Psoriasis

For more information, access Dr. Weinberg's editorial from the September 2014 issue, "Under Pressure."

For more information, access Dr. Weinberg's editorial from the September 2014 issue, "Under Pressure."

For more information, access Dr. Weinberg's editorial from the September 2014 issue, "Under Pressure."

The oral phosphodiesterase-4 inhibitor apremilast is now indicated for the treatment of moderate to severe plaque psoriasis.

On Sept. 23, the manufacturer, Celgene, announced that the Food and Drug Administration had approved the expanded indication for apremilast, which was initially approved in March 2014 for treating psoriatic arthritis. The new indication is for the treatment of patients with moderate to severe plaque psoriasis who are candidates for phototherapy or systemic therapy.

Approval was primarily based on the results of two multicenter, randomized, double-blind, placebo-controlled studies of adults with moderate to severe plaque psoriasis, according to Celgene. At 16 weeks, 33% and 29% of those randomized to the 30-mg, twice daily dose of apremilast had achieved at least a 75% reduction in the Psoriasis Area and Severity Index (PASI 75), compared with 5%-6% of those on placebo, according to the prescribing information.

The most common adverse events reported in studies, which affected at least 1% of treated patients and were more common than in patients on placebo, included diarrhea in 17% and nausea in 17%; other adverse events included upper respiratory infection, tension headache, and headache. The warnings and precautions section of the label includes the recommendation to be alert for the emergence or worsening of depression, suicidal thoughts, or other mood changes in patients treated with the drug, and to monitor weight regularly for significant weight loss. In studies, treatment with apremilast has been associated with an increase in reports of depression and significant weight loss.

Celgene markets apremilast as Otezla.

Serious adverse events associated with treatment should be reported to the FDA at 800-332-1088 or www.fda.gov/medwatch.

Information about the pregnancy registry of women exposed to the drug during pregnancy can be obtained at 877-311-8972.

The updated prescribing information is available at http://www.celgene.com/content/uploads/2014/09/psoriasis-pi.pdf

[email protected]

The oral phosphodiesterase-4 inhibitor apremilast is now indicated for the treatment of moderate to severe plaque psoriasis.

On Sept. 23, the manufacturer, Celgene, announced that the Food and Drug Administration had approved the expanded indication for apremilast, which was initially approved in March 2014 for treating psoriatic arthritis. The new indication is for the treatment of patients with moderate to severe plaque psoriasis who are candidates for phototherapy or systemic therapy.

Approval was primarily based on the results of two multicenter, randomized, double-blind, placebo-controlled studies of adults with moderate to severe plaque psoriasis, according to Celgene. At 16 weeks, 33% and 29% of those randomized to the 30-mg, twice daily dose of apremilast had achieved at least a 75% reduction in the Psoriasis Area and Severity Index (PASI 75), compared with 5%-6% of those on placebo, according to the prescribing information.

The most common adverse events reported in studies, which affected at least 1% of treated patients and were more common than in patients on placebo, included diarrhea in 17% and nausea in 17%; other adverse events included upper respiratory infection, tension headache, and headache. The warnings and precautions section of the label includes the recommendation to be alert for the emergence or worsening of depression, suicidal thoughts, or other mood changes in patients treated with the drug, and to monitor weight regularly for significant weight loss. In studies, treatment with apremilast has been associated with an increase in reports of depression and significant weight loss.

Celgene markets apremilast as Otezla.

Serious adverse events associated with treatment should be reported to the FDA at 800-332-1088 or www.fda.gov/medwatch.

Information about the pregnancy registry of women exposed to the drug during pregnancy can be obtained at 877-311-8972.

The updated prescribing information is available at http://www.celgene.com/content/uploads/2014/09/psoriasis-pi.pdf

[email protected]

The oral phosphodiesterase-4 inhibitor apremilast is now indicated for the treatment of moderate to severe plaque psoriasis.

On Sept. 23, the manufacturer, Celgene, announced that the Food and Drug Administration had approved the expanded indication for apremilast, which was initially approved in March 2014 for treating psoriatic arthritis. The new indication is for the treatment of patients with moderate to severe plaque psoriasis who are candidates for phototherapy or systemic therapy.

Approval was primarily based on the results of two multicenter, randomized, double-blind, placebo-controlled studies of adults with moderate to severe plaque psoriasis, according to Celgene. At 16 weeks, 33% and 29% of those randomized to the 30-mg, twice daily dose of apremilast had achieved at least a 75% reduction in the Psoriasis Area and Severity Index (PASI 75), compared with 5%-6% of those on placebo, according to the prescribing information.

The most common adverse events reported in studies, which affected at least 1% of treated patients and were more common than in patients on placebo, included diarrhea in 17% and nausea in 17%; other adverse events included upper respiratory infection, tension headache, and headache. The warnings and precautions section of the label includes the recommendation to be alert for the emergence or worsening of depression, suicidal thoughts, or other mood changes in patients treated with the drug, and to monitor weight regularly for significant weight loss. In studies, treatment with apremilast has been associated with an increase in reports of depression and significant weight loss.

Celgene markets apremilast as Otezla.

Serious adverse events associated with treatment should be reported to the FDA at 800-332-1088 or www.fda.gov/medwatch.

Information about the pregnancy registry of women exposed to the drug during pregnancy can be obtained at 877-311-8972.

The updated prescribing information is available at http://www.celgene.com/content/uploads/2014/09/psoriasis-pi.pdf

[email protected]

Therapies for Palmoplantar Pustular Psoriasis

There is limited evidence on therapies for palmoplantar pustular psoriasis (PPPP) and maintaining long-term remission. Sevrain et al (J Eur Acad Dermatol Venereol. 2014;28[suppl 5]:13-16) conducted a systematic literature search to identify trials in patients with PPPP that assessed therapeutic interventions (not including systemic biotherapy). They found that oral retinoid therapy (acitretin), photochemotherapy, or a combination of both; low-dose cyclosporine; or topical corticosteroids under occlusion appeared to help relieve symptoms of PPPP. Newer studies have noted the benefits of psoralen plus UVA, with better efficacy compared to UVB therapy. A 308-nm excimer laser has been shown to improve PPPP.

Practice Point: Although phototherapy, cyclosporine, and topical corticosteroids seem to be able to control PPPP, more randomized controlled trials are needed to better define treatment strategies for PPPP.

>>Read more at Journal of the European Academy of Dermatology and Venereology

Pediatric Pustular Psoriasis Cleared With Systemic Medications

Treatment of pediatric pustular psoriasis is challenging. Posso-De Los Rios and colleagues (Pediatr Dermatol. 2014;31:430-439) conducted a systematic review of systemic interventions for pediatric pustular psoriasis with a focus on clinical response and treatment outcomes. The most common therapies used for generalized pustular psoriasis were acitretin, cyclosporine, and methotrexate.

Practice Point: Acitretin, methotrexate, and cyclosporine seem to control generalized pustular psoriasis in the pediatric population; however, long-term data are lacking and physicians may encounter disease regression after discontinuing or tapering the medications.

>>Read more at Pediatric Dermatology

Biologics for Erythrodermic and Pustular Psoriasis

Levin et al (J Drugs Dermatol. 2014;13:342-354) sought to evaluate the efficacy and safety of biologics in the treatment of erythrodermic and generalized pustular psoriasis by reviewing the literature. In both psoriasis subtypes, infliximab was used to treat more than half of the reported cases. Other biologics that were successfully used included etanercept, ustekinumab, adalimumab, and anakinra.

Practice Point: Patients with erythrodermic or generalized pustular psoriasis may experience disease improvement with biologics.

>>Read more at Journal of Drugs in Dermatology

Therapies for Palmoplantar Pustular Psoriasis

There is limited evidence on therapies for palmoplantar pustular psoriasis (PPPP) and maintaining long-term remission. Sevrain et al (J Eur Acad Dermatol Venereol. 2014;28[suppl 5]:13-16) conducted a systematic literature search to identify trials in patients with PPPP that assessed therapeutic interventions (not including systemic biotherapy). They found that oral retinoid therapy (acitretin), photochemotherapy, or a combination of both; low-dose cyclosporine; or topical corticosteroids under occlusion appeared to help relieve symptoms of PPPP. Newer studies have noted the benefits of psoralen plus UVA, with better efficacy compared to UVB therapy. A 308-nm excimer laser has been shown to improve PPPP.

Practice Point: Although phototherapy, cyclosporine, and topical corticosteroids seem to be able to control PPPP, more randomized controlled trials are needed to better define treatment strategies for PPPP.

>>Read more at Journal of the European Academy of Dermatology and Venereology

Pediatric Pustular Psoriasis Cleared With Systemic Medications

Treatment of pediatric pustular psoriasis is challenging. Posso-De Los Rios and colleagues (Pediatr Dermatol. 2014;31:430-439) conducted a systematic review of systemic interventions for pediatric pustular psoriasis with a focus on clinical response and treatment outcomes. The most common therapies used for generalized pustular psoriasis were acitretin, cyclosporine, and methotrexate.

Practice Point: Acitretin, methotrexate, and cyclosporine seem to control generalized pustular psoriasis in the pediatric population; however, long-term data are lacking and physicians may encounter disease regression after discontinuing or tapering the medications.

>>Read more at Pediatric Dermatology

Biologics for Erythrodermic and Pustular Psoriasis

Levin et al (J Drugs Dermatol. 2014;13:342-354) sought to evaluate the efficacy and safety of biologics in the treatment of erythrodermic and generalized pustular psoriasis by reviewing the literature. In both psoriasis subtypes, infliximab was used to treat more than half of the reported cases. Other biologics that were successfully used included etanercept, ustekinumab, adalimumab, and anakinra.

Practice Point: Patients with erythrodermic or generalized pustular psoriasis may experience disease improvement with biologics.

>>Read more at Journal of Drugs in Dermatology

Therapies for Palmoplantar Pustular Psoriasis

There is limited evidence on therapies for palmoplantar pustular psoriasis (PPPP) and maintaining long-term remission. Sevrain et al (J Eur Acad Dermatol Venereol. 2014;28[suppl 5]:13-16) conducted a systematic literature search to identify trials in patients with PPPP that assessed therapeutic interventions (not including systemic biotherapy). They found that oral retinoid therapy (acitretin), photochemotherapy, or a combination of both; low-dose cyclosporine; or topical corticosteroids under occlusion appeared to help relieve symptoms of PPPP. Newer studies have noted the benefits of psoralen plus UVA, with better efficacy compared to UVB therapy. A 308-nm excimer laser has been shown to improve PPPP.

Practice Point: Although phototherapy, cyclosporine, and topical corticosteroids seem to be able to control PPPP, more randomized controlled trials are needed to better define treatment strategies for PPPP.

>>Read more at Journal of the European Academy of Dermatology and Venereology

Pediatric Pustular Psoriasis Cleared With Systemic Medications

Treatment of pediatric pustular psoriasis is challenging. Posso-De Los Rios and colleagues (Pediatr Dermatol. 2014;31:430-439) conducted a systematic review of systemic interventions for pediatric pustular psoriasis with a focus on clinical response and treatment outcomes. The most common therapies used for generalized pustular psoriasis were acitretin, cyclosporine, and methotrexate.

Practice Point: Acitretin, methotrexate, and cyclosporine seem to control generalized pustular psoriasis in the pediatric population; however, long-term data are lacking and physicians may encounter disease regression after discontinuing or tapering the medications.

>>Read more at Pediatric Dermatology

Biologics for Erythrodermic and Pustular Psoriasis

Levin et al (J Drugs Dermatol. 2014;13:342-354) sought to evaluate the efficacy and safety of biologics in the treatment of erythrodermic and generalized pustular psoriasis by reviewing the literature. In both psoriasis subtypes, infliximab was used to treat more than half of the reported cases. Other biologics that were successfully used included etanercept, ustekinumab, adalimumab, and anakinra.

Practice Point: Patients with erythrodermic or generalized pustular psoriasis may experience disease improvement with biologics.

>>Read more at Journal of Drugs in Dermatology

LAS VEGAS – A number of drugs are showing promise for the treatment of psoriatic arthritis, but broader improvements are needed with respect to treatment strategies, according to Dr. Iain McInnes.

Earlier diagnosis, appropriate therapies, and treating to target are among the topics he covered in a presentation on maximizing patient outcomes at the annual Perspectives in Rheumatic Diseases.

A recent study demonstrated that even a 6-month delay in the diagnosis of psoriatic arthritis is associated with worse long-term outcomes on several measures. In that study of 283 patients (Ann. Rheum. Dis. 2014 Feb. 13 [doi: 10.1136/annrheumdis-2013-204858]), the median lag time from disease onset to first rheumatological assessment was 1 year, with only 30% of patients being seen by a rheumatologist within 6 months.

Multiple stepwise regression analysis showed that late consulters had a greater risk of developing peripheral joint erosions (odds ratio, 4.25) and had worse Health Assessment Questionnaire scores (odds ratio, 2.2).

One finding that could help with earlier diagnosis is detection of early entheseal involvement, said Dr. McInnes, professor of medicine and director of the Institute of Infection, Immunity and Immunology at the University of Glasgow (Scotland).

Subclinical entheseal involvement appears to predict psoriatic arthritis in patients presenting with psoriasis, he said at the conference.

In one study, the mean Glasgow Ultrasound Enthesitis Scoring System (GUESS) score was 7.9 in patients with psoriasis, compared with 2.9 in controls, and in another study, thickness of the quadriceps tendon was a significant predictor of the development of psoriatic arthritis in those with psoriasis.

A key challenge in maximizing outcomes in psoriatic arthritis is that rheumatoid arthritis and psoriatic arthritis are typically treated as homogeneous for the purposes of drug development, but the two diseases have distinct clinical phenotypes and time course, tissue distribution, tissue cell/molecular features, genetic susceptibility, and probably impact of immune senescence.

In fact, while disease-modifying antirheumatic drugs are included in European League Against Rheumatsm (EULAR) treatment guidelines for psoriatic arthritis, the Methotrexate in Psoriatic Arthritis (MIPA) trial, a 6-month, double-blind, randomized, placebo-controlled trial of methotrexate, showed no benefit for key psoriatic arthritis endpoints at 3 and 6 months (Rheumatology 2012;51:1368-77).

Data on methotrexate combination therapy is limited, but existing clinical trials and registry data show no clear evidence of benefit. Methotrexate also has long-term toxicity issues.

In studies of patients who received anti–tumor necrosis factor therapy, 59%-69% of patients achieved 20% improvement (ACR 20 response), 37%-50% achieved 50% improvement (ACR 50 response), and up to 52% of patients achieved minimal disease activity at various time points. Also, radiographic progression was improved with anti-TNF therapy vs. placebo. However, TNF inhibitors lose efficacy over time in some patients, and are associated with an increased risk of infection.

Other disappointments or unmet needs in psoriatic arthritis are dichotomous skin and joint responses to biologics, lack of established predictors of response to biologics, lack of a cure, and difficulties in achieving sustained remission, Dr. McInnes said.

Future therapeutic options, including several drugs in development, include drugs that target cytokines and their receptors, such as ustekinumab, which targets IL-12/23; secukinumab and ixekizumab, which target IL-17; and brodalumab, which targets IL-17 receptor A. Other potential targets include IL-6 and the IL-6 receptor and IL-23 and the IL-23 receptor.

Studies of ustekinumab, for example, demonstrate beneficial effects on enthesitis, dactylitis, and modified van der Heijde-Sharp score.

Drugs that target intracellular signaling pathways are also being studied in psoriatic arthritis, including JAK family agents such as tofacitinib and phosphodiesterase inhibitors like apremilast.

As for strategies to improve outcomes, the Tight Control in Psoriatic Arthritis (TICOPA) study provided a rationale for treating to target. Current recommendations call for a target of remission or low disease activity.

The availability of highly effective biologics makes minimal level of disease activity a realistic treatment target, Dr. McInnes said.

The conference was held by Global Academy for Medical Education. Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

Dr. McInnes reported receiving research/grant support from Pfizer, Bristol-Myers Squibb, AstraZeneca, and Novo Nordisk, and serving as a consultant to Novartis, Bristol-Myers Squibb, Pfizer, and Galapagos. He is a member of scientific advisory boards for AstraZeneca, Crescendo Bioscience, and Janssen Biotech.

LAS VEGAS – A number of drugs are showing promise for the treatment of psoriatic arthritis, but broader improvements are needed with respect to treatment strategies, according to Dr. Iain McInnes.

Earlier diagnosis, appropriate therapies, and treating to target are among the topics he covered in a presentation on maximizing patient outcomes at the annual Perspectives in Rheumatic Diseases.

A recent study demonstrated that even a 6-month delay in the diagnosis of psoriatic arthritis is associated with worse long-term outcomes on several measures. In that study of 283 patients (Ann. Rheum. Dis. 2014 Feb. 13 [doi: 10.1136/annrheumdis-2013-204858]), the median lag time from disease onset to first rheumatological assessment was 1 year, with only 30% of patients being seen by a rheumatologist within 6 months.

Multiple stepwise regression analysis showed that late consulters had a greater risk of developing peripheral joint erosions (odds ratio, 4.25) and had worse Health Assessment Questionnaire scores (odds ratio, 2.2).

One finding that could help with earlier diagnosis is detection of early entheseal involvement, said Dr. McInnes, professor of medicine and director of the Institute of Infection, Immunity and Immunology at the University of Glasgow (Scotland).

Subclinical entheseal involvement appears to predict psoriatic arthritis in patients presenting with psoriasis, he said at the conference.

In one study, the mean Glasgow Ultrasound Enthesitis Scoring System (GUESS) score was 7.9 in patients with psoriasis, compared with 2.9 in controls, and in another study, thickness of the quadriceps tendon was a significant predictor of the development of psoriatic arthritis in those with psoriasis.

A key challenge in maximizing outcomes in psoriatic arthritis is that rheumatoid arthritis and psoriatic arthritis are typically treated as homogeneous for the purposes of drug development, but the two diseases have distinct clinical phenotypes and time course, tissue distribution, tissue cell/molecular features, genetic susceptibility, and probably impact of immune senescence.

In fact, while disease-modifying antirheumatic drugs are included in European League Against Rheumatsm (EULAR) treatment guidelines for psoriatic arthritis, the Methotrexate in Psoriatic Arthritis (MIPA) trial, a 6-month, double-blind, randomized, placebo-controlled trial of methotrexate, showed no benefit for key psoriatic arthritis endpoints at 3 and 6 months (Rheumatology 2012;51:1368-77).

Data on methotrexate combination therapy is limited, but existing clinical trials and registry data show no clear evidence of benefit. Methotrexate also has long-term toxicity issues.

In studies of patients who received anti–tumor necrosis factor therapy, 59%-69% of patients achieved 20% improvement (ACR 20 response), 37%-50% achieved 50% improvement (ACR 50 response), and up to 52% of patients achieved minimal disease activity at various time points. Also, radiographic progression was improved with anti-TNF therapy vs. placebo. However, TNF inhibitors lose efficacy over time in some patients, and are associated with an increased risk of infection.

Other disappointments or unmet needs in psoriatic arthritis are dichotomous skin and joint responses to biologics, lack of established predictors of response to biologics, lack of a cure, and difficulties in achieving sustained remission, Dr. McInnes said.

Future therapeutic options, including several drugs in development, include drugs that target cytokines and their receptors, such as ustekinumab, which targets IL-12/23; secukinumab and ixekizumab, which target IL-17; and brodalumab, which targets IL-17 receptor A. Other potential targets include IL-6 and the IL-6 receptor and IL-23 and the IL-23 receptor.

Studies of ustekinumab, for example, demonstrate beneficial effects on enthesitis, dactylitis, and modified van der Heijde-Sharp score.

Drugs that target intracellular signaling pathways are also being studied in psoriatic arthritis, including JAK family agents such as tofacitinib and phosphodiesterase inhibitors like apremilast.

As for strategies to improve outcomes, the Tight Control in Psoriatic Arthritis (TICOPA) study provided a rationale for treating to target. Current recommendations call for a target of remission or low disease activity.

The availability of highly effective biologics makes minimal level of disease activity a realistic treatment target, Dr. McInnes said.

The conference was held by Global Academy for Medical Education. Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

Dr. McInnes reported receiving research/grant support from Pfizer, Bristol-Myers Squibb, AstraZeneca, and Novo Nordisk, and serving as a consultant to Novartis, Bristol-Myers Squibb, Pfizer, and Galapagos. He is a member of scientific advisory boards for AstraZeneca, Crescendo Bioscience, and Janssen Biotech.

LAS VEGAS – A number of drugs are showing promise for the treatment of psoriatic arthritis, but broader improvements are needed with respect to treatment strategies, according to Dr. Iain McInnes.

Earlier diagnosis, appropriate therapies, and treating to target are among the topics he covered in a presentation on maximizing patient outcomes at the annual Perspectives in Rheumatic Diseases.

A recent study demonstrated that even a 6-month delay in the diagnosis of psoriatic arthritis is associated with worse long-term outcomes on several measures. In that study of 283 patients (Ann. Rheum. Dis. 2014 Feb. 13 [doi: 10.1136/annrheumdis-2013-204858]), the median lag time from disease onset to first rheumatological assessment was 1 year, with only 30% of patients being seen by a rheumatologist within 6 months.

Multiple stepwise regression analysis showed that late consulters had a greater risk of developing peripheral joint erosions (odds ratio, 4.25) and had worse Health Assessment Questionnaire scores (odds ratio, 2.2).

One finding that could help with earlier diagnosis is detection of early entheseal involvement, said Dr. McInnes, professor of medicine and director of the Institute of Infection, Immunity and Immunology at the University of Glasgow (Scotland).

Subclinical entheseal involvement appears to predict psoriatic arthritis in patients presenting with psoriasis, he said at the conference.

In one study, the mean Glasgow Ultrasound Enthesitis Scoring System (GUESS) score was 7.9 in patients with psoriasis, compared with 2.9 in controls, and in another study, thickness of the quadriceps tendon was a significant predictor of the development of psoriatic arthritis in those with psoriasis.

A key challenge in maximizing outcomes in psoriatic arthritis is that rheumatoid arthritis and psoriatic arthritis are typically treated as homogeneous for the purposes of drug development, but the two diseases have distinct clinical phenotypes and time course, tissue distribution, tissue cell/molecular features, genetic susceptibility, and probably impact of immune senescence.

In fact, while disease-modifying antirheumatic drugs are included in European League Against Rheumatsm (EULAR) treatment guidelines for psoriatic arthritis, the Methotrexate in Psoriatic Arthritis (MIPA) trial, a 6-month, double-blind, randomized, placebo-controlled trial of methotrexate, showed no benefit for key psoriatic arthritis endpoints at 3 and 6 months (Rheumatology 2012;51:1368-77).

Data on methotrexate combination therapy is limited, but existing clinical trials and registry data show no clear evidence of benefit. Methotrexate also has long-term toxicity issues.

In studies of patients who received anti–tumor necrosis factor therapy, 59%-69% of patients achieved 20% improvement (ACR 20 response), 37%-50% achieved 50% improvement (ACR 50 response), and up to 52% of patients achieved minimal disease activity at various time points. Also, radiographic progression was improved with anti-TNF therapy vs. placebo. However, TNF inhibitors lose efficacy over time in some patients, and are associated with an increased risk of infection.

Other disappointments or unmet needs in psoriatic arthritis are dichotomous skin and joint responses to biologics, lack of established predictors of response to biologics, lack of a cure, and difficulties in achieving sustained remission, Dr. McInnes said.

Future therapeutic options, including several drugs in development, include drugs that target cytokines and their receptors, such as ustekinumab, which targets IL-12/23; secukinumab and ixekizumab, which target IL-17; and brodalumab, which targets IL-17 receptor A. Other potential targets include IL-6 and the IL-6 receptor and IL-23 and the IL-23 receptor.

Studies of ustekinumab, for example, demonstrate beneficial effects on enthesitis, dactylitis, and modified van der Heijde-Sharp score.

Drugs that target intracellular signaling pathways are also being studied in psoriatic arthritis, including JAK family agents such as tofacitinib and phosphodiesterase inhibitors like apremilast.

As for strategies to improve outcomes, the Tight Control in Psoriatic Arthritis (TICOPA) study provided a rationale for treating to target. Current recommendations call for a target of remission or low disease activity.

The availability of highly effective biologics makes minimal level of disease activity a realistic treatment target, Dr. McInnes said.

The conference was held by Global Academy for Medical Education. Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

Dr. McInnes reported receiving research/grant support from Pfizer, Bristol-Myers Squibb, AstraZeneca, and Novo Nordisk, and serving as a consultant to Novartis, Bristol-Myers Squibb, Pfizer, and Galapagos. He is a member of scientific advisory boards for AstraZeneca, Crescendo Bioscience, and Janssen Biotech.

Patients with psoriatic arthritis who began taking disease-modifying antirheumatic drugs often changed regimens soon afterward, especially if they had started with nonbiologic treatments, researchers reported online in Arthritis Research and Therapy.

Only 31% of patients who started methotrexate or another nonbiologic disease-modifying antirheumatic drug (DMARD) for psoriatic arthritis stayed with their initial treatment for the next year, compared with 54% of patients who started on a biologic DMARD such as etanercept, infliximab, or golimumab, said Dr. Huabin F. Zhang at Celgene in Summit, N.J., and his associates.

The researchers analyzed U. S. health care claims data for 1,698 adults with psoriatic arthritis who were started on oral nonbiologic DMARDs and for 3,263 patients started on biologic DMARDs. In all, 69% of patients who started nonbiologic DMARDs and 46% of those who started biologic DMARDs discontinued, switched, or added on to their treatment within a year of starting therapy, they found. Patients most often switched to or added a biologic as opposed to a nonbiologic DMARD, the investigators said. Those who started on nonbiologics primarily took methotrexate, and "patient persistence with treatment was generally low and relatively brief," they said. Other studies have shown that use of nonbiologic DMARDs "erodes rapidly and progressively over time," they said (Arthritis Res. Ther. 2014 Aug. 22 [doi:10.1186/s13075-014-0420-5]).

Health insurance companies often require patients to take one or two nonbiologics before they will reimburse for a biologic DMARD, which could partially explain these findings, the researchers said. But the retrospective observational study did not capture data on side effects, safety concerns, or other reasons for treatment changes, they noted.

Celgene funded the study and employs Dr. Zhang. The other three coauthors reported receiving consultancy fees from Celgene.

Patients with psoriatic arthritis who began taking disease-modifying antirheumatic drugs often changed regimens soon afterward, especially if they had started with nonbiologic treatments, researchers reported online in Arthritis Research and Therapy.

Only 31% of patients who started methotrexate or another nonbiologic disease-modifying antirheumatic drug (DMARD) for psoriatic arthritis stayed with their initial treatment for the next year, compared with 54% of patients who started on a biologic DMARD such as etanercept, infliximab, or golimumab, said Dr. Huabin F. Zhang at Celgene in Summit, N.J., and his associates.

The researchers analyzed U. S. health care claims data for 1,698 adults with psoriatic arthritis who were started on oral nonbiologic DMARDs and for 3,263 patients started on biologic DMARDs. In all, 69% of patients who started nonbiologic DMARDs and 46% of those who started biologic DMARDs discontinued, switched, or added on to their treatment within a year of starting therapy, they found. Patients most often switched to or added a biologic as opposed to a nonbiologic DMARD, the investigators said. Those who started on nonbiologics primarily took methotrexate, and "patient persistence with treatment was generally low and relatively brief," they said. Other studies have shown that use of nonbiologic DMARDs "erodes rapidly and progressively over time," they said (Arthritis Res. Ther. 2014 Aug. 22 [doi:10.1186/s13075-014-0420-5]).

Health insurance companies often require patients to take one or two nonbiologics before they will reimburse for a biologic DMARD, which could partially explain these findings, the researchers said. But the retrospective observational study did not capture data on side effects, safety concerns, or other reasons for treatment changes, they noted.

Celgene funded the study and employs Dr. Zhang. The other three coauthors reported receiving consultancy fees from Celgene.

Patients with psoriatic arthritis who began taking disease-modifying antirheumatic drugs often changed regimens soon afterward, especially if they had started with nonbiologic treatments, researchers reported online in Arthritis Research and Therapy.

Only 31% of patients who started methotrexate or another nonbiologic disease-modifying antirheumatic drug (DMARD) for psoriatic arthritis stayed with their initial treatment for the next year, compared with 54% of patients who started on a biologic DMARD such as etanercept, infliximab, or golimumab, said Dr. Huabin F. Zhang at Celgene in Summit, N.J., and his associates.

The researchers analyzed U. S. health care claims data for 1,698 adults with psoriatic arthritis who were started on oral nonbiologic DMARDs and for 3,263 patients started on biologic DMARDs. In all, 69% of patients who started nonbiologic DMARDs and 46% of those who started biologic DMARDs discontinued, switched, or added on to their treatment within a year of starting therapy, they found. Patients most often switched to or added a biologic as opposed to a nonbiologic DMARD, the investigators said. Those who started on nonbiologics primarily took methotrexate, and "patient persistence with treatment was generally low and relatively brief," they said. Other studies have shown that use of nonbiologic DMARDs "erodes rapidly and progressively over time," they said (Arthritis Res. Ther. 2014 Aug. 22 [doi:10.1186/s13075-014-0420-5]).

Health insurance companies often require patients to take one or two nonbiologics before they will reimburse for a biologic DMARD, which could partially explain these findings, the researchers said. But the retrospective observational study did not capture data on side effects, safety concerns, or other reasons for treatment changes, they noted.

Celgene funded the study and employs Dr. Zhang. The other three coauthors reported receiving consultancy fees from Celgene.

VANCOUVER, B.C. – Results from some studies have concluded that treatment with conventional systemic or biologic therapy improves the elevated risk of cardiovascular disease in patients with psoriasis, but the association is not yet definitive, according to Dr. Robert Kalb.

"Current evidence is suggestive, but certainly our patients with psoriasis need intensive management of cardiovascular risk factors and appropriate psoriasis therapy, which may also produce benefits from a cardiovascular standpoint," Dr. Kalb said at the annual meeting of the Pacific Dermatologic Association.

Researchers who conducted the earliest study to explore the association between psoriasis and increased risk for cardiovascular death found that when they controlled for risk factors including age, sex, smoking, diabetes, hypertension, and hyperlipidemia, having psoriasis led to a hazard ratio of 1.57 for cardiovascular death (Eur. Heart J. 2010;31:1000-6). Since that time, six meta-analyses have appeared in the medical literature showing that psoriasis is linked to an increased risk of cardiovascular disease. Most of these studies defined severe psoriasis as patients who had received a systemic agent. Body surface area or other objective measures of psoriasis were not part of the definition, said Dr. Kalb, a dermatologist in group practice in Buffalo.

Emerging evidence supports the idea that increased risk factors are associated with the severity of psoriasis. As part of the landmark Incident Health Outcomes and Psoriasis Events (iHope) study, investigators found that patients with disease affecting 10% or more body surface area had an increased risk of myocardial infarction. One study defined psoriasis severity by body surface area (JAMA Dermatol. 2013;149:1173-9). The investigators found that the burdens of MI and other comorbid diseases increase with increasing disease severity, particularly in those with 10% body surface area or more affected.

Investigators are also working to determine if systemic therapy reduces the risk of MI in psoriasis patients. The Consortium of Rheumatology Researchers of North America (CORRONA) registry database found that in patients with rheumatoid arthritis, anti–tumor necrosis factor (TNF) agents reduced the risk of cardiovascular events (HR, 0.39), compared with nonbiologic disease-modifying antirheumatic drugs. Methotrexate did not reduce the risk of cardiovascular events, while the use of prednisone increased the risk (Ann. Rheum. Dis. 2011;70:576-82). Another review showed that anti-TNF therapy decreased the risk, but the use of methotrexate decreased the risk slightly more (Rheumatology 2011;50:518-31). "Reassuringly, there was no increased risk of congestive heart failure, which has always been [included] in the label of [anti-]TNF agents," Dr. Kalb said.

A cohort study of 25,554 patients with moderate to severe psoriasis used U.S. administrative and pharmacy claims data to examine the risk of acute myocardial infarction in those who underwent systemic therapy, compared with those who underwent phototherapy. The investigators found a trend toward an increased risk of MI in those who received systemic therapy, but there were no significant differences in risk between the two treatment groups (Br. J. Dermatol. 2011;165:1066-73). On the other hand, a retrospective, longitudinal cohort study of 2,400 patients with severe psoriasis in Denmark showed that the use of biologic agents and methotrexate was associated with fewer cardiovascular events (hazard ratios, 0.48 and 0.50, respectively), but the use of other antipsoriatic therapies – including cyclosporine, retinoids, phototherapy, and topicals – were not (J. Intern Med. 2013;273:197-204).

A retrospective cohort study of 8,845 Kaiser Permanente psoriasis patients set out to determine whether treatment with TNF inhibitors was associated with a decreased risk of MI, compared with those who did not receive TNF inhibitors (Arch. Dermatol. 2012;148:1244-50) . After adjusting for MI risk factors, the researchers found that those who received TNF inhibitors had a significantly lower risk of MI, compared with those who received topical therapy (adjusted HR, 0.50).

"Why do different studies reach different conclusions?" Dr. Kalb asked. "Different populations were studied, and there were differences in terms of how reference groups were defined and in the methods for categorizing therapy and severity of disease. Data from population studies are not yet sufficient to determine whether [anti-]TNF agents will reduce the incidence of MI."

One conundrum for researchers is how to measure this decreased risk. "What surrogate markers should we use?" Dr. Kalb asked. "One study showed a significant decrease in CRP [C-reactive protein] and ESR [erythrocyte sedimentation rate] in patients receiving therapy. The gold standard of decrease in mortality in this type of study will not be done because it requires thousands of patients studied over at least 10 years." However, in cardiology, 18-fluorodeoxyglucose PET scanning shows decreased inflammation in patients taking statins. Whether the same effect can be shown in psoriasis patients taking systemic medications for their disease remains unknown, but prospective studies are ongoing.

Dr. Kalb disclosed that he is an investigator and/or consultant for AbbVie, Amgen, Celgene, Dermira, Janssen, Leo, Merck, Pfizer, and Taro. He is also on the dermatology safety monitoring board for ApoPharma and Eli Lilly.

[email protected]

On Twitter @dougbrunk

VANCOUVER, B.C. – Results from some studies have concluded that treatment with conventional systemic or biologic therapy improves the elevated risk of cardiovascular disease in patients with psoriasis, but the association is not yet definitive, according to Dr. Robert Kalb.

"Current evidence is suggestive, but certainly our patients with psoriasis need intensive management of cardiovascular risk factors and appropriate psoriasis therapy, which may also produce benefits from a cardiovascular standpoint," Dr. Kalb said at the annual meeting of the Pacific Dermatologic Association.

Researchers who conducted the earliest study to explore the association between psoriasis and increased risk for cardiovascular death found that when they controlled for risk factors including age, sex, smoking, diabetes, hypertension, and hyperlipidemia, having psoriasis led to a hazard ratio of 1.57 for cardiovascular death (Eur. Heart J. 2010;31:1000-6). Since that time, six meta-analyses have appeared in the medical literature showing that psoriasis is linked to an increased risk of cardiovascular disease. Most of these studies defined severe psoriasis as patients who had received a systemic agent. Body surface area or other objective measures of psoriasis were not part of the definition, said Dr. Kalb, a dermatologist in group practice in Buffalo.

Emerging evidence supports the idea that increased risk factors are associated with the severity of psoriasis. As part of the landmark Incident Health Outcomes and Psoriasis Events (iHope) study, investigators found that patients with disease affecting 10% or more body surface area had an increased risk of myocardial infarction. One study defined psoriasis severity by body surface area (JAMA Dermatol. 2013;149:1173-9). The investigators found that the burdens of MI and other comorbid diseases increase with increasing disease severity, particularly in those with 10% body surface area or more affected.

Investigators are also working to determine if systemic therapy reduces the risk of MI in psoriasis patients. The Consortium of Rheumatology Researchers of North America (CORRONA) registry database found that in patients with rheumatoid arthritis, anti–tumor necrosis factor (TNF) agents reduced the risk of cardiovascular events (HR, 0.39), compared with nonbiologic disease-modifying antirheumatic drugs. Methotrexate did not reduce the risk of cardiovascular events, while the use of prednisone increased the risk (Ann. Rheum. Dis. 2011;70:576-82). Another review showed that anti-TNF therapy decreased the risk, but the use of methotrexate decreased the risk slightly more (Rheumatology 2011;50:518-31). "Reassuringly, there was no increased risk of congestive heart failure, which has always been [included] in the label of [anti-]TNF agents," Dr. Kalb said.

A cohort study of 25,554 patients with moderate to severe psoriasis used U.S. administrative and pharmacy claims data to examine the risk of acute myocardial infarction in those who underwent systemic therapy, compared with those who underwent phototherapy. The investigators found a trend toward an increased risk of MI in those who received systemic therapy, but there were no significant differences in risk between the two treatment groups (Br. J. Dermatol. 2011;165:1066-73). On the other hand, a retrospective, longitudinal cohort study of 2,400 patients with severe psoriasis in Denmark showed that the use of biologic agents and methotrexate was associated with fewer cardiovascular events (hazard ratios, 0.48 and 0.50, respectively), but the use of other antipsoriatic therapies – including cyclosporine, retinoids, phototherapy, and topicals – were not (J. Intern Med. 2013;273:197-204).

A retrospective cohort study of 8,845 Kaiser Permanente psoriasis patients set out to determine whether treatment with TNF inhibitors was associated with a decreased risk of MI, compared with those who did not receive TNF inhibitors (Arch. Dermatol. 2012;148:1244-50) . After adjusting for MI risk factors, the researchers found that those who received TNF inhibitors had a significantly lower risk of MI, compared with those who received topical therapy (adjusted HR, 0.50).

"Why do different studies reach different conclusions?" Dr. Kalb asked. "Different populations were studied, and there were differences in terms of how reference groups were defined and in the methods for categorizing therapy and severity of disease. Data from population studies are not yet sufficient to determine whether [anti-]TNF agents will reduce the incidence of MI."

One conundrum for researchers is how to measure this decreased risk. "What surrogate markers should we use?" Dr. Kalb asked. "One study showed a significant decrease in CRP [C-reactive protein] and ESR [erythrocyte sedimentation rate] in patients receiving therapy. The gold standard of decrease in mortality in this type of study will not be done because it requires thousands of patients studied over at least 10 years." However, in cardiology, 18-fluorodeoxyglucose PET scanning shows decreased inflammation in patients taking statins. Whether the same effect can be shown in psoriasis patients taking systemic medications for their disease remains unknown, but prospective studies are ongoing.

Dr. Kalb disclosed that he is an investigator and/or consultant for AbbVie, Amgen, Celgene, Dermira, Janssen, Leo, Merck, Pfizer, and Taro. He is also on the dermatology safety monitoring board for ApoPharma and Eli Lilly.

[email protected]

On Twitter @dougbrunk

VANCOUVER, B.C. – Results from some studies have concluded that treatment with conventional systemic or biologic therapy improves the elevated risk of cardiovascular disease in patients with psoriasis, but the association is not yet definitive, according to Dr. Robert Kalb.

"Current evidence is suggestive, but certainly our patients with psoriasis need intensive management of cardiovascular risk factors and appropriate psoriasis therapy, which may also produce benefits from a cardiovascular standpoint," Dr. Kalb said at the annual meeting of the Pacific Dermatologic Association.

Researchers who conducted the earliest study to explore the association between psoriasis and increased risk for cardiovascular death found that when they controlled for risk factors including age, sex, smoking, diabetes, hypertension, and hyperlipidemia, having psoriasis led to a hazard ratio of 1.57 for cardiovascular death (Eur. Heart J. 2010;31:1000-6). Since that time, six meta-analyses have appeared in the medical literature showing that psoriasis is linked to an increased risk of cardiovascular disease. Most of these studies defined severe psoriasis as patients who had received a systemic agent. Body surface area or other objective measures of psoriasis were not part of the definition, said Dr. Kalb, a dermatologist in group practice in Buffalo.

Emerging evidence supports the idea that increased risk factors are associated with the severity of psoriasis. As part of the landmark Incident Health Outcomes and Psoriasis Events (iHope) study, investigators found that patients with disease affecting 10% or more body surface area had an increased risk of myocardial infarction. One study defined psoriasis severity by body surface area (JAMA Dermatol. 2013;149:1173-9). The investigators found that the burdens of MI and other comorbid diseases increase with increasing disease severity, particularly in those with 10% body surface area or more affected.

Investigators are also working to determine if systemic therapy reduces the risk of MI in psoriasis patients. The Consortium of Rheumatology Researchers of North America (CORRONA) registry database found that in patients with rheumatoid arthritis, anti–tumor necrosis factor (TNF) agents reduced the risk of cardiovascular events (HR, 0.39), compared with nonbiologic disease-modifying antirheumatic drugs. Methotrexate did not reduce the risk of cardiovascular events, while the use of prednisone increased the risk (Ann. Rheum. Dis. 2011;70:576-82). Another review showed that anti-TNF therapy decreased the risk, but the use of methotrexate decreased the risk slightly more (Rheumatology 2011;50:518-31). "Reassuringly, there was no increased risk of congestive heart failure, which has always been [included] in the label of [anti-]TNF agents," Dr. Kalb said.

A cohort study of 25,554 patients with moderate to severe psoriasis used U.S. administrative and pharmacy claims data to examine the risk of acute myocardial infarction in those who underwent systemic therapy, compared with those who underwent phototherapy. The investigators found a trend toward an increased risk of MI in those who received systemic therapy, but there were no significant differences in risk between the two treatment groups (Br. J. Dermatol. 2011;165:1066-73). On the other hand, a retrospective, longitudinal cohort study of 2,400 patients with severe psoriasis in Denmark showed that the use of biologic agents and methotrexate was associated with fewer cardiovascular events (hazard ratios, 0.48 and 0.50, respectively), but the use of other antipsoriatic therapies – including cyclosporine, retinoids, phototherapy, and topicals – were not (J. Intern Med. 2013;273:197-204).

A retrospective cohort study of 8,845 Kaiser Permanente psoriasis patients set out to determine whether treatment with TNF inhibitors was associated with a decreased risk of MI, compared with those who did not receive TNF inhibitors (Arch. Dermatol. 2012;148:1244-50) . After adjusting for MI risk factors, the researchers found that those who received TNF inhibitors had a significantly lower risk of MI, compared with those who received topical therapy (adjusted HR, 0.50).

"Why do different studies reach different conclusions?" Dr. Kalb asked. "Different populations were studied, and there were differences in terms of how reference groups were defined and in the methods for categorizing therapy and severity of disease. Data from population studies are not yet sufficient to determine whether [anti-]TNF agents will reduce the incidence of MI."

One conundrum for researchers is how to measure this decreased risk. "What surrogate markers should we use?" Dr. Kalb asked. "One study showed a significant decrease in CRP [C-reactive protein] and ESR [erythrocyte sedimentation rate] in patients receiving therapy. The gold standard of decrease in mortality in this type of study will not be done because it requires thousands of patients studied over at least 10 years." However, in cardiology, 18-fluorodeoxyglucose PET scanning shows decreased inflammation in patients taking statins. Whether the same effect can be shown in psoriasis patients taking systemic medications for their disease remains unknown, but prospective studies are ongoing.

Dr. Kalb disclosed that he is an investigator and/or consultant for AbbVie, Amgen, Celgene, Dermira, Janssen, Leo, Merck, Pfizer, and Taro. He is also on the dermatology safety monitoring board for ApoPharma and Eli Lilly.

[email protected]

On Twitter @dougbrunk

One of the most important elements of a psoriasis patient’s medical history is the medication list. We are aware of the possible association between induction or exacerbation of psoriasis and intake of drugs including beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, lithium, and nonsteroidal anti-inflammatory drugs. However, we are lacking comprehensive data on these putative relationships.

Wu et al¹ evaluated the association of hypertension and antihypertensive medications with risk for psoriasis. The authors pointed out that psoriasis patients have an increased risk for hypertension, and medications for hypertension, especially beta-blockers, have been associated with the development of psoriasis. They noted, however, that there has been no prospective assessment of the association of existing hypertension and antihypertensive medications with risk for incident psoriasis.¹

The authors performed a prospective cohort study (June 1996 to June 1998) of 77,728 women from the Nurses’ Health Study who provided biennially updated data on hypertension and antihypertensive medications.¹ They documented 843 incidents of psoriasis during 1,066,339 person-years of follow-up. Women with hypertension tended to be older and had a higher body mass index. In addition, they had proportionately higher prevalence rates of cardiovascular disease, type 2 diabetes mellitus, and hypercholesterolemia. They also were less physically active than subjects without hypertension. Compared with those with normal blood pressure, women with hypertension lasting 6 years or more were at higher risk for development of psoriasis (hazard ratio [HR], 1.27; 95% confidence interval [CI], 1.03-1.57). In stratified analysis, the risk for psoriasis was higher among hypertensive women without medication use (HR, 1.49; 95% CI, 1.15-1.92) and among hypertensive women with current medication use (HR, 1.31; 95% CI, 1.10-1.55) when compared with those without hypertension and without medication use.¹

Among the individual antihypertensive drugs, only beta-blockers were associated with an increased risk for psoriasis.¹ Of interest, this association persisted in a duration-dependent manner, with a higher risk for psoriasis found among women who regularly used beta-blockers with a duration of use of 6 years or more (HR, 1.39; 95% CI, 1.11-1.73; P for trend=.009). No association was found between any other individual hypertension medication and the development of psoriasis.¹

The authors concluded that their study provided evidence that a history of long-term hypertension was associated with an increased risk for psoriasis.¹ Among the individual medications analyzed in the study, only beta-blockers were linked to an increased risk for psoriasis after long-term regular use (≥6 years). They noted that these findings provided insights into the relationship between hypertension, medications for the condition, and psoriasis. However, further work is necessary to confirm these findings and clarify the biological mechanisms that may explain these links.¹

As we further evaluate the associations between psoriasis and systemic comorbidities, we are learning more about the complex interrelationship between these conditions. The findings reported by Wu et al¹ serve as another reminder that clinicians should be proactive in having psoriasis patients actively monitor their blood pressure, either with the dermatologist or with the primary care physician. This type of novel prospective information serves as another piece of the puzzle in our comprehensive management of psoriasis.

One of the most important elements of a psoriasis patient’s medical history is the medication list. We are aware of the possible association between induction or exacerbation of psoriasis and intake of drugs including beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, lithium, and nonsteroidal anti-inflammatory drugs. However, we are lacking comprehensive data on these putative relationships.

Wu et al¹ evaluated the association of hypertension and antihypertensive medications with risk for psoriasis. The authors pointed out that psoriasis patients have an increased risk for hypertension, and medications for hypertension, especially beta-blockers, have been associated with the development of psoriasis. They noted, however, that there has been no prospective assessment of the association of existing hypertension and antihypertensive medications with risk for incident psoriasis.¹

The authors performed a prospective cohort study (June 1996 to June 1998) of 77,728 women from the Nurses’ Health Study who provided biennially updated data on hypertension and antihypertensive medications.¹ They documented 843 incidents of psoriasis during 1,066,339 person-years of follow-up. Women with hypertension tended to be older and had a higher body mass index. In addition, they had proportionately higher prevalence rates of cardiovascular disease, type 2 diabetes mellitus, and hypercholesterolemia. They also were less physically active than subjects without hypertension. Compared with those with normal blood pressure, women with hypertension lasting 6 years or more were at higher risk for development of psoriasis (hazard ratio [HR], 1.27; 95% confidence interval [CI], 1.03-1.57). In stratified analysis, the risk for psoriasis was higher among hypertensive women without medication use (HR, 1.49; 95% CI, 1.15-1.92) and among hypertensive women with current medication use (HR, 1.31; 95% CI, 1.10-1.55) when compared with those without hypertension and without medication use.¹

Among the individual antihypertensive drugs, only beta-blockers were associated with an increased risk for psoriasis.¹ Of interest, this association persisted in a duration-dependent manner, with a higher risk for psoriasis found among women who regularly used beta-blockers with a duration of use of 6 years or more (HR, 1.39; 95% CI, 1.11-1.73; P for trend=.009). No association was found between any other individual hypertension medication and the development of psoriasis.¹

The authors concluded that their study provided evidence that a history of long-term hypertension was associated with an increased risk for psoriasis.¹ Among the individual medications analyzed in the study, only beta-blockers were linked to an increased risk for psoriasis after long-term regular use (≥6 years). They noted that these findings provided insights into the relationship between hypertension, medications for the condition, and psoriasis. However, further work is necessary to confirm these findings and clarify the biological mechanisms that may explain these links.¹

As we further evaluate the associations between psoriasis and systemic comorbidities, we are learning more about the complex interrelationship between these conditions. The findings reported by Wu et al¹ serve as another reminder that clinicians should be proactive in having psoriasis patients actively monitor their blood pressure, either with the dermatologist or with the primary care physician. This type of novel prospective information serves as another piece of the puzzle in our comprehensive management of psoriasis.

One of the most important elements of a psoriasis patient’s medical history is the medication list. We are aware of the possible association between induction or exacerbation of psoriasis and intake of drugs including beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, lithium, and nonsteroidal anti-inflammatory drugs. However, we are lacking comprehensive data on these putative relationships.

Wu et al¹ evaluated the association of hypertension and antihypertensive medications with risk for psoriasis. The authors pointed out that psoriasis patients have an increased risk for hypertension, and medications for hypertension, especially beta-blockers, have been associated with the development of psoriasis. They noted, however, that there has been no prospective assessment of the association of existing hypertension and antihypertensive medications with risk for incident psoriasis.¹

The authors performed a prospective cohort study (June 1996 to June 1998) of 77,728 women from the Nurses’ Health Study who provided biennially updated data on hypertension and antihypertensive medications.¹ They documented 843 incidents of psoriasis during 1,066,339 person-years of follow-up. Women with hypertension tended to be older and had a higher body mass index. In addition, they had proportionately higher prevalence rates of cardiovascular disease, type 2 diabetes mellitus, and hypercholesterolemia. They also were less physically active than subjects without hypertension. Compared with those with normal blood pressure, women with hypertension lasting 6 years or more were at higher risk for development of psoriasis (hazard ratio [HR], 1.27; 95% confidence interval [CI], 1.03-1.57). In stratified analysis, the risk for psoriasis was higher among hypertensive women without medication use (HR, 1.49; 95% CI, 1.15-1.92) and among hypertensive women with current medication use (HR, 1.31; 95% CI, 1.10-1.55) when compared with those without hypertension and without medication use.¹

Among the individual antihypertensive drugs, only beta-blockers were associated with an increased risk for psoriasis.¹ Of interest, this association persisted in a duration-dependent manner, with a higher risk for psoriasis found among women who regularly used beta-blockers with a duration of use of 6 years or more (HR, 1.39; 95% CI, 1.11-1.73; P for trend=.009). No association was found between any other individual hypertension medication and the development of psoriasis.¹

The authors concluded that their study provided evidence that a history of long-term hypertension was associated with an increased risk for psoriasis.¹ Among the individual medications analyzed in the study, only beta-blockers were linked to an increased risk for psoriasis after long-term regular use (≥6 years). They noted that these findings provided insights into the relationship between hypertension, medications for the condition, and psoriasis. However, further work is necessary to confirm these findings and clarify the biological mechanisms that may explain these links.¹

As we further evaluate the associations between psoriasis and systemic comorbidities, we are learning more about the complex interrelationship between these conditions. The findings reported by Wu et al¹ serve as another reminder that clinicians should be proactive in having psoriasis patients actively monitor their blood pressure, either with the dermatologist or with the primary care physician. This type of novel prospective information serves as another piece of the puzzle in our comprehensive management of psoriasis.

Erythrodermic psoriasis is a severe form of psoriasis associated with higher morbidity and mortality rates compared to other forms of psoriasis. Cutaneous signs of erythrodermic psoriasis include erythema, edema, and superficial desquamation. Scabies is a common ectoparasitic disease that is diagnosed by the presence of pruritus and typical clinical signs including burrows, vesicles, and erythematous papules. Erythematous papules usually are distributed on the abdomen, thoracic region, axillae, and medial thighs and are characterized by more intense pruritus, especially at night. The course of scabies may be altered in patients with desquamative inflammatory skin disease such as psoriasis. Pruritus may be absent and typical scabies lesions may be concealed due to the preexisting disease, resulting in delayed diagnosis.
 

Case Reports

Patient 1

A 13-year-old adolescent boy with psoriasis of 4 years’ duration presented to our outpatient clinic with severe widespread erythema and mild desquamation (Figure 1). The patient was hospitalized following a diagnosis of erythrodermic psoriasis. His medical history was remarkable for recurrent episodes of bronchitis, and his family history included 2 siblings with psoriasis. Physical examination revealed no abnormalities, except for a fever (temperature, 38.0°C). A complete blood cell count revealed an elevated absolute eosinophil count (9260 cells/µL [reference range, 0–700 cells/µL]) corresponding to 48.4% (reference range, 0%–7%) of blood cells. There were no pathological findings in the serum biochemistry; complete urine analysis; throat, sputum, and urine cultures; stool analysis for parasites; or chest radiography. A VDRL test, hepatitis markers, and anti–human immunodeficiency virus test were negative. Antistreptolysin O titer; thyroid function tests; hormone profile; and IgG, IgA, IgM, C3, C4, and total IgE levels were within reference range. Peripheral blood smear, abdominal ultrasonography, electrocardiography, and echocardiography were performed; no cardiac pathology was observed. Cyclosporine 200 mg daily was initiated for treatment of erythrodermic psoriasis.

Figure 1. Severe widespread erythema and mild desquamation in a 13-year-old adolescent boy with psoriasis.

One week after the initiation of treatment the patient’s fever improved. At 2-week follow-up, a complete blood cell count demonstrated more marked eosinophilia, and the percentage of eosinophils at weekly intervals over the next 3 weeks increased to 51.2%, 63.0%, and 71.7%, respectively. The patient presented 2 weeks later with a chief concern of pruritus. Histologic examination of a lesional biopsy specimen revealed psoriasiform epithelial hyperplasia with scabies mites in the stratum corneum (Figure 2). Mites also were noted on direct microscopic examination of scrapings performed with the suspicion of scabies. The patient was treated with permethrin cream 5%. Although all of the patients and staff in the ward also were administered topical permethrin to prevent a scabies epidemic, 2 inpatients who had been discharged before the diagnosis of scabies presented to our outpatient clinic approximately 1 month later with scabies. At 6-month follow-up, the patient’s eosinophil count was within reference range (0.237cells/µL; 3.78%); pruritus and lesions were not observed.

Figure 2. Findings from a lesional biopsy specimen demonstrated epidermal psoriasiform changes and eosinophils in the dermis. Mites were present in the stratum corneum (H&E, original magnification ×100). Figure 2. Findings from a lesional biopsy specimen demonstrated epidermal psoriasiform changes and eosinophils in the dermis. Mites were present in the stratum corneum (H&E, original magnification ×100).

Patient 2

A 26-year-old woman with psoriasis of 5 years’ duration was hospitalized for treatment of erythrodermic psoriasis at the same time as patient 1, her brother. On dermatologic examination, severe widespread erythema, scaling, and edema were noted (Figure 3). Physical examination revealed a fever (temperature, 38.5°C). Hypoalbuminemia and high C-reactive protein levels were present in serum biochemistry. Eosinophil counts were within reference range (0.346 cells/µL; 1.88%). No pathological findings were noted in the complete urine analysis; throat, sputum, and urine cultures; stool analysis for parasites; or chest radiography. A VDRL test, hepatitis markers, and anti–human immunodeficiency virus test were negative. Antistreptolysin O titer; thyroid function tests; hormone profile; and IgG, IgA, IgM, C3, C4, and total IgE levels were within reference range. Cyclosporine 200 mg daily was initiated for treatment of erythrodermic psoriasis. On days 20 and 45 of treatment, eosinophil levels were 8.26% (0.994 cells/mL) and 17.5% (1620 cells/mL), respectively. The patient’s erythema and edema remarkably decreased at the end of the first month of treatment with cyclosporine, but simultaneous onset of pruritus and increasing eosinophil levels despite treatment with cyclosporine were noted. Scabies mites were demonstrated on microscopic examination of skin scrapings from the dorsal aspect of the hand (Figure 4), and the patient was treated with permethrin cream 5%. At 6-month follow-up, eosinophil levels were within reference range (0.317 cells/mL; 4.75%); pruritus and lesions were not observed.

Figure 3. Severe widespread erythema, scaling, and edema in a 26-year-old woman with psoriasis.

Figure 4. A mite and an egg were noted on direct microscopic examination of skin scrapings from the dorsal aspect of the hand (original magnification ×400).

Comment

Erythrodermic psoriasis is a severe form of psoriasis. In the 2010 consensus of the National Psoriasis Foundation medical board, it was reported that cyclosporine and infliximab are the fastest and most effective agents in treating erythrodermic psoriasis.¹

Progressive increases in the number of eosinophils prompted us to screen our patients for causes of hypereosinophilia. Increased eosinophil counts have not been linked to treatment with cyclosporine. In contrast, it has been detected that cyclosporine reduces the number of eosinophils in many eosinophilic dermatoses.²

There is no hematologic finding for scabies; therefore, clinical findings are most important in the diagnosis. Crusted scabies is a special form of scabies seen in immunocompromised patients that is characterized by excessive numbers of scabies mites. Peripheral eosinophilia may be observed in this form of the disease.³ In classic scabies, eosinophilia is uncommon in peripheral blood. In contrast with these data, there are 2 cases in the literature of scabies secondary to disorders of keratinization without immune deficiency with different clinical presentations.⁴ In these patients, the most striking and only finding at the time of diagnosis was substantial eosinophilia. These cases were reported with emphasis on eosinophilia as the first sign of scabies infestation in patients with severe hyperkeratosis.⁴ In our patients, the spread of infection may have been facilitated by the immunosuppressive effects of cyclosporine in addition to the existing disease. Crusted scabies after use of cyclosporine for atopic dermatitis has been reported. It was emphasized that suppression of scratching and immunosuppression due to cyclospor-ine caused the spread of scabies mites in the skin.⁵

Burrows, vesicles, and erythematous papules are typical lesions seen in scabies. Erythematous papules usually are distributed on the abdomen, thoracic region, axillae, and medial thighs and are characterized by more intense pruritus, especially at night. In our patients, widespread erythema and scaling were noted, and pruritus was thought to be due to psoriasis lesions. Because of excessive scaling in the stratum corneum from psoriasis, the clinical features of scabies were concealed and the classic clinical signs of scabies were not present. The patients’ hypereosinophilia led us to investigate the cause. A lesional biopsy and direct microscopy demonstrated scabies mites.

Conclusion

The relationship between psoriasis and scabies previously has been reported in the literature as scabies with crusts mimicking rupioid psoriasis.⁶ However, our patients developed scabies in the setting of psoriasis. Severe scabies can present as erythroderma.⁷ We believe the diagnosis of scabies in our patients would have been more complicated without the preexisting psoriasis, as biopsies of erythrodermic psoriasis often are nonspecific and may contain eosinophils in the inflammatory infiltrate. Although pruritus may be interpreted as a result of the primary dermatologic disease, the presence of hypereosinophilia may suggest scabies in erythrodermic patients. For this reason, peripheral eosinophilia may suggest scabies in patients with erythematous scaly inflammatory skin diseases who are treated with immunosuppressive agents, and a search for scabies mites in skin scrapings should be undertaken.

Erythrodermic psoriasis is a severe form of psoriasis associated with higher morbidity and mortality rates compared to other forms of psoriasis. Cutaneous signs of erythrodermic psoriasis include erythema, edema, and superficial desquamation. Scabies is a common ectoparasitic disease that is diagnosed by the presence of pruritus and typical clinical signs including burrows, vesicles, and erythematous papules. Erythematous papules usually are distributed on the abdomen, thoracic region, axillae, and medial thighs and are characterized by more intense pruritus, especially at night. The course of scabies may be altered in patients with desquamative inflammatory skin disease such as psoriasis. Pruritus may be absent and typical scabies lesions may be concealed due to the preexisting disease, resulting in delayed diagnosis.
 

Case Reports

Patient 1

A 13-year-old adolescent boy with psoriasis of 4 years’ duration presented to our outpatient clinic with severe widespread erythema and mild desquamation (Figure 1). The patient was hospitalized following a diagnosis of erythrodermic psoriasis. His medical history was remarkable for recurrent episodes of bronchitis, and his family history included 2 siblings with psoriasis. Physical examination revealed no abnormalities, except for a fever (temperature, 38.0°C). A complete blood cell count revealed an elevated absolute eosinophil count (9260 cells/µL [reference range, 0–700 cells/µL]) corresponding to 48.4% (reference range, 0%–7%) of blood cells. There were no pathological findings in the serum biochemistry; complete urine analysis; throat, sputum, and urine cultures; stool analysis for parasites; or chest radiography. A VDRL test, hepatitis markers, and anti–human immunodeficiency virus test were negative. Antistreptolysin O titer; thyroid function tests; hormone profile; and IgG, IgA, IgM, C3, C4, and total IgE levels were within reference range. Peripheral blood smear, abdominal ultrasonography, electrocardiography, and echocardiography were performed; no cardiac pathology was observed. Cyclosporine 200 mg daily was initiated for treatment of erythrodermic psoriasis.

Figure 1. Severe widespread erythema and mild desquamation in a 13-year-old adolescent boy with psoriasis.

One week after the initiation of treatment the patient’s fever improved. At 2-week follow-up, a complete blood cell count demonstrated more marked eosinophilia, and the percentage of eosinophils at weekly intervals over the next 3 weeks increased to 51.2%, 63.0%, and 71.7%, respectively. The patient presented 2 weeks later with a chief concern of pruritus. Histologic examination of a lesional biopsy specimen revealed psoriasiform epithelial hyperplasia with scabies mites in the stratum corneum (Figure 2). Mites also were noted on direct microscopic examination of scrapings performed with the suspicion of scabies. The patient was treated with permethrin cream 5%. Although all of the patients and staff in the ward also were administered topical permethrin to prevent a scabies epidemic, 2 inpatients who had been discharged before the diagnosis of scabies presented to our outpatient clinic approximately 1 month later with scabies. At 6-month follow-up, the patient’s eosinophil count was within reference range (0.237cells/µL; 3.78%); pruritus and lesions were not observed.

Figure 2. Findings from a lesional biopsy specimen demonstrated epidermal psoriasiform changes and eosinophils in the dermis. Mites were present in the stratum corneum (H&E, original magnification ×100). Figure 2. Findings from a lesional biopsy specimen demonstrated epidermal psoriasiform changes and eosinophils in the dermis. Mites were present in the stratum corneum (H&E, original magnification ×100).

Patient 2

A 26-year-old woman with psoriasis of 5 years’ duration was hospitalized for treatment of erythrodermic psoriasis at the same time as patient 1, her brother. On dermatologic examination, severe widespread erythema, scaling, and edema were noted (Figure 3). Physical examination revealed a fever (temperature, 38.5°C). Hypoalbuminemia and high C-reactive protein levels were present in serum biochemistry. Eosinophil counts were within reference range (0.346 cells/µL; 1.88%). No pathological findings were noted in the complete urine analysis; throat, sputum, and urine cultures; stool analysis for parasites; or chest radiography. A VDRL test, hepatitis markers, and anti–human immunodeficiency virus test were negative. Antistreptolysin O titer; thyroid function tests; hormone profile; and IgG, IgA, IgM, C3, C4, and total IgE levels were within reference range. Cyclosporine 200 mg daily was initiated for treatment of erythrodermic psoriasis. On days 20 and 45 of treatment, eosinophil levels were 8.26% (0.994 cells/mL) and 17.5% (1620 cells/mL), respectively. The patient’s erythema and edema remarkably decreased at the end of the first month of treatment with cyclosporine, but simultaneous onset of pruritus and increasing eosinophil levels despite treatment with cyclosporine were noted. Scabies mites were demonstrated on microscopic examination of skin scrapings from the dorsal aspect of the hand (Figure 4), and the patient was treated with permethrin cream 5%. At 6-month follow-up, eosinophil levels were within reference range (0.317 cells/mL; 4.75%); pruritus and lesions were not observed.

Figure 3. Severe widespread erythema, scaling, and edema in a 26-year-old woman with psoriasis.

Figure 4. A mite and an egg were noted on direct microscopic examination of skin scrapings from the dorsal aspect of the hand (original magnification ×400).

Comment

Erythrodermic psoriasis is a severe form of psoriasis. In the 2010 consensus of the National Psoriasis Foundation medical board, it was reported that cyclosporine and infliximab are the fastest and most effective agents in treating erythrodermic psoriasis.¹

Progressive increases in the number of eosinophils prompted us to screen our patients for causes of hypereosinophilia. Increased eosinophil counts have not been linked to treatment with cyclosporine. In contrast, it has been detected that cyclosporine reduces the number of eosinophils in many eosinophilic dermatoses.²

There is no hematologic finding for scabies; therefore, clinical findings are most important in the diagnosis. Crusted scabies is a special form of scabies seen in immunocompromised patients that is characterized by excessive numbers of scabies mites. Peripheral eosinophilia may be observed in this form of the disease.³ In classic scabies, eosinophilia is uncommon in peripheral blood. In contrast with these data, there are 2 cases in the literature of scabies secondary to disorders of keratinization without immune deficiency with different clinical presentations.⁴ In these patients, the most striking and only finding at the time of diagnosis was substantial eosinophilia. These cases were reported with emphasis on eosinophilia as the first sign of scabies infestation in patients with severe hyperkeratosis.⁴ In our patients, the spread of infection may have been facilitated by the immunosuppressive effects of cyclosporine in addition to the existing disease. Crusted scabies after use of cyclosporine for atopic dermatitis has been reported. It was emphasized that suppression of scratching and immunosuppression due to cyclospor-ine caused the spread of scabies mites in the skin.⁵

Burrows, vesicles, and erythematous papules are typical lesions seen in scabies. Erythematous papules usually are distributed on the abdomen, thoracic region, axillae, and medial thighs and are characterized by more intense pruritus, especially at night. In our patients, widespread erythema and scaling were noted, and pruritus was thought to be due to psoriasis lesions. Because of excessive scaling in the stratum corneum from psoriasis, the clinical features of scabies were concealed and the classic clinical signs of scabies were not present. The patients’ hypereosinophilia led us to investigate the cause. A lesional biopsy and direct microscopy demonstrated scabies mites.

Conclusion

The relationship between psoriasis and scabies previously has been reported in the literature as scabies with crusts mimicking rupioid psoriasis.⁶ However, our patients developed scabies in the setting of psoriasis. Severe scabies can present as erythroderma.⁷ We believe the diagnosis of scabies in our patients would have been more complicated without the preexisting psoriasis, as biopsies of erythrodermic psoriasis often are nonspecific and may contain eosinophils in the inflammatory infiltrate. Although pruritus may be interpreted as a result of the primary dermatologic disease, the presence of hypereosinophilia may suggest scabies in erythrodermic patients. For this reason, peripheral eosinophilia may suggest scabies in patients with erythematous scaly inflammatory skin diseases who are treated with immunosuppressive agents, and a search for scabies mites in skin scrapings should be undertaken.

Erythrodermic psoriasis is a severe form of psoriasis associated with higher morbidity and mortality rates compared to other forms of psoriasis. Cutaneous signs of erythrodermic psoriasis include erythema, edema, and superficial desquamation. Scabies is a common ectoparasitic disease that is diagnosed by the presence of pruritus and typical clinical signs including burrows, vesicles, and erythematous papules. Erythematous papules usually are distributed on the abdomen, thoracic region, axillae, and medial thighs and are characterized by more intense pruritus, especially at night. The course of scabies may be altered in patients with desquamative inflammatory skin disease such as psoriasis. Pruritus may be absent and typical scabies lesions may be concealed due to the preexisting disease, resulting in delayed diagnosis.
 

Case Reports

Patient 1

A 13-year-old adolescent boy with psoriasis of 4 years’ duration presented to our outpatient clinic with severe widespread erythema and mild desquamation (Figure 1). The patient was hospitalized following a diagnosis of erythrodermic psoriasis. His medical history was remarkable for recurrent episodes of bronchitis, and his family history included 2 siblings with psoriasis. Physical examination revealed no abnormalities, except for a fever (temperature, 38.0°C). A complete blood cell count revealed an elevated absolute eosinophil count (9260 cells/µL [reference range, 0–700 cells/µL]) corresponding to 48.4% (reference range, 0%–7%) of blood cells. There were no pathological findings in the serum biochemistry; complete urine analysis; throat, sputum, and urine cultures; stool analysis for parasites; or chest radiography. A VDRL test, hepatitis markers, and anti–human immunodeficiency virus test were negative. Antistreptolysin O titer; thyroid function tests; hormone profile; and IgG, IgA, IgM, C3, C4, and total IgE levels were within reference range. Peripheral blood smear, abdominal ultrasonography, electrocardiography, and echocardiography were performed; no cardiac pathology was observed. Cyclosporine 200 mg daily was initiated for treatment of erythrodermic psoriasis.

Figure 1. Severe widespread erythema and mild desquamation in a 13-year-old adolescent boy with psoriasis.

One week after the initiation of treatment the patient’s fever improved. At 2-week follow-up, a complete blood cell count demonstrated more marked eosinophilia, and the percentage of eosinophils at weekly intervals over the next 3 weeks increased to 51.2%, 63.0%, and 71.7%, respectively. The patient presented 2 weeks later with a chief concern of pruritus. Histologic examination of a lesional biopsy specimen revealed psoriasiform epithelial hyperplasia with scabies mites in the stratum corneum (Figure 2). Mites also were noted on direct microscopic examination of scrapings performed with the suspicion of scabies. The patient was treated with permethrin cream 5%. Although all of the patients and staff in the ward also were administered topical permethrin to prevent a scabies epidemic, 2 inpatients who had been discharged before the diagnosis of scabies presented to our outpatient clinic approximately 1 month later with scabies. At 6-month follow-up, the patient’s eosinophil count was within reference range (0.237cells/µL; 3.78%); pruritus and lesions were not observed.

Figure 2. Findings from a lesional biopsy specimen demonstrated epidermal psoriasiform changes and eosinophils in the dermis. Mites were present in the stratum corneum (H&E, original magnification ×100). Figure 2. Findings from a lesional biopsy specimen demonstrated epidermal psoriasiform changes and eosinophils in the dermis. Mites were present in the stratum corneum (H&E, original magnification ×100).

Patient 2

A 26-year-old woman with psoriasis of 5 years’ duration was hospitalized for treatment of erythrodermic psoriasis at the same time as patient 1, her brother. On dermatologic examination, severe widespread erythema, scaling, and edema were noted (Figure 3). Physical examination revealed a fever (temperature, 38.5°C). Hypoalbuminemia and high C-reactive protein levels were present in serum biochemistry. Eosinophil counts were within reference range (0.346 cells/µL; 1.88%). No pathological findings were noted in the complete urine analysis; throat, sputum, and urine cultures; stool analysis for parasites; or chest radiography. A VDRL test, hepatitis markers, and anti–human immunodeficiency virus test were negative. Antistreptolysin O titer; thyroid function tests; hormone profile; and IgG, IgA, IgM, C3, C4, and total IgE levels were within reference range. Cyclosporine 200 mg daily was initiated for treatment of erythrodermic psoriasis. On days 20 and 45 of treatment, eosinophil levels were 8.26% (0.994 cells/mL) and 17.5% (1620 cells/mL), respectively. The patient’s erythema and edema remarkably decreased at the end of the first month of treatment with cyclosporine, but simultaneous onset of pruritus and increasing eosinophil levels despite treatment with cyclosporine were noted. Scabies mites were demonstrated on microscopic examination of skin scrapings from the dorsal aspect of the hand (Figure 4), and the patient was treated with permethrin cream 5%. At 6-month follow-up, eosinophil levels were within reference range (0.317 cells/mL; 4.75%); pruritus and lesions were not observed.

Figure 3. Severe widespread erythema, scaling, and edema in a 26-year-old woman with psoriasis.

Figure 4. A mite and an egg were noted on direct microscopic examination of skin scrapings from the dorsal aspect of the hand (original magnification ×400).

Comment

Erythrodermic psoriasis is a severe form of psoriasis. In the 2010 consensus of the National Psoriasis Foundation medical board, it was reported that cyclosporine and infliximab are the fastest and most effective agents in treating erythrodermic psoriasis.¹

Progressive increases in the number of eosinophils prompted us to screen our patients for causes of hypereosinophilia. Increased eosinophil counts have not been linked to treatment with cyclosporine. In contrast, it has been detected that cyclosporine reduces the number of eosinophils in many eosinophilic dermatoses.²

There is no hematologic finding for scabies; therefore, clinical findings are most important in the diagnosis. Crusted scabies is a special form of scabies seen in immunocompromised patients that is characterized by excessive numbers of scabies mites. Peripheral eosinophilia may be observed in this form of the disease.³ In classic scabies, eosinophilia is uncommon in peripheral blood. In contrast with these data, there are 2 cases in the literature of scabies secondary to disorders of keratinization without immune deficiency with different clinical presentations.⁴ In these patients, the most striking and only finding at the time of diagnosis was substantial eosinophilia. These cases were reported with emphasis on eosinophilia as the first sign of scabies infestation in patients with severe hyperkeratosis.⁴ In our patients, the spread of infection may have been facilitated by the immunosuppressive effects of cyclosporine in addition to the existing disease. Crusted scabies after use of cyclosporine for atopic dermatitis has been reported. It was emphasized that suppression of scratching and immunosuppression due to cyclospor-ine caused the spread of scabies mites in the skin.⁵

Burrows, vesicles, and erythematous papules are typical lesions seen in scabies. Erythematous papules usually are distributed on the abdomen, thoracic region, axillae, and medial thighs and are characterized by more intense pruritus, especially at night. In our patients, widespread erythema and scaling were noted, and pruritus was thought to be due to psoriasis lesions. Because of excessive scaling in the stratum corneum from psoriasis, the clinical features of scabies were concealed and the classic clinical signs of scabies were not present. The patients’ hypereosinophilia led us to investigate the cause. A lesional biopsy and direct microscopy demonstrated scabies mites.

Conclusion

The relationship between psoriasis and scabies previously has been reported in the literature as scabies with crusts mimicking rupioid psoriasis.⁶ However, our patients developed scabies in the setting of psoriasis. Severe scabies can present as erythroderma.⁷ We believe the diagnosis of scabies in our patients would have been more complicated without the preexisting psoriasis, as biopsies of erythrodermic psoriasis often are nonspecific and may contain eosinophils in the inflammatory infiltrate. Although pruritus may be interpreted as a result of the primary dermatologic disease, the presence of hypereosinophilia may suggest scabies in erythrodermic patients. For this reason, peripheral eosinophilia may suggest scabies in patients with erythematous scaly inflammatory skin diseases who are treated with immunosuppressive agents, and a search for scabies mites in skin scrapings should be undertaken.

Psoriasis affects 1% to 2% of individuals in the United States, typically within the third decade of life.^1,2 Psoriasis lesions may be persistent or relapsing plaques or pustules. The epidermal thickening that often is noted in psoriasis is secondary to the elongation of rete ridges. Parakeratosis, which also is often noted in psoriasis, is the accumulation of cells with retained nuclei within the cornified layer. Localized pustular psoriasis is a variant of psoriasis that displays scaling erythematous plaques studded with pustules. The pustules are most frequently observed on the palms, soles, and nails of affected individuals.¹ Palmoplantar pustular psoriasis is most commonly seen in women in their fifth and sixth decades of life.³ One agent commonly used in the treatment of psoriasis is methotrexate, a prodrug that is converted to polyglutamyl derivatives and acts as a dihydrofolate reductase inhibitor.^4,5 We report a case of palmoplantar pustular psoriasis that was triggered by initiation of a beta-blocker. The patient’s condition was controlled with a low-dose methotrexate regimen.

Case Report

A 76-year-old woman with a history of hypertension, hyperlipidemia, and hypothyroidism presented with erythema and pustules on the bilateral palms and soles 6 weeks following initiation of a beta-blocker. On discontinuation of the beta-blocker, the lesions showed minimal improvement without resolution. The patient then was started on fluocinonide ointment 0.05% and acitretin 25 mg 3 times weekly. Improvement (25%) was noted over the course of 9 months; acitretin then was increased to 25 mg 4 times weekly, but no change was noted (Figure). Acitretin then was discontinued and she was started on methotrexate 2.5 mg weekly, followed by improvement of the lesions on the palms and soles. This regimen was continued and the patient was stable at 2-year follow-up with moderate hyperpigmentation of the palms and minimal hyperpigmentation of the soles, both without erythema or exudates.

Palmoplantar pustular psoriasis on the soles of both feet prior to treatment with methotrexate.

Comment

Palmoplantar pustular psoriasis is a rare form of psoriasis; it may, however, be induced by a variety of medications.⁶ A causal relationship to psoriasis has been documented with beta-blockers, lithium, tetracyclines, nonsteroidal anti-inflammatory drugs, adalimumab, and synthetic antimalarials. Other drugs linked to psoriasis are angiotensin-converting enzyme inhibitors, interferons, and terbinafine.⁷ Anti–tumor necrosis factor a agents such as in-fliximab and etanercept also have been reported to induce pustular psoriasis.⁶ These drugs have been reported to aggravate preexisting psoriasis, provoke lesions in uninvolved skin in individuals with psoriasis, and induce psoriasis in patients without a personal or family history of psoriasis.⁸ The pathogenesis of psoriasis triggered by beta-blockers is thought to be due to decreased intraepidermal cyclic adenosine monophosphate, leading to an increase in epidermal cell turnover.⁷

Palmoplantar pustular psoriasis is a debilitating chronic illness that can span decades.⁹ Not only can it be socially stigmatizing, but it also interferes with patients’ quality of life.¹⁰ Various therapies are used to treat this condition including coal tar, topical corticosteroids with or without polythene occlusion, photochemotherapy, tetracyclines, systemic retinoids, cyclosporine, biologics, and methotrexate.⁹ There currently is no therapeutic standard for controlling this disease, as treatment often is fraught with medication resistance and intolerance as well as frequent relapses. Many medications also are used without firm evidence proving they are beneficial.¹¹

Despite the advent of biologics, methotrexate remains commonly used in the treatment of psoriasis as monotherapy or in combination with other drugs. In comparison to biologics, methotrexate is less expensive, has established efficacy data, and can be administered orally.¹² Although it was previously believed that the antiproliferative action of methotrexate via antifolate metabolism led to improvement of psoriatic lesions, in vitro data point to the anti-inflammatory activity of methotrexate playing the more dominant role in disease improvement. Methotrexate also inhibits 5-aminoimidazole-4-carboxamide ribonucleotide transformylase, leading to the buildup of adeno-sine in tissue and consequently contributing to its anti-inflammatory properties.¹²

In psoriasis patients, methotrexate is commonly used in dosages up to 30 mg weekly.⁵ Our patient demonstrates a rare case of palmoplantar pustular psoriasis that was well controlled using low-dose methotrexate (2.5 mg weekly). Some cases report low doses of 15 to 20 mg for long-term control in psoriasis.¹³ However, the successful use of doses as low as 2.5 mg for control of any variant of psoriasis is rare.

Conclusion

Although it has been shown to be effective in the treatment of psoriasis, the use of methotrexate is not benign; it has been associated with hepatotoxicity and bone marrow toxicity.¹² It is important for dermatologists to recognize that pustular psoriasis can be treated with low-dose methotrexate to avoid potentially toxic effects of higher doses of methotrexate, which is especially true in cases of drug-induced disease, as seen in our patient.

Psoriasis affects 1% to 2% of individuals in the United States, typically within the third decade of life.^1,2 Psoriasis lesions may be persistent or relapsing plaques or pustules. The epidermal thickening that often is noted in psoriasis is secondary to the elongation of rete ridges. Parakeratosis, which also is often noted in psoriasis, is the accumulation of cells with retained nuclei within the cornified layer. Localized pustular psoriasis is a variant of psoriasis that displays scaling erythematous plaques studded with pustules. The pustules are most frequently observed on the palms, soles, and nails of affected individuals.¹ Palmoplantar pustular psoriasis is most commonly seen in women in their fifth and sixth decades of life.³ One agent commonly used in the treatment of psoriasis is methotrexate, a prodrug that is converted to polyglutamyl derivatives and acts as a dihydrofolate reductase inhibitor.^4,5 We report a case of palmoplantar pustular psoriasis that was triggered by initiation of a beta-blocker. The patient’s condition was controlled with a low-dose methotrexate regimen.

Case Report

A 76-year-old woman with a history of hypertension, hyperlipidemia, and hypothyroidism presented with erythema and pustules on the bilateral palms and soles 6 weeks following initiation of a beta-blocker. On discontinuation of the beta-blocker, the lesions showed minimal improvement without resolution. The patient then was started on fluocinonide ointment 0.05% and acitretin 25 mg 3 times weekly. Improvement (25%) was noted over the course of 9 months; acitretin then was increased to 25 mg 4 times weekly, but no change was noted (Figure). Acitretin then was discontinued and she was started on methotrexate 2.5 mg weekly, followed by improvement of the lesions on the palms and soles. This regimen was continued and the patient was stable at 2-year follow-up with moderate hyperpigmentation of the palms and minimal hyperpigmentation of the soles, both without erythema or exudates.

Palmoplantar pustular psoriasis on the soles of both feet prior to treatment with methotrexate.

Comment

Palmoplantar pustular psoriasis is a rare form of psoriasis; it may, however, be induced by a variety of medications.⁶ A causal relationship to psoriasis has been documented with beta-blockers, lithium, tetracyclines, nonsteroidal anti-inflammatory drugs, adalimumab, and synthetic antimalarials. Other drugs linked to psoriasis are angiotensin-converting enzyme inhibitors, interferons, and terbinafine.⁷ Anti–tumor necrosis factor a agents such as in-fliximab and etanercept also have been reported to induce pustular psoriasis.⁶ These drugs have been reported to aggravate preexisting psoriasis, provoke lesions in uninvolved skin in individuals with psoriasis, and induce psoriasis in patients without a personal or family history of psoriasis.⁸ The pathogenesis of psoriasis triggered by beta-blockers is thought to be due to decreased intraepidermal cyclic adenosine monophosphate, leading to an increase in epidermal cell turnover.⁷

Palmoplantar pustular psoriasis is a debilitating chronic illness that can span decades.⁹ Not only can it be socially stigmatizing, but it also interferes with patients’ quality of life.¹⁰ Various therapies are used to treat this condition including coal tar, topical corticosteroids with or without polythene occlusion, photochemotherapy, tetracyclines, systemic retinoids, cyclosporine, biologics, and methotrexate.⁹ There currently is no therapeutic standard for controlling this disease, as treatment often is fraught with medication resistance and intolerance as well as frequent relapses. Many medications also are used without firm evidence proving they are beneficial.¹¹

Despite the advent of biologics, methotrexate remains commonly used in the treatment of psoriasis as monotherapy or in combination with other drugs. In comparison to biologics, methotrexate is less expensive, has established efficacy data, and can be administered orally.¹² Although it was previously believed that the antiproliferative action of methotrexate via antifolate metabolism led to improvement of psoriatic lesions, in vitro data point to the anti-inflammatory activity of methotrexate playing the more dominant role in disease improvement. Methotrexate also inhibits 5-aminoimidazole-4-carboxamide ribonucleotide transformylase, leading to the buildup of adeno-sine in tissue and consequently contributing to its anti-inflammatory properties.¹²

In psoriasis patients, methotrexate is commonly used in dosages up to 30 mg weekly.⁵ Our patient demonstrates a rare case of palmoplantar pustular psoriasis that was well controlled using low-dose methotrexate (2.5 mg weekly). Some cases report low doses of 15 to 20 mg for long-term control in psoriasis.¹³ However, the successful use of doses as low as 2.5 mg for control of any variant of psoriasis is rare.

Conclusion

Although it has been shown to be effective in the treatment of psoriasis, the use of methotrexate is not benign; it has been associated with hepatotoxicity and bone marrow toxicity.¹² It is important for dermatologists to recognize that pustular psoriasis can be treated with low-dose methotrexate to avoid potentially toxic effects of higher doses of methotrexate, which is especially true in cases of drug-induced disease, as seen in our patient.

Psoriasis affects 1% to 2% of individuals in the United States, typically within the third decade of life.^1,2 Psoriasis lesions may be persistent or relapsing plaques or pustules. The epidermal thickening that often is noted in psoriasis is secondary to the elongation of rete ridges. Parakeratosis, which also is often noted in psoriasis, is the accumulation of cells with retained nuclei within the cornified layer. Localized pustular psoriasis is a variant of psoriasis that displays scaling erythematous plaques studded with pustules. The pustules are most frequently observed on the palms, soles, and nails of affected individuals.¹ Palmoplantar pustular psoriasis is most commonly seen in women in their fifth and sixth decades of life.³ One agent commonly used in the treatment of psoriasis is methotrexate, a prodrug that is converted to polyglutamyl derivatives and acts as a dihydrofolate reductase inhibitor.^4,5 We report a case of palmoplantar pustular psoriasis that was triggered by initiation of a beta-blocker. The patient’s condition was controlled with a low-dose methotrexate regimen.

Case Report

A 76-year-old woman with a history of hypertension, hyperlipidemia, and hypothyroidism presented with erythema and pustules on the bilateral palms and soles 6 weeks following initiation of a beta-blocker. On discontinuation of the beta-blocker, the lesions showed minimal improvement without resolution. The patient then was started on fluocinonide ointment 0.05% and acitretin 25 mg 3 times weekly. Improvement (25%) was noted over the course of 9 months; acitretin then was increased to 25 mg 4 times weekly, but no change was noted (Figure). Acitretin then was discontinued and she was started on methotrexate 2.5 mg weekly, followed by improvement of the lesions on the palms and soles. This regimen was continued and the patient was stable at 2-year follow-up with moderate hyperpigmentation of the palms and minimal hyperpigmentation of the soles, both without erythema or exudates.

Palmoplantar pustular psoriasis on the soles of both feet prior to treatment with methotrexate.

Comment

Palmoplantar pustular psoriasis is a rare form of psoriasis; it may, however, be induced by a variety of medications.⁶ A causal relationship to psoriasis has been documented with beta-blockers, lithium, tetracyclines, nonsteroidal anti-inflammatory drugs, adalimumab, and synthetic antimalarials. Other drugs linked to psoriasis are angiotensin-converting enzyme inhibitors, interferons, and terbinafine.⁷ Anti–tumor necrosis factor a agents such as in-fliximab and etanercept also have been reported to induce pustular psoriasis.⁶ These drugs have been reported to aggravate preexisting psoriasis, provoke lesions in uninvolved skin in individuals with psoriasis, and induce psoriasis in patients without a personal or family history of psoriasis.⁸ The pathogenesis of psoriasis triggered by beta-blockers is thought to be due to decreased intraepidermal cyclic adenosine monophosphate, leading to an increase in epidermal cell turnover.⁷

Palmoplantar pustular psoriasis is a debilitating chronic illness that can span decades.⁹ Not only can it be socially stigmatizing, but it also interferes with patients’ quality of life.¹⁰ Various therapies are used to treat this condition including coal tar, topical corticosteroids with or without polythene occlusion, photochemotherapy, tetracyclines, systemic retinoids, cyclosporine, biologics, and methotrexate.⁹ There currently is no therapeutic standard for controlling this disease, as treatment often is fraught with medication resistance and intolerance as well as frequent relapses. Many medications also are used without firm evidence proving they are beneficial.¹¹

Despite the advent of biologics, methotrexate remains commonly used in the treatment of psoriasis as monotherapy or in combination with other drugs. In comparison to biologics, methotrexate is less expensive, has established efficacy data, and can be administered orally.¹² Although it was previously believed that the antiproliferative action of methotrexate via antifolate metabolism led to improvement of psoriatic lesions, in vitro data point to the anti-inflammatory activity of methotrexate playing the more dominant role in disease improvement. Methotrexate also inhibits 5-aminoimidazole-4-carboxamide ribonucleotide transformylase, leading to the buildup of adeno-sine in tissue and consequently contributing to its anti-inflammatory properties.¹²

In psoriasis patients, methotrexate is commonly used in dosages up to 30 mg weekly.⁵ Our patient demonstrates a rare case of palmoplantar pustular psoriasis that was well controlled using low-dose methotrexate (2.5 mg weekly). Some cases report low doses of 15 to 20 mg for long-term control in psoriasis.¹³ However, the successful use of doses as low as 2.5 mg for control of any variant of psoriasis is rare.

Conclusion

Although it has been shown to be effective in the treatment of psoriasis, the use of methotrexate is not benign; it has been associated with hepatotoxicity and bone marrow toxicity.¹² It is important for dermatologists to recognize that pustular psoriasis can be treated with low-dose methotrexate to avoid potentially toxic effects of higher doses of methotrexate, which is especially true in cases of drug-induced disease, as seen in our patient.