Psoriasis

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.

dbrunk@frontlinemedcom.com

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.

dbrunk@frontlinemedcom.com

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.

dbrunk@frontlinemedcom.com

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.

Case Report

A 28-year-old man presented to the dermatology department with cone-shaped, oyster shell–like skin lesions on the scalp, trunk, arms, and legs of 1 month’s duration. He denied any fever, pruritus, pain, joint stiffness, or arthralgia. His family history was remarkable for psoriasis in his paternal grandfather and uncle.

A few years prior to the eruption, the patient developed a rash in the bilateral inguinal area but did not seek medical attention. One month prior to presentation, the rash began to spread to the scalp, trunk, arms, and legs. He was treated in the emergency department with a 5-day course of oral prednisone without any noticeable improvement. At the time of presentation to the dermatology clinic, he was found to have multiple well-demarcated erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crusts (Figure 1). Rapid plasma reagin testing was negative. A 4-mm punch biopsy specimen from the right upper arm demonstrated thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (Figure 2). In the stratum corneum, there was seroexudate with numerous red blood cells between the parakeratosis.

Figure 1. Multiple well-demarcated erythematous plaques with hyperkeratotic crust on the back (A). Closer view of erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crust (B).

Figure 2. Thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (H&E, original magnification ×100).

The patient was diagnosed with rupioid psoriasis. The lesions dramatically improved with methotrexate 10 mg weekly and topical steroids. Two months following diagnosis the patient presented with persistent hyperkeratotic lesions on the back, as he had difficulty reaching the lesions to apply topical medications; intralesional steroid injections were added. This regimen resulted in near-complete resolution maintained at his most recent follow-up 2 years following diagnosis in our clinic.

Comment

Rupia is based on the Greek word rhupos, which means dirt or filth. The term rupioid has been used to describe well-demarcated, cone-shaped plaques with thick, dark, lamellate, and adherent crusts on the skin somewhat resembling oyster or limpet shells. Histologically, a serosanguineous exudate along with thick skin helps to impart a “dirty” appearance to rupioid lesions. Rupioid manifestations have been clinically observed in a variety of diseases, including rupioid psoriasis,^1-3 reactive arthritis,⁴ disseminated histoplasmosis,⁵ keratotic scabies,⁶ secondary syphilis,⁷ and photosensitive skin lesions in association with aminoaciduria.⁸ To diagnose the underlying infectious or inflammatory diseases beneath the thick crusts, skin biopsy and a blood test for syphilis may be necessary.

Rupioid psoriasis is a morphologic subtype of plaque psoriasis with hyperkeratotic lesions that resemble an oyster or limpet shell. Patients with thick plaque psoriasis are more likely to be male with a higher incidence of nail disease and psoriatic arthritis as well as a greater body surface area affected than patients with thin plaque psoriasis.¹ Although most cases of rupioid psoriasis were associated with psoriatic arthritis,³ our patient showed no evidence of psoriatic arthritis or nail changes.

Reactive arthritis may have a similar appearance to rupioid psoriasis but may be distinguished by a geographic relief map configuration with coalescing, keratotic and desquamating lesions, as well as associated urethritis, arthritis, and conjunctivitis.⁴ A rupioid eruption was reported as a manifestation of disseminated histoplasmosis with dirty-appearing, heaped-up, crusted lesions present on the cheeks, nose, and forehead on clinical examination and several intracellular and extracellular oval structures on histologic examination with periodic acid–Schiff and Gomori methenamine-silver stain.⁵ Malignant or rupioid syphilis refers to the stage in which papulopustules of pustular syphilis undergo central necrosis due to endarteritis obliterans and intravascular thrombosis.⁷

In our case, the patient’s psoriasis could have flared after discontinuation of the prednisone that was administered by the emergency department physician. Most cases have been treated with combined systemic and topical therapy.⁹ For systemic treatment, cyclosporine, intramuscular or oral methotrexate, adalimumab, and ustekinumab³ have been used with remarkable improvement. Hyperkeratotic types of psoriasis are generally thought to be resistant to topical therapy because of poor penetration of applied agents; however, a case of rupioid psoriasis without arthritis was successfully treated with topical steroids without concomitant systemic medications.²

Conclusion

Rupioid psoriasis is a morphological subtype of plaque psoriasis with hyperkeratotic lesions that resemble a limpet shell. Rupioid skin manifestations may be seen in a variety of diseases including rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, and photosensitive skin lesions associated with aminoaciduria. Diagnosis of rupioid psoriasis often requires additional testing such as skin biopsy, skin scraping, and blood tests, and it typically requires systemic therapy for treatment.

Case Report

A 28-year-old man presented to the dermatology department with cone-shaped, oyster shell–like skin lesions on the scalp, trunk, arms, and legs of 1 month’s duration. He denied any fever, pruritus, pain, joint stiffness, or arthralgia. His family history was remarkable for psoriasis in his paternal grandfather and uncle.

A few years prior to the eruption, the patient developed a rash in the bilateral inguinal area but did not seek medical attention. One month prior to presentation, the rash began to spread to the scalp, trunk, arms, and legs. He was treated in the emergency department with a 5-day course of oral prednisone without any noticeable improvement. At the time of presentation to the dermatology clinic, he was found to have multiple well-demarcated erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crusts (Figure 1). Rapid plasma reagin testing was negative. A 4-mm punch biopsy specimen from the right upper arm demonstrated thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (Figure 2). In the stratum corneum, there was seroexudate with numerous red blood cells between the parakeratosis.

Figure 1. Multiple well-demarcated erythematous plaques with hyperkeratotic crust on the back (A). Closer view of erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crust (B).

Figure 2. Thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (H&E, original magnification ×100).

The patient was diagnosed with rupioid psoriasis. The lesions dramatically improved with methotrexate 10 mg weekly and topical steroids. Two months following diagnosis the patient presented with persistent hyperkeratotic lesions on the back, as he had difficulty reaching the lesions to apply topical medications; intralesional steroid injections were added. This regimen resulted in near-complete resolution maintained at his most recent follow-up 2 years following diagnosis in our clinic.

Comment

Rupia is based on the Greek word rhupos, which means dirt or filth. The term rupioid has been used to describe well-demarcated, cone-shaped plaques with thick, dark, lamellate, and adherent crusts on the skin somewhat resembling oyster or limpet shells. Histologically, a serosanguineous exudate along with thick skin helps to impart a “dirty” appearance to rupioid lesions. Rupioid manifestations have been clinically observed in a variety of diseases, including rupioid psoriasis,^1-3 reactive arthritis,⁴ disseminated histoplasmosis,⁵ keratotic scabies,⁶ secondary syphilis,⁷ and photosensitive skin lesions in association with aminoaciduria.⁸ To diagnose the underlying infectious or inflammatory diseases beneath the thick crusts, skin biopsy and a blood test for syphilis may be necessary.

Rupioid psoriasis is a morphologic subtype of plaque psoriasis with hyperkeratotic lesions that resemble an oyster or limpet shell. Patients with thick plaque psoriasis are more likely to be male with a higher incidence of nail disease and psoriatic arthritis as well as a greater body surface area affected than patients with thin plaque psoriasis.¹ Although most cases of rupioid psoriasis were associated with psoriatic arthritis,³ our patient showed no evidence of psoriatic arthritis or nail changes.

Reactive arthritis may have a similar appearance to rupioid psoriasis but may be distinguished by a geographic relief map configuration with coalescing, keratotic and desquamating lesions, as well as associated urethritis, arthritis, and conjunctivitis.⁴ A rupioid eruption was reported as a manifestation of disseminated histoplasmosis with dirty-appearing, heaped-up, crusted lesions present on the cheeks, nose, and forehead on clinical examination and several intracellular and extracellular oval structures on histologic examination with periodic acid–Schiff and Gomori methenamine-silver stain.⁵ Malignant or rupioid syphilis refers to the stage in which papulopustules of pustular syphilis undergo central necrosis due to endarteritis obliterans and intravascular thrombosis.⁷

In our case, the patient’s psoriasis could have flared after discontinuation of the prednisone that was administered by the emergency department physician. Most cases have been treated with combined systemic and topical therapy.⁹ For systemic treatment, cyclosporine, intramuscular or oral methotrexate, adalimumab, and ustekinumab³ have been used with remarkable improvement. Hyperkeratotic types of psoriasis are generally thought to be resistant to topical therapy because of poor penetration of applied agents; however, a case of rupioid psoriasis without arthritis was successfully treated with topical steroids without concomitant systemic medications.²

Conclusion

Rupioid psoriasis is a morphological subtype of plaque psoriasis with hyperkeratotic lesions that resemble a limpet shell. Rupioid skin manifestations may be seen in a variety of diseases including rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, and photosensitive skin lesions associated with aminoaciduria. Diagnosis of rupioid psoriasis often requires additional testing such as skin biopsy, skin scraping, and blood tests, and it typically requires systemic therapy for treatment.

Case Report

A 28-year-old man presented to the dermatology department with cone-shaped, oyster shell–like skin lesions on the scalp, trunk, arms, and legs of 1 month’s duration. He denied any fever, pruritus, pain, joint stiffness, or arthralgia. His family history was remarkable for psoriasis in his paternal grandfather and uncle.

A few years prior to the eruption, the patient developed a rash in the bilateral inguinal area but did not seek medical attention. One month prior to presentation, the rash began to spread to the scalp, trunk, arms, and legs. He was treated in the emergency department with a 5-day course of oral prednisone without any noticeable improvement. At the time of presentation to the dermatology clinic, he was found to have multiple well-demarcated erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crusts (Figure 1). Rapid plasma reagin testing was negative. A 4-mm punch biopsy specimen from the right upper arm demonstrated thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (Figure 2). In the stratum corneum, there was seroexudate with numerous red blood cells between the parakeratosis.

Figure 1. Multiple well-demarcated erythematous plaques with hyperkeratotic crust on the back (A). Closer view of erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crust (B).

Figure 2. Thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (H&E, original magnification ×100).

The patient was diagnosed with rupioid psoriasis. The lesions dramatically improved with methotrexate 10 mg weekly and topical steroids. Two months following diagnosis the patient presented with persistent hyperkeratotic lesions on the back, as he had difficulty reaching the lesions to apply topical medications; intralesional steroid injections were added. This regimen resulted in near-complete resolution maintained at his most recent follow-up 2 years following diagnosis in our clinic.

Comment

Rupia is based on the Greek word rhupos, which means dirt or filth. The term rupioid has been used to describe well-demarcated, cone-shaped plaques with thick, dark, lamellate, and adherent crusts on the skin somewhat resembling oyster or limpet shells. Histologically, a serosanguineous exudate along with thick skin helps to impart a “dirty” appearance to rupioid lesions. Rupioid manifestations have been clinically observed in a variety of diseases, including rupioid psoriasis,^1-3 reactive arthritis,⁴ disseminated histoplasmosis,⁵ keratotic scabies,⁶ secondary syphilis,⁷ and photosensitive skin lesions in association with aminoaciduria.⁸ To diagnose the underlying infectious or inflammatory diseases beneath the thick crusts, skin biopsy and a blood test for syphilis may be necessary.

Rupioid psoriasis is a morphologic subtype of plaque psoriasis with hyperkeratotic lesions that resemble an oyster or limpet shell. Patients with thick plaque psoriasis are more likely to be male with a higher incidence of nail disease and psoriatic arthritis as well as a greater body surface area affected than patients with thin plaque psoriasis.¹ Although most cases of rupioid psoriasis were associated with psoriatic arthritis,³ our patient showed no evidence of psoriatic arthritis or nail changes.

Reactive arthritis may have a similar appearance to rupioid psoriasis but may be distinguished by a geographic relief map configuration with coalescing, keratotic and desquamating lesions, as well as associated urethritis, arthritis, and conjunctivitis.⁴ A rupioid eruption was reported as a manifestation of disseminated histoplasmosis with dirty-appearing, heaped-up, crusted lesions present on the cheeks, nose, and forehead on clinical examination and several intracellular and extracellular oval structures on histologic examination with periodic acid–Schiff and Gomori methenamine-silver stain.⁵ Malignant or rupioid syphilis refers to the stage in which papulopustules of pustular syphilis undergo central necrosis due to endarteritis obliterans and intravascular thrombosis.⁷

In our case, the patient’s psoriasis could have flared after discontinuation of the prednisone that was administered by the emergency department physician. Most cases have been treated with combined systemic and topical therapy.⁹ For systemic treatment, cyclosporine, intramuscular or oral methotrexate, adalimumab, and ustekinumab³ have been used with remarkable improvement. Hyperkeratotic types of psoriasis are generally thought to be resistant to topical therapy because of poor penetration of applied agents; however, a case of rupioid psoriasis without arthritis was successfully treated with topical steroids without concomitant systemic medications.²

Conclusion

Rupioid psoriasis is a morphological subtype of plaque psoriasis with hyperkeratotic lesions that resemble a limpet shell. Rupioid skin manifestations may be seen in a variety of diseases including rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, and photosensitive skin lesions associated with aminoaciduria. Diagnosis of rupioid psoriasis often requires additional testing such as skin biopsy, skin scraping, and blood tests, and it typically requires systemic therapy for treatment.

Psoriasis Associated With Obesity in Adults

The National Health and Nutrition Examination Surveys were reviewed to better understand the burden of psoriasis. Helmick et al (Am J Prev Med. 2014;47:37-45) examined psoriasis prevalence, severity, disparities, health-related quality of life, and selected comorbidities in 10,676 adults aged 20 to 59 years from 2003-2006 and 2009-2010. Related to patient diet and weight, they noted that psoriasis was associated with obesity.

Practice Point: The association between psoriasis and obesity warrants further research, as the disease is a large public health concern.

>>Read more at American Journal of Preventive Medicine

Dietary Plan With Physical Exercise Reduces Psoriasis Severity

Among the risk factors for psoriasis are increased body mass index and weight gain. The prevalence of obesity in patients with psoriasis is higher than in the general population. Naldi et al (Br J Dermatol. 2014;170:634-642) assessed the impact of a dietary intervention combined with physical exercise for weight loss on improving psoriasis in overweight or obese patients. Patients were randomized to receive either a 20-week quantitative and qualitative dietary plan associated with physical exercise for weight loss or simple informative counseling at baseline about the utility of weight loss for clinical control of psoriatic disease. They reported that the median reduction in psoriasis area and severity index scores was significantly higher in the dietary intervention arm compared with the information-only arm (P=.02).

Practice Point: A dietary plan associated with physical exercise for obese or overweight psoriasis patients may help reduce disease severity.

>>Read more at British Journal of Dermatology

Improvement in Psoriasis With a Low-Energy Diet

Psoriasis severity increases with weight gain. Jensen et al (JAMA Dermatol. 2013;149:795-801) sought to measure the effect of weight reduction on the severity of psoriasis in obese patients. The intervention group received a low-energy diet for 8 weeks to induce weight loss, followed by 8 weeks of reintroduction of normal food intake. The control group was instructed to continue eating ordinary healthy foods. Results based on psoriasis area and severity index and dermatology life quality index scores were in favor of the low-energy diet group.

Practice Point: A low-energy diet may improve the severity of psoriasis in obese patients.

>>Read more at JAMA Dermatology

Psoriasis Associated With Obesity in Adults

The National Health and Nutrition Examination Surveys were reviewed to better understand the burden of psoriasis. Helmick et al (Am J Prev Med. 2014;47:37-45) examined psoriasis prevalence, severity, disparities, health-related quality of life, and selected comorbidities in 10,676 adults aged 20 to 59 years from 2003-2006 and 2009-2010. Related to patient diet and weight, they noted that psoriasis was associated with obesity.

Practice Point: The association between psoriasis and obesity warrants further research, as the disease is a large public health concern.

>>Read more at American Journal of Preventive Medicine

Dietary Plan With Physical Exercise Reduces Psoriasis Severity

Among the risk factors for psoriasis are increased body mass index and weight gain. The prevalence of obesity in patients with psoriasis is higher than in the general population. Naldi et al (Br J Dermatol. 2014;170:634-642) assessed the impact of a dietary intervention combined with physical exercise for weight loss on improving psoriasis in overweight or obese patients. Patients were randomized to receive either a 20-week quantitative and qualitative dietary plan associated with physical exercise for weight loss or simple informative counseling at baseline about the utility of weight loss for clinical control of psoriatic disease. They reported that the median reduction in psoriasis area and severity index scores was significantly higher in the dietary intervention arm compared with the information-only arm (P=.02).

Practice Point: A dietary plan associated with physical exercise for obese or overweight psoriasis patients may help reduce disease severity.

>>Read more at British Journal of Dermatology

Improvement in Psoriasis With a Low-Energy Diet

Psoriasis severity increases with weight gain. Jensen et al (JAMA Dermatol. 2013;149:795-801) sought to measure the effect of weight reduction on the severity of psoriasis in obese patients. The intervention group received a low-energy diet for 8 weeks to induce weight loss, followed by 8 weeks of reintroduction of normal food intake. The control group was instructed to continue eating ordinary healthy foods. Results based on psoriasis area and severity index and dermatology life quality index scores were in favor of the low-energy diet group.

Practice Point: A low-energy diet may improve the severity of psoriasis in obese patients.

>>Read more at JAMA Dermatology

Psoriasis Associated With Obesity in Adults

The National Health and Nutrition Examination Surveys were reviewed to better understand the burden of psoriasis. Helmick et al (Am J Prev Med. 2014;47:37-45) examined psoriasis prevalence, severity, disparities, health-related quality of life, and selected comorbidities in 10,676 adults aged 20 to 59 years from 2003-2006 and 2009-2010. Related to patient diet and weight, they noted that psoriasis was associated with obesity.

Practice Point: The association between psoriasis and obesity warrants further research, as the disease is a large public health concern.

>>Read more at American Journal of Preventive Medicine

Dietary Plan With Physical Exercise Reduces Psoriasis Severity

Among the risk factors for psoriasis are increased body mass index and weight gain. The prevalence of obesity in patients with psoriasis is higher than in the general population. Naldi et al (Br J Dermatol. 2014;170:634-642) assessed the impact of a dietary intervention combined with physical exercise for weight loss on improving psoriasis in overweight or obese patients. Patients were randomized to receive either a 20-week quantitative and qualitative dietary plan associated with physical exercise for weight loss or simple informative counseling at baseline about the utility of weight loss for clinical control of psoriatic disease. They reported that the median reduction in psoriasis area and severity index scores was significantly higher in the dietary intervention arm compared with the information-only arm (P=.02).

Practice Point: A dietary plan associated with physical exercise for obese or overweight psoriasis patients may help reduce disease severity.

>>Read more at British Journal of Dermatology

Improvement in Psoriasis With a Low-Energy Diet

Psoriasis severity increases with weight gain. Jensen et al (JAMA Dermatol. 2013;149:795-801) sought to measure the effect of weight reduction on the severity of psoriasis in obese patients. The intervention group received a low-energy diet for 8 weeks to induce weight loss, followed by 8 weeks of reintroduction of normal food intake. The control group was instructed to continue eating ordinary healthy foods. Results based on psoriasis area and severity index and dermatology life quality index scores were in favor of the low-energy diet group.

Practice Point: A low-energy diet may improve the severity of psoriasis in obese patients.

>>Read more at JAMA Dermatology

CHICAGO – Malignancy rates in patients with psoriasis outstrip those in the general population, based on data from a retrospective analysis of commercial claims.

Rates for all cancers were similar among patients undergoing different psoriasis treatments, with the exception of nonmelanoma skin cancer and lymphoma.

Rates for these two cancers were more variable across treatment groups, but were still above those in the general public, Dr. Alexa B. Kimball reported at the American Academy of Dermatology summer meeting.

The increased cancer risk may be associated with chronic inflammation, a hallmark of psoriasis, and exposure to some psoriasis therapies such as phototherapy with psoralen plus ultraviolet, cyclosporine, and methotrexate, she noted in the study’s background information.

Previous studies also have suggested that patients with psoriasis may be at increased risk for some cancers such as respiratory tract, urinary tract, and liver cancers, non-Hodgkin’s lymphoma, and skin cancers.

To evaluate the incidence of malignancy, the investigators obtained data from the MarketScan Commercial and Medicare Supplemental claims databases for patients with a diagnosis of psoriasis on or before Dec. 31, 2006, and at least one prescription claim for etanercept (Enbrel), adalimumab (Humira), infliximab (Remicade), ustekinumab (Stelara), nonbiologic therapies, or phototherapy.

The general population cohort included patients at least 18 years old as of 2005 or at enrollment in the health care plan. Both cohorts had 12 months’ continuous enrollment in the health care plan from Jan. 1, 2005, through Dec. 31, 2006.

Follow-up for a patient ended at the first cancer event, disenrollment from the health care plan, or after 5 years from the index date.

Patients with psoriasis had a 5-year malignancy rate of 115.5 cases/10,000 person-years, compared with 96/10,000 person-years for the general population, reported Dr. Kimball of Massachusetts General Hospital, Boston.

Excluding nonmelanoma skin cancer and lymphoma, incidence rates were similar across treatment groups: etanercept (100.2/10,000), adalimumab (94.6/10,000), infliximab (138.1/10,000), ustekinumab (100.6/10,000), nonbiologics (116.8/10,000), and phototherapy (117.3/10,000).

"These large database queries continue to be reassuring that most systemic therapies are not changing the risk for common cancers, excluding lymphoma and skin cancer, which we continue to examine separately," Dr. Kimball said in an interview.

Nonmelanoma skin cancer was far and away the most common malignancy in psoriasis patients, occurring at a rate of 147.2/10,000 person-years vs. 94.2/10,000 person-years among the general public. Rates were highest in patients treated with adalimumab (234.2/10,000 person-years) and ustekinumab (233.3/10,000) and lowest in those treated with etanercept (155.9/10,000).

"Even with the large size of the database, the number of skin cancers remains small, so making conclusions about specific therapies may be premature," she said.

Incidence rates of lymphoma were considerably lower, but again higher in psoriasis patients than the general public (11.1/10,000 vs. 6.6/10,000). Rates of this hematologic cancer were highest with ustekinumab (25.1/10,000) and, once again, lowest with etanercept (6.9/10,000), according to the poster.

In all, 5,857 patients received nonbiologic therapies, 6,856 received etanercept, 3,314 adalimumab, 1,044 infliximab, 526 ustekinumab, and 5,156 were treated with phototherapy.

Dr. Kimball is a consultant for several pharmaceutical companies including Amgen, the study sponsor.

pwendling@frontlinemedcom.com

CHICAGO – Malignancy rates in patients with psoriasis outstrip those in the general population, based on data from a retrospective analysis of commercial claims.

Rates for all cancers were similar among patients undergoing different psoriasis treatments, with the exception of nonmelanoma skin cancer and lymphoma.

Rates for these two cancers were more variable across treatment groups, but were still above those in the general public, Dr. Alexa B. Kimball reported at the American Academy of Dermatology summer meeting.

The increased cancer risk may be associated with chronic inflammation, a hallmark of psoriasis, and exposure to some psoriasis therapies such as phototherapy with psoralen plus ultraviolet, cyclosporine, and methotrexate, she noted in the study’s background information.

Previous studies also have suggested that patients with psoriasis may be at increased risk for some cancers such as respiratory tract, urinary tract, and liver cancers, non-Hodgkin’s lymphoma, and skin cancers.

To evaluate the incidence of malignancy, the investigators obtained data from the MarketScan Commercial and Medicare Supplemental claims databases for patients with a diagnosis of psoriasis on or before Dec. 31, 2006, and at least one prescription claim for etanercept (Enbrel), adalimumab (Humira), infliximab (Remicade), ustekinumab (Stelara), nonbiologic therapies, or phototherapy.

The general population cohort included patients at least 18 years old as of 2005 or at enrollment in the health care plan. Both cohorts had 12 months’ continuous enrollment in the health care plan from Jan. 1, 2005, through Dec. 31, 2006.

Follow-up for a patient ended at the first cancer event, disenrollment from the health care plan, or after 5 years from the index date.

Patients with psoriasis had a 5-year malignancy rate of 115.5 cases/10,000 person-years, compared with 96/10,000 person-years for the general population, reported Dr. Kimball of Massachusetts General Hospital, Boston.

Excluding nonmelanoma skin cancer and lymphoma, incidence rates were similar across treatment groups: etanercept (100.2/10,000), adalimumab (94.6/10,000), infliximab (138.1/10,000), ustekinumab (100.6/10,000), nonbiologics (116.8/10,000), and phototherapy (117.3/10,000).

"These large database queries continue to be reassuring that most systemic therapies are not changing the risk for common cancers, excluding lymphoma and skin cancer, which we continue to examine separately," Dr. Kimball said in an interview.

Nonmelanoma skin cancer was far and away the most common malignancy in psoriasis patients, occurring at a rate of 147.2/10,000 person-years vs. 94.2/10,000 person-years among the general public. Rates were highest in patients treated with adalimumab (234.2/10,000 person-years) and ustekinumab (233.3/10,000) and lowest in those treated with etanercept (155.9/10,000).

"Even with the large size of the database, the number of skin cancers remains small, so making conclusions about specific therapies may be premature," she said.

Incidence rates of lymphoma were considerably lower, but again higher in psoriasis patients than the general public (11.1/10,000 vs. 6.6/10,000). Rates of this hematologic cancer were highest with ustekinumab (25.1/10,000) and, once again, lowest with etanercept (6.9/10,000), according to the poster.

In all, 5,857 patients received nonbiologic therapies, 6,856 received etanercept, 3,314 adalimumab, 1,044 infliximab, 526 ustekinumab, and 5,156 were treated with phototherapy.

Dr. Kimball is a consultant for several pharmaceutical companies including Amgen, the study sponsor.

pwendling@frontlinemedcom.com

CHICAGO – Malignancy rates in patients with psoriasis outstrip those in the general population, based on data from a retrospective analysis of commercial claims.

Rates for all cancers were similar among patients undergoing different psoriasis treatments, with the exception of nonmelanoma skin cancer and lymphoma.

Rates for these two cancers were more variable across treatment groups, but were still above those in the general public, Dr. Alexa B. Kimball reported at the American Academy of Dermatology summer meeting.

The increased cancer risk may be associated with chronic inflammation, a hallmark of psoriasis, and exposure to some psoriasis therapies such as phototherapy with psoralen plus ultraviolet, cyclosporine, and methotrexate, she noted in the study’s background information.

Previous studies also have suggested that patients with psoriasis may be at increased risk for some cancers such as respiratory tract, urinary tract, and liver cancers, non-Hodgkin’s lymphoma, and skin cancers.

To evaluate the incidence of malignancy, the investigators obtained data from the MarketScan Commercial and Medicare Supplemental claims databases for patients with a diagnosis of psoriasis on or before Dec. 31, 2006, and at least one prescription claim for etanercept (Enbrel), adalimumab (Humira), infliximab (Remicade), ustekinumab (Stelara), nonbiologic therapies, or phototherapy.

The general population cohort included patients at least 18 years old as of 2005 or at enrollment in the health care plan. Both cohorts had 12 months’ continuous enrollment in the health care plan from Jan. 1, 2005, through Dec. 31, 2006.

Follow-up for a patient ended at the first cancer event, disenrollment from the health care plan, or after 5 years from the index date.

Patients with psoriasis had a 5-year malignancy rate of 115.5 cases/10,000 person-years, compared with 96/10,000 person-years for the general population, reported Dr. Kimball of Massachusetts General Hospital, Boston.

Excluding nonmelanoma skin cancer and lymphoma, incidence rates were similar across treatment groups: etanercept (100.2/10,000), adalimumab (94.6/10,000), infliximab (138.1/10,000), ustekinumab (100.6/10,000), nonbiologics (116.8/10,000), and phototherapy (117.3/10,000).

"These large database queries continue to be reassuring that most systemic therapies are not changing the risk for common cancers, excluding lymphoma and skin cancer, which we continue to examine separately," Dr. Kimball said in an interview.

Nonmelanoma skin cancer was far and away the most common malignancy in psoriasis patients, occurring at a rate of 147.2/10,000 person-years vs. 94.2/10,000 person-years among the general public. Rates were highest in patients treated with adalimumab (234.2/10,000 person-years) and ustekinumab (233.3/10,000) and lowest in those treated with etanercept (155.9/10,000).

"Even with the large size of the database, the number of skin cancers remains small, so making conclusions about specific therapies may be premature," she said.

Incidence rates of lymphoma were considerably lower, but again higher in psoriasis patients than the general public (11.1/10,000 vs. 6.6/10,000). Rates of this hematologic cancer were highest with ustekinumab (25.1/10,000) and, once again, lowest with etanercept (6.9/10,000), according to the poster.

In all, 5,857 patients received nonbiologic therapies, 6,856 received etanercept, 3,314 adalimumab, 1,044 infliximab, 526 ustekinumab, and 5,156 were treated with phototherapy.

Dr. Kimball is a consultant for several pharmaceutical companies including Amgen, the study sponsor.

pwendling@frontlinemedcom.com

Psoriatic arthritis patients with detectable anti-adalimumab antibodies have significantly lower serum adalimumab concentrations and poorer clinical outcomes at 28 weeks and 52 weeks of treatment, than did patients without antibodies in a prospective cohort study of 103 patients.

At week 52, the 23 patients with detectable anti-adalimumab antibodies had a median adalimumab concentration of 0.9 mg/L, compared with 9.4 mg/L in the 80 patients without detectable antibodies, as well as significantly higher C-reactive protein, Psoriasis Area Severity Index score, and 28-joint Disease Activity Score.

The researchers, led by Erik H. Vogelzang of the Jan van Breemen Research Institute/Reade in Amsterdam, also found that patients on adalimumab monotherapy had significantly lower median adalimumab concentrations at 28 and 52 weeks, compared with patients taking adalimumab and concomitant methotrexate (Ann. Rheum. Dis. 2014 [doi:10.1136/annrheumdis-2014-205554]).

"Further studies regarding measuring drug concentrations would be relevant, since this could give more insight on the cause of inadequate response, especially since treatment options in PsA [psoriatic arthritis] are limited," the investigators wrote.

The study was partly supported by AbbVie and Pfizer. The authors declared a range of consultancies, lecture fees, and research grants from the pharmaceutical industry.

Psoriatic arthritis patients with detectable anti-adalimumab antibodies have significantly lower serum adalimumab concentrations and poorer clinical outcomes at 28 weeks and 52 weeks of treatment, than did patients without antibodies in a prospective cohort study of 103 patients.

At week 52, the 23 patients with detectable anti-adalimumab antibodies had a median adalimumab concentration of 0.9 mg/L, compared with 9.4 mg/L in the 80 patients without detectable antibodies, as well as significantly higher C-reactive protein, Psoriasis Area Severity Index score, and 28-joint Disease Activity Score.

The researchers, led by Erik H. Vogelzang of the Jan van Breemen Research Institute/Reade in Amsterdam, also found that patients on adalimumab monotherapy had significantly lower median adalimumab concentrations at 28 and 52 weeks, compared with patients taking adalimumab and concomitant methotrexate (Ann. Rheum. Dis. 2014 [doi:10.1136/annrheumdis-2014-205554]).

"Further studies regarding measuring drug concentrations would be relevant, since this could give more insight on the cause of inadequate response, especially since treatment options in PsA [psoriatic arthritis] are limited," the investigators wrote.

The study was partly supported by AbbVie and Pfizer. The authors declared a range of consultancies, lecture fees, and research grants from the pharmaceutical industry.

Psoriatic arthritis patients with detectable anti-adalimumab antibodies have significantly lower serum adalimumab concentrations and poorer clinical outcomes at 28 weeks and 52 weeks of treatment, than did patients without antibodies in a prospective cohort study of 103 patients.

At week 52, the 23 patients with detectable anti-adalimumab antibodies had a median adalimumab concentration of 0.9 mg/L, compared with 9.4 mg/L in the 80 patients without detectable antibodies, as well as significantly higher C-reactive protein, Psoriasis Area Severity Index score, and 28-joint Disease Activity Score.

The researchers, led by Erik H. Vogelzang of the Jan van Breemen Research Institute/Reade in Amsterdam, also found that patients on adalimumab monotherapy had significantly lower median adalimumab concentrations at 28 and 52 weeks, compared with patients taking adalimumab and concomitant methotrexate (Ann. Rheum. Dis. 2014 [doi:10.1136/annrheumdis-2014-205554]).

"Further studies regarding measuring drug concentrations would be relevant, since this could give more insight on the cause of inadequate response, especially since treatment options in PsA [psoriatic arthritis] are limited," the investigators wrote.

The study was partly supported by AbbVie and Pfizer. The authors declared a range of consultancies, lecture fees, and research grants from the pharmaceutical industry.