Psoriasis

The expanded use of targeted anticancer agents such as sorafenib has revealed a growing spectrum of adverse cutaneous eruptions. We describe 3 patients with sorafenib-induced psoriasiform dermatitis and review the literature of only 10 other similar reported cases based on a search of PubMed, Web of Science, and American Society of Clinical Oncology abstracts using the terms psoriasis or psoriasiform dermatitis and sorafenib.^1-10 We seek to increase awareness of this particular drug eruption in response to sorafenib and to describe potential effective treatment options, especially when sorafenib cannot be discontinued.

Case Reports

Patient 1
A 68-year-old man with chronic hepatitis B infection and hepatocellular carcinoma (HCC) was started on sorafenib 400 mg daily. After 2 months of treatment, he developed painful hyperkeratotic lesions on the bilateral palms and soles with formation of calluses and superficial blisters on an erythematous base that was consistent with hand-foot skin reaction (HFSR). He also had numerous erythematous thin papules and plaques with adherent white scale and yellow crust on the bilateral thighs, lower legs, forearms, dorsal hands, abdomen, back, and buttocks (Figure 1). He had no personal or family history of psoriasis, and blood tests were unremarkable. Histologic analysis of punch biopsies from the buttocks and right leg revealed focal parakeratosis with neutrophils and serous crust, acanthosis, mild spongiosis, and lymphocytes at the dermoepidermal junction and surrounding dermal vessels, consistent with psoriasiform dermatitis (Figure 2). Sorafenib was discontinued and the eruption began to resolve within a week. A lower dose of sorafenib (200 mg daily) was attempted and the psoriasiform eruption recurred.

Patient 2
An 82-year-old man with chronic hepatitis B infection and HCC with lung metastasis was treated with sorafenib 400 mg daily. One week after treatment, he developed painful, thick, erythematous lesions on acral surfaces, consistent with HFSR. The sorafenib dose was decreased to 200 mg daily and HFSR resolved. Four months later, he developed well-demarcated, erythematous, scaly plaques with peripheral pustules on the right thigh (Figure 3) and right shin. He had no personal or family history of psoriasis, and blood tests were unremarkable. Samples from the pustules were taken for bacterial culture and fungal stain, but both were negative. Histologic analysis of a punch biopsy from the right thigh revealed necrotic parakeratosis, spongiform pustules, mild acanthosis, and a perivascular lymphocytic infiltrate with many neutrophils in the dermis. These findings suggested a diagnosis of pustular psoriasis, pustular drug eruption, or acute generalized exanthematous pustulosis. Treatment was initiated with mometasone cream. The patient subsequently developed hemoptysis and ascites from sorafenib. Sorafenib was discontinued and his skin eruption gradually resolved.

Comment

Sorafenib is an oral tyrosine kinase inhibitor that blocks tumor cell proliferation and angiogenesis due to its activity against vascular endothelial growth factor (VEGF) receptor, platelet-derived growth factor receptor, stem cell growth factor receptor, and rapidly accelerated fibrosarcoma kinases.¹¹ It is primarily used for the treatment of solid tumors, such as advanced renal cell carcinoma, unresectable HCC, and thyroid carcinoma, and more recently has been expanded for treatment of AML due to potential inhibition of FMS-like tyrosine kinase 3 receptor. Although dermatologic toxicity is a common adverse event during treatment with sorafenib,¹¹ reports of psoriasiform drug eruptions are rare.

Review of Cases
Based on our literature search, there are 10 previously reported cases of psoriasiform drug eruption secondary to sorafenib. Of the 13 total cases (including the 3 patients in this report), 7 patients had a history of psoriasis; most were middle-aged men; and the treatment with sorafenib was for solid tumors, primarily HCC with the exception of patient 3 from the current report who was treated for AML (Table). In all cases, the dose of sorafenib ranged from 200 to 800 mg daily. In 5 cases, HFSR preceded (as with patient 2 in the current report) or presented concurrently (as with patient 1 in the current report) with the onset of psoriasiform rash.^1,3,5

Vascular endothelial growth factor is overexpressed on psoriatic keratinocytes, contributes to epidermal hyperplasia, and induces angiogenesis in the dermis.¹² The development of psoriasiform eruptions in patients treated with sorafenib seems paradoxical, as this drug has been considered as potential therapy for psoriasis due to its ability to block VEGF receptor signaling. Indeed, an improvement of psoriasis has been reported in 1 case of a patient treated with sorafenib¹³ and in multiple patients with psoriasis treated with other VEGF antagonists (eg, bevacizumab).¹⁴ The underlying mechanisms by which sorafenib induced or exacerbated psoriasis are not entirely clear. Palmoplantar hyperkeratosis, keratosis pilaris–like eruption, multiple cysts, eruptive keratoacanthomas, and squamous cell carcinoma have been described in patients treated with sorafenib, supporting the hypothesis that treatment with sorafenib alters keratinocyte proliferation and differentiation.¹⁵ In addition, B-Raf inhibitors such as imatinib are known to induce or exacerbate psoriasiform dermatitis.¹⁶ The activity of sorafenib resulting in psoriasis may be specific to RAF kinase inhibition, as there are no reports in the literature that describe psoriasiform dermatitis with agents that preferentially block other sorafenib targets such as VEGF receptor, stem cell growth factor receptor, or platelet-derived growth factor receptor. Future studies are needed to fully elucidate the underlying mechanisms by which sorafenib induces or exacerbates psoriasiform dermatitis and whether the severity of the drug eruption correlates with the antitumor efficacy of sorafenib.

Conclusion

Although psoriasiform drug eruptions secondary to sorafenib are not life-threatening, they impact quality of life with associated pain, pruritus, infection, and limitation of daily activities. Dose reduction or discontinuation of sorafenib resulted in resolution of the psoriasiform dermatitis; however, as demonstrated in 3 cases (including patient 3),^1,2 psoriasiform dermatitis can be managed while maintaining the patient on sorafenib so that treatment of the malignancy is not compromised.

The expanded use of targeted anticancer agents such as sorafenib has revealed a growing spectrum of adverse cutaneous eruptions. We describe 3 patients with sorafenib-induced psoriasiform dermatitis and review the literature of only 10 other similar reported cases based on a search of PubMed, Web of Science, and American Society of Clinical Oncology abstracts using the terms psoriasis or psoriasiform dermatitis and sorafenib.^1-10 We seek to increase awareness of this particular drug eruption in response to sorafenib and to describe potential effective treatment options, especially when sorafenib cannot be discontinued.

Case Reports

Patient 1
A 68-year-old man with chronic hepatitis B infection and hepatocellular carcinoma (HCC) was started on sorafenib 400 mg daily. After 2 months of treatment, he developed painful hyperkeratotic lesions on the bilateral palms and soles with formation of calluses and superficial blisters on an erythematous base that was consistent with hand-foot skin reaction (HFSR). He also had numerous erythematous thin papules and plaques with adherent white scale and yellow crust on the bilateral thighs, lower legs, forearms, dorsal hands, abdomen, back, and buttocks (Figure 1). He had no personal or family history of psoriasis, and blood tests were unremarkable. Histologic analysis of punch biopsies from the buttocks and right leg revealed focal parakeratosis with neutrophils and serous crust, acanthosis, mild spongiosis, and lymphocytes at the dermoepidermal junction and surrounding dermal vessels, consistent with psoriasiform dermatitis (Figure 2). Sorafenib was discontinued and the eruption began to resolve within a week. A lower dose of sorafenib (200 mg daily) was attempted and the psoriasiform eruption recurred.

Patient 2
An 82-year-old man with chronic hepatitis B infection and HCC with lung metastasis was treated with sorafenib 400 mg daily. One week after treatment, he developed painful, thick, erythematous lesions on acral surfaces, consistent with HFSR. The sorafenib dose was decreased to 200 mg daily and HFSR resolved. Four months later, he developed well-demarcated, erythematous, scaly plaques with peripheral pustules on the right thigh (Figure 3) and right shin. He had no personal or family history of psoriasis, and blood tests were unremarkable. Samples from the pustules were taken for bacterial culture and fungal stain, but both were negative. Histologic analysis of a punch biopsy from the right thigh revealed necrotic parakeratosis, spongiform pustules, mild acanthosis, and a perivascular lymphocytic infiltrate with many neutrophils in the dermis. These findings suggested a diagnosis of pustular psoriasis, pustular drug eruption, or acute generalized exanthematous pustulosis. Treatment was initiated with mometasone cream. The patient subsequently developed hemoptysis and ascites from sorafenib. Sorafenib was discontinued and his skin eruption gradually resolved.

Comment

Sorafenib is an oral tyrosine kinase inhibitor that blocks tumor cell proliferation and angiogenesis due to its activity against vascular endothelial growth factor (VEGF) receptor, platelet-derived growth factor receptor, stem cell growth factor receptor, and rapidly accelerated fibrosarcoma kinases.¹¹ It is primarily used for the treatment of solid tumors, such as advanced renal cell carcinoma, unresectable HCC, and thyroid carcinoma, and more recently has been expanded for treatment of AML due to potential inhibition of FMS-like tyrosine kinase 3 receptor. Although dermatologic toxicity is a common adverse event during treatment with sorafenib,¹¹ reports of psoriasiform drug eruptions are rare.

Review of Cases
Based on our literature search, there are 10 previously reported cases of psoriasiform drug eruption secondary to sorafenib. Of the 13 total cases (including the 3 patients in this report), 7 patients had a history of psoriasis; most were middle-aged men; and the treatment with sorafenib was for solid tumors, primarily HCC with the exception of patient 3 from the current report who was treated for AML (Table). In all cases, the dose of sorafenib ranged from 200 to 800 mg daily. In 5 cases, HFSR preceded (as with patient 2 in the current report) or presented concurrently (as with patient 1 in the current report) with the onset of psoriasiform rash.^1,3,5

Vascular endothelial growth factor is overexpressed on psoriatic keratinocytes, contributes to epidermal hyperplasia, and induces angiogenesis in the dermis.¹² The development of psoriasiform eruptions in patients treated with sorafenib seems paradoxical, as this drug has been considered as potential therapy for psoriasis due to its ability to block VEGF receptor signaling. Indeed, an improvement of psoriasis has been reported in 1 case of a patient treated with sorafenib¹³ and in multiple patients with psoriasis treated with other VEGF antagonists (eg, bevacizumab).¹⁴ The underlying mechanisms by which sorafenib induced or exacerbated psoriasis are not entirely clear. Palmoplantar hyperkeratosis, keratosis pilaris–like eruption, multiple cysts, eruptive keratoacanthomas, and squamous cell carcinoma have been described in patients treated with sorafenib, supporting the hypothesis that treatment with sorafenib alters keratinocyte proliferation and differentiation.¹⁵ In addition, B-Raf inhibitors such as imatinib are known to induce or exacerbate psoriasiform dermatitis.¹⁶ The activity of sorafenib resulting in psoriasis may be specific to RAF kinase inhibition, as there are no reports in the literature that describe psoriasiform dermatitis with agents that preferentially block other sorafenib targets such as VEGF receptor, stem cell growth factor receptor, or platelet-derived growth factor receptor. Future studies are needed to fully elucidate the underlying mechanisms by which sorafenib induces or exacerbates psoriasiform dermatitis and whether the severity of the drug eruption correlates with the antitumor efficacy of sorafenib.

Conclusion

Although psoriasiform drug eruptions secondary to sorafenib are not life-threatening, they impact quality of life with associated pain, pruritus, infection, and limitation of daily activities. Dose reduction or discontinuation of sorafenib resulted in resolution of the psoriasiform dermatitis; however, as demonstrated in 3 cases (including patient 3),^1,2 psoriasiform dermatitis can be managed while maintaining the patient on sorafenib so that treatment of the malignancy is not compromised.

The expanded use of targeted anticancer agents such as sorafenib has revealed a growing spectrum of adverse cutaneous eruptions. We describe 3 patients with sorafenib-induced psoriasiform dermatitis and review the literature of only 10 other similar reported cases based on a search of PubMed, Web of Science, and American Society of Clinical Oncology abstracts using the terms psoriasis or psoriasiform dermatitis and sorafenib.^1-10 We seek to increase awareness of this particular drug eruption in response to sorafenib and to describe potential effective treatment options, especially when sorafenib cannot be discontinued.

Case Reports

Patient 1
A 68-year-old man with chronic hepatitis B infection and hepatocellular carcinoma (HCC) was started on sorafenib 400 mg daily. After 2 months of treatment, he developed painful hyperkeratotic lesions on the bilateral palms and soles with formation of calluses and superficial blisters on an erythematous base that was consistent with hand-foot skin reaction (HFSR). He also had numerous erythematous thin papules and plaques with adherent white scale and yellow crust on the bilateral thighs, lower legs, forearms, dorsal hands, abdomen, back, and buttocks (Figure 1). He had no personal or family history of psoriasis, and blood tests were unremarkable. Histologic analysis of punch biopsies from the buttocks and right leg revealed focal parakeratosis with neutrophils and serous crust, acanthosis, mild spongiosis, and lymphocytes at the dermoepidermal junction and surrounding dermal vessels, consistent with psoriasiform dermatitis (Figure 2). Sorafenib was discontinued and the eruption began to resolve within a week. A lower dose of sorafenib (200 mg daily) was attempted and the psoriasiform eruption recurred.

Patient 2
An 82-year-old man with chronic hepatitis B infection and HCC with lung metastasis was treated with sorafenib 400 mg daily. One week after treatment, he developed painful, thick, erythematous lesions on acral surfaces, consistent with HFSR. The sorafenib dose was decreased to 200 mg daily and HFSR resolved. Four months later, he developed well-demarcated, erythematous, scaly plaques with peripheral pustules on the right thigh (Figure 3) and right shin. He had no personal or family history of psoriasis, and blood tests were unremarkable. Samples from the pustules were taken for bacterial culture and fungal stain, but both were negative. Histologic analysis of a punch biopsy from the right thigh revealed necrotic parakeratosis, spongiform pustules, mild acanthosis, and a perivascular lymphocytic infiltrate with many neutrophils in the dermis. These findings suggested a diagnosis of pustular psoriasis, pustular drug eruption, or acute generalized exanthematous pustulosis. Treatment was initiated with mometasone cream. The patient subsequently developed hemoptysis and ascites from sorafenib. Sorafenib was discontinued and his skin eruption gradually resolved.

Comment

Sorafenib is an oral tyrosine kinase inhibitor that blocks tumor cell proliferation and angiogenesis due to its activity against vascular endothelial growth factor (VEGF) receptor, platelet-derived growth factor receptor, stem cell growth factor receptor, and rapidly accelerated fibrosarcoma kinases.¹¹ It is primarily used for the treatment of solid tumors, such as advanced renal cell carcinoma, unresectable HCC, and thyroid carcinoma, and more recently has been expanded for treatment of AML due to potential inhibition of FMS-like tyrosine kinase 3 receptor. Although dermatologic toxicity is a common adverse event during treatment with sorafenib,¹¹ reports of psoriasiform drug eruptions are rare.

Review of Cases
Based on our literature search, there are 10 previously reported cases of psoriasiform drug eruption secondary to sorafenib. Of the 13 total cases (including the 3 patients in this report), 7 patients had a history of psoriasis; most were middle-aged men; and the treatment with sorafenib was for solid tumors, primarily HCC with the exception of patient 3 from the current report who was treated for AML (Table). In all cases, the dose of sorafenib ranged from 200 to 800 mg daily. In 5 cases, HFSR preceded (as with patient 2 in the current report) or presented concurrently (as with patient 1 in the current report) with the onset of psoriasiform rash.^1,3,5

Vascular endothelial growth factor is overexpressed on psoriatic keratinocytes, contributes to epidermal hyperplasia, and induces angiogenesis in the dermis.¹² The development of psoriasiform eruptions in patients treated with sorafenib seems paradoxical, as this drug has been considered as potential therapy for psoriasis due to its ability to block VEGF receptor signaling. Indeed, an improvement of psoriasis has been reported in 1 case of a patient treated with sorafenib¹³ and in multiple patients with psoriasis treated with other VEGF antagonists (eg, bevacizumab).¹⁴ The underlying mechanisms by which sorafenib induced or exacerbated psoriasis are not entirely clear. Palmoplantar hyperkeratosis, keratosis pilaris–like eruption, multiple cysts, eruptive keratoacanthomas, and squamous cell carcinoma have been described in patients treated with sorafenib, supporting the hypothesis that treatment with sorafenib alters keratinocyte proliferation and differentiation.¹⁵ In addition, B-Raf inhibitors such as imatinib are known to induce or exacerbate psoriasiform dermatitis.¹⁶ The activity of sorafenib resulting in psoriasis may be specific to RAF kinase inhibition, as there are no reports in the literature that describe psoriasiform dermatitis with agents that preferentially block other sorafenib targets such as VEGF receptor, stem cell growth factor receptor, or platelet-derived growth factor receptor. Future studies are needed to fully elucidate the underlying mechanisms by which sorafenib induces or exacerbates psoriasiform dermatitis and whether the severity of the drug eruption correlates with the antitumor efficacy of sorafenib.

Conclusion

Although psoriasiform drug eruptions secondary to sorafenib are not life-threatening, they impact quality of life with associated pain, pruritus, infection, and limitation of daily activities. Dose reduction or discontinuation of sorafenib resulted in resolution of the psoriasiform dermatitis; however, as demonstrated in 3 cases (including patient 3),^1,2 psoriasiform dermatitis can be managed while maintaining the patient on sorafenib so that treatment of the malignancy is not compromised.

Higher body mass index and moderate – but not heavy – drinking may increase the risk of individuals with psoriasis going on to develop psoriatic arthritis, a study has found.

Around one in five people with psoriasis will develop psoriatic arthritis (PsA), wrote Amelia Green of the University of Bath (England) and coauthors in the British Journal of Dermatology.

Previous studies have explored possible links between obesity, alcohol consumption, or smoking, and an increased risk of developing psoriatic arthritis. However, some of these studies found conflicting results or had limitations such as measuring only a single exposure.

In a cohort study, the Ms. Green and her colleagues examined data from the U.K. Clinical Practice Research Datalink for 90,189 individuals with psoriasis, 1,409 of whom were subsequently also diagnosed with psoriatic arthritis.

The analysis showed a significant association between increasing body mass index (BMI) and increasing odds of developing psoriatic arthritis. Compared with individuals with a BMI below 25 kg/m², those with a BMI of 25.0-29.9 had a 79% greater odds of psoriatic arthritis, those with a BMI of 30.0-34.9 had a 2.10-fold greater odds, and those with a BMI at or above 35 had a 2.68-fold greater odds of developing psoriatic arthritis (P for trend less than .001). Adjustment for potential confounders such as sex, age, duration and severity of psoriasis, diabetes, smoking, and alcohol use slightly attenuated the association, but it remained statistically significant.

Researchers also examined the cumulative effect of lower BMIs over time, and found that over a 10-year period, reductions in BMI were associated with reductions in the risk of developing PsA, compared with remaining at the same BMI over that time.

“Here we have shown for the first time that losing weight over time could reduce the risk of developing PsA in a population with documented psoriasis,” the authors wrote. “As the effect of obesity on the risk of developing PsA may in fact occur with some delay and change over time, our analysis took into account both updated BMI measurements over time and the possible nonlinear and cumulative effects of BMI, which have not previously been investigated.”

Commenting on the mechanisms underlying the association between obesity and the development of PsA, the authors noted that adipose tissue is a source of inflammatory mediators such as adipokines and proinflammatory cytokines, which could lead to the development of PsA. Increasing body weight also could cause microtraumas of the connective tissue between tendon and bone, which may act as an initiating pathogenic event for PsA.

Moderate drinkers – defined as 0.1–3.0 drinks per day ­– had 57% higher odds of developing PsA when compared with nondrinkers, but former drinkers or heavy drinkers did not have an increased risk.

The study also didn’t see any effect of either past or current smoking on the risk of PsA, although there was a nonsignificant interaction with obesity that hinted at increased odds.

“While we found no association between smoking status and the development of PsA in people with psoriasis, further analysis revealed that the effect of smoking on the risk of PsA was possibly mediated through the effect of BMI on PsA; in other words, the protective effect of smoking may be associated with lower BMI among smokers,” the authors wrote.

Patients who developed PsA were also more likely to be younger (mean age of 44.7 years vs. 48.5 years), have severe psoriasis, and have had the disease for a shorter duration.

The study was funded by the National Institute for Health Research, and the authors declared grants from the funder during the conduct of the study. No other conflicts of interest were declared.

SOURCE: Green A et al. Br J Dermatol. 2019 Jun 18. doi: 10.1111/bjd.18227

Higher body mass index and moderate – but not heavy – drinking may increase the risk of individuals with psoriasis going on to develop psoriatic arthritis, a study has found.

Around one in five people with psoriasis will develop psoriatic arthritis (PsA), wrote Amelia Green of the University of Bath (England) and coauthors in the British Journal of Dermatology.

Previous studies have explored possible links between obesity, alcohol consumption, or smoking, and an increased risk of developing psoriatic arthritis. However, some of these studies found conflicting results or had limitations such as measuring only a single exposure.

In a cohort study, the Ms. Green and her colleagues examined data from the U.K. Clinical Practice Research Datalink for 90,189 individuals with psoriasis, 1,409 of whom were subsequently also diagnosed with psoriatic arthritis.

The analysis showed a significant association between increasing body mass index (BMI) and increasing odds of developing psoriatic arthritis. Compared with individuals with a BMI below 25 kg/m², those with a BMI of 25.0-29.9 had a 79% greater odds of psoriatic arthritis, those with a BMI of 30.0-34.9 had a 2.10-fold greater odds, and those with a BMI at or above 35 had a 2.68-fold greater odds of developing psoriatic arthritis (P for trend less than .001). Adjustment for potential confounders such as sex, age, duration and severity of psoriasis, diabetes, smoking, and alcohol use slightly attenuated the association, but it remained statistically significant.

Researchers also examined the cumulative effect of lower BMIs over time, and found that over a 10-year period, reductions in BMI were associated with reductions in the risk of developing PsA, compared with remaining at the same BMI over that time.

“Here we have shown for the first time that losing weight over time could reduce the risk of developing PsA in a population with documented psoriasis,” the authors wrote. “As the effect of obesity on the risk of developing PsA may in fact occur with some delay and change over time, our analysis took into account both updated BMI measurements over time and the possible nonlinear and cumulative effects of BMI, which have not previously been investigated.”

Commenting on the mechanisms underlying the association between obesity and the development of PsA, the authors noted that adipose tissue is a source of inflammatory mediators such as adipokines and proinflammatory cytokines, which could lead to the development of PsA. Increasing body weight also could cause microtraumas of the connective tissue between tendon and bone, which may act as an initiating pathogenic event for PsA.

Moderate drinkers – defined as 0.1–3.0 drinks per day ­– had 57% higher odds of developing PsA when compared with nondrinkers, but former drinkers or heavy drinkers did not have an increased risk.

The study also didn’t see any effect of either past or current smoking on the risk of PsA, although there was a nonsignificant interaction with obesity that hinted at increased odds.

“While we found no association between smoking status and the development of PsA in people with psoriasis, further analysis revealed that the effect of smoking on the risk of PsA was possibly mediated through the effect of BMI on PsA; in other words, the protective effect of smoking may be associated with lower BMI among smokers,” the authors wrote.

Patients who developed PsA were also more likely to be younger (mean age of 44.7 years vs. 48.5 years), have severe psoriasis, and have had the disease for a shorter duration.

The study was funded by the National Institute for Health Research, and the authors declared grants from the funder during the conduct of the study. No other conflicts of interest were declared.

SOURCE: Green A et al. Br J Dermatol. 2019 Jun 18. doi: 10.1111/bjd.18227

Higher body mass index and moderate – but not heavy – drinking may increase the risk of individuals with psoriasis going on to develop psoriatic arthritis, a study has found.

Around one in five people with psoriasis will develop psoriatic arthritis (PsA), wrote Amelia Green of the University of Bath (England) and coauthors in the British Journal of Dermatology.

Previous studies have explored possible links between obesity, alcohol consumption, or smoking, and an increased risk of developing psoriatic arthritis. However, some of these studies found conflicting results or had limitations such as measuring only a single exposure.

In a cohort study, the Ms. Green and her colleagues examined data from the U.K. Clinical Practice Research Datalink for 90,189 individuals with psoriasis, 1,409 of whom were subsequently also diagnosed with psoriatic arthritis.

The analysis showed a significant association between increasing body mass index (BMI) and increasing odds of developing psoriatic arthritis. Compared with individuals with a BMI below 25 kg/m², those with a BMI of 25.0-29.9 had a 79% greater odds of psoriatic arthritis, those with a BMI of 30.0-34.9 had a 2.10-fold greater odds, and those with a BMI at or above 35 had a 2.68-fold greater odds of developing psoriatic arthritis (P for trend less than .001). Adjustment for potential confounders such as sex, age, duration and severity of psoriasis, diabetes, smoking, and alcohol use slightly attenuated the association, but it remained statistically significant.

Researchers also examined the cumulative effect of lower BMIs over time, and found that over a 10-year period, reductions in BMI were associated with reductions in the risk of developing PsA, compared with remaining at the same BMI over that time.

“Here we have shown for the first time that losing weight over time could reduce the risk of developing PsA in a population with documented psoriasis,” the authors wrote. “As the effect of obesity on the risk of developing PsA may in fact occur with some delay and change over time, our analysis took into account both updated BMI measurements over time and the possible nonlinear and cumulative effects of BMI, which have not previously been investigated.”

Commenting on the mechanisms underlying the association between obesity and the development of PsA, the authors noted that adipose tissue is a source of inflammatory mediators such as adipokines and proinflammatory cytokines, which could lead to the development of PsA. Increasing body weight also could cause microtraumas of the connective tissue between tendon and bone, which may act as an initiating pathogenic event for PsA.

Moderate drinkers – defined as 0.1–3.0 drinks per day ­– had 57% higher odds of developing PsA when compared with nondrinkers, but former drinkers or heavy drinkers did not have an increased risk.

The study also didn’t see any effect of either past or current smoking on the risk of PsA, although there was a nonsignificant interaction with obesity that hinted at increased odds.

“While we found no association between smoking status and the development of PsA in people with psoriasis, further analysis revealed that the effect of smoking on the risk of PsA was possibly mediated through the effect of BMI on PsA; in other words, the protective effect of smoking may be associated with lower BMI among smokers,” the authors wrote.

Patients who developed PsA were also more likely to be younger (mean age of 44.7 years vs. 48.5 years), have severe psoriasis, and have had the disease for a shorter duration.

The study was funded by the National Institute for Health Research, and the authors declared grants from the funder during the conduct of the study. No other conflicts of interest were declared.

SOURCE: Green A et al. Br J Dermatol. 2019 Jun 18. doi: 10.1111/bjd.18227

AUSTIN, TEX. – The way Kelly M. Cordoro sees it, the most difficult part of managing pediatric patients with severe psoriasis is not in the logistics of prescribing a drug, it’s deciding which drug to use for which patient.

“You can look up the dosing and frequency of these drugs; all of that’s available,” she said at the annual meeting of the Society for Pediatric Dermatology. “But how do we think about which drug for which patient? What are the considerations?”

Dr. Cordoro, professor of dermatology and pediatrics at the University of California, San Francisco, described psoriasis as an autoamplifying inflammatory cascade involving innate and adaptive immunity and noted that various components of that cascade represent treatment targets. “We don’t have a true comprehension of the pathophysiology of psoriasis, but as we learn the pathways, we’re targeting them,” she said. “You can target keratinocyte proliferation with drugs like retinoids and phototherapy. You can broadly target T cells, neutrophils, and dendritic cells with methotrexate, cyclosporine, and phototherapy. The newer drugs target the cytokine milieu, including TNF [tumor necrosis factor]–alpha, IL [interleukin]–17A, IL-12, and IL-23.”

There is no one right answer for which drug to prescribe, she continued, except in the cases of certain comorbidities, contraindications, and genetic variants. “For example, if a patient has psoriatic arthritis, then you have methotrexate and all of the biologics that might be disease modifying,” she said. “If a patient has inflammatory bowel disease, it’s critical to know that IL-17 inhibitors will flare that disease, but anti-TNF and IL-12 and IL-23 inhibitors are okay. If a patient has liver and kidney disease, you want to avoid methotrexate and cyclosporine. If there’s a female of childbearing potential you want to be very cautious with using retinoids. I think the harder question for us is, How about the rest of the patients?”

In addition to a drug’s mechanism of action, patient- and family-related factors play a role in deciding which agent to use. For example, does the patient prefer an oral or an injectable agent? Is the patient able to travel to a phototherapy center? Is it feasible for the family to manage visits for lab work and direct clinical monitoring? Does the family have a high level of health literacy and are you communicating with them in ways that facilitate shared decision making?

“The best way to choose a systemic therapy is to develop an individualized assessment of overall disease burden,” said Dr. Cordoro, who is also division chief of pediatric dermatology at UCSF. “Include psychological burden and subjective data in addition to objective measures like body surface area. Look for triggers. Infants are more commonly affected by viral infections and, in a subset, monogenic forms of psoriasis such as deficiency of interleukin 1 receptor antagonist [DIRA]. In general, we try to take a conservative approach in the developing child. As children hit early adolescence and become post pubertal, you have to start thinking about the psychosocial impact [of psoriasis], and we have to start treating patients with the consideration that chronic uncontrolled inflammation can potentially lead to comorbidities down the road. We see this in adults with severe psoriasis and early onset cardiovascular disease, the so-called psoriatic march from chronic inflammation to cardiovascular disease.”

Dr. Cordoro advises clinicians to rethink the conventional “therapeutic ladder” concept and embrace the idea of “finding the right tool for the job right now.” If a patient presents with a flare from a known trigger such as a strep infection, “maybe you want to treat with something more conservative,” she said. “Once you treat, and if the trigger has been managed, they might be better. But some patients will need the most aggressive treatment right out of the gate.”

Tried and true systemic therapies for psoriasis include methotrexate, cyclosporine, acitretin, and phototherapy, but none is approved by the Food and Drug Administration for use in children. “These drugs have decades of experience behind them,” Dr. Cordoro said. “Methotrexate is slow to start but has a sustained profile, so if you can get the patient to respond, that response tends to persist. Methotrexate also prevents the formation of antidrug antibodies, which is important if you are considering use of a biologic agent later on.”

Cyclosporine is best if you need a rapid rescue drug to get the disease under control before moving on to other options. “One in four patients relapse once cyclosporine is discontinued, so the benefit may not be as sustained as with methotrexate,” she said. “Acitretin is a really nice choice when you can’t or don’t want to immunosuppress the patient, and phototherapy is good if you can get it. The advantages of systemic therapies are that they’re easy on, easy off, and you can combine medications in severe situations. Almost all of these drugs can be combined with another, with few exceptions. I would caution that over immunosuppression is the biggest risk ... so this must be done carefully and only when necessary.”

Biologic agents such as TNF inhibitors and IL-12/23 inhibitors are playing an increasing role in pediatric psoriasis. They can be expensive and difficult for some insurance plans to cover, but offer the convenience of better efficacy and less frequent lab monitoring than conventional systemics. In the United States, etanercept and ustekinumab are approved for moderate to severe pediatric plaque psoriasis in patients as young as age 4 and 12 years, respectively. TNF inhibitors have accumulated the most data in children, while data are accumulating in trials of IL-17 inhibitors, IL-23 inhibitors, and PDE4 inhibitors.

“These drugs have reassuring safety profiles; low rates of infection and adverse reactions,” Dr. Cordoro said of biologic agents. “They’ve changed the landscape completely because now the expectation is complete or near-complete clearance. In contrast to the systemic agents, which may be started and stopped repeatedly, you need to think about continuous therapy, because these drugs are immunogenic,” she noted. “Whether antibodies against them become neutralizing or not is a different case. If a patient does have antibodies, it does not mean you have to stop the drug. Dose escalation can help. Increasing frequency of use of the drug can help, but patients will develop antibodies and it may result in loss of efficacy or reactions to the drug,” she added.

“When you’re thinking about using a biologic agent, think about patients who are chronic, moderate to severe, and who will need more long-term therapy. Most importantly, treatment should be individualized, as there is no ‘one size fits all’ approach.”

Dr. Cordoro disclosed that she is a member of the Celgene Corporation Scientific Steering Committee.

dbrunk@mdedge.com

AUSTIN, TEX. – The way Kelly M. Cordoro sees it, the most difficult part of managing pediatric patients with severe psoriasis is not in the logistics of prescribing a drug, it’s deciding which drug to use for which patient.

“You can look up the dosing and frequency of these drugs; all of that’s available,” she said at the annual meeting of the Society for Pediatric Dermatology. “But how do we think about which drug for which patient? What are the considerations?”

Dr. Cordoro, professor of dermatology and pediatrics at the University of California, San Francisco, described psoriasis as an autoamplifying inflammatory cascade involving innate and adaptive immunity and noted that various components of that cascade represent treatment targets. “We don’t have a true comprehension of the pathophysiology of psoriasis, but as we learn the pathways, we’re targeting them,” she said. “You can target keratinocyte proliferation with drugs like retinoids and phototherapy. You can broadly target T cells, neutrophils, and dendritic cells with methotrexate, cyclosporine, and phototherapy. The newer drugs target the cytokine milieu, including TNF [tumor necrosis factor]–alpha, IL [interleukin]–17A, IL-12, and IL-23.”

There is no one right answer for which drug to prescribe, she continued, except in the cases of certain comorbidities, contraindications, and genetic variants. “For example, if a patient has psoriatic arthritis, then you have methotrexate and all of the biologics that might be disease modifying,” she said. “If a patient has inflammatory bowel disease, it’s critical to know that IL-17 inhibitors will flare that disease, but anti-TNF and IL-12 and IL-23 inhibitors are okay. If a patient has liver and kidney disease, you want to avoid methotrexate and cyclosporine. If there’s a female of childbearing potential you want to be very cautious with using retinoids. I think the harder question for us is, How about the rest of the patients?”

In addition to a drug’s mechanism of action, patient- and family-related factors play a role in deciding which agent to use. For example, does the patient prefer an oral or an injectable agent? Is the patient able to travel to a phototherapy center? Is it feasible for the family to manage visits for lab work and direct clinical monitoring? Does the family have a high level of health literacy and are you communicating with them in ways that facilitate shared decision making?

“The best way to choose a systemic therapy is to develop an individualized assessment of overall disease burden,” said Dr. Cordoro, who is also division chief of pediatric dermatology at UCSF. “Include psychological burden and subjective data in addition to objective measures like body surface area. Look for triggers. Infants are more commonly affected by viral infections and, in a subset, monogenic forms of psoriasis such as deficiency of interleukin 1 receptor antagonist [DIRA]. In general, we try to take a conservative approach in the developing child. As children hit early adolescence and become post pubertal, you have to start thinking about the psychosocial impact [of psoriasis], and we have to start treating patients with the consideration that chronic uncontrolled inflammation can potentially lead to comorbidities down the road. We see this in adults with severe psoriasis and early onset cardiovascular disease, the so-called psoriatic march from chronic inflammation to cardiovascular disease.”

Dr. Cordoro advises clinicians to rethink the conventional “therapeutic ladder” concept and embrace the idea of “finding the right tool for the job right now.” If a patient presents with a flare from a known trigger such as a strep infection, “maybe you want to treat with something more conservative,” she said. “Once you treat, and if the trigger has been managed, they might be better. But some patients will need the most aggressive treatment right out of the gate.”

Tried and true systemic therapies for psoriasis include methotrexate, cyclosporine, acitretin, and phototherapy, but none is approved by the Food and Drug Administration for use in children. “These drugs have decades of experience behind them,” Dr. Cordoro said. “Methotrexate is slow to start but has a sustained profile, so if you can get the patient to respond, that response tends to persist. Methotrexate also prevents the formation of antidrug antibodies, which is important if you are considering use of a biologic agent later on.”

Cyclosporine is best if you need a rapid rescue drug to get the disease under control before moving on to other options. “One in four patients relapse once cyclosporine is discontinued, so the benefit may not be as sustained as with methotrexate,” she said. “Acitretin is a really nice choice when you can’t or don’t want to immunosuppress the patient, and phototherapy is good if you can get it. The advantages of systemic therapies are that they’re easy on, easy off, and you can combine medications in severe situations. Almost all of these drugs can be combined with another, with few exceptions. I would caution that over immunosuppression is the biggest risk ... so this must be done carefully and only when necessary.”

Biologic agents such as TNF inhibitors and IL-12/23 inhibitors are playing an increasing role in pediatric psoriasis. They can be expensive and difficult for some insurance plans to cover, but offer the convenience of better efficacy and less frequent lab monitoring than conventional systemics. In the United States, etanercept and ustekinumab are approved for moderate to severe pediatric plaque psoriasis in patients as young as age 4 and 12 years, respectively. TNF inhibitors have accumulated the most data in children, while data are accumulating in trials of IL-17 inhibitors, IL-23 inhibitors, and PDE4 inhibitors.

“These drugs have reassuring safety profiles; low rates of infection and adverse reactions,” Dr. Cordoro said of biologic agents. “They’ve changed the landscape completely because now the expectation is complete or near-complete clearance. In contrast to the systemic agents, which may be started and stopped repeatedly, you need to think about continuous therapy, because these drugs are immunogenic,” she noted. “Whether antibodies against them become neutralizing or not is a different case. If a patient does have antibodies, it does not mean you have to stop the drug. Dose escalation can help. Increasing frequency of use of the drug can help, but patients will develop antibodies and it may result in loss of efficacy or reactions to the drug,” she added.

“When you’re thinking about using a biologic agent, think about patients who are chronic, moderate to severe, and who will need more long-term therapy. Most importantly, treatment should be individualized, as there is no ‘one size fits all’ approach.”

Dr. Cordoro disclosed that she is a member of the Celgene Corporation Scientific Steering Committee.

dbrunk@mdedge.com

AUSTIN, TEX. – The way Kelly M. Cordoro sees it, the most difficult part of managing pediatric patients with severe psoriasis is not in the logistics of prescribing a drug, it’s deciding which drug to use for which patient.

“You can look up the dosing and frequency of these drugs; all of that’s available,” she said at the annual meeting of the Society for Pediatric Dermatology. “But how do we think about which drug for which patient? What are the considerations?”

Dr. Cordoro, professor of dermatology and pediatrics at the University of California, San Francisco, described psoriasis as an autoamplifying inflammatory cascade involving innate and adaptive immunity and noted that various components of that cascade represent treatment targets. “We don’t have a true comprehension of the pathophysiology of psoriasis, but as we learn the pathways, we’re targeting them,” she said. “You can target keratinocyte proliferation with drugs like retinoids and phototherapy. You can broadly target T cells, neutrophils, and dendritic cells with methotrexate, cyclosporine, and phototherapy. The newer drugs target the cytokine milieu, including TNF [tumor necrosis factor]–alpha, IL [interleukin]–17A, IL-12, and IL-23.”

There is no one right answer for which drug to prescribe, she continued, except in the cases of certain comorbidities, contraindications, and genetic variants. “For example, if a patient has psoriatic arthritis, then you have methotrexate and all of the biologics that might be disease modifying,” she said. “If a patient has inflammatory bowel disease, it’s critical to know that IL-17 inhibitors will flare that disease, but anti-TNF and IL-12 and IL-23 inhibitors are okay. If a patient has liver and kidney disease, you want to avoid methotrexate and cyclosporine. If there’s a female of childbearing potential you want to be very cautious with using retinoids. I think the harder question for us is, How about the rest of the patients?”

In addition to a drug’s mechanism of action, patient- and family-related factors play a role in deciding which agent to use. For example, does the patient prefer an oral or an injectable agent? Is the patient able to travel to a phototherapy center? Is it feasible for the family to manage visits for lab work and direct clinical monitoring? Does the family have a high level of health literacy and are you communicating with them in ways that facilitate shared decision making?

“The best way to choose a systemic therapy is to develop an individualized assessment of overall disease burden,” said Dr. Cordoro, who is also division chief of pediatric dermatology at UCSF. “Include psychological burden and subjective data in addition to objective measures like body surface area. Look for triggers. Infants are more commonly affected by viral infections and, in a subset, monogenic forms of psoriasis such as deficiency of interleukin 1 receptor antagonist [DIRA]. In general, we try to take a conservative approach in the developing child. As children hit early adolescence and become post pubertal, you have to start thinking about the psychosocial impact [of psoriasis], and we have to start treating patients with the consideration that chronic uncontrolled inflammation can potentially lead to comorbidities down the road. We see this in adults with severe psoriasis and early onset cardiovascular disease, the so-called psoriatic march from chronic inflammation to cardiovascular disease.”

Dr. Cordoro advises clinicians to rethink the conventional “therapeutic ladder” concept and embrace the idea of “finding the right tool for the job right now.” If a patient presents with a flare from a known trigger such as a strep infection, “maybe you want to treat with something more conservative,” she said. “Once you treat, and if the trigger has been managed, they might be better. But some patients will need the most aggressive treatment right out of the gate.”

Tried and true systemic therapies for psoriasis include methotrexate, cyclosporine, acitretin, and phototherapy, but none is approved by the Food and Drug Administration for use in children. “These drugs have decades of experience behind them,” Dr. Cordoro said. “Methotrexate is slow to start but has a sustained profile, so if you can get the patient to respond, that response tends to persist. Methotrexate also prevents the formation of antidrug antibodies, which is important if you are considering use of a biologic agent later on.”

Cyclosporine is best if you need a rapid rescue drug to get the disease under control before moving on to other options. “One in four patients relapse once cyclosporine is discontinued, so the benefit may not be as sustained as with methotrexate,” she said. “Acitretin is a really nice choice when you can’t or don’t want to immunosuppress the patient, and phototherapy is good if you can get it. The advantages of systemic therapies are that they’re easy on, easy off, and you can combine medications in severe situations. Almost all of these drugs can be combined with another, with few exceptions. I would caution that over immunosuppression is the biggest risk ... so this must be done carefully and only when necessary.”

Biologic agents such as TNF inhibitors and IL-12/23 inhibitors are playing an increasing role in pediatric psoriasis. They can be expensive and difficult for some insurance plans to cover, but offer the convenience of better efficacy and less frequent lab monitoring than conventional systemics. In the United States, etanercept and ustekinumab are approved for moderate to severe pediatric plaque psoriasis in patients as young as age 4 and 12 years, respectively. TNF inhibitors have accumulated the most data in children, while data are accumulating in trials of IL-17 inhibitors, IL-23 inhibitors, and PDE4 inhibitors.

“These drugs have reassuring safety profiles; low rates of infection and adverse reactions,” Dr. Cordoro said of biologic agents. “They’ve changed the landscape completely because now the expectation is complete or near-complete clearance. In contrast to the systemic agents, which may be started and stopped repeatedly, you need to think about continuous therapy, because these drugs are immunogenic,” she noted. “Whether antibodies against them become neutralizing or not is a different case. If a patient does have antibodies, it does not mean you have to stop the drug. Dose escalation can help. Increasing frequency of use of the drug can help, but patients will develop antibodies and it may result in loss of efficacy or reactions to the drug,” she added.

“When you’re thinking about using a biologic agent, think about patients who are chronic, moderate to severe, and who will need more long-term therapy. Most importantly, treatment should be individualized, as there is no ‘one size fits all’ approach.”

Dr. Cordoro disclosed that she is a member of the Celgene Corporation Scientific Steering Committee.

dbrunk@mdedge.com

Verrucous psoriasis: A rare variant of psoriasis masquerading as verrucous carcinoma.

Garvie K, McGinley Simpson M, Logemann N, Lackey J. JAAD Case Rep. 2019 Aug 5;5(8):723-725.

Verrucous psoriasis is a rare variant of psoriasis characterized by hyperkeratotic, papillomatous plaques that clinically resemble verrucous carcinoma in lesion appearance and distribution. It is amenable to medical treatments. Conversely, verrucous carcinoma, a rare subtype of well-differentiated squamous cell carcinoma, is treated with surgical excision. Histologically, they may be difficult to differentiate. This case report presents a patient with verrucous psoriasis of the heal that was initially diagnosed as verrucous carcinoma and excised.

Re-Categorization of Psoriasis Severity: Delphi Consensus from the International Psoriasis Council.

Strober B, Ryan C, van de Kerkhof P, et al. J Am Acad Dermatol. 2019 Aug 16.

This consensus statement on the classification of psoriasis severity preferentially ranked seven severity definitions. This most preferred statement rejects the mild, moderate and severe categories in favor of a dichotomous definition: Psoriasis patients should be classified as either candidates for topical therapy or candidates for systemic therapy; the latter are patients who meet at least one of the following criteria: 1) BSA > 10%, 2) Disease involving special areas, 3) Failure of topical therapy.

Gluten intake and risk of psoriasis, psoriatic arthritis and atopic dermatitis among US women.

Drucker AM, Qureshi AA, Thompson JM, Li T, Cho E. J Am Acad Dermatol. 2019 Aug 9.

Associations between gluten intake and psoriasis, psoriatic arthritis and atopic dermatitis are poorly understood. Gluten content of participants' diet was calculated every four years using food frequency questionnaires. Disease outcomes were assessed by self-report and subsequently validated.

Psoriasis and Mortality in the US: Data from the National Health and Nutrition Examination Survey.

Semenov YR, Herbosa CM, Rogers AT, et al. J Am Acad Dermatol. 2019 Aug 12.

In this retrospective population-based cohort study of adults and adolescents > 10 years (n=13,031) who participated in National Health and Nutrition Examination Surveys (2003-2006; 2009-2010), psoriasis was present in 2.7% of the study population. Over an average 52.3 months median follow-up, psoriasis was significantly associated with increased mortality risk. This relationship is partially mediated by an increased prevalence of cardiovascular, infectious, and neoplastic disorders seen among psoriatics.

Ostraceous Psoriasis Presenting as Koebner Phenomenon in a Tattoo.

Reinhart J, Willett M, Gibbs N. J Drugs Dermatol. 2019 Aug 1;18(8):825-826.

Psoriasis ostracea is defined as having pronounced adherent scales resembling an oyster shell. Many ostraceous cases occur as generalized outbreaks in patients with long-standing history of psoriasis. Rarely does this variant occur as a direct flare from a cutaneous insult. In these situations, when a pre-existing dermatosis appears in response to a traumatic insult to skin, the process is referred to as the Koebner phenomenon. In addition to lichen planus and vitiligo, psoriasis is a commonly known condition that can present as a Koebner reaction. In this atypical case, the authors present a 21-year-old male with remarkable ostraceous psoriatic lesions precipitated by an upper arm tattoo, demonstrating the Koebner phenomenon.

Verrucous psoriasis: A rare variant of psoriasis masquerading as verrucous carcinoma.

Garvie K, McGinley Simpson M, Logemann N, Lackey J. JAAD Case Rep. 2019 Aug 5;5(8):723-725.

Verrucous psoriasis is a rare variant of psoriasis characterized by hyperkeratotic, papillomatous plaques that clinically resemble verrucous carcinoma in lesion appearance and distribution. It is amenable to medical treatments. Conversely, verrucous carcinoma, a rare subtype of well-differentiated squamous cell carcinoma, is treated with surgical excision. Histologically, they may be difficult to differentiate. This case report presents a patient with verrucous psoriasis of the heal that was initially diagnosed as verrucous carcinoma and excised.

Re-Categorization of Psoriasis Severity: Delphi Consensus from the International Psoriasis Council.

Strober B, Ryan C, van de Kerkhof P, et al. J Am Acad Dermatol. 2019 Aug 16.

This consensus statement on the classification of psoriasis severity preferentially ranked seven severity definitions. This most preferred statement rejects the mild, moderate and severe categories in favor of a dichotomous definition: Psoriasis patients should be classified as either candidates for topical therapy or candidates for systemic therapy; the latter are patients who meet at least one of the following criteria: 1) BSA > 10%, 2) Disease involving special areas, 3) Failure of topical therapy.

Gluten intake and risk of psoriasis, psoriatic arthritis and atopic dermatitis among US women.

Drucker AM, Qureshi AA, Thompson JM, Li T, Cho E. J Am Acad Dermatol. 2019 Aug 9.

Associations between gluten intake and psoriasis, psoriatic arthritis and atopic dermatitis are poorly understood. Gluten content of participants' diet was calculated every four years using food frequency questionnaires. Disease outcomes were assessed by self-report and subsequently validated.

Psoriasis and Mortality in the US: Data from the National Health and Nutrition Examination Survey.

Semenov YR, Herbosa CM, Rogers AT, et al. J Am Acad Dermatol. 2019 Aug 12.

In this retrospective population-based cohort study of adults and adolescents > 10 years (n=13,031) who participated in National Health and Nutrition Examination Surveys (2003-2006; 2009-2010), psoriasis was present in 2.7% of the study population. Over an average 52.3 months median follow-up, psoriasis was significantly associated with increased mortality risk. This relationship is partially mediated by an increased prevalence of cardiovascular, infectious, and neoplastic disorders seen among psoriatics.

Ostraceous Psoriasis Presenting as Koebner Phenomenon in a Tattoo.

Reinhart J, Willett M, Gibbs N. J Drugs Dermatol. 2019 Aug 1;18(8):825-826.

Psoriasis ostracea is defined as having pronounced adherent scales resembling an oyster shell. Many ostraceous cases occur as generalized outbreaks in patients with long-standing history of psoriasis. Rarely does this variant occur as a direct flare from a cutaneous insult. In these situations, when a pre-existing dermatosis appears in response to a traumatic insult to skin, the process is referred to as the Koebner phenomenon. In addition to lichen planus and vitiligo, psoriasis is a commonly known condition that can present as a Koebner reaction. In this atypical case, the authors present a 21-year-old male with remarkable ostraceous psoriatic lesions precipitated by an upper arm tattoo, demonstrating the Koebner phenomenon.

Verrucous psoriasis: A rare variant of psoriasis masquerading as verrucous carcinoma.

Garvie K, McGinley Simpson M, Logemann N, Lackey J. JAAD Case Rep. 2019 Aug 5;5(8):723-725.

Verrucous psoriasis is a rare variant of psoriasis characterized by hyperkeratotic, papillomatous plaques that clinically resemble verrucous carcinoma in lesion appearance and distribution. It is amenable to medical treatments. Conversely, verrucous carcinoma, a rare subtype of well-differentiated squamous cell carcinoma, is treated with surgical excision. Histologically, they may be difficult to differentiate. This case report presents a patient with verrucous psoriasis of the heal that was initially diagnosed as verrucous carcinoma and excised.

Re-Categorization of Psoriasis Severity: Delphi Consensus from the International Psoriasis Council.

Strober B, Ryan C, van de Kerkhof P, et al. J Am Acad Dermatol. 2019 Aug 16.

This consensus statement on the classification of psoriasis severity preferentially ranked seven severity definitions. This most preferred statement rejects the mild, moderate and severe categories in favor of a dichotomous definition: Psoriasis patients should be classified as either candidates for topical therapy or candidates for systemic therapy; the latter are patients who meet at least one of the following criteria: 1) BSA > 10%, 2) Disease involving special areas, 3) Failure of topical therapy.

Gluten intake and risk of psoriasis, psoriatic arthritis and atopic dermatitis among US women.

Drucker AM, Qureshi AA, Thompson JM, Li T, Cho E. J Am Acad Dermatol. 2019 Aug 9.

Associations between gluten intake and psoriasis, psoriatic arthritis and atopic dermatitis are poorly understood. Gluten content of participants' diet was calculated every four years using food frequency questionnaires. Disease outcomes were assessed by self-report and subsequently validated.

Psoriasis and Mortality in the US: Data from the National Health and Nutrition Examination Survey.

Semenov YR, Herbosa CM, Rogers AT, et al. J Am Acad Dermatol. 2019 Aug 12.

In this retrospective population-based cohort study of adults and adolescents > 10 years (n=13,031) who participated in National Health and Nutrition Examination Surveys (2003-2006; 2009-2010), psoriasis was present in 2.7% of the study population. Over an average 52.3 months median follow-up, psoriasis was significantly associated with increased mortality risk. This relationship is partially mediated by an increased prevalence of cardiovascular, infectious, and neoplastic disorders seen among psoriatics.

Ostraceous Psoriasis Presenting as Koebner Phenomenon in a Tattoo.

Reinhart J, Willett M, Gibbs N. J Drugs Dermatol. 2019 Aug 1;18(8):825-826.

Psoriasis ostracea is defined as having pronounced adherent scales resembling an oyster shell. Many ostraceous cases occur as generalized outbreaks in patients with long-standing history of psoriasis. Rarely does this variant occur as a direct flare from a cutaneous insult. In these situations, when a pre-existing dermatosis appears in response to a traumatic insult to skin, the process is referred to as the Koebner phenomenon. In addition to lichen planus and vitiligo, psoriasis is a commonly known condition that can present as a Koebner reaction. In this atypical case, the authors present a 21-year-old male with remarkable ostraceous psoriatic lesions precipitated by an upper arm tattoo, demonstrating the Koebner phenomenon.

Biologics improved coronary inflammation as well as psoriasis symptoms, according to data from the perivascular fat attenuation index in 134 adults identified using coronary CT angiography.

Oxford Academic Cardiovascular CT Core Lab and Lab of Inflammation and Cardiometabolic Diseases at NHLBI

“The perivascular fat attenuation index [FAI] is a [CT]-based, novel, noninvasive imaging technique that allows for direct visualization and quantification of coronary inflammation using differential mapping of attenuation gradients in pericoronary fat,” wrote Youssef A. Elnabawi, MD, of the National Heart, Lung, and Blood Institute and colleagues. Biologics have been associated with reduced noncalcified coronary plaques in psoriasis patients, which suggests possible reduction in coronary inflammation as well.

In a study published in JAMA Cardiology, the researchers analyzed data from 134 adults with moderate to severe psoriasis who received no biologic therapy for at least 3 months before starting the study. Of these, 52 chose not to receive biologics, and served as controls while being treated with topical or light therapies. The participants are part of the Psoriasis Atherosclerosis Cardiometabolic Initiative, an ongoing, prospective cohort study. The average age of the patients was 51 years, and 63% were male.

The 82 patients given biologics received anti–tumor necrosis factor–alpha, anti–interleukin-12/23, or anti-IL-17 for 1 year. Overall, patients on biologics showed a significant decrease in FAI from a median of –71.22 Hounsfield units (HU) at baseline to a median of –76.06 at 1 year. These patients also showed significant improvement in Psoriasis Area and Severity Index scores, from a median of 7.7 at baseline to a median of 3.2 at 1 year. The control patients not on biologics showed no significant changes in FAI, with a median of –71.98 HU at baseline and –72.66 HU at 1 year.

The changes were consistent among the various biologics used, and The median FAI for patients on anti–tumor necrosis factor–alpha changed from –71.25 at baseline to –75.49 at 1 year; median FAI for both IL-12/23 and anti-IL-17 treatment groups changed from –71.18 HU at baseline to –76.92 at 1 year.

In addition, only patients treated with biologics showed a significant reduction in median C-reactive protein levels from baseline (2.2 mg/L vs. 1.3 mg/L). The changes in FAI were not associated with the presence of coronary plaques, the researchers noted.

The study findings were limited by several factors, including the observational design, small size, and lack of data on cardiovascular endpoints. “Future studies will be needed to explore whether the residual CV risk detected by perivascular FAI can be attenuated using targeted anti-inflammatory interventions,” they wrote.

However, the results suggest that biologics impact coronary vasculature at the microenvironmental level, and that FAI can be a noninvasive, cost-effective way to stratify patients at increased risk for cardiovascular disease, the researchers noted.


“We believe that the strength of perivascular FAI in risk stratifying patients with increased coronary inflammation will allow for better identification of patients at increased risk of future myocardial events that are not captured by traditional CV risk factors,” they wrote.

The study was funded by the National Institutes of Health, several research foundations, Elsevier, Colgate-Palmolive, and Genentech. Dr. Elnabawi had no financial conflicts to disclose; several coauthors reported relationships with multiple companies. One coauthor disclosed a pending and licensed patent to a novel tool for cardiovascular risk stratification based on the CT attenuation of perivascular tissue (OxScore) and a pending and licensed patent to perivascular texture index.

SOURCE: Elnabawi YA et al. JAMA Cardiol. 2019 Jul 31. doi: 10.1001/jamacardio.2019.2589.

Biologics improved coronary inflammation as well as psoriasis symptoms, according to data from the perivascular fat attenuation index in 134 adults identified using coronary CT angiography.

Oxford Academic Cardiovascular CT Core Lab and Lab of Inflammation and Cardiometabolic Diseases at NHLBI

“The perivascular fat attenuation index [FAI] is a [CT]-based, novel, noninvasive imaging technique that allows for direct visualization and quantification of coronary inflammation using differential mapping of attenuation gradients in pericoronary fat,” wrote Youssef A. Elnabawi, MD, of the National Heart, Lung, and Blood Institute and colleagues. Biologics have been associated with reduced noncalcified coronary plaques in psoriasis patients, which suggests possible reduction in coronary inflammation as well.

In a study published in JAMA Cardiology, the researchers analyzed data from 134 adults with moderate to severe psoriasis who received no biologic therapy for at least 3 months before starting the study. Of these, 52 chose not to receive biologics, and served as controls while being treated with topical or light therapies. The participants are part of the Psoriasis Atherosclerosis Cardiometabolic Initiative, an ongoing, prospective cohort study. The average age of the patients was 51 years, and 63% were male.

The 82 patients given biologics received anti–tumor necrosis factor–alpha, anti–interleukin-12/23, or anti-IL-17 for 1 year. Overall, patients on biologics showed a significant decrease in FAI from a median of –71.22 Hounsfield units (HU) at baseline to a median of –76.06 at 1 year. These patients also showed significant improvement in Psoriasis Area and Severity Index scores, from a median of 7.7 at baseline to a median of 3.2 at 1 year. The control patients not on biologics showed no significant changes in FAI, with a median of –71.98 HU at baseline and –72.66 HU at 1 year.

The changes were consistent among the various biologics used, and The median FAI for patients on anti–tumor necrosis factor–alpha changed from –71.25 at baseline to –75.49 at 1 year; median FAI for both IL-12/23 and anti-IL-17 treatment groups changed from –71.18 HU at baseline to –76.92 at 1 year.

In addition, only patients treated with biologics showed a significant reduction in median C-reactive protein levels from baseline (2.2 mg/L vs. 1.3 mg/L). The changes in FAI were not associated with the presence of coronary plaques, the researchers noted.

The study findings were limited by several factors, including the observational design, small size, and lack of data on cardiovascular endpoints. “Future studies will be needed to explore whether the residual CV risk detected by perivascular FAI can be attenuated using targeted anti-inflammatory interventions,” they wrote.

However, the results suggest that biologics impact coronary vasculature at the microenvironmental level, and that FAI can be a noninvasive, cost-effective way to stratify patients at increased risk for cardiovascular disease, the researchers noted.


“We believe that the strength of perivascular FAI in risk stratifying patients with increased coronary inflammation will allow for better identification of patients at increased risk of future myocardial events that are not captured by traditional CV risk factors,” they wrote.

The study was funded by the National Institutes of Health, several research foundations, Elsevier, Colgate-Palmolive, and Genentech. Dr. Elnabawi had no financial conflicts to disclose; several coauthors reported relationships with multiple companies. One coauthor disclosed a pending and licensed patent to a novel tool for cardiovascular risk stratification based on the CT attenuation of perivascular tissue (OxScore) and a pending and licensed patent to perivascular texture index.

SOURCE: Elnabawi YA et al. JAMA Cardiol. 2019 Jul 31. doi: 10.1001/jamacardio.2019.2589.

Biologics improved coronary inflammation as well as psoriasis symptoms, according to data from the perivascular fat attenuation index in 134 adults identified using coronary CT angiography.

Oxford Academic Cardiovascular CT Core Lab and Lab of Inflammation and Cardiometabolic Diseases at NHLBI

“The perivascular fat attenuation index [FAI] is a [CT]-based, novel, noninvasive imaging technique that allows for direct visualization and quantification of coronary inflammation using differential mapping of attenuation gradients in pericoronary fat,” wrote Youssef A. Elnabawi, MD, of the National Heart, Lung, and Blood Institute and colleagues. Biologics have been associated with reduced noncalcified coronary plaques in psoriasis patients, which suggests possible reduction in coronary inflammation as well.

In a study published in JAMA Cardiology, the researchers analyzed data from 134 adults with moderate to severe psoriasis who received no biologic therapy for at least 3 months before starting the study. Of these, 52 chose not to receive biologics, and served as controls while being treated with topical or light therapies. The participants are part of the Psoriasis Atherosclerosis Cardiometabolic Initiative, an ongoing, prospective cohort study. The average age of the patients was 51 years, and 63% were male.

The 82 patients given biologics received anti–tumor necrosis factor–alpha, anti–interleukin-12/23, or anti-IL-17 for 1 year. Overall, patients on biologics showed a significant decrease in FAI from a median of –71.22 Hounsfield units (HU) at baseline to a median of –76.06 at 1 year. These patients also showed significant improvement in Psoriasis Area and Severity Index scores, from a median of 7.7 at baseline to a median of 3.2 at 1 year. The control patients not on biologics showed no significant changes in FAI, with a median of –71.98 HU at baseline and –72.66 HU at 1 year.

The changes were consistent among the various biologics used, and The median FAI for patients on anti–tumor necrosis factor–alpha changed from –71.25 at baseline to –75.49 at 1 year; median FAI for both IL-12/23 and anti-IL-17 treatment groups changed from –71.18 HU at baseline to –76.92 at 1 year.

In addition, only patients treated with biologics showed a significant reduction in median C-reactive protein levels from baseline (2.2 mg/L vs. 1.3 mg/L). The changes in FAI were not associated with the presence of coronary plaques, the researchers noted.

The study findings were limited by several factors, including the observational design, small size, and lack of data on cardiovascular endpoints. “Future studies will be needed to explore whether the residual CV risk detected by perivascular FAI can be attenuated using targeted anti-inflammatory interventions,” they wrote.

However, the results suggest that biologics impact coronary vasculature at the microenvironmental level, and that FAI can be a noninvasive, cost-effective way to stratify patients at increased risk for cardiovascular disease, the researchers noted.


“We believe that the strength of perivascular FAI in risk stratifying patients with increased coronary inflammation will allow for better identification of patients at increased risk of future myocardial events that are not captured by traditional CV risk factors,” they wrote.

The study was funded by the National Institutes of Health, several research foundations, Elsevier, Colgate-Palmolive, and Genentech. Dr. Elnabawi had no financial conflicts to disclose; several coauthors reported relationships with multiple companies. One coauthor disclosed a pending and licensed patent to a novel tool for cardiovascular risk stratification based on the CT attenuation of perivascular tissue (OxScore) and a pending and licensed patent to perivascular texture index.

SOURCE: Elnabawi YA et al. JAMA Cardiol. 2019 Jul 31. doi: 10.1001/jamacardio.2019.2589.

Facial involvement and the severity of psoriasis.

Passos AN, de A Rêgo VRP, Duarte GV, Santos E Miranda RC, de O Rocha B, de F S P de Oliveira M. Int J Dermatol. 2019 Jul 26.

The aim of this cross-sectional study is to compare the severity of psoriasis, measured by the Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI), in patients with and without facial lesions.

Genital Psoriasis: Impact on Quality of Life and Treatment Options.

Kelly A, Ryan C. Am J Clin Dermatol. 2019 Jul 16

Psoriasis involving the genital skin occurs in up to two-thirds of psoriasis patients but is often overlooked by physicians. Furthermore, psoriasis objective and subjective severity indexes for common plaque psoriasis often neglect the impact this small area of psoriasis can have on a patient. It can have a significant impact on patients' psychosocial function due to intrusive physical symptoms such as genital itch and pain, and a detrimental impact on sexual health and impaired relationships.

Lifestyle changes for treating psoriasis.

Ko SH, Chi CC, Yeh ML, Wang SH, Tsai YS, Hsu MY. Cochrane Database Syst Rev. 2019 Jul 16

The objective of this review is to assess the effects of lifestyle changes for psoriasis, including weight reduction, alcohol abstinence, smoking cessation, dietary modification, exercise, and other lifestyle change interventions. Dietary intervention may reduce the severity of psoriasis (low-quality evidence) and probably improves quality of life and reduces BMI (moderate-quality evidence) in obese people when compared with usual care, while combined dietary intervention and exercise programme probably improves psoriasis severity and BMI when compared with information only (moderate-quality evidence).

The Incidence Rates and Risk Factors of Parkinson's Disease in Patients with Psoriasis: A Nationwide Population-based Cohort Study.

Lee JH, Han K, Gee HY. J Am Acad Dermatol. 2019 Jul 11.

This was a nationwide population-based cohort study to determine the incidence rates and risk factors of Parkinson's disease in patients with psoriasis. The psoriasis group showed a significantly increased risk of developing Parkinson's disease. The risk of Parkinson's disease was significantly high among the psoriasis patients who were not receiving systemic therapy and was low among the psoriasis patients on systemic therapy.

Psoriasis-associated itch: etiology, assessment, impact, and management.

Pithadia DJ, Reynolds KA, Lee EB, Wu JJ. J Dermatolog Treat. 2019 Jul 5:1-9.

Pruritus, a very broad, subjective, and complex symptom, troubles the majority of patients with psoriasis. However, the subjective and multidimensional nature of the symptom renders it challenging for patients to appropriately communicate their experiences with itch to providers. This review explores current perspectives regarding the underlying mechanisms, assessment tools, burden, and treatment modalities for psoriatic pruritus. It emphasizes the significance of incorporating a standardized, thorough, and verified metric that incorporates severity, distribution, and character of pruritus as well as its effects on various aspects of quality of life. It also underscores the importance of continued research to fully understand the pathogenesis of psoriatic itch for establishment of novel, targeted therapeutics.

Facial involvement and the severity of psoriasis.

Passos AN, de A Rêgo VRP, Duarte GV, Santos E Miranda RC, de O Rocha B, de F S P de Oliveira M. Int J Dermatol. 2019 Jul 26.

The aim of this cross-sectional study is to compare the severity of psoriasis, measured by the Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI), in patients with and without facial lesions.

Genital Psoriasis: Impact on Quality of Life and Treatment Options.

Kelly A, Ryan C. Am J Clin Dermatol. 2019 Jul 16

Psoriasis involving the genital skin occurs in up to two-thirds of psoriasis patients but is often overlooked by physicians. Furthermore, psoriasis objective and subjective severity indexes for common plaque psoriasis often neglect the impact this small area of psoriasis can have on a patient. It can have a significant impact on patients' psychosocial function due to intrusive physical symptoms such as genital itch and pain, and a detrimental impact on sexual health and impaired relationships.

Lifestyle changes for treating psoriasis.

Ko SH, Chi CC, Yeh ML, Wang SH, Tsai YS, Hsu MY. Cochrane Database Syst Rev. 2019 Jul 16

The objective of this review is to assess the effects of lifestyle changes for psoriasis, including weight reduction, alcohol abstinence, smoking cessation, dietary modification, exercise, and other lifestyle change interventions. Dietary intervention may reduce the severity of psoriasis (low-quality evidence) and probably improves quality of life and reduces BMI (moderate-quality evidence) in obese people when compared with usual care, while combined dietary intervention and exercise programme probably improves psoriasis severity and BMI when compared with information only (moderate-quality evidence).

The Incidence Rates and Risk Factors of Parkinson's Disease in Patients with Psoriasis: A Nationwide Population-based Cohort Study.

Lee JH, Han K, Gee HY. J Am Acad Dermatol. 2019 Jul 11.

This was a nationwide population-based cohort study to determine the incidence rates and risk factors of Parkinson's disease in patients with psoriasis. The psoriasis group showed a significantly increased risk of developing Parkinson's disease. The risk of Parkinson's disease was significantly high among the psoriasis patients who were not receiving systemic therapy and was low among the psoriasis patients on systemic therapy.

Psoriasis-associated itch: etiology, assessment, impact, and management.

Pithadia DJ, Reynolds KA, Lee EB, Wu JJ. J Dermatolog Treat. 2019 Jul 5:1-9.

Pruritus, a very broad, subjective, and complex symptom, troubles the majority of patients with psoriasis. However, the subjective and multidimensional nature of the symptom renders it challenging for patients to appropriately communicate their experiences with itch to providers. This review explores current perspectives regarding the underlying mechanisms, assessment tools, burden, and treatment modalities for psoriatic pruritus. It emphasizes the significance of incorporating a standardized, thorough, and verified metric that incorporates severity, distribution, and character of pruritus as well as its effects on various aspects of quality of life. It also underscores the importance of continued research to fully understand the pathogenesis of psoriatic itch for establishment of novel, targeted therapeutics.

Facial involvement and the severity of psoriasis.

Passos AN, de A Rêgo VRP, Duarte GV, Santos E Miranda RC, de O Rocha B, de F S P de Oliveira M. Int J Dermatol. 2019 Jul 26.

The aim of this cross-sectional study is to compare the severity of psoriasis, measured by the Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI), in patients with and without facial lesions.

Genital Psoriasis: Impact on Quality of Life and Treatment Options.

Kelly A, Ryan C. Am J Clin Dermatol. 2019 Jul 16

Psoriasis involving the genital skin occurs in up to two-thirds of psoriasis patients but is often overlooked by physicians. Furthermore, psoriasis objective and subjective severity indexes for common plaque psoriasis often neglect the impact this small area of psoriasis can have on a patient. It can have a significant impact on patients' psychosocial function due to intrusive physical symptoms such as genital itch and pain, and a detrimental impact on sexual health and impaired relationships.

Lifestyle changes for treating psoriasis.

Ko SH, Chi CC, Yeh ML, Wang SH, Tsai YS, Hsu MY. Cochrane Database Syst Rev. 2019 Jul 16

The objective of this review is to assess the effects of lifestyle changes for psoriasis, including weight reduction, alcohol abstinence, smoking cessation, dietary modification, exercise, and other lifestyle change interventions. Dietary intervention may reduce the severity of psoriasis (low-quality evidence) and probably improves quality of life and reduces BMI (moderate-quality evidence) in obese people when compared with usual care, while combined dietary intervention and exercise programme probably improves psoriasis severity and BMI when compared with information only (moderate-quality evidence).

The Incidence Rates and Risk Factors of Parkinson's Disease in Patients with Psoriasis: A Nationwide Population-based Cohort Study.

Lee JH, Han K, Gee HY. J Am Acad Dermatol. 2019 Jul 11.

This was a nationwide population-based cohort study to determine the incidence rates and risk factors of Parkinson's disease in patients with psoriasis. The psoriasis group showed a significantly increased risk of developing Parkinson's disease. The risk of Parkinson's disease was significantly high among the psoriasis patients who were not receiving systemic therapy and was low among the psoriasis patients on systemic therapy.

Psoriasis-associated itch: etiology, assessment, impact, and management.

Pithadia DJ, Reynolds KA, Lee EB, Wu JJ. J Dermatolog Treat. 2019 Jul 5:1-9.

Pruritus, a very broad, subjective, and complex symptom, troubles the majority of patients with psoriasis. However, the subjective and multidimensional nature of the symptom renders it challenging for patients to appropriately communicate their experiences with itch to providers. This review explores current perspectives regarding the underlying mechanisms, assessment tools, burden, and treatment modalities for psoriatic pruritus. It emphasizes the significance of incorporating a standardized, thorough, and verified metric that incorporates severity, distribution, and character of pruritus as well as its effects on various aspects of quality of life. It also underscores the importance of continued research to fully understand the pathogenesis of psoriatic itch for establishment of novel, targeted therapeutics.