun protection with vitamin D supplementation, avoidance of drug triggers, and smoking cessation, as well as pharmacotherapy. The importance of wearing sun protective hats and garments with sunscreen use cannot be understated.¹ Smoking cessation should be advised because smoking reduces the efficacy of antimalarial treatment and potentially increases the likelihood of patients requiring a second antimalarial drug. Quinacrine often is noted in both the dermatology and rheumatology literature to be used for escalating cutaneous lupus erythematosus care when hydroxychloroquine is ineffective or not tolerated, but no US manufacturer produces this medication; thus, compounding is required, which may be financially prohibitive, making this recommendation difficult to translate into clinical practice.⁵ Firstline therapy for acute flares is high-potency topical corticosteroids. If lesions are primarily on areas other than the face, a medium-potency topical steroid may be used. Topical calcineurin inhibitors or intralesional corticosteroids may be used if minimal improvement is seen after initial topical corticosteroid therapy. Treatment for widespread disease or disease that is resistant to local treatment is systemic therapy with antimalarial agents, followed by antimetabolites, systemic retinoids, thalidomide, or dapsone.^1,2 The Cutaneous Lupus Erythematosus Disease Area and Severity Index is a valid tool to gauge the degree of disease and to help with disease progression and treatment response by noting the features of the plaques.¹

Patients also should be educated that this disease can last for years, and long-standing DLE plaques infrequently can give rise to squamous cell carcinoma. In addition, isolated DLE can progress to SLE in 5% to 28% of patients.²

The differential diagnosis in our patient included other diseases with violaceous annular lesions and central clearing. Majocchi granuloma usually presents in areas of prior trauma, possibly due to shaving the face in our patient, or in the setting of topical corticosteroid use or immunosuppression. Scaling often is present within lesions, and histology shows fungal elements.⁶ Cutaneous sarcoidosis usually presents on the face, with scarring alopecia when appearing on the scalp; histology shows noncaseating granulomas, and 70% of patients with cutaneous symptoms will have systemic sarcoidosis.⁷ Granuloma annulare most commonly presents on the extremities, and histology shows lymphohistiocytic granulomas in a palisaded or interstitial pattern with connective-tissue degeneration and mucinous deposits.⁸ Annular psoriasis often is scaly and symmetric with parakeratosis, epidermal hyperplasia, dilated dermal capillaries, loss of granular layer, perivascular mononuclear cell infiltrate, and elongation of rete ridges on histology.⁹ Drug-induced lupus erythematosus always should be considered in patients taking triggering drugs such as antihypertensives, lipid-lowering drugs, antifungals, anti–tumor necrosis factor drugs, and proton pump inhibitors—the latter being a drug our patient was taking.¹⁰

The Diagnosis: Discoid Lupus Erythematosus

The biopsies demonstrated vacuolar interface changes with superficial and deep perivascular and periadnexal inflammation as well as increased background mucin deposition. The clinical morphology and distributions of the plaques limited to the photoexposed areas of the head suggested a diagnosis of discoid lupus erythematosus (DLE). The interface changes on histopathology supported this clinical impression. Our patient was treated with limited application of triamcinolone ointment 0.1% twice daily around the ears and neck, tacrolimus ointment 0.1% twice daily on the face, and hydroxychloroquine, as well as sun protection instructions. Smoking cessation was strongly advised.

Discoid lupus erythematosus is a disorder with chronic, erythematous, scaly, coin-shaped (discoid) plaques and is the most common form of chronic cutaneous lupus erythematosus.¹ Lesions usually present on sun-exposed areas of the face, scalp, neck, ears, lips, or upper torso. They expand slowly with an active peripheral margin and a central scar that can result in induration, pigmentation changes, telangiectases, pruritus, or tenderness. Hair-bearing areas may be involved, causing hair loss due to follicular plugging; irreversible scarring alopecia can result. Facial DLE often spares the nasolabial folds. Ear involvement characteristically includes the conchal bowl and the outer external auditory canal. Discoid lupus erythematosus is considered localized if most of the head and neck region is involved or generalized if lesions also are present below the neck. Risk factors for DLE include genetic and environmental factors such as UV exposure, hormones, or exposure to toxins such as cigarette smoke.¹ The disorder most commonly affects females and has a higher prevalence in patients of African descent than in Asian and White patients. Disease can occur at any age but usually occurs between 20 and 40 years of age.² Discoid lupus erythematosus and other forms of chronic cutaneous lupus can occur independently or in conjunction with systemic lupus erythematosus (SLE), and approximately 15% to 30% of SLE patients develop DLE.¹

Discoid lupus erythematosus is clinically diagnosed by the presentation of plaques in the characteristic distribution with confirmation via skin biopsy.¹ Elman et al³ created a system for DLE classification that was only clinical and did not involve histopathology. Histologically, DLE often includes basement membrane thickening, follicular keratin plugs, mucin deposition, and vacuolar change with an interface, and a perivascular and periadnexal lymphocytic infiltrate.^3,4 Antibodies such as antinuclear antibodies, rheumatoid factor, anti–double-stranded DNA, anti-Smith, and Sjögren syndrome A and B antibodies may be present (albeit with low positive frequency) in cutaneous lupus erythematosus.4 Characteristics of SLE also may be present, helping to confirm the diagnosis. Because there is an association of DLE with SLE, various laboratory tests should be ordered, including complete blood cell count, renal function panel, inflammatory markers, antibodies, and urinalysis for proteinuria.^2,4

Treatment of DLE consists of preventative measures, such as sun protection with vitamin D supplementation, avoidance of drug triggers, and smoking cessation, as well as pharmacotherapy. The importance of wearing sun protective hats and garments with sunscreen use cannot be understated.¹ Smoking cessation should be advised because smoking reduces the efficacy of antimalarial treatment and potentially increases the likelihood of patients requiring a second antimalarial drug. Quinacrine often is noted in both the dermatology and rheumatology literature to be used for escalating cutaneous lupus erythematosus care when hydroxychloroquine is ineffective or not tolerated, but no US manufacturer produces this medication; thus, compounding is required, which may be financially prohibitive, making this recommendation difficult to translate into clinical practice.⁵ Firstline therapy for acute flares is high-potency topical corticosteroids. If lesions are primarily on areas other than the face, a medium-potency topical steroid may be used. Topical calcineurin inhibitors or intralesional corticosteroids may be used if minimal improvement is seen after initial topical corticosteroid therapy. Treatment for widespread disease or disease that is resistant to local treatment is systemic therapy with antimalarial agents, followed by antimetabolites, systemic retinoids, thalidomide, or dapsone.^1,2 The Cutaneous Lupus Erythematosus Disease Area and Severity Index is a valid tool to gauge the degree of disease and to help with disease progression and treatment response by noting the features of the plaques.¹

Patients also should be educated that this disease can last for years, and long-standing DLE plaques infrequently can give rise to squamous cell carcinoma. In addition, isolated DLE can progress to SLE in 5% to 28% of patients.²

The differential diagnosis in our patient included other diseases with violaceous annular lesions and central clearing. Majocchi granuloma usually presents in areas of prior trauma, possibly due to shaving the face in our patient, or in the setting of topical corticosteroid use or immunosuppression. Scaling often is present within lesions, and histology shows fungal elements.⁶ Cutaneous sarcoidosis usually presents on the face, with scarring alopecia when appearing on the scalp; histology shows noncaseating granulomas, and 70% of patients with cutaneous symptoms will have systemic sarcoidosis.⁷ Granuloma annulare most commonly presents on the extremities, and histology shows lymphohistiocytic granulomas in a palisaded or interstitial pattern with connective-tissue degeneration and mucinous deposits.⁸ Annular psoriasis often is scaly and symmetric with parakeratosis, epidermal hyperplasia, dilated dermal capillaries, loss of granular layer, perivascular mononuclear cell infiltrate, and elongation of rete ridges on histology.⁹ Drug-induced lupus erythematosus always should be considered in patients taking triggering drugs such as antihypertensives, lipid-lowering drugs, antifungals, anti–tumor necrosis factor drugs, and proton pump inhibitors—the latter being a drug our patient was taking.¹⁰

The Diagnosis: Discoid Lupus Erythematosus

The biopsies demonstrated vacuolar interface changes with superficial and deep perivascular and periadnexal inflammation as well as increased background mucin deposition. The clinical morphology and distributions of the plaques limited to the photoexposed areas of the head suggested a diagnosis of discoid lupus erythematosus (DLE). The interface changes on histopathology supported this clinical impression. Our patient was treated with limited application of triamcinolone ointment 0.1% twice daily around the ears and neck, tacrolimus ointment 0.1% twice daily on the face, and hydroxychloroquine, as well as sun protection instructions. Smoking cessation was strongly advised.

Discoid lupus erythematosus is a disorder with chronic, erythematous, scaly, coin-shaped (discoid) plaques and is the most common form of chronic cutaneous lupus erythematosus.¹ Lesions usually present on sun-exposed areas of the face, scalp, neck, ears, lips, or upper torso. They expand slowly with an active peripheral margin and a central scar that can result in induration, pigmentation changes, telangiectases, pruritus, or tenderness. Hair-bearing areas may be involved, causing hair loss due to follicular plugging; irreversible scarring alopecia can result. Facial DLE often spares the nasolabial folds. Ear involvement characteristically includes the conchal bowl and the outer external auditory canal. Discoid lupus erythematosus is considered localized if most of the head and neck region is involved or generalized if lesions also are present below the neck. Risk factors for DLE include genetic and environmental factors such as UV exposure, hormones, or exposure to toxins such as cigarette smoke.¹ The disorder most commonly affects females and has a higher prevalence in patients of African descent than in Asian and White patients. Disease can occur at any age but usually occurs between 20 and 40 years of age.² Discoid lupus erythematosus and other forms of chronic cutaneous lupus can occur independently or in conjunction with systemic lupus erythematosus (SLE), and approximately 15% to 30% of SLE patients develop DLE.¹

Discoid lupus erythematosus is clinically diagnosed by the presentation of plaques in the characteristic distribution with confirmation via skin biopsy.¹ Elman et al³ created a system for DLE classification that was only clinical and did not involve histopathology. Histologically, DLE often includes basement membrane thickening, follicular keratin plugs, mucin deposition, and vacuolar change with an interface, and a perivascular and periadnexal lymphocytic infiltrate.^3,4 Antibodies such as antinuclear antibodies, rheumatoid factor, anti–double-stranded DNA, anti-Smith, and Sjögren syndrome A and B antibodies may be present (albeit with low positive frequency) in cutaneous lupus erythematosus.4 Characteristics of SLE also may be present, helping to confirm the diagnosis. Because there is an association of DLE with SLE, various laboratory tests should be ordered, including complete blood cell count, renal function panel, inflammatory markers, antibodies, and urinalysis for proteinuria.^2,4

Treatment of DLE consists of preventative measures, such as sun protection with vitamin D supplementation, avoidance of drug triggers, and smoking cessation, as well as pharmacotherapy. The importance of wearing sun protective hats and garments with sunscreen use cannot be understated.¹ Smoking cessation should be advised because smoking reduces the efficacy of antimalarial treatment and potentially increases the likelihood of patients requiring a second antimalarial drug. Quinacrine often is noted in both the dermatology and rheumatology literature to be used for escalating cutaneous lupus erythematosus care when hydroxychloroquine is ineffective or not tolerated, but no US manufacturer produces this medication; thus, compounding is required, which may be financially prohibitive, making this recommendation difficult to translate into clinical practice.⁵ Firstline therapy for acute flares is high-potency topical corticosteroids. If lesions are primarily on areas other than the face, a medium-potency topical steroid may be used. Topical calcineurin inhibitors or intralesional corticosteroids may be used if minimal improvement is seen after initial topical corticosteroid therapy. Treatment for widespread disease or disease that is resistant to local treatment is systemic therapy with antimalarial agents, followed by antimetabolites, systemic retinoids, thalidomide, or dapsone.^1,2 The Cutaneous Lupus Erythematosus Disease Area and Severity Index is a valid tool to gauge the degree of disease and to help with disease progression and treatment response by noting the features of the plaques.¹

Patients also should be educated that this disease can last for years, and long-standing DLE plaques infrequently can give rise to squamous cell carcinoma. In addition, isolated DLE can progress to SLE in 5% to 28% of patients.²

The differential diagnosis in our patient included other diseases with violaceous annular lesions and central clearing. Majocchi granuloma usually presents in areas of prior trauma, possibly due to shaving the face in our patient, or in the setting of topical corticosteroid use or immunosuppression. Scaling often is present within lesions, and histology shows fungal elements.⁶ Cutaneous sarcoidosis usually presents on the face, with scarring alopecia when appearing on the scalp; histology shows noncaseating granulomas, and 70% of patients with cutaneous symptoms will have systemic sarcoidosis.⁷ Granuloma annulare most commonly presents on the extremities, and histology shows lymphohistiocytic granulomas in a palisaded or interstitial pattern with connective-tissue degeneration and mucinous deposits.⁸ Annular psoriasis often is scaly and symmetric with parakeratosis, epidermal hyperplasia, dilated dermal capillaries, loss of granular layer, perivascular mononuclear cell infiltrate, and elongation of rete ridges on histology.⁹ Drug-induced lupus erythematosus always should be considered in patients taking triggering drugs such as antihypertensives, lipid-lowering drugs, antifungals, anti–tumor necrosis factor drugs, and proton pump inhibitors—the latter being a drug our patient was taking.¹⁰