Psoriasis

Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease.¹ The majority of BP cases are idiopathic and occur in patients older than 60 years. The disease is characterized by the development of circulating IgG autoantibodies reacting with the BP180 antigen of the basement membrane zone.¹ Psoriasis vulgaris (PV) is a common, chronic, immune-mediated disease affecting approximately 2% of the world’s population including children and adults.² Both entities may coexist with internal disorders such as hypertension, diabetes mellitus, coronary heart disease, congestive heart failure, hyperlipidemia, and cerebrovascular accident. It has been postulated that BP more often coexists with neurological disorders, such as stroke and Parkinson disease,³ whereas PV usually is associated with cardiovascular disorders and diabetes mellitus.² We report the case of a 35-year-old man with chronic PV and metabolic syndrome who developed BP that was successfully treated with methotrexate (MTX).

Case Report

A 35-year-old man with a 15-year history of PV, class 3 obesity (body mass index, 69.2), and thrombosis of the left leg was referred to the dermatology department due to a sudden extensive erythematous and bullous eruption located on the trunk, arms, and legs with involvement of the oral mucosa that had started 4 weeks prior. The skin lesions were accompanied by severe pruritus. On admission to the hospital, the patient presented with stable psoriatic plaques located on the trunk, arms, and proximal part of the lower legs with a psoriasis area severity index score of 11.8 (Figure 1A). He also had disseminated tense blisters and erosions partially arranged in an annular pattern located on the border of the psoriatic plaques as well as on an erythematous base or within unaffected skin (Figure 1B). Additionally, a few small erosions were present on the oral mucosa.

The patient’s father had a history of PV, but there was no family history of obesity or autoimmune blistering disorders. On physical examination, central obesity was noted with a waist circumference of 180 cm and a body mass index of 69.2; his blood pressure was 220/150 mm Hg. Laboratory tests revealed leukocytosis (20.06×10⁹/L [reference range, 4.5–11.0×10⁹/L]) with neutrophilia (16.2×10⁹/L [reference range, 1.6–7.6×10⁹/L]; 80.9% [reference range, 40.0%–70.0%]), eosinophilia (1.01×10⁹/L [reference range, 0–0.5×10⁹/L]), elevated C-reactive protein levels (49.4 mg/L [reference range, 0.0–9.0 mg/L]), elevated erythrocyte sedimentation rate (35 mm/h [reference range, 0–12 mm/h]), elevated γ-glutamyltransferase (66 U/L [reference range, 0–55 U/L]), decreased high-density lipoprotein levels (38 mg/dL [reference range, ≥40 mg/dL]), elevated fasting plasma glucose (116 mg/dL or 6.4 mmol/L [reference range, 70–99 mg/dL or 3.9–5.5 mmol/L]), elevated total IgE (1540 µg/L [reference range, 0–1000 µg/L]), elevated D-dimer (3.21 µg/mL [reference range, <0.5 µg/mL]), and low free triiodothyronine levels (130 pg/dL [reference range, 171–371 pg/dL]). The total protein level was 6.5 g/dL (reference range, 6.0–8.0 g/dL) and albumin level was 3.2 g/dL (reference range, 4.02–4.76 g/dL). A chest radiograph showed no abnormalities.

Based on the physical examination and laboratory testing, it was determined that the patient fulfilled 4 of 5 criteria for metabolic syndrome described by the International Diabetes Federation in 2006 (Table).⁴ Direct immunofluorescence performed on normal-appearing perilesional skin demonstrated linear IgG and C3 deposits along the basement membrane zone. Indirect immunofluorescence detected circulating IgG autoantibodies at a titer of 1:80. Serum studies using biochip mosaics⁵ revealed the reactivity of circulating IgG antibodies to the epidermal side of salt-split skin and with antigen dots of tetrameric BP180-NC16a, which prompted the diagnosis of BP (Figure 2).

Oral treatment with MTX 12.5 mg once weekly with clobetasol propionate cream applied to affected skin was initiated for 4 weeks. The PV resolved completely and blister formation stopped. A few weeks later BP reappeared, even though the patient was still taking MTX. The treatment failure may have been related to the patient’s class 3 obesity; therefore, the dose was increased to 20 mg once weekly for 8 weeks, which led to rapid healing of BP erosions. The patient was monitored for 2 months with no symptoms of recurrence.

Comment

Psoriasis Comorbidities

The correlation between PV and cardiovascular disorders such as myocardial infarction, cerebrovascular accident, and pulmonary embolism has been well established and is widely accepted.² It also has been documented that the risk for metabolic syndrome with components such as diabetes mellitus, hypertension, lipid abnormalities, obesity, and arteriosclerosis is notably increased in PV patients.⁶ Moreover, associated internal disorders are responsible for a 3- to 4-year reduction in life expectancy in patients with moderate to severe PV.⁷

Correlation of PV and BP

Psoriasis also may coexist with autoimmune disorders such as rheumatoid arthritis, lupus erythematosus, and blistering disorders.⁸ There are more than 60 known cases reporting PV in association with various types of subepidermal blistering diseases, including pemphigus vulgaris, epidermolysis bullosa acquisita, anti-p200 pemphigoid, and BP.^8,9 The pathogenetic relationship between BP and PV remains obscure. In most published cases, PV preceded BP by 5 to 30 years, possibly ascribable to patients being diagnosed with PV at a younger age.⁹ In general, patients with BP and PV are younger than patients with BP only, with a mean age of 62 years.⁹ Because our patient was in his mid-30s when he developed BP, in such cases physicians should take under consideration any triggering factors (eg, drugs). Physical examination and detailed laboratory findings allowed us to make the patient aware of the potential for development of metabolic syndrome. This condition in combination with PV could be a predisposing factor for BP development. According to more recent research, PV is considered a generalized inflammatory process rather than a disorder limited to the skin and joints.¹⁰ The chronic inflammatory process in psoriatic skin results in exposure of autoantigens, leading to an immune response and the production of BP antibodies. The neutrophil elastase enzyme present in psoriatic lesions also may take part in dermoepidermal junction degradation and blister formation of BP.¹¹ According to other observations, some antipsoriatic therapies (eg, psoralen plus UVA, UVB, dithranol, coal tar) could be associated with development of BP.¹² Moreover, it was shown that psoralen plus UVA therapy, which is widely used in PV treatment, alters the cytokine profile from helper T cells T_H1 to T_H2.¹² T_H2-dependent cytokines predominate the sera and erosions in BP patients and seem to be notably relevant to the pathophysiology of the disease.¹³ The history of our patient’s psoriatic treatment included only topical corticosteroids, keratolytic agents, and occasionally dithranol and coal tar; however, UV phototherapy or any other systemic therapies had never been utilized. Three previously reported cases of patients with PV and BP also revealed no history of UV phototherapy,^8,9 which suggests that mechanisms responsible for coexistence of PV and BP are more complex. It has been proven that proinflammatory cytokines secreted by T_H1 and T_H17 cells, in particular tumor necrosis factor α, IL-17, IL-22, and IL-23, play an important role in the development of psoriatic lesions.¹⁰ On the other hand, these cytokines are known to contribute to vascular inflammation, leading to development of arteriosclerosis, as well as to regulate adipogenesis and obesity.^14,15 Arakawa et al¹⁶ reported increased expression of IL-17 in lesional skin in BP. They concluded that IL-17 may contribute to the recruitment of eosinophils and neutrophils and tissue damage in BP. Therefore, it is highly likely that IL-17 might be a common factor underlying the coexistence of BP with PV and metabolic syndrome. More such reports are required for better understanding this association.

BP Treatment

Selecting a therapy for BP with coexistent PV is challenging, especially in patients with extreme obesity and metabolic syndrome. It is well established that obesity correlates with a higher incidence of PV and more severe disease. On the other hand, obesity also influences response to therapy. Systemic corticosteroids are contraindicated in psoriasis patients because of severe side effects, such as rebound phenomenon of psoriatic lesions and risk for development of generalized pustular PV. Although systemic corticosteroids are effective in BP, high-dose therapy may potentially be life-threatening, particularly in these obese patients with conditions such as hypertension and diabetes mellitus, among others,¹ as was observed in our case. Taking into consideration the above mentioned conditions and our experience on such cases, the current patient had received MTX (12.5 mg once weekly) and clobetasol propionate cream, which led to the rapid healing of the psoriatic plaques, whereas BP was more resistant to this therapy. This response may be explained by our patient’s class 3 obesity (body mass index, 69.2). Therefore, the dose of MTX was increased to 20 mg once weekly and was successful. The decision to use MTX was supported by evidence that this medicine may reduce the risk for arteriosclerosis and cardiovascular disorders.¹⁷

There are some alternative therapeutic options for patients with coexisting BP and PV, such as cyclosporine,¹⁸ combination low-dose cyclosporine and low-dose systemic corticosteroids,¹⁹ dapsone,²⁰ azathioprine,²¹ mycophenolate mofetil,²² and acitretin.²³ It also has been shown that biologics (eg, ustekinumab) may be a successful solution in patients with PV and antilaminin-γ1 pemphigoid.²⁴ However, these alternative therapeutic regimens could not be considered in our patient because of serious coexisting internal disorders.

Conclusion

We present a case of concomitant BP and PV in a patient with metabolic syndrome. Although the pathogenic role of this unique coexistence is not fully understood, MTX proved suitable and effective in this single case. Further studies should be performed to elucidate the pathogenic relationship and therapeutic solutions for cases with coexisting PV, BP, and metabolic syndrome.

Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease.¹ The majority of BP cases are idiopathic and occur in patients older than 60 years. The disease is characterized by the development of circulating IgG autoantibodies reacting with the BP180 antigen of the basement membrane zone.¹ Psoriasis vulgaris (PV) is a common, chronic, immune-mediated disease affecting approximately 2% of the world’s population including children and adults.² Both entities may coexist with internal disorders such as hypertension, diabetes mellitus, coronary heart disease, congestive heart failure, hyperlipidemia, and cerebrovascular accident. It has been postulated that BP more often coexists with neurological disorders, such as stroke and Parkinson disease,³ whereas PV usually is associated with cardiovascular disorders and diabetes mellitus.² We report the case of a 35-year-old man with chronic PV and metabolic syndrome who developed BP that was successfully treated with methotrexate (MTX).

Case Report

A 35-year-old man with a 15-year history of PV, class 3 obesity (body mass index, 69.2), and thrombosis of the left leg was referred to the dermatology department due to a sudden extensive erythematous and bullous eruption located on the trunk, arms, and legs with involvement of the oral mucosa that had started 4 weeks prior. The skin lesions were accompanied by severe pruritus. On admission to the hospital, the patient presented with stable psoriatic plaques located on the trunk, arms, and proximal part of the lower legs with a psoriasis area severity index score of 11.8 (Figure 1A). He also had disseminated tense blisters and erosions partially arranged in an annular pattern located on the border of the psoriatic plaques as well as on an erythematous base or within unaffected skin (Figure 1B). Additionally, a few small erosions were present on the oral mucosa.

The patient’s father had a history of PV, but there was no family history of obesity or autoimmune blistering disorders. On physical examination, central obesity was noted with a waist circumference of 180 cm and a body mass index of 69.2; his blood pressure was 220/150 mm Hg. Laboratory tests revealed leukocytosis (20.06×10⁹/L [reference range, 4.5–11.0×10⁹/L]) with neutrophilia (16.2×10⁹/L [reference range, 1.6–7.6×10⁹/L]; 80.9% [reference range, 40.0%–70.0%]), eosinophilia (1.01×10⁹/L [reference range, 0–0.5×10⁹/L]), elevated C-reactive protein levels (49.4 mg/L [reference range, 0.0–9.0 mg/L]), elevated erythrocyte sedimentation rate (35 mm/h [reference range, 0–12 mm/h]), elevated γ-glutamyltransferase (66 U/L [reference range, 0–55 U/L]), decreased high-density lipoprotein levels (38 mg/dL [reference range, ≥40 mg/dL]), elevated fasting plasma glucose (116 mg/dL or 6.4 mmol/L [reference range, 70–99 mg/dL or 3.9–5.5 mmol/L]), elevated total IgE (1540 µg/L [reference range, 0–1000 µg/L]), elevated D-dimer (3.21 µg/mL [reference range, <0.5 µg/mL]), and low free triiodothyronine levels (130 pg/dL [reference range, 171–371 pg/dL]). The total protein level was 6.5 g/dL (reference range, 6.0–8.0 g/dL) and albumin level was 3.2 g/dL (reference range, 4.02–4.76 g/dL). A chest radiograph showed no abnormalities.

Based on the physical examination and laboratory testing, it was determined that the patient fulfilled 4 of 5 criteria for metabolic syndrome described by the International Diabetes Federation in 2006 (Table).⁴ Direct immunofluorescence performed on normal-appearing perilesional skin demonstrated linear IgG and C3 deposits along the basement membrane zone. Indirect immunofluorescence detected circulating IgG autoantibodies at a titer of 1:80. Serum studies using biochip mosaics⁵ revealed the reactivity of circulating IgG antibodies to the epidermal side of salt-split skin and with antigen dots of tetrameric BP180-NC16a, which prompted the diagnosis of BP (Figure 2).

Oral treatment with MTX 12.5 mg once weekly with clobetasol propionate cream applied to affected skin was initiated for 4 weeks. The PV resolved completely and blister formation stopped. A few weeks later BP reappeared, even though the patient was still taking MTX. The treatment failure may have been related to the patient’s class 3 obesity; therefore, the dose was increased to 20 mg once weekly for 8 weeks, which led to rapid healing of BP erosions. The patient was monitored for 2 months with no symptoms of recurrence.

Comment

Psoriasis Comorbidities

The correlation between PV and cardiovascular disorders such as myocardial infarction, cerebrovascular accident, and pulmonary embolism has been well established and is widely accepted.² It also has been documented that the risk for metabolic syndrome with components such as diabetes mellitus, hypertension, lipid abnormalities, obesity, and arteriosclerosis is notably increased in PV patients.⁶ Moreover, associated internal disorders are responsible for a 3- to 4-year reduction in life expectancy in patients with moderate to severe PV.⁷

Correlation of PV and BP

Psoriasis also may coexist with autoimmune disorders such as rheumatoid arthritis, lupus erythematosus, and blistering disorders.⁸ There are more than 60 known cases reporting PV in association with various types of subepidermal blistering diseases, including pemphigus vulgaris, epidermolysis bullosa acquisita, anti-p200 pemphigoid, and BP.^8,9 The pathogenetic relationship between BP and PV remains obscure. In most published cases, PV preceded BP by 5 to 30 years, possibly ascribable to patients being diagnosed with PV at a younger age.⁹ In general, patients with BP and PV are younger than patients with BP only, with a mean age of 62 years.⁹ Because our patient was in his mid-30s when he developed BP, in such cases physicians should take under consideration any triggering factors (eg, drugs). Physical examination and detailed laboratory findings allowed us to make the patient aware of the potential for development of metabolic syndrome. This condition in combination with PV could be a predisposing factor for BP development. According to more recent research, PV is considered a generalized inflammatory process rather than a disorder limited to the skin and joints.¹⁰ The chronic inflammatory process in psoriatic skin results in exposure of autoantigens, leading to an immune response and the production of BP antibodies. The neutrophil elastase enzyme present in psoriatic lesions also may take part in dermoepidermal junction degradation and blister formation of BP.¹¹ According to other observations, some antipsoriatic therapies (eg, psoralen plus UVA, UVB, dithranol, coal tar) could be associated with development of BP.¹² Moreover, it was shown that psoralen plus UVA therapy, which is widely used in PV treatment, alters the cytokine profile from helper T cells T_H1 to T_H2.¹² T_H2-dependent cytokines predominate the sera and erosions in BP patients and seem to be notably relevant to the pathophysiology of the disease.¹³ The history of our patient’s psoriatic treatment included only topical corticosteroids, keratolytic agents, and occasionally dithranol and coal tar; however, UV phototherapy or any other systemic therapies had never been utilized. Three previously reported cases of patients with PV and BP also revealed no history of UV phototherapy,^8,9 which suggests that mechanisms responsible for coexistence of PV and BP are more complex. It has been proven that proinflammatory cytokines secreted by T_H1 and T_H17 cells, in particular tumor necrosis factor α, IL-17, IL-22, and IL-23, play an important role in the development of psoriatic lesions.¹⁰ On the other hand, these cytokines are known to contribute to vascular inflammation, leading to development of arteriosclerosis, as well as to regulate adipogenesis and obesity.^14,15 Arakawa et al¹⁶ reported increased expression of IL-17 in lesional skin in BP. They concluded that IL-17 may contribute to the recruitment of eosinophils and neutrophils and tissue damage in BP. Therefore, it is highly likely that IL-17 might be a common factor underlying the coexistence of BP with PV and metabolic syndrome. More such reports are required for better understanding this association.

BP Treatment

Selecting a therapy for BP with coexistent PV is challenging, especially in patients with extreme obesity and metabolic syndrome. It is well established that obesity correlates with a higher incidence of PV and more severe disease. On the other hand, obesity also influences response to therapy. Systemic corticosteroids are contraindicated in psoriasis patients because of severe side effects, such as rebound phenomenon of psoriatic lesions and risk for development of generalized pustular PV. Although systemic corticosteroids are effective in BP, high-dose therapy may potentially be life-threatening, particularly in these obese patients with conditions such as hypertension and diabetes mellitus, among others,¹ as was observed in our case. Taking into consideration the above mentioned conditions and our experience on such cases, the current patient had received MTX (12.5 mg once weekly) and clobetasol propionate cream, which led to the rapid healing of the psoriatic plaques, whereas BP was more resistant to this therapy. This response may be explained by our patient’s class 3 obesity (body mass index, 69.2). Therefore, the dose of MTX was increased to 20 mg once weekly and was successful. The decision to use MTX was supported by evidence that this medicine may reduce the risk for arteriosclerosis and cardiovascular disorders.¹⁷

There are some alternative therapeutic options for patients with coexisting BP and PV, such as cyclosporine,¹⁸ combination low-dose cyclosporine and low-dose systemic corticosteroids,¹⁹ dapsone,²⁰ azathioprine,²¹ mycophenolate mofetil,²² and acitretin.²³ It also has been shown that biologics (eg, ustekinumab) may be a successful solution in patients with PV and antilaminin-γ1 pemphigoid.²⁴ However, these alternative therapeutic regimens could not be considered in our patient because of serious coexisting internal disorders.

Conclusion

We present a case of concomitant BP and PV in a patient with metabolic syndrome. Although the pathogenic role of this unique coexistence is not fully understood, MTX proved suitable and effective in this single case. Further studies should be performed to elucidate the pathogenic relationship and therapeutic solutions for cases with coexisting PV, BP, and metabolic syndrome.

Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease.¹ The majority of BP cases are idiopathic and occur in patients older than 60 years. The disease is characterized by the development of circulating IgG autoantibodies reacting with the BP180 antigen of the basement membrane zone.¹ Psoriasis vulgaris (PV) is a common, chronic, immune-mediated disease affecting approximately 2% of the world’s population including children and adults.² Both entities may coexist with internal disorders such as hypertension, diabetes mellitus, coronary heart disease, congestive heart failure, hyperlipidemia, and cerebrovascular accident. It has been postulated that BP more often coexists with neurological disorders, such as stroke and Parkinson disease,³ whereas PV usually is associated with cardiovascular disorders and diabetes mellitus.² We report the case of a 35-year-old man with chronic PV and metabolic syndrome who developed BP that was successfully treated with methotrexate (MTX).

Case Report

A 35-year-old man with a 15-year history of PV, class 3 obesity (body mass index, 69.2), and thrombosis of the left leg was referred to the dermatology department due to a sudden extensive erythematous and bullous eruption located on the trunk, arms, and legs with involvement of the oral mucosa that had started 4 weeks prior. The skin lesions were accompanied by severe pruritus. On admission to the hospital, the patient presented with stable psoriatic plaques located on the trunk, arms, and proximal part of the lower legs with a psoriasis area severity index score of 11.8 (Figure 1A). He also had disseminated tense blisters and erosions partially arranged in an annular pattern located on the border of the psoriatic plaques as well as on an erythematous base or within unaffected skin (Figure 1B). Additionally, a few small erosions were present on the oral mucosa.

The patient’s father had a history of PV, but there was no family history of obesity or autoimmune blistering disorders. On physical examination, central obesity was noted with a waist circumference of 180 cm and a body mass index of 69.2; his blood pressure was 220/150 mm Hg. Laboratory tests revealed leukocytosis (20.06×10⁹/L [reference range, 4.5–11.0×10⁹/L]) with neutrophilia (16.2×10⁹/L [reference range, 1.6–7.6×10⁹/L]; 80.9% [reference range, 40.0%–70.0%]), eosinophilia (1.01×10⁹/L [reference range, 0–0.5×10⁹/L]), elevated C-reactive protein levels (49.4 mg/L [reference range, 0.0–9.0 mg/L]), elevated erythrocyte sedimentation rate (35 mm/h [reference range, 0–12 mm/h]), elevated γ-glutamyltransferase (66 U/L [reference range, 0–55 U/L]), decreased high-density lipoprotein levels (38 mg/dL [reference range, ≥40 mg/dL]), elevated fasting plasma glucose (116 mg/dL or 6.4 mmol/L [reference range, 70–99 mg/dL or 3.9–5.5 mmol/L]), elevated total IgE (1540 µg/L [reference range, 0–1000 µg/L]), elevated D-dimer (3.21 µg/mL [reference range, <0.5 µg/mL]), and low free triiodothyronine levels (130 pg/dL [reference range, 171–371 pg/dL]). The total protein level was 6.5 g/dL (reference range, 6.0–8.0 g/dL) and albumin level was 3.2 g/dL (reference range, 4.02–4.76 g/dL). A chest radiograph showed no abnormalities.

Based on the physical examination and laboratory testing, it was determined that the patient fulfilled 4 of 5 criteria for metabolic syndrome described by the International Diabetes Federation in 2006 (Table).⁴ Direct immunofluorescence performed on normal-appearing perilesional skin demonstrated linear IgG and C3 deposits along the basement membrane zone. Indirect immunofluorescence detected circulating IgG autoantibodies at a titer of 1:80. Serum studies using biochip mosaics⁵ revealed the reactivity of circulating IgG antibodies to the epidermal side of salt-split skin and with antigen dots of tetrameric BP180-NC16a, which prompted the diagnosis of BP (Figure 2).

Oral treatment with MTX 12.5 mg once weekly with clobetasol propionate cream applied to affected skin was initiated for 4 weeks. The PV resolved completely and blister formation stopped. A few weeks later BP reappeared, even though the patient was still taking MTX. The treatment failure may have been related to the patient’s class 3 obesity; therefore, the dose was increased to 20 mg once weekly for 8 weeks, which led to rapid healing of BP erosions. The patient was monitored for 2 months with no symptoms of recurrence.

Comment

Psoriasis Comorbidities

The correlation between PV and cardiovascular disorders such as myocardial infarction, cerebrovascular accident, and pulmonary embolism has been well established and is widely accepted.² It also has been documented that the risk for metabolic syndrome with components such as diabetes mellitus, hypertension, lipid abnormalities, obesity, and arteriosclerosis is notably increased in PV patients.⁶ Moreover, associated internal disorders are responsible for a 3- to 4-year reduction in life expectancy in patients with moderate to severe PV.⁷

Correlation of PV and BP

Psoriasis also may coexist with autoimmune disorders such as rheumatoid arthritis, lupus erythematosus, and blistering disorders.⁸ There are more than 60 known cases reporting PV in association with various types of subepidermal blistering diseases, including pemphigus vulgaris, epidermolysis bullosa acquisita, anti-p200 pemphigoid, and BP.^8,9 The pathogenetic relationship between BP and PV remains obscure. In most published cases, PV preceded BP by 5 to 30 years, possibly ascribable to patients being diagnosed with PV at a younger age.⁹ In general, patients with BP and PV are younger than patients with BP only, with a mean age of 62 years.⁹ Because our patient was in his mid-30s when he developed BP, in such cases physicians should take under consideration any triggering factors (eg, drugs). Physical examination and detailed laboratory findings allowed us to make the patient aware of the potential for development of metabolic syndrome. This condition in combination with PV could be a predisposing factor for BP development. According to more recent research, PV is considered a generalized inflammatory process rather than a disorder limited to the skin and joints.¹⁰ The chronic inflammatory process in psoriatic skin results in exposure of autoantigens, leading to an immune response and the production of BP antibodies. The neutrophil elastase enzyme present in psoriatic lesions also may take part in dermoepidermal junction degradation and blister formation of BP.¹¹ According to other observations, some antipsoriatic therapies (eg, psoralen plus UVA, UVB, dithranol, coal tar) could be associated with development of BP.¹² Moreover, it was shown that psoralen plus UVA therapy, which is widely used in PV treatment, alters the cytokine profile from helper T cells T_H1 to T_H2.¹² T_H2-dependent cytokines predominate the sera and erosions in BP patients and seem to be notably relevant to the pathophysiology of the disease.¹³ The history of our patient’s psoriatic treatment included only topical corticosteroids, keratolytic agents, and occasionally dithranol and coal tar; however, UV phototherapy or any other systemic therapies had never been utilized. Three previously reported cases of patients with PV and BP also revealed no history of UV phototherapy,^8,9 which suggests that mechanisms responsible for coexistence of PV and BP are more complex. It has been proven that proinflammatory cytokines secreted by T_H1 and T_H17 cells, in particular tumor necrosis factor α, IL-17, IL-22, and IL-23, play an important role in the development of psoriatic lesions.¹⁰ On the other hand, these cytokines are known to contribute to vascular inflammation, leading to development of arteriosclerosis, as well as to regulate adipogenesis and obesity.^14,15 Arakawa et al¹⁶ reported increased expression of IL-17 in lesional skin in BP. They concluded that IL-17 may contribute to the recruitment of eosinophils and neutrophils and tissue damage in BP. Therefore, it is highly likely that IL-17 might be a common factor underlying the coexistence of BP with PV and metabolic syndrome. More such reports are required for better understanding this association.

BP Treatment

Selecting a therapy for BP with coexistent PV is challenging, especially in patients with extreme obesity and metabolic syndrome. It is well established that obesity correlates with a higher incidence of PV and more severe disease. On the other hand, obesity also influences response to therapy. Systemic corticosteroids are contraindicated in psoriasis patients because of severe side effects, such as rebound phenomenon of psoriatic lesions and risk for development of generalized pustular PV. Although systemic corticosteroids are effective in BP, high-dose therapy may potentially be life-threatening, particularly in these obese patients with conditions such as hypertension and diabetes mellitus, among others,¹ as was observed in our case. Taking into consideration the above mentioned conditions and our experience on such cases, the current patient had received MTX (12.5 mg once weekly) and clobetasol propionate cream, which led to the rapid healing of the psoriatic plaques, whereas BP was more resistant to this therapy. This response may be explained by our patient’s class 3 obesity (body mass index, 69.2). Therefore, the dose of MTX was increased to 20 mg once weekly and was successful. The decision to use MTX was supported by evidence that this medicine may reduce the risk for arteriosclerosis and cardiovascular disorders.¹⁷

There are some alternative therapeutic options for patients with coexisting BP and PV, such as cyclosporine,¹⁸ combination low-dose cyclosporine and low-dose systemic corticosteroids,¹⁹ dapsone,²⁰ azathioprine,²¹ mycophenolate mofetil,²² and acitretin.²³ It also has been shown that biologics (eg, ustekinumab) may be a successful solution in patients with PV and antilaminin-γ1 pemphigoid.²⁴ However, these alternative therapeutic regimens could not be considered in our patient because of serious coexisting internal disorders.

Conclusion

We present a case of concomitant BP and PV in a patient with metabolic syndrome. Although the pathogenic role of this unique coexistence is not fully understood, MTX proved suitable and effective in this single case. Further studies should be performed to elucidate the pathogenic relationship and therapeutic solutions for cases with coexisting PV, BP, and metabolic syndrome.

When using biologic therapies for psoriasis, it is important to evaluate long-term efficacy (>4 years of follow-up). Biologic drug survival in psoriasis reflects long-term performance in real-life settings. Prior studies have yielded inconsistent results.

Vilarrasa et al (J Am Acad Dermatol. 2016;74:1066-1072) conducted an observational retrospective study called ORBIT (Outcome and Retention Rate of Biologic Treatments for Psoriasis) to determine drug survival (the mean length of time patients remain on a drug) in a cohort of 427 patients (63.5% male; mean age, 50.2 years) with moderate to severe psoriasis vulgaris (mean baseline psoriasis area and severity index [PASI], 16.4). In addition to determining mean drug survival times for etanercept, infliximab, adalimumab, and ustekinumab, investigators searched for variables that positively or negatively affected drug survival times. Data were extracted from clinical records of patients treated with biologic agents over a 4-year period. Drug survival was analyzed using the Kaplan-Meier method and the influence of several covariates was assessed using Cox regression.

The investigators evaluated 703 treatment courses. The overall median drug survival was 31.0 months. Cumulative probability of drug survival was lower in obese patients (23.0 months; 95% CI, 17.4-28.6) than in patients with body mass index less than 30 (37.3 months; 95% CI, 29.4-45.1; P=.001). Drug survival was significantly higher for ustekinumab than for any other biologic agent (log-rank test, P<.001). Multivariate analysis showed that obesity, etanercept treatment, and strict adherence to approved doses were associated with an increased probability of drug withdrawal, whereas ustekinumab treatment and PASI 75 and PASI 90 responses at week 16 prolonged drug survival. Data were collected retrospectively.

What’s the issue?

These results should help to educate patients and to manage expectations about drug efficacy. They should also give guidance to physicians. Patients who respond rapidly to biologics—PASI 70 or PASI 90 clearance during the induction phase—are more likely to enjoy long-term remission. In contrast, those with a high body mass index should be advised that their psoriasis may take longer to respond to treatment and may need combination therapy for optimal clearance.

We want to know your views! Tell us what you think.

When using biologic therapies for psoriasis, it is important to evaluate long-term efficacy (>4 years of follow-up). Biologic drug survival in psoriasis reflects long-term performance in real-life settings. Prior studies have yielded inconsistent results.

Vilarrasa et al (J Am Acad Dermatol. 2016;74:1066-1072) conducted an observational retrospective study called ORBIT (Outcome and Retention Rate of Biologic Treatments for Psoriasis) to determine drug survival (the mean length of time patients remain on a drug) in a cohort of 427 patients (63.5% male; mean age, 50.2 years) with moderate to severe psoriasis vulgaris (mean baseline psoriasis area and severity index [PASI], 16.4). In addition to determining mean drug survival times for etanercept, infliximab, adalimumab, and ustekinumab, investigators searched for variables that positively or negatively affected drug survival times. Data were extracted from clinical records of patients treated with biologic agents over a 4-year period. Drug survival was analyzed using the Kaplan-Meier method and the influence of several covariates was assessed using Cox regression.

The investigators evaluated 703 treatment courses. The overall median drug survival was 31.0 months. Cumulative probability of drug survival was lower in obese patients (23.0 months; 95% CI, 17.4-28.6) than in patients with body mass index less than 30 (37.3 months; 95% CI, 29.4-45.1; P=.001). Drug survival was significantly higher for ustekinumab than for any other biologic agent (log-rank test, P<.001). Multivariate analysis showed that obesity, etanercept treatment, and strict adherence to approved doses were associated with an increased probability of drug withdrawal, whereas ustekinumab treatment and PASI 75 and PASI 90 responses at week 16 prolonged drug survival. Data were collected retrospectively.

What’s the issue?

These results should help to educate patients and to manage expectations about drug efficacy. They should also give guidance to physicians. Patients who respond rapidly to biologics—PASI 70 or PASI 90 clearance during the induction phase—are more likely to enjoy long-term remission. In contrast, those with a high body mass index should be advised that their psoriasis may take longer to respond to treatment and may need combination therapy for optimal clearance.

We want to know your views! Tell us what you think.

When using biologic therapies for psoriasis, it is important to evaluate long-term efficacy (>4 years of follow-up). Biologic drug survival in psoriasis reflects long-term performance in real-life settings. Prior studies have yielded inconsistent results.

Vilarrasa et al (J Am Acad Dermatol. 2016;74:1066-1072) conducted an observational retrospective study called ORBIT (Outcome and Retention Rate of Biologic Treatments for Psoriasis) to determine drug survival (the mean length of time patients remain on a drug) in a cohort of 427 patients (63.5% male; mean age, 50.2 years) with moderate to severe psoriasis vulgaris (mean baseline psoriasis area and severity index [PASI], 16.4). In addition to determining mean drug survival times for etanercept, infliximab, adalimumab, and ustekinumab, investigators searched for variables that positively or negatively affected drug survival times. Data were extracted from clinical records of patients treated with biologic agents over a 4-year period. Drug survival was analyzed using the Kaplan-Meier method and the influence of several covariates was assessed using Cox regression.

The investigators evaluated 703 treatment courses. The overall median drug survival was 31.0 months. Cumulative probability of drug survival was lower in obese patients (23.0 months; 95% CI, 17.4-28.6) than in patients with body mass index less than 30 (37.3 months; 95% CI, 29.4-45.1; P=.001). Drug survival was significantly higher for ustekinumab than for any other biologic agent (log-rank test, P<.001). Multivariate analysis showed that obesity, etanercept treatment, and strict adherence to approved doses were associated with an increased probability of drug withdrawal, whereas ustekinumab treatment and PASI 75 and PASI 90 responses at week 16 prolonged drug survival. Data were collected retrospectively.

What’s the issue?

These results should help to educate patients and to manage expectations about drug efficacy. They should also give guidance to physicians. Patients who respond rapidly to biologics—PASI 70 or PASI 90 clearance during the induction phase—are more likely to enjoy long-term remission. In contrast, those with a high body mass index should be advised that their psoriasis may take longer to respond to treatment and may need combination therapy for optimal clearance.

We want to know your views! Tell us what you think.

Myth: Psoriasis Is Infectious The precise cause of psoriasis is unknown, but researchers believe the immune system and genetics play major roles in its development, according to the National Psoriasis Foundation. The skin cells in patients with psoriasis grow at an abnormally fast rate, which causes the buildup of psoriasis lesions. Usually, something triggers psoriasis to flare.

A common misconception among patients is that psoriasis is caused by an infection. Psoriasis is not contagious and psoriasis lesions are not infectious.

However, psoriasis patients are more prone to infections than those without psoriasis. Risk factors for serious infections in psoriasis patients include immune dysregulation, systemic immunosuppressive medications, and comorbid health conditions such as diabetes mellitus or obesity. A 2016 study revealed an increased incidence of serious infections (eg, cellulitis, herpes simplex virus infection, any fungal infection, infectious arthritis, methicillin-resistant Staphylococcus aureus) in hospitalized patients with psoriasis. Higher rates were seen among nonwhite and non-privately insured patients.

In a 2011 study, the likelihood of infectious diseases in patients with psoriasis was twice as high as the reference population. The risk was highest in patients with more severe psoriasis but was not associated with recent systemic antipsoriatic drug dispensing. Respiratory tract, abdominal, and skin infections occurred most frequently in patients with psoriasis.

Poor access to adequate dermatologic care may contribute to higher rates of infections. Dermatologists must closely monitor patients with psoriasis for infection. More research is needed to develop interventions for prevention.

Expert Commentary Psoriasis patients have long faced discrimination because of an  irrational fear that their disease was somehow contagious. In fact this is completely false. This highlights the need for education of the public, so that they understand the true causes and nature of the disease.
—Jeffrey M. Weinberg, MD (New York, New York)

Myth: Psoriasis Is Infectious The precise cause of psoriasis is unknown, but researchers believe the immune system and genetics play major roles in its development, according to the National Psoriasis Foundation. The skin cells in patients with psoriasis grow at an abnormally fast rate, which causes the buildup of psoriasis lesions. Usually, something triggers psoriasis to flare.

A common misconception among patients is that psoriasis is caused by an infection. Psoriasis is not contagious and psoriasis lesions are not infectious.

However, psoriasis patients are more prone to infections than those without psoriasis. Risk factors for serious infections in psoriasis patients include immune dysregulation, systemic immunosuppressive medications, and comorbid health conditions such as diabetes mellitus or obesity. A 2016 study revealed an increased incidence of serious infections (eg, cellulitis, herpes simplex virus infection, any fungal infection, infectious arthritis, methicillin-resistant Staphylococcus aureus) in hospitalized patients with psoriasis. Higher rates were seen among nonwhite and non-privately insured patients.

In a 2011 study, the likelihood of infectious diseases in patients with psoriasis was twice as high as the reference population. The risk was highest in patients with more severe psoriasis but was not associated with recent systemic antipsoriatic drug dispensing. Respiratory tract, abdominal, and skin infections occurred most frequently in patients with psoriasis.

Poor access to adequate dermatologic care may contribute to higher rates of infections. Dermatologists must closely monitor patients with psoriasis for infection. More research is needed to develop interventions for prevention.

Expert Commentary Psoriasis patients have long faced discrimination because of an  irrational fear that their disease was somehow contagious. In fact this is completely false. This highlights the need for education of the public, so that they understand the true causes and nature of the disease.
—Jeffrey M. Weinberg, MD (New York, New York)

Myth: Psoriasis Is Infectious The precise cause of psoriasis is unknown, but researchers believe the immune system and genetics play major roles in its development, according to the National Psoriasis Foundation. The skin cells in patients with psoriasis grow at an abnormally fast rate, which causes the buildup of psoriasis lesions. Usually, something triggers psoriasis to flare.

A common misconception among patients is that psoriasis is caused by an infection. Psoriasis is not contagious and psoriasis lesions are not infectious.

However, psoriasis patients are more prone to infections than those without psoriasis. Risk factors for serious infections in psoriasis patients include immune dysregulation, systemic immunosuppressive medications, and comorbid health conditions such as diabetes mellitus or obesity. A 2016 study revealed an increased incidence of serious infections (eg, cellulitis, herpes simplex virus infection, any fungal infection, infectious arthritis, methicillin-resistant Staphylococcus aureus) in hospitalized patients with psoriasis. Higher rates were seen among nonwhite and non-privately insured patients.

In a 2011 study, the likelihood of infectious diseases in patients with psoriasis was twice as high as the reference population. The risk was highest in patients with more severe psoriasis but was not associated with recent systemic antipsoriatic drug dispensing. Respiratory tract, abdominal, and skin infections occurred most frequently in patients with psoriasis.

Poor access to adequate dermatologic care may contribute to higher rates of infections. Dermatologists must closely monitor patients with psoriasis for infection. More research is needed to develop interventions for prevention.

Expert Commentary Psoriasis patients have long faced discrimination because of an  irrational fear that their disease was somehow contagious. In fact this is completely false. This highlights the need for education of the public, so that they understand the true causes and nature of the disease.
—Jeffrey M. Weinberg, MD (New York, New York)

The US Food and Drug Administration uses the term boxed warning to highlight potentially dangerous situations associated with prescription drugs. A boxed warning is used when “[T]here is an adverse reaction so serious in proportion to the potential benefit from the drug (e.g., a fatal, life-threatening or permanently disabling adverse reaction) that it is essential that it be considered in assessing the risks and benefits of using the drug.”¹ However, drugs are not the only potential cause of severe adverse outcomes in patients with psoriasis. Untreated psoriasis also is a well-established cause of serious morbidity and mortality. What are the risks of inadequate psoriasis treatment?

Psoriasis is associated with an increased risk for cardiovascular disease.^2-4 Patients with psoriasis also have a higher prevalence of classic cardiovascular risk factors including smoking, diabetes mellitus, hypertension, obesity, and hyperlipidemia.^5,6 Psoriasis is a T-cell mediated disease process driven by IL-23 and T_H17 helper cell–derived proinflammatory cytokines, sharing certain genetic aspects with metabolic syndrome.⁶ Cytokine actions on insulin signaling, lipid metabolism, and adipogenesis may underlie the increased prevalence of metabolic syndrome and cardiovascular risk factors in patients with psoriasis. In addition to treating the cutaneous manifestations of psoriasis, reducing inflammation in these patients reduces C-reactive protein and lipid peroxidation and increases high-density lipoprotein levels.⁶ Tumor necrosis factor α blockers decrease the risk for cardiovascular disease in patients with psoriasis.^7,8 Lower than expected rates of cardiovascular disease also have been reported in a large cohort of psoriasis patients (ie, PSOLAR [Psoriasis Longitudinal Assessment and Registry] registry) being treated with either ustekinumab or tumor necrosis factor α blockers.⁹

Psoriatic arthritis is a chronic inflammatory disease in which active inflammation results in progressive joint destruction.¹⁰ Tumor necrosis factor α inhibitors suppress disease progression, preserve function, and delay destruction of the joints. Ustekinumab also helps control psoriatic arthritis and inhibits radiographic progression of joint disease.¹¹

Importantly, untreated moderate to severe psoriasis is associated with several comorbidities that may lead to early death such as heart attacks and strokes.¹² Furthermore, patients not taking biologic medications may have higher death rates than patients taking biologic medications.⁹ Psoriasis also is associated with tremendous suffering and negative psychosocial effects. The mental and physical impact of the disease is comparable to other major medical conditions (eg, cancer, arthritis, hypertension, heart disease, diabetes, depression).¹³ Patients also may experience physical discomfort from pain and itching.¹⁴ Children with psoriasis may experience bullying, which is associated with an increased number of depressive episodes, thereby increasing their risk for developing psychiatric conditions such as depression and anxiety as adults.¹⁵ The stigma associated with psoriasis may affect patients’ ability to build relationships. Patients with psoriasis experience higher divorce rates than patients with other chronic medical conditions, and direct involvement of genital regions may negatively impact patients’ sex lives. Patients have noted that the stigma of psoriasis also is associated with the inability to obtain employment.¹⁵ Almost one-third of patients with psoriasis who are either not working or are retired base their work status on their skin condition.¹⁶ Furthermore, psoriasis may contribute to economic burden for patients due to indirect costs associated with work absenteeism.¹⁷

Adequate treatment of psoriasis improves patients’ physical and psychological health as well as their ability to function in the workplace. However, despite the benefits of treatment, 30% of patients with severe psoriasis and 53% of patients with moderate psoriasis receive no treatment or only topical medications instead of systemic therapies.¹⁶ The potential adverse events of inadequate psoriasis treatment far outweigh any potential benefits of withholding treatment. Perhaps a boxed warning should be issued for inadequate treatment of psoriasis patients.

The US Food and Drug Administration uses the term boxed warning to highlight potentially dangerous situations associated with prescription drugs. A boxed warning is used when “[T]here is an adverse reaction so serious in proportion to the potential benefit from the drug (e.g., a fatal, life-threatening or permanently disabling adverse reaction) that it is essential that it be considered in assessing the risks and benefits of using the drug.”¹ However, drugs are not the only potential cause of severe adverse outcomes in patients with psoriasis. Untreated psoriasis also is a well-established cause of serious morbidity and mortality. What are the risks of inadequate psoriasis treatment?

Psoriasis is associated with an increased risk for cardiovascular disease.^2-4 Patients with psoriasis also have a higher prevalence of classic cardiovascular risk factors including smoking, diabetes mellitus, hypertension, obesity, and hyperlipidemia.^5,6 Psoriasis is a T-cell mediated disease process driven by IL-23 and T_H17 helper cell–derived proinflammatory cytokines, sharing certain genetic aspects with metabolic syndrome.⁶ Cytokine actions on insulin signaling, lipid metabolism, and adipogenesis may underlie the increased prevalence of metabolic syndrome and cardiovascular risk factors in patients with psoriasis. In addition to treating the cutaneous manifestations of psoriasis, reducing inflammation in these patients reduces C-reactive protein and lipid peroxidation and increases high-density lipoprotein levels.⁶ Tumor necrosis factor α blockers decrease the risk for cardiovascular disease in patients with psoriasis.^7,8 Lower than expected rates of cardiovascular disease also have been reported in a large cohort of psoriasis patients (ie, PSOLAR [Psoriasis Longitudinal Assessment and Registry] registry) being treated with either ustekinumab or tumor necrosis factor α blockers.⁹

Psoriatic arthritis is a chronic inflammatory disease in which active inflammation results in progressive joint destruction.¹⁰ Tumor necrosis factor α inhibitors suppress disease progression, preserve function, and delay destruction of the joints. Ustekinumab also helps control psoriatic arthritis and inhibits radiographic progression of joint disease.¹¹

Importantly, untreated moderate to severe psoriasis is associated with several comorbidities that may lead to early death such as heart attacks and strokes.¹² Furthermore, patients not taking biologic medications may have higher death rates than patients taking biologic medications.⁹ Psoriasis also is associated with tremendous suffering and negative psychosocial effects. The mental and physical impact of the disease is comparable to other major medical conditions (eg, cancer, arthritis, hypertension, heart disease, diabetes, depression).¹³ Patients also may experience physical discomfort from pain and itching.¹⁴ Children with psoriasis may experience bullying, which is associated with an increased number of depressive episodes, thereby increasing their risk for developing psychiatric conditions such as depression and anxiety as adults.¹⁵ The stigma associated with psoriasis may affect patients’ ability to build relationships. Patients with psoriasis experience higher divorce rates than patients with other chronic medical conditions, and direct involvement of genital regions may negatively impact patients’ sex lives. Patients have noted that the stigma of psoriasis also is associated with the inability to obtain employment.¹⁵ Almost one-third of patients with psoriasis who are either not working or are retired base their work status on their skin condition.¹⁶ Furthermore, psoriasis may contribute to economic burden for patients due to indirect costs associated with work absenteeism.¹⁷

Adequate treatment of psoriasis improves patients’ physical and psychological health as well as their ability to function in the workplace. However, despite the benefits of treatment, 30% of patients with severe psoriasis and 53% of patients with moderate psoriasis receive no treatment or only topical medications instead of systemic therapies.¹⁶ The potential adverse events of inadequate psoriasis treatment far outweigh any potential benefits of withholding treatment. Perhaps a boxed warning should be issued for inadequate treatment of psoriasis patients.

The US Food and Drug Administration uses the term boxed warning to highlight potentially dangerous situations associated with prescription drugs. A boxed warning is used when “[T]here is an adverse reaction so serious in proportion to the potential benefit from the drug (e.g., a fatal, life-threatening or permanently disabling adverse reaction) that it is essential that it be considered in assessing the risks and benefits of using the drug.”¹ However, drugs are not the only potential cause of severe adverse outcomes in patients with psoriasis. Untreated psoriasis also is a well-established cause of serious morbidity and mortality. What are the risks of inadequate psoriasis treatment?

Psoriasis is associated with an increased risk for cardiovascular disease.^2-4 Patients with psoriasis also have a higher prevalence of classic cardiovascular risk factors including smoking, diabetes mellitus, hypertension, obesity, and hyperlipidemia.^5,6 Psoriasis is a T-cell mediated disease process driven by IL-23 and T_H17 helper cell–derived proinflammatory cytokines, sharing certain genetic aspects with metabolic syndrome.⁶ Cytokine actions on insulin signaling, lipid metabolism, and adipogenesis may underlie the increased prevalence of metabolic syndrome and cardiovascular risk factors in patients with psoriasis. In addition to treating the cutaneous manifestations of psoriasis, reducing inflammation in these patients reduces C-reactive protein and lipid peroxidation and increases high-density lipoprotein levels.⁶ Tumor necrosis factor α blockers decrease the risk for cardiovascular disease in patients with psoriasis.^7,8 Lower than expected rates of cardiovascular disease also have been reported in a large cohort of psoriasis patients (ie, PSOLAR [Psoriasis Longitudinal Assessment and Registry] registry) being treated with either ustekinumab or tumor necrosis factor α blockers.⁹

Psoriatic arthritis is a chronic inflammatory disease in which active inflammation results in progressive joint destruction.¹⁰ Tumor necrosis factor α inhibitors suppress disease progression, preserve function, and delay destruction of the joints. Ustekinumab also helps control psoriatic arthritis and inhibits radiographic progression of joint disease.¹¹

Importantly, untreated moderate to severe psoriasis is associated with several comorbidities that may lead to early death such as heart attacks and strokes.¹² Furthermore, patients not taking biologic medications may have higher death rates than patients taking biologic medications.⁹ Psoriasis also is associated with tremendous suffering and negative psychosocial effects. The mental and physical impact of the disease is comparable to other major medical conditions (eg, cancer, arthritis, hypertension, heart disease, diabetes, depression).¹³ Patients also may experience physical discomfort from pain and itching.¹⁴ Children with psoriasis may experience bullying, which is associated with an increased number of depressive episodes, thereby increasing their risk for developing psychiatric conditions such as depression and anxiety as adults.¹⁵ The stigma associated with psoriasis may affect patients’ ability to build relationships. Patients with psoriasis experience higher divorce rates than patients with other chronic medical conditions, and direct involvement of genital regions may negatively impact patients’ sex lives. Patients have noted that the stigma of psoriasis also is associated with the inability to obtain employment.¹⁵ Almost one-third of patients with psoriasis who are either not working or are retired base their work status on their skin condition.¹⁶ Furthermore, psoriasis may contribute to economic burden for patients due to indirect costs associated with work absenteeism.¹⁷

Adequate treatment of psoriasis improves patients’ physical and psychological health as well as their ability to function in the workplace. However, despite the benefits of treatment, 30% of patients with severe psoriasis and 53% of patients with moderate psoriasis receive no treatment or only topical medications instead of systemic therapies.¹⁶ The potential adverse events of inadequate psoriasis treatment far outweigh any potential benefits of withholding treatment. Perhaps a boxed warning should be issued for inadequate treatment of psoriasis patients.

Psoriasis patients may have more success with a second tumor necrosis factor (TNF) antagonist after failure with a first, report Paul S. Yamauchi, MD, PhD, and coauthors.

Investigators analyzed 15 studies evaluating the efficacy of switching TNF antagonists after primary or secondary failure. Response rates at 24 weeks for a second antagonist were 30%-74% for a 75% improvement in Psoriasis Area and Severity Index score, and 20%-70% for achieving a Physician Global Assessment score of 0/1. Mean improvements in Dermatology Life Quality Index ranged from –3.5 to –13, Dr. Yamauchi and colleagues reported.

©AzriSuratmin/Thinkstock

Patients who experienced secondary failure with initial treatment generally achieved better responses than those with primary failure, the authors said.

Though response rates to a second anti-TNF agent were lower than for a first, “a substantial proportion of patients in every study achieved treatment success,” they added.

Read the full article in the Journal of the American Academy of Dermatology.

dermnews@frontlinemedcom.com

Psoriasis patients may have more success with a second tumor necrosis factor (TNF) antagonist after failure with a first, report Paul S. Yamauchi, MD, PhD, and coauthors.

Investigators analyzed 15 studies evaluating the efficacy of switching TNF antagonists after primary or secondary failure. Response rates at 24 weeks for a second antagonist were 30%-74% for a 75% improvement in Psoriasis Area and Severity Index score, and 20%-70% for achieving a Physician Global Assessment score of 0/1. Mean improvements in Dermatology Life Quality Index ranged from –3.5 to –13, Dr. Yamauchi and colleagues reported.

©AzriSuratmin/Thinkstock

Patients who experienced secondary failure with initial treatment generally achieved better responses than those with primary failure, the authors said.

Though response rates to a second anti-TNF agent were lower than for a first, “a substantial proportion of patients in every study achieved treatment success,” they added.

Read the full article in the Journal of the American Academy of Dermatology.

dermnews@frontlinemedcom.com

Psoriasis patients may have more success with a second tumor necrosis factor (TNF) antagonist after failure with a first, report Paul S. Yamauchi, MD, PhD, and coauthors.

Investigators analyzed 15 studies evaluating the efficacy of switching TNF antagonists after primary or secondary failure. Response rates at 24 weeks for a second antagonist were 30%-74% for a 75% improvement in Psoriasis Area and Severity Index score, and 20%-70% for achieving a Physician Global Assessment score of 0/1. Mean improvements in Dermatology Life Quality Index ranged from –3.5 to –13, Dr. Yamauchi and colleagues reported.

©AzriSuratmin/Thinkstock

Patients who experienced secondary failure with initial treatment generally achieved better responses than those with primary failure, the authors said.

Though response rates to a second anti-TNF agent were lower than for a first, “a substantial proportion of patients in every study achieved treatment success,” they added.

Read the full article in the Journal of the American Academy of Dermatology.

dermnews@frontlinemedcom.com

A biosimilar of etanercept received clearance for marketing from the Food and Drug Administration on Aug. 30 for all of the inflammatory disease indications held by the reference originator etanercept product, Enbrel, according to an announcement from the agency.

Approval for all of Enbrel’s indications – rheumatoid arthritis, plaque psoriasis, psoriatic arthritis, ankylosing spondylitis, and polyarticular juvenile idiopathic arthritis – was initially met with skepticism by members of the agency’s Arthritis Advisory Committee at a meeting in July because the biosimilar was compared against Enbrel in patients with plaque psoriasis only, but eventually all panel members voted to recommend approval.

The approval allows the biosimilar etanercept, called etanercept-szzs, to be marketed as a biosimilar only, not as an interchangeable product. The FDA has not yet developed guidance for manufacturers to follow to get approval for interchangeability, which means that a biosimilar “may be substituted for the reference product by a pharmacist without the intervention of the health care provider who prescribed the reference product,” according to the agency.

“We carefully evaluate the structural and functional characteristics of these complex molecules. Patients and providers can have confidence that there are no clinically meaningful differences in safety and efficacy from the reference product,” Janet Woodcock, MD, director of the FDA’s Center for Drug Evaluation and Research, said in the agency’s announcement.

Etanercept-szzs will be marketed by Sandoz as Erelzi. Erelzi’s prescribing information can be found here. The biosimilar is currently undergoing review with the European Medicines Agency.

jevans@frontlinemedcom.com

A biosimilar of etanercept received clearance for marketing from the Food and Drug Administration on Aug. 30 for all of the inflammatory disease indications held by the reference originator etanercept product, Enbrel, according to an announcement from the agency.

Approval for all of Enbrel’s indications – rheumatoid arthritis, plaque psoriasis, psoriatic arthritis, ankylosing spondylitis, and polyarticular juvenile idiopathic arthritis – was initially met with skepticism by members of the agency’s Arthritis Advisory Committee at a meeting in July because the biosimilar was compared against Enbrel in patients with plaque psoriasis only, but eventually all panel members voted to recommend approval.

The approval allows the biosimilar etanercept, called etanercept-szzs, to be marketed as a biosimilar only, not as an interchangeable product. The FDA has not yet developed guidance for manufacturers to follow to get approval for interchangeability, which means that a biosimilar “may be substituted for the reference product by a pharmacist without the intervention of the health care provider who prescribed the reference product,” according to the agency.

“We carefully evaluate the structural and functional characteristics of these complex molecules. Patients and providers can have confidence that there are no clinically meaningful differences in safety and efficacy from the reference product,” Janet Woodcock, MD, director of the FDA’s Center for Drug Evaluation and Research, said in the agency’s announcement.

Etanercept-szzs will be marketed by Sandoz as Erelzi. Erelzi’s prescribing information can be found here. The biosimilar is currently undergoing review with the European Medicines Agency.

jevans@frontlinemedcom.com

A biosimilar of etanercept received clearance for marketing from the Food and Drug Administration on Aug. 30 for all of the inflammatory disease indications held by the reference originator etanercept product, Enbrel, according to an announcement from the agency.

Approval for all of Enbrel’s indications – rheumatoid arthritis, plaque psoriasis, psoriatic arthritis, ankylosing spondylitis, and polyarticular juvenile idiopathic arthritis – was initially met with skepticism by members of the agency’s Arthritis Advisory Committee at a meeting in July because the biosimilar was compared against Enbrel in patients with plaque psoriasis only, but eventually all panel members voted to recommend approval.

The approval allows the biosimilar etanercept, called etanercept-szzs, to be marketed as a biosimilar only, not as an interchangeable product. The FDA has not yet developed guidance for manufacturers to follow to get approval for interchangeability, which means that a biosimilar “may be substituted for the reference product by a pharmacist without the intervention of the health care provider who prescribed the reference product,” according to the agency.

“We carefully evaluate the structural and functional characteristics of these complex molecules. Patients and providers can have confidence that there are no clinically meaningful differences in safety and efficacy from the reference product,” Janet Woodcock, MD, director of the FDA’s Center for Drug Evaluation and Research, said in the agency’s announcement.

Etanercept-szzs will be marketed by Sandoz as Erelzi. Erelzi’s prescribing information can be found here. The biosimilar is currently undergoing review with the European Medicines Agency.

jevans@frontlinemedcom.com

Two different doses of the humanized monoclonal antibody ixekizumab improved signs and symptoms of active psoriatic arthritis in a phase III manufacturer-sponsored trial of patients who had not taken a biologic drug before.

The agent selectively binds and neutralizes interleukin (IL)-17A, which promotes joint inflammation and damage via several mechanisms. So the study findings support the view that IL-17A is a key cytokine in the pathogenesis of psoriatic arthritis and an appropriate therapeutic target, said Philip J. Mease, MD, of the department of rheumatology at Swedish Medical Center and the University of Washington, Seattle, and his associates.

They are performing the ongoing, 3-year, randomized, double-blind trial (SPIRIT-P1) comparing responses with an 80-mg dose of ixekizumab every 2 weeks (103 patients), an 80-mg dose every 4 weeks (107 patients), a 40-mg dose of adalimumab (Humira) every 2 weeks (101 patients, active control group), and matching placebo (106 patients, placebo-control group). Each of the two ixekizumab arms received a starting dose of 160 mg given as two injections at week 0. This report presented the findings after the initial 24-week, double-blind treatment period of the trial.

The study participants are adults with active psoriatic arthritis who had never been treated with biologic agents and who continued taking their usual doses of conventional disease-modifying antirheumatic drugs, oral corticosteroids, opiates, and/or nonsteroidal anti-inflammatory drugs/Cox-2 inhibitors during the study. The mean patient age was 49.5 years. Of the 382 who completed this portion of the study, 57 showed an inadequate response and required rescue medication, including 10 on the lower dose of ixekizumab, 11 on the higher dose of ixekizumab, 9 taking adalimumab, and 27 taking placebo.

The primary efficacy endpoint, ACR20 response at week 24, was met by 62.1% of the higher-dose ixekizumab group, 57.9% of the lower-dose ixekizumab group, and 57.4% of the adalimumab group, all of which were significantly greater than the 30.2% rate in the placebo group. Both doses of the study drug as well as the active control drug also improved secondary endpoints: reducing mean levels of disease activity as measured by the 28-joint Disease Activity Score using on C-reactive protein, improving patient-reported physical function on the Health Assessment Questionnaire–Disability Index, and improving disease-related physical health as measured by the SF-36, the investigators said (Ann Rheum Dis. 2016 Aug 23. doi: 10.1136/annrheumdis-2016-209709).

In addition, the progression of structural joint damage, as assessed on radiographs of bone erosions and joint-space narrowing in the hands and feet, was significantly less with the three active treatments than with placebo. Among patients with the most extensive disease, a significantly greater percentage achieved Psoriasis Area and Severity Index 75 level of improvement with the three active treatments than with placebo. And among patients with nail involvement, mean improvements in Nail Psoriasis Severity Index scores were significantly higher with the three active treatments than with placebo.

Adverse effects included grade 1 and 2 neutropenia, herpes zoster involving the eyelid, gastroenteritis, esophageal candidiasis, and depression-related symptoms. All infections resolved with treatment, and none required discontinuation of the study drug.

This study was funded and sponsored by Eli Lilly, maker of ixekizumab. Dr. Mease reported receiving grants, personal fees, and other support from Eli Lilly, AbbVie, Amgen, Bristol Myers Squibb, Celgene, Crescendo, Genentech, Janssen, Pfizer, UCB Pharma, Merck, Novartis, and Corrona. His associates reported ties to numerous industry sources.

Two different doses of the humanized monoclonal antibody ixekizumab improved signs and symptoms of active psoriatic arthritis in a phase III manufacturer-sponsored trial of patients who had not taken a biologic drug before.

The agent selectively binds and neutralizes interleukin (IL)-17A, which promotes joint inflammation and damage via several mechanisms. So the study findings support the view that IL-17A is a key cytokine in the pathogenesis of psoriatic arthritis and an appropriate therapeutic target, said Philip J. Mease, MD, of the department of rheumatology at Swedish Medical Center and the University of Washington, Seattle, and his associates.

They are performing the ongoing, 3-year, randomized, double-blind trial (SPIRIT-P1) comparing responses with an 80-mg dose of ixekizumab every 2 weeks (103 patients), an 80-mg dose every 4 weeks (107 patients), a 40-mg dose of adalimumab (Humira) every 2 weeks (101 patients, active control group), and matching placebo (106 patients, placebo-control group). Each of the two ixekizumab arms received a starting dose of 160 mg given as two injections at week 0. This report presented the findings after the initial 24-week, double-blind treatment period of the trial.

The study participants are adults with active psoriatic arthritis who had never been treated with biologic agents and who continued taking their usual doses of conventional disease-modifying antirheumatic drugs, oral corticosteroids, opiates, and/or nonsteroidal anti-inflammatory drugs/Cox-2 inhibitors during the study. The mean patient age was 49.5 years. Of the 382 who completed this portion of the study, 57 showed an inadequate response and required rescue medication, including 10 on the lower dose of ixekizumab, 11 on the higher dose of ixekizumab, 9 taking adalimumab, and 27 taking placebo.

The primary efficacy endpoint, ACR20 response at week 24, was met by 62.1% of the higher-dose ixekizumab group, 57.9% of the lower-dose ixekizumab group, and 57.4% of the adalimumab group, all of which were significantly greater than the 30.2% rate in the placebo group. Both doses of the study drug as well as the active control drug also improved secondary endpoints: reducing mean levels of disease activity as measured by the 28-joint Disease Activity Score using on C-reactive protein, improving patient-reported physical function on the Health Assessment Questionnaire–Disability Index, and improving disease-related physical health as measured by the SF-36, the investigators said (Ann Rheum Dis. 2016 Aug 23. doi: 10.1136/annrheumdis-2016-209709).

In addition, the progression of structural joint damage, as assessed on radiographs of bone erosions and joint-space narrowing in the hands and feet, was significantly less with the three active treatments than with placebo. Among patients with the most extensive disease, a significantly greater percentage achieved Psoriasis Area and Severity Index 75 level of improvement with the three active treatments than with placebo. And among patients with nail involvement, mean improvements in Nail Psoriasis Severity Index scores were significantly higher with the three active treatments than with placebo.

Adverse effects included grade 1 and 2 neutropenia, herpes zoster involving the eyelid, gastroenteritis, esophageal candidiasis, and depression-related symptoms. All infections resolved with treatment, and none required discontinuation of the study drug.

This study was funded and sponsored by Eli Lilly, maker of ixekizumab. Dr. Mease reported receiving grants, personal fees, and other support from Eli Lilly, AbbVie, Amgen, Bristol Myers Squibb, Celgene, Crescendo, Genentech, Janssen, Pfizer, UCB Pharma, Merck, Novartis, and Corrona. His associates reported ties to numerous industry sources.

Two different doses of the humanized monoclonal antibody ixekizumab improved signs and symptoms of active psoriatic arthritis in a phase III manufacturer-sponsored trial of patients who had not taken a biologic drug before.

The agent selectively binds and neutralizes interleukin (IL)-17A, which promotes joint inflammation and damage via several mechanisms. So the study findings support the view that IL-17A is a key cytokine in the pathogenesis of psoriatic arthritis and an appropriate therapeutic target, said Philip J. Mease, MD, of the department of rheumatology at Swedish Medical Center and the University of Washington, Seattle, and his associates.

They are performing the ongoing, 3-year, randomized, double-blind trial (SPIRIT-P1) comparing responses with an 80-mg dose of ixekizumab every 2 weeks (103 patients), an 80-mg dose every 4 weeks (107 patients), a 40-mg dose of adalimumab (Humira) every 2 weeks (101 patients, active control group), and matching placebo (106 patients, placebo-control group). Each of the two ixekizumab arms received a starting dose of 160 mg given as two injections at week 0. This report presented the findings after the initial 24-week, double-blind treatment period of the trial.

The study participants are adults with active psoriatic arthritis who had never been treated with biologic agents and who continued taking their usual doses of conventional disease-modifying antirheumatic drugs, oral corticosteroids, opiates, and/or nonsteroidal anti-inflammatory drugs/Cox-2 inhibitors during the study. The mean patient age was 49.5 years. Of the 382 who completed this portion of the study, 57 showed an inadequate response and required rescue medication, including 10 on the lower dose of ixekizumab, 11 on the higher dose of ixekizumab, 9 taking adalimumab, and 27 taking placebo.

The primary efficacy endpoint, ACR20 response at week 24, was met by 62.1% of the higher-dose ixekizumab group, 57.9% of the lower-dose ixekizumab group, and 57.4% of the adalimumab group, all of which were significantly greater than the 30.2% rate in the placebo group. Both doses of the study drug as well as the active control drug also improved secondary endpoints: reducing mean levels of disease activity as measured by the 28-joint Disease Activity Score using on C-reactive protein, improving patient-reported physical function on the Health Assessment Questionnaire–Disability Index, and improving disease-related physical health as measured by the SF-36, the investigators said (Ann Rheum Dis. 2016 Aug 23. doi: 10.1136/annrheumdis-2016-209709).

In addition, the progression of structural joint damage, as assessed on radiographs of bone erosions and joint-space narrowing in the hands and feet, was significantly less with the three active treatments than with placebo. Among patients with the most extensive disease, a significantly greater percentage achieved Psoriasis Area and Severity Index 75 level of improvement with the three active treatments than with placebo. And among patients with nail involvement, mean improvements in Nail Psoriasis Severity Index scores were significantly higher with the three active treatments than with placebo.

Adverse effects included grade 1 and 2 neutropenia, herpes zoster involving the eyelid, gastroenteritis, esophageal candidiasis, and depression-related symptoms. All infections resolved with treatment, and none required discontinuation of the study drug.

This study was funded and sponsored by Eli Lilly, maker of ixekizumab. Dr. Mease reported receiving grants, personal fees, and other support from Eli Lilly, AbbVie, Amgen, Bristol Myers Squibb, Celgene, Crescendo, Genentech, Janssen, Pfizer, UCB Pharma, Merck, Novartis, and Corrona. His associates reported ties to numerous industry sources.

Psoriasis increased the measures of coronary artery calcium at a level similar to that seen in type 2 diabetes mellitus, independent of cardiovascular disease risk factors, based on data from a trio of cross-sectional studies including 387 adults. .

“Psoriasis and type 2 diabetes share similar cardiovascular risk profiles, which may predispose patients to developing coronary atherosclerosis at a relatively young age,” wrote Bobbak Mansouri, MD, of Baylor University Medical Center in Dallas and his associates (JAMA Dermatol. 2016. [doi: 10.1001/jamadermatol.2016.2907]).

©eenevski/thinkstockphotos

The researchers compared coronary artery calcium (CAC) levels in patients with psoriasis, patients with type 2 diabetes, and healthy controls. CAC has become an accepted measure of atherosclerosis and “the cornerstone for screening the risk of future cardiac events and improving cardiovascular risk stratification beyond traditional risk factors, especially in higher-risk groups,” according to the investigators. The average age of the patients was 52 years, 50% were female, and at least 92% were white.

The researchers used a hierarchical Tobit regression analysis to determine the association between disease and CAC level, as measured by the Agatston score. After controlling for confounding variables, including cardiovascular risk factors (low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, fasting blood glucose, systolic blood pressure, and tobacco use), the association with CAC was similar in psoriasis patients and type 2 diabetes patients (Tobit regression ratio [TRR], 0.89 and 0.79, respectively).

In a logistic multivariate regression analysis, patients with either psoriasis or type 2 diabetes were approximately twice as likely to have evidence of CAC as were healthy controls (odds ratio, 2.35 and 2.18, respectively), and psoriasis remained independently associated with the presence of CAC.

“When we added use of systemic or biological therapy to the models, the TRR and OR increased; however, these analyses were exploratory,” wrote Dr. Mansouri and his associates.

The study was limited by factors including the cross-sectional design and lack of diversity in the patient population, the investigators noted. However, the results suggest that “CAC assessment may be considered in patients with psoriasis who have two or more traditional cardiovascular risk factors given the high prevalence of CAC observed in this study,” they said.

Dr. Mansouri disclosed serving on an advisory board and receiving an honorarium from Celgene, maker of the psoriasis drug apremilast (Otezl). Study coauthors disclosed financial relationships with multiple pharmaceutical companies.

Psoriasis increased the measures of coronary artery calcium at a level similar to that seen in type 2 diabetes mellitus, independent of cardiovascular disease risk factors, based on data from a trio of cross-sectional studies including 387 adults. .

“Psoriasis and type 2 diabetes share similar cardiovascular risk profiles, which may predispose patients to developing coronary atherosclerosis at a relatively young age,” wrote Bobbak Mansouri, MD, of Baylor University Medical Center in Dallas and his associates (JAMA Dermatol. 2016. [doi: 10.1001/jamadermatol.2016.2907]).

©eenevski/thinkstockphotos

The researchers compared coronary artery calcium (CAC) levels in patients with psoriasis, patients with type 2 diabetes, and healthy controls. CAC has become an accepted measure of atherosclerosis and “the cornerstone for screening the risk of future cardiac events and improving cardiovascular risk stratification beyond traditional risk factors, especially in higher-risk groups,” according to the investigators. The average age of the patients was 52 years, 50% were female, and at least 92% were white.

The researchers used a hierarchical Tobit regression analysis to determine the association between disease and CAC level, as measured by the Agatston score. After controlling for confounding variables, including cardiovascular risk factors (low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, fasting blood glucose, systolic blood pressure, and tobacco use), the association with CAC was similar in psoriasis patients and type 2 diabetes patients (Tobit regression ratio [TRR], 0.89 and 0.79, respectively).

In a logistic multivariate regression analysis, patients with either psoriasis or type 2 diabetes were approximately twice as likely to have evidence of CAC as were healthy controls (odds ratio, 2.35 and 2.18, respectively), and psoriasis remained independently associated with the presence of CAC.

“When we added use of systemic or biological therapy to the models, the TRR and OR increased; however, these analyses were exploratory,” wrote Dr. Mansouri and his associates.

The study was limited by factors including the cross-sectional design and lack of diversity in the patient population, the investigators noted. However, the results suggest that “CAC assessment may be considered in patients with psoriasis who have two or more traditional cardiovascular risk factors given the high prevalence of CAC observed in this study,” they said.

Dr. Mansouri disclosed serving on an advisory board and receiving an honorarium from Celgene, maker of the psoriasis drug apremilast (Otezl). Study coauthors disclosed financial relationships with multiple pharmaceutical companies.

Psoriasis increased the measures of coronary artery calcium at a level similar to that seen in type 2 diabetes mellitus, independent of cardiovascular disease risk factors, based on data from a trio of cross-sectional studies including 387 adults. .

“Psoriasis and type 2 diabetes share similar cardiovascular risk profiles, which may predispose patients to developing coronary atherosclerosis at a relatively young age,” wrote Bobbak Mansouri, MD, of Baylor University Medical Center in Dallas and his associates (JAMA Dermatol. 2016. [doi: 10.1001/jamadermatol.2016.2907]).

©eenevski/thinkstockphotos

The researchers compared coronary artery calcium (CAC) levels in patients with psoriasis, patients with type 2 diabetes, and healthy controls. CAC has become an accepted measure of atherosclerosis and “the cornerstone for screening the risk of future cardiac events and improving cardiovascular risk stratification beyond traditional risk factors, especially in higher-risk groups,” according to the investigators. The average age of the patients was 52 years, 50% were female, and at least 92% were white.

The researchers used a hierarchical Tobit regression analysis to determine the association between disease and CAC level, as measured by the Agatston score. After controlling for confounding variables, including cardiovascular risk factors (low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, fasting blood glucose, systolic blood pressure, and tobacco use), the association with CAC was similar in psoriasis patients and type 2 diabetes patients (Tobit regression ratio [TRR], 0.89 and 0.79, respectively).

In a logistic multivariate regression analysis, patients with either psoriasis or type 2 diabetes were approximately twice as likely to have evidence of CAC as were healthy controls (odds ratio, 2.35 and 2.18, respectively), and psoriasis remained independently associated with the presence of CAC.

“When we added use of systemic or biological therapy to the models, the TRR and OR increased; however, these analyses were exploratory,” wrote Dr. Mansouri and his associates.

The study was limited by factors including the cross-sectional design and lack of diversity in the patient population, the investigators noted. However, the results suggest that “CAC assessment may be considered in patients with psoriasis who have two or more traditional cardiovascular risk factors given the high prevalence of CAC observed in this study,” they said.

Dr. Mansouri disclosed serving on an advisory board and receiving an honorarium from Celgene, maker of the psoriasis drug apremilast (Otezl). Study coauthors disclosed financial relationships with multiple pharmaceutical companies.

Myth: Psoriasis Cannot Be Treated

At the Summer Meeting of the American Academy of Dermatology in Boston, Massachusetts (July 28-31, 2016), Dr. Alexa Kimball presented on dermatology research advances at the plenary session and referenced the revolution in psoriasis treatment that has been experienced in the last several years, noting that dermatologists previously were relegated to treating patients with tar treatments. Today, many options for the treatment of psoriasis exist, though the disease is not curable.

According to the Mayo Clinic, psoriasis treatment is aimed at stopping the skin cells from growing so quickly, which reduces inflammation and plaque formation, and removing scales and smoothing skin. It is important for patients to understand the different treatment options so that they are aware that a variety of therapies may be tried until the right regimen with the fewest potential side effects is found. Options include:

• Biologics: given by injection or intravenous infusion for moderate to severe psoriasis that has not responded to other treatments

• Experimental medications: new medications undergoing clinical trials

• Oral treatments: inhibit specific molecules associated with inflammation and can be taken by mouth rather than injection or infusion (eg, retinoids, methotrexate, cyclosporine)

• Phototherapy or other light therapy: involves exposing the skin to UV light on a regular basis and under medical supervision (eg, UVB phototherapy, narrowband UVB therapy, psoralen plus UVA, excimer laser)

• Systemics: given orally or by injection and work throughout the body for moderate to severe psoriasis

• Topicals: applied to the skin and typically used for mild to moderate psoriasis (eg, topical corticosteroids, vitamin D analogues, anthralin, topical retinoids, calcineurin inhibitors, salicylic acid, coal tar, moisturizers)

In a 2014 analysis of data from the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey of the National Center for Health Statistics, the frequency of phototherapy treatments for psoriasis significantly decreased from 1993 to 2010 (P<.001), while the frequency of biologics significantly increased, becoming the most frequently used treatment from 2008 to 2010 (P<.0001).

However, psoriasis has been noted to be undertreated. A 2007 survey of 1657 psoriasis patients (28% with severe disease and 41% with moderate disease) from the National Psoriasis Foundation contact database indicated that 39% of respondents with severe psoriasis and 37% with moderate psoriasis were not currently receiving any treatment. Among those receiving treatment, only 43% with severe psoriasis received either traditional systemic therapy, biologic therapy, or phototherapy.

Access to care and cost of treatment are some of the reasons why psoriasis may go untreated. In 2013 the National Psoriasis Foundation reported results of a survey of 5600 patients with psoriasis and psoriatic arthritis, which revealed that patients did not see a specialist (ie, dermatologist, rheumatologist) to treat their disease because they had given up on treatment (28%), it was too expensive (21%), or it was too much of a hassle (11%). Although approximately 91% of patients were covered by medical insurance, the majority spent more than $2500 per year in out-of-pocket costs for their disease.

Patient satisfaction with treatment also is a concern. A 2002 National Psoriasis Foundation survey reported that 33% of patients are unsatisfied with current treatments and 78% do not use more aggressive therapies to treat their disease because of their side effects and lack of effectiveness. The advent of biologic therapies and new oral treatments has afforded psoriasis patients the opportunity to have a frank discussion with their health care provider if they are not satisfied with treatment or are not seeing the type of improvement that would make a substantial impact on their quality of life. Additionally, over time skin may become resistant to various treatments. Therefore, open communication with psoriasis patients is key.

Expert Commentary

We are in the midst of a second revolution in the treatment of psoriasis. We have multiple new biologic and oral agents available for the treatment of this condition. In addition, there are a large number of treatments currently in development. Not only can psoriasis be treated, it can be treated highly effectively and safely.

—Jeffrey M. Weinberg, MD (New York, New York)

Myth: Psoriasis Cannot Be Treated

At the Summer Meeting of the American Academy of Dermatology in Boston, Massachusetts (July 28-31, 2016), Dr. Alexa Kimball presented on dermatology research advances at the plenary session and referenced the revolution in psoriasis treatment that has been experienced in the last several years, noting that dermatologists previously were relegated to treating patients with tar treatments. Today, many options for the treatment of psoriasis exist, though the disease is not curable.

According to the Mayo Clinic, psoriasis treatment is aimed at stopping the skin cells from growing so quickly, which reduces inflammation and plaque formation, and removing scales and smoothing skin. It is important for patients to understand the different treatment options so that they are aware that a variety of therapies may be tried until the right regimen with the fewest potential side effects is found. Options include:

• Biologics: given by injection or intravenous infusion for moderate to severe psoriasis that has not responded to other treatments

• Experimental medications: new medications undergoing clinical trials

• Oral treatments: inhibit specific molecules associated with inflammation and can be taken by mouth rather than injection or infusion (eg, retinoids, methotrexate, cyclosporine)

• Phototherapy or other light therapy: involves exposing the skin to UV light on a regular basis and under medical supervision (eg, UVB phototherapy, narrowband UVB therapy, psoralen plus UVA, excimer laser)

• Systemics: given orally or by injection and work throughout the body for moderate to severe psoriasis

• Topicals: applied to the skin and typically used for mild to moderate psoriasis (eg, topical corticosteroids, vitamin D analogues, anthralin, topical retinoids, calcineurin inhibitors, salicylic acid, coal tar, moisturizers)

In a 2014 analysis of data from the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey of the National Center for Health Statistics, the frequency of phototherapy treatments for psoriasis significantly decreased from 1993 to 2010 (P<.001), while the frequency of biologics significantly increased, becoming the most frequently used treatment from 2008 to 2010 (P<.0001).

However, psoriasis has been noted to be undertreated. A 2007 survey of 1657 psoriasis patients (28% with severe disease and 41% with moderate disease) from the National Psoriasis Foundation contact database indicated that 39% of respondents with severe psoriasis and 37% with moderate psoriasis were not currently receiving any treatment. Among those receiving treatment, only 43% with severe psoriasis received either traditional systemic therapy, biologic therapy, or phototherapy.

Access to care and cost of treatment are some of the reasons why psoriasis may go untreated. In 2013 the National Psoriasis Foundation reported results of a survey of 5600 patients with psoriasis and psoriatic arthritis, which revealed that patients did not see a specialist (ie, dermatologist, rheumatologist) to treat their disease because they had given up on treatment (28%), it was too expensive (21%), or it was too much of a hassle (11%). Although approximately 91% of patients were covered by medical insurance, the majority spent more than $2500 per year in out-of-pocket costs for their disease.

Patient satisfaction with treatment also is a concern. A 2002 National Psoriasis Foundation survey reported that 33% of patients are unsatisfied with current treatments and 78% do not use more aggressive therapies to treat their disease because of their side effects and lack of effectiveness. The advent of biologic therapies and new oral treatments has afforded psoriasis patients the opportunity to have a frank discussion with their health care provider if they are not satisfied with treatment or are not seeing the type of improvement that would make a substantial impact on their quality of life. Additionally, over time skin may become resistant to various treatments. Therefore, open communication with psoriasis patients is key.

Expert Commentary

We are in the midst of a second revolution in the treatment of psoriasis. We have multiple new biologic and oral agents available for the treatment of this condition. In addition, there are a large number of treatments currently in development. Not only can psoriasis be treated, it can be treated highly effectively and safely.

—Jeffrey M. Weinberg, MD (New York, New York)

Myth: Psoriasis Cannot Be Treated

At the Summer Meeting of the American Academy of Dermatology in Boston, Massachusetts (July 28-31, 2016), Dr. Alexa Kimball presented on dermatology research advances at the plenary session and referenced the revolution in psoriasis treatment that has been experienced in the last several years, noting that dermatologists previously were relegated to treating patients with tar treatments. Today, many options for the treatment of psoriasis exist, though the disease is not curable.

According to the Mayo Clinic, psoriasis treatment is aimed at stopping the skin cells from growing so quickly, which reduces inflammation and plaque formation, and removing scales and smoothing skin. It is important for patients to understand the different treatment options so that they are aware that a variety of therapies may be tried until the right regimen with the fewest potential side effects is found. Options include:

• Biologics: given by injection or intravenous infusion for moderate to severe psoriasis that has not responded to other treatments

• Experimental medications: new medications undergoing clinical trials

• Oral treatments: inhibit specific molecules associated with inflammation and can be taken by mouth rather than injection or infusion (eg, retinoids, methotrexate, cyclosporine)

• Phototherapy or other light therapy: involves exposing the skin to UV light on a regular basis and under medical supervision (eg, UVB phototherapy, narrowband UVB therapy, psoralen plus UVA, excimer laser)

• Systemics: given orally or by injection and work throughout the body for moderate to severe psoriasis

• Topicals: applied to the skin and typically used for mild to moderate psoriasis (eg, topical corticosteroids, vitamin D analogues, anthralin, topical retinoids, calcineurin inhibitors, salicylic acid, coal tar, moisturizers)

In a 2014 analysis of data from the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey of the National Center for Health Statistics, the frequency of phototherapy treatments for psoriasis significantly decreased from 1993 to 2010 (P<.001), while the frequency of biologics significantly increased, becoming the most frequently used treatment from 2008 to 2010 (P<.0001).

However, psoriasis has been noted to be undertreated. A 2007 survey of 1657 psoriasis patients (28% with severe disease and 41% with moderate disease) from the National Psoriasis Foundation contact database indicated that 39% of respondents with severe psoriasis and 37% with moderate psoriasis were not currently receiving any treatment. Among those receiving treatment, only 43% with severe psoriasis received either traditional systemic therapy, biologic therapy, or phototherapy.

Access to care and cost of treatment are some of the reasons why psoriasis may go untreated. In 2013 the National Psoriasis Foundation reported results of a survey of 5600 patients with psoriasis and psoriatic arthritis, which revealed that patients did not see a specialist (ie, dermatologist, rheumatologist) to treat their disease because they had given up on treatment (28%), it was too expensive (21%), or it was too much of a hassle (11%). Although approximately 91% of patients were covered by medical insurance, the majority spent more than $2500 per year in out-of-pocket costs for their disease.

Patient satisfaction with treatment also is a concern. A 2002 National Psoriasis Foundation survey reported that 33% of patients are unsatisfied with current treatments and 78% do not use more aggressive therapies to treat their disease because of their side effects and lack of effectiveness. The advent of biologic therapies and new oral treatments has afforded psoriasis patients the opportunity to have a frank discussion with their health care provider if they are not satisfied with treatment or are not seeing the type of improvement that would make a substantial impact on their quality of life. Additionally, over time skin may become resistant to various treatments. Therefore, open communication with psoriasis patients is key.

Expert Commentary

We are in the midst of a second revolution in the treatment of psoriasis. We have multiple new biologic and oral agents available for the treatment of this condition. In addition, there are a large number of treatments currently in development. Not only can psoriasis be treated, it can be treated highly effectively and safely.

—Jeffrey M. Weinberg, MD (New York, New York)

For the last decade, we have considered the cardioprotective benefit of biologics, especially in patients with chronic inflammatory diseases. Due to accelerated coronary artery disease, inflammatory pathways of psoriasis share connections with the mechanisms of atherosclerosis.

In a July 7 article published online in JAMA Dermatology, Hjuler et al investigated the association of biological therapy with changes in coronary artery disease progression, measured by serial coronary computed tomography (CT). Patients with severe psoriasis were enrolled in a single-center, prospective, controlled, observer-blinded clinical study. Between April 2011 and June 2014, biologic therapy (intervention group) and a matched control that did not receive the same therapy (control group) were initiated. Biological therapies included adalimumab, etanercept, infliximab, and ustekinumab, along with the possibility to switch between treatments to ensure inflammation control.

At baseline and 13-month follow-up, 28 treated patients (mean age [SD], 49.2 [10.2] years; 71% men; mean psoriasis area severity index [PASI][SD], 15.4 [4.3]) and 28 controls (mean age [SD], 52.8 [10.6] years; 71% men; mean PASI [SD], 12.4 [3.9]) underwent noncontrast coronary artery calcium (CAC) CT and contrast-enhanced coronary CT angiography. Changes in CAC score, number of coronary plaques, severity of luminal narrowing, composition, and vessel wall volume were measured.

In the intervention group, the CAC scores remained stable (mean yearly CAC change [SD], -16 [56]; P=.15) and progressed in the control group (14 [29]; P=.02). The severity of luminal narrowing in the diseased segments remained unchanged in the intervention group (Wilcoxon W=76; n=483; P=.39) but increased at follow-up in the control group (Wilcoxon W=281; n=414; P=.02). Luminal abnormalities remained unchanged in both groups.

The authors concluded that clinically effective treatment with biologic agents is associated with reduced coronary artery diseases in patients with severe psoriasis. These findings support a beneficial effect of biologic anti-inflammatory agents in preventing cardiovascular disease progression in addition to disease control in inflammatory diseases.

What’s the issue?

These findings give continued support to the cardioprotective effects of biologics in inflammatory diseases. How will these data change your prescribing habits?

We want to know your views! Tell us what you think.

For the last decade, we have considered the cardioprotective benefit of biologics, especially in patients with chronic inflammatory diseases. Due to accelerated coronary artery disease, inflammatory pathways of psoriasis share connections with the mechanisms of atherosclerosis.

In a July 7 article published online in JAMA Dermatology, Hjuler et al investigated the association of biological therapy with changes in coronary artery disease progression, measured by serial coronary computed tomography (CT). Patients with severe psoriasis were enrolled in a single-center, prospective, controlled, observer-blinded clinical study. Between April 2011 and June 2014, biologic therapy (intervention group) and a matched control that did not receive the same therapy (control group) were initiated. Biological therapies included adalimumab, etanercept, infliximab, and ustekinumab, along with the possibility to switch between treatments to ensure inflammation control.

At baseline and 13-month follow-up, 28 treated patients (mean age [SD], 49.2 [10.2] years; 71% men; mean psoriasis area severity index [PASI][SD], 15.4 [4.3]) and 28 controls (mean age [SD], 52.8 [10.6] years; 71% men; mean PASI [SD], 12.4 [3.9]) underwent noncontrast coronary artery calcium (CAC) CT and contrast-enhanced coronary CT angiography. Changes in CAC score, number of coronary plaques, severity of luminal narrowing, composition, and vessel wall volume were measured.

In the intervention group, the CAC scores remained stable (mean yearly CAC change [SD], -16 [56]; P=.15) and progressed in the control group (14 [29]; P=.02). The severity of luminal narrowing in the diseased segments remained unchanged in the intervention group (Wilcoxon W=76; n=483; P=.39) but increased at follow-up in the control group (Wilcoxon W=281; n=414; P=.02). Luminal abnormalities remained unchanged in both groups.

The authors concluded that clinically effective treatment with biologic agents is associated with reduced coronary artery diseases in patients with severe psoriasis. These findings support a beneficial effect of biologic anti-inflammatory agents in preventing cardiovascular disease progression in addition to disease control in inflammatory diseases.

What’s the issue?

These findings give continued support to the cardioprotective effects of biologics in inflammatory diseases. How will these data change your prescribing habits?

We want to know your views! Tell us what you think.

For the last decade, we have considered the cardioprotective benefit of biologics, especially in patients with chronic inflammatory diseases. Due to accelerated coronary artery disease, inflammatory pathways of psoriasis share connections with the mechanisms of atherosclerosis.

In a July 7 article published online in JAMA Dermatology, Hjuler et al investigated the association of biological therapy with changes in coronary artery disease progression, measured by serial coronary computed tomography (CT). Patients with severe psoriasis were enrolled in a single-center, prospective, controlled, observer-blinded clinical study. Between April 2011 and June 2014, biologic therapy (intervention group) and a matched control that did not receive the same therapy (control group) were initiated. Biological therapies included adalimumab, etanercept, infliximab, and ustekinumab, along with the possibility to switch between treatments to ensure inflammation control.

At baseline and 13-month follow-up, 28 treated patients (mean age [SD], 49.2 [10.2] years; 71% men; mean psoriasis area severity index [PASI][SD], 15.4 [4.3]) and 28 controls (mean age [SD], 52.8 [10.6] years; 71% men; mean PASI [SD], 12.4 [3.9]) underwent noncontrast coronary artery calcium (CAC) CT and contrast-enhanced coronary CT angiography. Changes in CAC score, number of coronary plaques, severity of luminal narrowing, composition, and vessel wall volume were measured.

In the intervention group, the CAC scores remained stable (mean yearly CAC change [SD], -16 [56]; P=.15) and progressed in the control group (14 [29]; P=.02). The severity of luminal narrowing in the diseased segments remained unchanged in the intervention group (Wilcoxon W=76; n=483; P=.39) but increased at follow-up in the control group (Wilcoxon W=281; n=414; P=.02). Luminal abnormalities remained unchanged in both groups.

The authors concluded that clinically effective treatment with biologic agents is associated with reduced coronary artery diseases in patients with severe psoriasis. These findings support a beneficial effect of biologic anti-inflammatory agents in preventing cardiovascular disease progression in addition to disease control in inflammatory diseases.

What’s the issue?

These findings give continued support to the cardioprotective effects of biologics in inflammatory diseases. How will these data change your prescribing habits?

We want to know your views! Tell us what you think.