Psoriasis

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

hsplete@frontlinemedcom.com

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

hsplete@frontlinemedcom.com

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

hsplete@frontlinemedcom.com

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

hsplete@frontlinemedcom.com

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

hsplete@frontlinemedcom.com

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

hsplete@frontlinemedcom.com

The metabolic syndrome and insulin resistance are not just common among patients with psoriatic arthritis, but both also correlate with the severity of the inflammatory musculoskeletal disease, according to a single-center, cross-sectional cohort study.

In the study of 283 consecutive white patients with longstanding psoriatic arthritis who attended a rheumatology clinic during a 1-year period, 44% were found to have the metabolic syndrome and 16% to have insulin resistance. "Our findings are novel and support our pretest hypothesis that the risk of metabolic syndrome and insulin resistance increases with the severity of underlying psoriatic arthritis, probably reflecting the increasing burden of inflammation," said Dr. Muhammad Haroon of the department of rheumatology and his associates at St. Vincent’s University Hospital, Dublin.

Psoriatic arthritis is known to be associated with heightened cardiovascular risk, and CV diseases are the leading causes of death in patients with psoriatic arthritis. Until now, however, the prevalences of these two major CV risk factors have not been well studied in patients with psoriatic arthritis. "We hypothesized, therefore, that there might be a greater burden of metabolic syndrome and insulin resistance in psoriatic arthritis, and consequently of cardiovascular diseases because of a greater inflammatory load," Dr. Haroon and his colleagues wrote (J. Rheumatol. 2014;41:1357-65).

The patients had psoriatic arthritis for a duration of at least 10 years (mean of 19 years), and just over half of the patients were women. Their mean age was 54.6 years.

A total of 124 patients (44%) were found to have the metabolic syndrome. "Even more alarming was the finding that about 50% of these newly diagnosed patients with metabolic syndrome had a combination of 4 or 5 of these risk features," the investigators said. In particular, elevated blood pressure (74%), greater waist circumference (56%), and elevated triglycerides (44%) were common among these psoriatic arthritis patients.

On multivariate analysis, metabolic syndrome was significantly associated with more severe disease, higher smoking pack-years, and worse EuroQol-5 dimension (EQ-5D). Metabolic syndrome was significantly associated with severe disease, even after adjustment for the presence of insulin resistance.

A total of 41 patients (16%) had insulin resistance of the 263 for whom insulin resistance data were available, which on multivariate analysis was significantly associated more severe disease, older age at the onset of psoriasis, and higher body-mass index, even after adjusting for the presence of metabolic syndrome.

Both the metabolic syndrome and insulin resistance were more frequent among patients with the most severe psoriatic arthritis, as measured by current and previous skin assessments; inflammatory markers; measures of disease activity; the number of deformed joints; and the presence of dactylitis, enthesitis, peripheral joint erosions, osteolysis, and sacroiliitis, the investigators said.

The study findings suggest, but do not establish, that "the higher burden of inflammatory arthritis or the combination of severe psoriatic disease features play major roles in the development of the metabolic syndrome and/or insulin resistance," Dr. Haroon and his associates said.

Their observations "can also help inform risk stratification" of patients with psoriatic arthritis, they added.

No disclosures were provided.

The metabolic syndrome and insulin resistance are not just common among patients with psoriatic arthritis, but both also correlate with the severity of the inflammatory musculoskeletal disease, according to a single-center, cross-sectional cohort study.

In the study of 283 consecutive white patients with longstanding psoriatic arthritis who attended a rheumatology clinic during a 1-year period, 44% were found to have the metabolic syndrome and 16% to have insulin resistance. "Our findings are novel and support our pretest hypothesis that the risk of metabolic syndrome and insulin resistance increases with the severity of underlying psoriatic arthritis, probably reflecting the increasing burden of inflammation," said Dr. Muhammad Haroon of the department of rheumatology and his associates at St. Vincent’s University Hospital, Dublin.

Psoriatic arthritis is known to be associated with heightened cardiovascular risk, and CV diseases are the leading causes of death in patients with psoriatic arthritis. Until now, however, the prevalences of these two major CV risk factors have not been well studied in patients with psoriatic arthritis. "We hypothesized, therefore, that there might be a greater burden of metabolic syndrome and insulin resistance in psoriatic arthritis, and consequently of cardiovascular diseases because of a greater inflammatory load," Dr. Haroon and his colleagues wrote (J. Rheumatol. 2014;41:1357-65).

The patients had psoriatic arthritis for a duration of at least 10 years (mean of 19 years), and just over half of the patients were women. Their mean age was 54.6 years.

A total of 124 patients (44%) were found to have the metabolic syndrome. "Even more alarming was the finding that about 50% of these newly diagnosed patients with metabolic syndrome had a combination of 4 or 5 of these risk features," the investigators said. In particular, elevated blood pressure (74%), greater waist circumference (56%), and elevated triglycerides (44%) were common among these psoriatic arthritis patients.

On multivariate analysis, metabolic syndrome was significantly associated with more severe disease, higher smoking pack-years, and worse EuroQol-5 dimension (EQ-5D). Metabolic syndrome was significantly associated with severe disease, even after adjustment for the presence of insulin resistance.

A total of 41 patients (16%) had insulin resistance of the 263 for whom insulin resistance data were available, which on multivariate analysis was significantly associated more severe disease, older age at the onset of psoriasis, and higher body-mass index, even after adjusting for the presence of metabolic syndrome.

Both the metabolic syndrome and insulin resistance were more frequent among patients with the most severe psoriatic arthritis, as measured by current and previous skin assessments; inflammatory markers; measures of disease activity; the number of deformed joints; and the presence of dactylitis, enthesitis, peripheral joint erosions, osteolysis, and sacroiliitis, the investigators said.

The study findings suggest, but do not establish, that "the higher burden of inflammatory arthritis or the combination of severe psoriatic disease features play major roles in the development of the metabolic syndrome and/or insulin resistance," Dr. Haroon and his associates said.

Their observations "can also help inform risk stratification" of patients with psoriatic arthritis, they added.

No disclosures were provided.

The metabolic syndrome and insulin resistance are not just common among patients with psoriatic arthritis, but both also correlate with the severity of the inflammatory musculoskeletal disease, according to a single-center, cross-sectional cohort study.

In the study of 283 consecutive white patients with longstanding psoriatic arthritis who attended a rheumatology clinic during a 1-year period, 44% were found to have the metabolic syndrome and 16% to have insulin resistance. "Our findings are novel and support our pretest hypothesis that the risk of metabolic syndrome and insulin resistance increases with the severity of underlying psoriatic arthritis, probably reflecting the increasing burden of inflammation," said Dr. Muhammad Haroon of the department of rheumatology and his associates at St. Vincent’s University Hospital, Dublin.

Psoriatic arthritis is known to be associated with heightened cardiovascular risk, and CV diseases are the leading causes of death in patients with psoriatic arthritis. Until now, however, the prevalences of these two major CV risk factors have not been well studied in patients with psoriatic arthritis. "We hypothesized, therefore, that there might be a greater burden of metabolic syndrome and insulin resistance in psoriatic arthritis, and consequently of cardiovascular diseases because of a greater inflammatory load," Dr. Haroon and his colleagues wrote (J. Rheumatol. 2014;41:1357-65).

The patients had psoriatic arthritis for a duration of at least 10 years (mean of 19 years), and just over half of the patients were women. Their mean age was 54.6 years.

A total of 124 patients (44%) were found to have the metabolic syndrome. "Even more alarming was the finding that about 50% of these newly diagnosed patients with metabolic syndrome had a combination of 4 or 5 of these risk features," the investigators said. In particular, elevated blood pressure (74%), greater waist circumference (56%), and elevated triglycerides (44%) were common among these psoriatic arthritis patients.

On multivariate analysis, metabolic syndrome was significantly associated with more severe disease, higher smoking pack-years, and worse EuroQol-5 dimension (EQ-5D). Metabolic syndrome was significantly associated with severe disease, even after adjustment for the presence of insulin resistance.

A total of 41 patients (16%) had insulin resistance of the 263 for whom insulin resistance data were available, which on multivariate analysis was significantly associated more severe disease, older age at the onset of psoriasis, and higher body-mass index, even after adjusting for the presence of metabolic syndrome.

Both the metabolic syndrome and insulin resistance were more frequent among patients with the most severe psoriatic arthritis, as measured by current and previous skin assessments; inflammatory markers; measures of disease activity; the number of deformed joints; and the presence of dactylitis, enthesitis, peripheral joint erosions, osteolysis, and sacroiliitis, the investigators said.

The study findings suggest, but do not establish, that "the higher burden of inflammatory arthritis or the combination of severe psoriatic disease features play major roles in the development of the metabolic syndrome and/or insulin resistance," Dr. Haroon and his associates said.

Their observations "can also help inform risk stratification" of patients with psoriatic arthritis, they added.

No disclosures were provided.

Women with a 6-year or longer history of hypertension, and women with a 6-year or longer use of beta-blocker medications to treat hypertension, may be at increased risk of developing psoriasis, compared with women who have normal blood pressure, according to data from more than 77,000 women.

"Women with hypertension tended to be older; had higher [body mass indexes]; had proportionately higher prevalence rates of cardiovascular disease, type 2 diabetes, and hypercholesterolemia; and were less physically active than those without hypertension," the researchers wrote.

The report was published online July 2 in JAMA Dermatology [doi:10.1001/jamadermatol.2013.9957].

Dr. Shaowei Wu of Brown University, Providence, R.I., and colleagues performed a prospective cohort study of 77,728 women participating in the Nurses’ Health Study between June 1996 and June 2008. The women provided biennially updated data on hypertension and antihypertensive medications. The researchers identified 843 psoriasis cases during more than 1 million person-years of follow-up.

Women with hypertension lasting 6 years or more were at higher risk of developing psoriasis than were normotensive women [HR 1.27]. In further analysis, researchers found "a higher risk of psoriasis among hypertensive women without medication use [HR 1.49] and among hypertensive women with current medication use [HR 1.31] when compared with normotensive women without medication use." In an analysis of individual antihypertensive medications, beta-blockers were the only drugs associated with psoriasis development. Although this association disappeared in a fully-adjusted model, it "persisted in a duration-dependent manner" [HR 1.39] among women taking the medications for 6 years or more, and this trend was statistically significant.

"Special attention on psoriasis screening may be needed for patients with long-term duration of hypertension and related antihypertensive medication use in clinical practices," the authors wrote. The findings "provide novel insights into the association among hypertension, antihypertensive medications, and psoriasis," they said. "However, further work is necessary to confirm our findings and clarify the biological mechanisms that underlie these associations."

The study was supported in part by the National Institutes of Health. Senior author Dr. Abrar Qureshi has served as a consultant for Abbott, Centocor, Novartis, and the Centers for Disease Control and Prevention.

Women with a 6-year or longer history of hypertension, and women with a 6-year or longer use of beta-blocker medications to treat hypertension, may be at increased risk of developing psoriasis, compared with women who have normal blood pressure, according to data from more than 77,000 women.

"Women with hypertension tended to be older; had higher [body mass indexes]; had proportionately higher prevalence rates of cardiovascular disease, type 2 diabetes, and hypercholesterolemia; and were less physically active than those without hypertension," the researchers wrote.

The report was published online July 2 in JAMA Dermatology [doi:10.1001/jamadermatol.2013.9957].

Dr. Shaowei Wu of Brown University, Providence, R.I., and colleagues performed a prospective cohort study of 77,728 women participating in the Nurses’ Health Study between June 1996 and June 2008. The women provided biennially updated data on hypertension and antihypertensive medications. The researchers identified 843 psoriasis cases during more than 1 million person-years of follow-up.

Women with hypertension lasting 6 years or more were at higher risk of developing psoriasis than were normotensive women [HR 1.27]. In further analysis, researchers found "a higher risk of psoriasis among hypertensive women without medication use [HR 1.49] and among hypertensive women with current medication use [HR 1.31] when compared with normotensive women without medication use." In an analysis of individual antihypertensive medications, beta-blockers were the only drugs associated with psoriasis development. Although this association disappeared in a fully-adjusted model, it "persisted in a duration-dependent manner" [HR 1.39] among women taking the medications for 6 years or more, and this trend was statistically significant.

"Special attention on psoriasis screening may be needed for patients with long-term duration of hypertension and related antihypertensive medication use in clinical practices," the authors wrote. The findings "provide novel insights into the association among hypertension, antihypertensive medications, and psoriasis," they said. "However, further work is necessary to confirm our findings and clarify the biological mechanisms that underlie these associations."

The study was supported in part by the National Institutes of Health. Senior author Dr. Abrar Qureshi has served as a consultant for Abbott, Centocor, Novartis, and the Centers for Disease Control and Prevention.

Women with a 6-year or longer history of hypertension, and women with a 6-year or longer use of beta-blocker medications to treat hypertension, may be at increased risk of developing psoriasis, compared with women who have normal blood pressure, according to data from more than 77,000 women.

"Women with hypertension tended to be older; had higher [body mass indexes]; had proportionately higher prevalence rates of cardiovascular disease, type 2 diabetes, and hypercholesterolemia; and were less physically active than those without hypertension," the researchers wrote.

The report was published online July 2 in JAMA Dermatology [doi:10.1001/jamadermatol.2013.9957].

Dr. Shaowei Wu of Brown University, Providence, R.I., and colleagues performed a prospective cohort study of 77,728 women participating in the Nurses’ Health Study between June 1996 and June 2008. The women provided biennially updated data on hypertension and antihypertensive medications. The researchers identified 843 psoriasis cases during more than 1 million person-years of follow-up.

Women with hypertension lasting 6 years or more were at higher risk of developing psoriasis than were normotensive women [HR 1.27]. In further analysis, researchers found "a higher risk of psoriasis among hypertensive women without medication use [HR 1.49] and among hypertensive women with current medication use [HR 1.31] when compared with normotensive women without medication use." In an analysis of individual antihypertensive medications, beta-blockers were the only drugs associated with psoriasis development. Although this association disappeared in a fully-adjusted model, it "persisted in a duration-dependent manner" [HR 1.39] among women taking the medications for 6 years or more, and this trend was statistically significant.

"Special attention on psoriasis screening may be needed for patients with long-term duration of hypertension and related antihypertensive medication use in clinical practices," the authors wrote. The findings "provide novel insights into the association among hypertension, antihypertensive medications, and psoriasis," they said. "However, further work is necessary to confirm our findings and clarify the biological mechanisms that underlie these associations."

The study was supported in part by the National Institutes of Health. Senior author Dr. Abrar Qureshi has served as a consultant for Abbott, Centocor, Novartis, and the Centers for Disease Control and Prevention.

Case Report

A 35-year-old man with chronic plaque-type psoriasis presented for treatment of a flare-up caused by a combination of hot tub use and 3 missed etanercept injections. The patient had been prescribed subcutaneous etanercept (50 mg once weekly) approximately 2 years prior to presentation for treatment of psoriasis and had used it consistently with 2 brief periods of discontinuation due to upper respiratory infections; treatment was discontinued for 2 weeks until the infections resolved and was restarted at the same dose. Recent hot tub use induced localized folliculitis of the leg and caused koebnerization of his psoriasis. Treatment with etanercept (50 mg twice weekly) was reinitiated, but after 1 month of therapy, the patient developed a nodulocystic eruption on the face. The patient discontinued use of etanercept and subsequently was started on oral minocycline (50 mgonce daily) by his primary care physician. After 6 weeks of minocycline therapy, the patient reported gradual improvement of his cystic acne. At follow-up, physical examination revealed approximately 15 erythematous cystic papules and nodules on the bilateral cheeks. The dose of oral minocycline was increased to 100 mg twice daily and his face subsequently cleared after 12 weeks of treatment.

On rechallenge with etanercept (50 mg weekly) after a separate flare-up of his psoriasis and psoriatic arthritis, the patient again developed nodulocystic acne within 3 weeks of restarting the medication, which confirmed the association between etanercept and the eruption. Etanercept was subsequently discontinued and the patient was started on ustekinumab for treatment of psoriasis and psoriatic arthritis as well as minocycline (100 mg twice daily) for treatment of nodulocystic acne. His acne subsequently cleared after 12 weeks of therapy. The patient’s psoriasis currently is well controlled on a regimen of methotrexate 20 mg weekly, as continued use of ustekinumab was not covered by his health insurance policy.

Comment

Etanercept, along with infliximab and adalimumab, is a tumor necrosis factor α (TNF-α) antagonist. Tumor necrosis factor α is a major cytokine of the immune system that is deregulated in autoimmune disorders, causing inflammation and a variety of systemic effects. Inhibition of TNF-α results in a decrease in inflammatory markers such as IL-1 and IL-6, leading to a reduction in endothelial permeability and leukocyte migration.¹ Etanercept is unique in that it is a fully humanized soluble fusion protein consisting of a TNF-α receptor linked to the Fc region of IgG1, whereas infliximab and adalimumab are monoclonal antibodies that target TNF-α. Etanercept works by acting as a decoy receptor for TNF-α, thereby preventing it from binding cell surface receptors and subsequently decreasing inflammation. It is an approved treatment of rheumatoid arthritis, polyarticular juvenile rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and plaque psoriasis.²

Many drugs have been implicated in acneform eruptions mimicking acne vulgaris, such as corticosteroids, cyclosporine, antipsychotics, anticonvulsants, epidermal growth factor receptor inhibitors, antidepressants, danazol, antituberculosis drugs, quinidine, azathioprine, testosterone, and TNF-α antagonists.¹ The TNF-α antagonists that have been associated with acne are infliximab and adalimumab, especially when used to treat Crohn disease or rheumatoid arthritis, though there also are reports of acneform eruptions when using these drugs to treat psoriasis.^1,3 There have been reports of the use of etanercept in treating severe acne and acne conglobata^4,5; our case documents etanercept-induced acne associated with psoriasis treatment. Theoretically, anti–TNF-α agents should suppress acne rather than induce it due to their inhibition of the inflammatory markers TNF-α, IL-1a, and IFN-γ, which are thought to play a role in hypercornification of the infundibulum.⁶ Thus the mechanism of TNF-α antagonists and associated acneform eruptions remains unknown. This observation should prompt further research to investigate the correlation between the use of TNF-α inhibitors, specifically etanercept, and cystic acne.

Case Report

A 35-year-old man with chronic plaque-type psoriasis presented for treatment of a flare-up caused by a combination of hot tub use and 3 missed etanercept injections. The patient had been prescribed subcutaneous etanercept (50 mg once weekly) approximately 2 years prior to presentation for treatment of psoriasis and had used it consistently with 2 brief periods of discontinuation due to upper respiratory infections; treatment was discontinued for 2 weeks until the infections resolved and was restarted at the same dose. Recent hot tub use induced localized folliculitis of the leg and caused koebnerization of his psoriasis. Treatment with etanercept (50 mg twice weekly) was reinitiated, but after 1 month of therapy, the patient developed a nodulocystic eruption on the face. The patient discontinued use of etanercept and subsequently was started on oral minocycline (50 mgonce daily) by his primary care physician. After 6 weeks of minocycline therapy, the patient reported gradual improvement of his cystic acne. At follow-up, physical examination revealed approximately 15 erythematous cystic papules and nodules on the bilateral cheeks. The dose of oral minocycline was increased to 100 mg twice daily and his face subsequently cleared after 12 weeks of treatment.

On rechallenge with etanercept (50 mg weekly) after a separate flare-up of his psoriasis and psoriatic arthritis, the patient again developed nodulocystic acne within 3 weeks of restarting the medication, which confirmed the association between etanercept and the eruption. Etanercept was subsequently discontinued and the patient was started on ustekinumab for treatment of psoriasis and psoriatic arthritis as well as minocycline (100 mg twice daily) for treatment of nodulocystic acne. His acne subsequently cleared after 12 weeks of therapy. The patient’s psoriasis currently is well controlled on a regimen of methotrexate 20 mg weekly, as continued use of ustekinumab was not covered by his health insurance policy.

Comment

Etanercept, along with infliximab and adalimumab, is a tumor necrosis factor α (TNF-α) antagonist. Tumor necrosis factor α is a major cytokine of the immune system that is deregulated in autoimmune disorders, causing inflammation and a variety of systemic effects. Inhibition of TNF-α results in a decrease in inflammatory markers such as IL-1 and IL-6, leading to a reduction in endothelial permeability and leukocyte migration.¹ Etanercept is unique in that it is a fully humanized soluble fusion protein consisting of a TNF-α receptor linked to the Fc region of IgG1, whereas infliximab and adalimumab are monoclonal antibodies that target TNF-α. Etanercept works by acting as a decoy receptor for TNF-α, thereby preventing it from binding cell surface receptors and subsequently decreasing inflammation. It is an approved treatment of rheumatoid arthritis, polyarticular juvenile rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and plaque psoriasis.²

Many drugs have been implicated in acneform eruptions mimicking acne vulgaris, such as corticosteroids, cyclosporine, antipsychotics, anticonvulsants, epidermal growth factor receptor inhibitors, antidepressants, danazol, antituberculosis drugs, quinidine, azathioprine, testosterone, and TNF-α antagonists.¹ The TNF-α antagonists that have been associated with acne are infliximab and adalimumab, especially when used to treat Crohn disease or rheumatoid arthritis, though there also are reports of acneform eruptions when using these drugs to treat psoriasis.^1,3 There have been reports of the use of etanercept in treating severe acne and acne conglobata^4,5; our case documents etanercept-induced acne associated with psoriasis treatment. Theoretically, anti–TNF-α agents should suppress acne rather than induce it due to their inhibition of the inflammatory markers TNF-α, IL-1a, and IFN-γ, which are thought to play a role in hypercornification of the infundibulum.⁶ Thus the mechanism of TNF-α antagonists and associated acneform eruptions remains unknown. This observation should prompt further research to investigate the correlation between the use of TNF-α inhibitors, specifically etanercept, and cystic acne.

Case Report

A 35-year-old man with chronic plaque-type psoriasis presented for treatment of a flare-up caused by a combination of hot tub use and 3 missed etanercept injections. The patient had been prescribed subcutaneous etanercept (50 mg once weekly) approximately 2 years prior to presentation for treatment of psoriasis and had used it consistently with 2 brief periods of discontinuation due to upper respiratory infections; treatment was discontinued for 2 weeks until the infections resolved and was restarted at the same dose. Recent hot tub use induced localized folliculitis of the leg and caused koebnerization of his psoriasis. Treatment with etanercept (50 mg twice weekly) was reinitiated, but after 1 month of therapy, the patient developed a nodulocystic eruption on the face. The patient discontinued use of etanercept and subsequently was started on oral minocycline (50 mgonce daily) by his primary care physician. After 6 weeks of minocycline therapy, the patient reported gradual improvement of his cystic acne. At follow-up, physical examination revealed approximately 15 erythematous cystic papules and nodules on the bilateral cheeks. The dose of oral minocycline was increased to 100 mg twice daily and his face subsequently cleared after 12 weeks of treatment.

On rechallenge with etanercept (50 mg weekly) after a separate flare-up of his psoriasis and psoriatic arthritis, the patient again developed nodulocystic acne within 3 weeks of restarting the medication, which confirmed the association between etanercept and the eruption. Etanercept was subsequently discontinued and the patient was started on ustekinumab for treatment of psoriasis and psoriatic arthritis as well as minocycline (100 mg twice daily) for treatment of nodulocystic acne. His acne subsequently cleared after 12 weeks of therapy. The patient’s psoriasis currently is well controlled on a regimen of methotrexate 20 mg weekly, as continued use of ustekinumab was not covered by his health insurance policy.

Comment

Etanercept, along with infliximab and adalimumab, is a tumor necrosis factor α (TNF-α) antagonist. Tumor necrosis factor α is a major cytokine of the immune system that is deregulated in autoimmune disorders, causing inflammation and a variety of systemic effects. Inhibition of TNF-α results in a decrease in inflammatory markers such as IL-1 and IL-6, leading to a reduction in endothelial permeability and leukocyte migration.¹ Etanercept is unique in that it is a fully humanized soluble fusion protein consisting of a TNF-α receptor linked to the Fc region of IgG1, whereas infliximab and adalimumab are monoclonal antibodies that target TNF-α. Etanercept works by acting as a decoy receptor for TNF-α, thereby preventing it from binding cell surface receptors and subsequently decreasing inflammation. It is an approved treatment of rheumatoid arthritis, polyarticular juvenile rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and plaque psoriasis.²

Many drugs have been implicated in acneform eruptions mimicking acne vulgaris, such as corticosteroids, cyclosporine, antipsychotics, anticonvulsants, epidermal growth factor receptor inhibitors, antidepressants, danazol, antituberculosis drugs, quinidine, azathioprine, testosterone, and TNF-α antagonists.¹ The TNF-α antagonists that have been associated with acne are infliximab and adalimumab, especially when used to treat Crohn disease or rheumatoid arthritis, though there also are reports of acneform eruptions when using these drugs to treat psoriasis.^1,3 There have been reports of the use of etanercept in treating severe acne and acne conglobata^4,5; our case documents etanercept-induced acne associated with psoriasis treatment. Theoretically, anti–TNF-α agents should suppress acne rather than induce it due to their inhibition of the inflammatory markers TNF-α, IL-1a, and IFN-γ, which are thought to play a role in hypercornification of the infundibulum.⁶ Thus the mechanism of TNF-α antagonists and associated acneform eruptions remains unknown. This observation should prompt further research to investigate the correlation between the use of TNF-α inhibitors, specifically etanercept, and cystic acne.

The National Psoriasis Foundation has relaunched its psoriatic arthritis program to aggressively address the disparities in diagnosis and treatment for psoriatic arthritis patients in the United States.

"There are significantly fewer resources for people with psoriatic arthritis than for those with rheumatoid arthritis," despite similar symptoms and prevalence, according to a press release issued by the foundation June 26.

The National Psoriasis Foundation PsA Project states four goals: Reduce the time to diagnosis of PsA; improve clinician understanding of PsA symptoms, treatment options, and the effect of the disease on quality of life; reduce barriers to treatment; and help patients better manage their disease.

Specifically, the foundation aims to reduce from 4 years to 1 year the average time to diagnosis for PsA patients, reduce from 50% to 30% the percentage of patients who report PsA is a problem in their everyday lives; and double the number of PsA patients receiving proper treatment, the number of National Institutes of Health scientists studying psoriatic disease, and the health resources available for PsA patients.

hsplete@frontlinemedcom.com

The National Psoriasis Foundation has relaunched its psoriatic arthritis program to aggressively address the disparities in diagnosis and treatment for psoriatic arthritis patients in the United States.

"There are significantly fewer resources for people with psoriatic arthritis than for those with rheumatoid arthritis," despite similar symptoms and prevalence, according to a press release issued by the foundation June 26.

The National Psoriasis Foundation PsA Project states four goals: Reduce the time to diagnosis of PsA; improve clinician understanding of PsA symptoms, treatment options, and the effect of the disease on quality of life; reduce barriers to treatment; and help patients better manage their disease.

Specifically, the foundation aims to reduce from 4 years to 1 year the average time to diagnosis for PsA patients, reduce from 50% to 30% the percentage of patients who report PsA is a problem in their everyday lives; and double the number of PsA patients receiving proper treatment, the number of National Institutes of Health scientists studying psoriatic disease, and the health resources available for PsA patients.

hsplete@frontlinemedcom.com

The National Psoriasis Foundation has relaunched its psoriatic arthritis program to aggressively address the disparities in diagnosis and treatment for psoriatic arthritis patients in the United States.

"There are significantly fewer resources for people with psoriatic arthritis than for those with rheumatoid arthritis," despite similar symptoms and prevalence, according to a press release issued by the foundation June 26.

The National Psoriasis Foundation PsA Project states four goals: Reduce the time to diagnosis of PsA; improve clinician understanding of PsA symptoms, treatment options, and the effect of the disease on quality of life; reduce barriers to treatment; and help patients better manage their disease.

Specifically, the foundation aims to reduce from 4 years to 1 year the average time to diagnosis for PsA patients, reduce from 50% to 30% the percentage of patients who report PsA is a problem in their everyday lives; and double the number of PsA patients receiving proper treatment, the number of National Institutes of Health scientists studying psoriatic disease, and the health resources available for PsA patients.

hsplete@frontlinemedcom.com

Median starting doses of infliximab in psoriatic arthritis patients in two nationwide registries were below the recommended dose of 5 mg/kg every 8 weeks, but outcomes suggest that a low starting dose with subsequent step-up is an effective treatment strategy, according to an observational cohort study based on the registries.

In 376 Danish patients in the Danish Rheumatologic Database (DANBIO) registry and 86 Icelandic patients in the Center for Rheumatology Research (ICEBIO) registry, starting infliximab doses were less than 3 mg/kg in 29% and 74%, respectively, 3-5 mg/kg in 42% and 27%, respectively, and greater than 5 mg/kg in 10% and 0%, respectively (starting doses in the remaining patients were not registered). In those cohorts, median starting doses were 3.1 mg/kg and 2.3 mg/kg, respectively, Dr. Bente Glintborg of the Copenhagen Center for Arthritis Research and Glostrup (Denmark) Hospital and her colleagues reported (Rheumatology 2014 June 17 [doi:10.1093/rheumatology/keu252]).

Treatment was maintained after 12 months in 58% and 66% of the Danish and Icelandic patients, respectively (and was highest in those taking concomitant methotrexate). At 12 months, the median doses were 3.3 and 2.9 mg/kg, respectively, and time until dose escalation, response rates, drug survival, and disease activity at 12 months did not differ based on starting dose. Dosing was sustained at below the recommended level in more than 70% of the patients, the investigators found.

Recommended starting doses of infliximab are higher for psoriatic arthritis than for rheumatoid arthritis (5 mg/kg vs. 3 mg/kg) based on randomized trial data, but data on the effectiveness of lower doses are lacking. The current findings suggest that the approach often used in RA – a lower starting dose with gradual escalation – is also effective in psoriatic arthritis, they concluded.

Dr. Glintborg reported having no disclosures. Other study authors reported receiving research grants, serving on a speakers’ bureau, providing consultancy, or serving as an adviser or investigator to a variety of manufacturers of biologic drugs.

Median starting doses of infliximab in psoriatic arthritis patients in two nationwide registries were below the recommended dose of 5 mg/kg every 8 weeks, but outcomes suggest that a low starting dose with subsequent step-up is an effective treatment strategy, according to an observational cohort study based on the registries.

In 376 Danish patients in the Danish Rheumatologic Database (DANBIO) registry and 86 Icelandic patients in the Center for Rheumatology Research (ICEBIO) registry, starting infliximab doses were less than 3 mg/kg in 29% and 74%, respectively, 3-5 mg/kg in 42% and 27%, respectively, and greater than 5 mg/kg in 10% and 0%, respectively (starting doses in the remaining patients were not registered). In those cohorts, median starting doses were 3.1 mg/kg and 2.3 mg/kg, respectively, Dr. Bente Glintborg of the Copenhagen Center for Arthritis Research and Glostrup (Denmark) Hospital and her colleagues reported (Rheumatology 2014 June 17 [doi:10.1093/rheumatology/keu252]).

Treatment was maintained after 12 months in 58% and 66% of the Danish and Icelandic patients, respectively (and was highest in those taking concomitant methotrexate). At 12 months, the median doses were 3.3 and 2.9 mg/kg, respectively, and time until dose escalation, response rates, drug survival, and disease activity at 12 months did not differ based on starting dose. Dosing was sustained at below the recommended level in more than 70% of the patients, the investigators found.

Recommended starting doses of infliximab are higher for psoriatic arthritis than for rheumatoid arthritis (5 mg/kg vs. 3 mg/kg) based on randomized trial data, but data on the effectiveness of lower doses are lacking. The current findings suggest that the approach often used in RA – a lower starting dose with gradual escalation – is also effective in psoriatic arthritis, they concluded.

Dr. Glintborg reported having no disclosures. Other study authors reported receiving research grants, serving on a speakers’ bureau, providing consultancy, or serving as an adviser or investigator to a variety of manufacturers of biologic drugs.

Median starting doses of infliximab in psoriatic arthritis patients in two nationwide registries were below the recommended dose of 5 mg/kg every 8 weeks, but outcomes suggest that a low starting dose with subsequent step-up is an effective treatment strategy, according to an observational cohort study based on the registries.

In 376 Danish patients in the Danish Rheumatologic Database (DANBIO) registry and 86 Icelandic patients in the Center for Rheumatology Research (ICEBIO) registry, starting infliximab doses were less than 3 mg/kg in 29% and 74%, respectively, 3-5 mg/kg in 42% and 27%, respectively, and greater than 5 mg/kg in 10% and 0%, respectively (starting doses in the remaining patients were not registered). In those cohorts, median starting doses were 3.1 mg/kg and 2.3 mg/kg, respectively, Dr. Bente Glintborg of the Copenhagen Center for Arthritis Research and Glostrup (Denmark) Hospital and her colleagues reported (Rheumatology 2014 June 17 [doi:10.1093/rheumatology/keu252]).

Treatment was maintained after 12 months in 58% and 66% of the Danish and Icelandic patients, respectively (and was highest in those taking concomitant methotrexate). At 12 months, the median doses were 3.3 and 2.9 mg/kg, respectively, and time until dose escalation, response rates, drug survival, and disease activity at 12 months did not differ based on starting dose. Dosing was sustained at below the recommended level in more than 70% of the patients, the investigators found.

Recommended starting doses of infliximab are higher for psoriatic arthritis than for rheumatoid arthritis (5 mg/kg vs. 3 mg/kg) based on randomized trial data, but data on the effectiveness of lower doses are lacking. The current findings suggest that the approach often used in RA – a lower starting dose with gradual escalation – is also effective in psoriatic arthritis, they concluded.

Dr. Glintborg reported having no disclosures. Other study authors reported receiving research grants, serving on a speakers’ bureau, providing consultancy, or serving as an adviser or investigator to a variety of manufacturers of biologic drugs.

The tumor necrosis factor–alpha antagonists infliximab, adalimumab, and certolizumab did not raise the risk of cancer in a nationwide Danish cohort study of patients with inflammatory bowel disease who were followed for approximately 10 years, according to a report published online June 17 in JAMA.

At present, the effectiveness of these agents in inflammatory bowel disease (IBD) must be weighed against their potential adverse effects, which include immunosuppression that is suspected to increase the risk of cancer. But few studies have examined this risk, and those that have done so have had short (less than 1 year) exposure and follow-up times, said Dr. Nynne Nyboe Andersen of the department of epidemiology research, Statens Serum Institut, Copenhagen, and her associates.

They assessed the risks of any cancer and of 11 individual cancers in 56,146 IBD patients aged 15 and older living in Denmark in 1999-2012, of whom 4,553 took TNF-alpha antagonists. Median follow-up was 9.3 years, and median duration of therapy with TNF-alpha antagonists was 3.7 years. The two study groups were propensity matched for year of birth, sex, socioeconomic status, comorbidities, use of other medications, subtype of IBD, and history of gastrointestinal or anal fistula, abscess, fissure, or surgery.

A total of 6.7% of the patients who never took TNF-alpha antagonists developed cancer during follow-up, compared with 1.8% of patients who took the drugs, indicating no increase in cancer risk associated with TNF-alpha antagonists. Further analyses of the data found no association between use of these agents and the risk of overall cancer, regardless of the patient’s sex, age, the duration of therapy, or the cumulative dose, and sensitivity analyses confirmed these results, the investigators said (JAMA 2014 June 17 [doi:10.1001/jama.2014.5613]).

There also was no association between use of TNF-alpha antagonists and any individual cancer. "However, it should be noted that because of the relatively small sample size and the small number of cancer cases in our study, statistical power was limited in subgroup analyses of site-specific cancers," Dr. Andersen and her associates said.

"Stratifying for cancer risk according to years since first exposure, no specific time-dependent pattern was observed in our study. However, considering the often protracted progression of cancer, an increased risk in the long term cannot be excluded, and future studies with longer follow-up are needed," they added.

The Lundbeck Foundation, Danish Cancer Society, Crohn’s and Colitis Association of Denmark, and Danish Council of Independent Research supported the study. Dr. Andersen reported receiving funding from Merck Sharp & Dohme; her associates reported ties to Merck Sharp & Dohme, Tillotts, Calpro, Ferring, and AbbVie.

The tumor necrosis factor–alpha antagonists infliximab, adalimumab, and certolizumab did not raise the risk of cancer in a nationwide Danish cohort study of patients with inflammatory bowel disease who were followed for approximately 10 years, according to a report published online June 17 in JAMA.

At present, the effectiveness of these agents in inflammatory bowel disease (IBD) must be weighed against their potential adverse effects, which include immunosuppression that is suspected to increase the risk of cancer. But few studies have examined this risk, and those that have done so have had short (less than 1 year) exposure and follow-up times, said Dr. Nynne Nyboe Andersen of the department of epidemiology research, Statens Serum Institut, Copenhagen, and her associates.

They assessed the risks of any cancer and of 11 individual cancers in 56,146 IBD patients aged 15 and older living in Denmark in 1999-2012, of whom 4,553 took TNF-alpha antagonists. Median follow-up was 9.3 years, and median duration of therapy with TNF-alpha antagonists was 3.7 years. The two study groups were propensity matched for year of birth, sex, socioeconomic status, comorbidities, use of other medications, subtype of IBD, and history of gastrointestinal or anal fistula, abscess, fissure, or surgery.

A total of 6.7% of the patients who never took TNF-alpha antagonists developed cancer during follow-up, compared with 1.8% of patients who took the drugs, indicating no increase in cancer risk associated with TNF-alpha antagonists. Further analyses of the data found no association between use of these agents and the risk of overall cancer, regardless of the patient’s sex, age, the duration of therapy, or the cumulative dose, and sensitivity analyses confirmed these results, the investigators said (JAMA 2014 June 17 [doi:10.1001/jama.2014.5613]).

There also was no association between use of TNF-alpha antagonists and any individual cancer. "However, it should be noted that because of the relatively small sample size and the small number of cancer cases in our study, statistical power was limited in subgroup analyses of site-specific cancers," Dr. Andersen and her associates said.

"Stratifying for cancer risk according to years since first exposure, no specific time-dependent pattern was observed in our study. However, considering the often protracted progression of cancer, an increased risk in the long term cannot be excluded, and future studies with longer follow-up are needed," they added.

The Lundbeck Foundation, Danish Cancer Society, Crohn’s and Colitis Association of Denmark, and Danish Council of Independent Research supported the study. Dr. Andersen reported receiving funding from Merck Sharp & Dohme; her associates reported ties to Merck Sharp & Dohme, Tillotts, Calpro, Ferring, and AbbVie.

The tumor necrosis factor–alpha antagonists infliximab, adalimumab, and certolizumab did not raise the risk of cancer in a nationwide Danish cohort study of patients with inflammatory bowel disease who were followed for approximately 10 years, according to a report published online June 17 in JAMA.

At present, the effectiveness of these agents in inflammatory bowel disease (IBD) must be weighed against their potential adverse effects, which include immunosuppression that is suspected to increase the risk of cancer. But few studies have examined this risk, and those that have done so have had short (less than 1 year) exposure and follow-up times, said Dr. Nynne Nyboe Andersen of the department of epidemiology research, Statens Serum Institut, Copenhagen, and her associates.

They assessed the risks of any cancer and of 11 individual cancers in 56,146 IBD patients aged 15 and older living in Denmark in 1999-2012, of whom 4,553 took TNF-alpha antagonists. Median follow-up was 9.3 years, and median duration of therapy with TNF-alpha antagonists was 3.7 years. The two study groups were propensity matched for year of birth, sex, socioeconomic status, comorbidities, use of other medications, subtype of IBD, and history of gastrointestinal or anal fistula, abscess, fissure, or surgery.

A total of 6.7% of the patients who never took TNF-alpha antagonists developed cancer during follow-up, compared with 1.8% of patients who took the drugs, indicating no increase in cancer risk associated with TNF-alpha antagonists. Further analyses of the data found no association between use of these agents and the risk of overall cancer, regardless of the patient’s sex, age, the duration of therapy, or the cumulative dose, and sensitivity analyses confirmed these results, the investigators said (JAMA 2014 June 17 [doi:10.1001/jama.2014.5613]).

There also was no association between use of TNF-alpha antagonists and any individual cancer. "However, it should be noted that because of the relatively small sample size and the small number of cancer cases in our study, statistical power was limited in subgroup analyses of site-specific cancers," Dr. Andersen and her associates said.

"Stratifying for cancer risk according to years since first exposure, no specific time-dependent pattern was observed in our study. However, considering the often protracted progression of cancer, an increased risk in the long term cannot be excluded, and future studies with longer follow-up are needed," they added.

The Lundbeck Foundation, Danish Cancer Society, Crohn’s and Colitis Association of Denmark, and Danish Council of Independent Research supported the study. Dr. Andersen reported receiving funding from Merck Sharp & Dohme; her associates reported ties to Merck Sharp & Dohme, Tillotts, Calpro, Ferring, and AbbVie.

Thanks to anti–tumor necrosis factor inhibitors and other highly effective biologic therapies, rheumatologists are increasingly embracing treat to target, a strategy in which patients are closely monitored and medications adjusted until a patient has the least disease activity possible.

Ample evidence from randomized, controlled trials has shown treat to target – sometimes referred to as tight control – to result in better outcomes than standard therapy in rheumatoid arthritis patients.

But in psoriatic arthritis (PsA), a more heterogeneous disorder with skin and nail manifestations as well as joint and connective tissue involvement, remission has historically been less well defined. Only in recent years have endpoints been developed and validated for minimal disease activity in PsA, and evidence in support of a treat-to-target approach is now slowly trickling in.

Mary Jo M. Dales/Frontline Medical News

At the annual European Congress of Rheumatology, Dr. Arthur Kavanaugh of the University of California, San Diego, presented results from a 5-year extension of a randomized, controlled trial of golimumab in patients with PsA that showed better long-term outcomes in those able to achieve minimal disease activity (MDA) through a treat-to-target strategy.

"I think [the study] does provide some evidence suggesting that treat to target could well be a valuable goal for PsA, Dr. Kavanaugh said. "Right now, RA has the advantage of more studies showing this."

Dr. Kavanaugh and his colleagues’ study used data from an open-label extension of a clinical trial in which about 400 patients were randomized to receive golimumab at 50 mg or 100 mg, or placebo; all placebo patients were crossed over to golimumab treatment at 24 weeks and during the long-term, open-label extension of the trial, were followed for as long as 252 weeks. Patients were assessed at 14, 24, and 52 weeks, then yearly until week 252. The investigators used a validated composite endpoint that included measures of skin, joint, and enthesis involvement.

About half of the patients (44.2% of those randomized to placebo and 51.7% of those randomized to active treatment) achieved persistent MDA over three or more consecutive time points during follow-up, and investigators saw significantly better clinically meaningful Health Assessment Questionnaire improvement and less radiographic progression in patients who had achieved MDA, regardless of treatment allocation.

Patients who achieved MDA after crossing over had improvements that were similar to those who started on golimumab at baseline, suggesting that delayed treatment initiation does not result in a worsening of physical function or radiographic progression.

"When it comes to patients, we cannot always control when we will see them in the course of disease," Dr. Kavanaugh said. "These data suggest that even though a patient may show up with months of uncontrolled disease, it is still a viable goal to treat them to try to get MDA."

Dr. Kavanaugh said that further studies in PsA patients were needed to confirm that treat-to-target strategies resulted in better long-term disease outcomes. "As always in medicine, it is important to have verification from multiple studies. It would be helpful to have data from studies using medications with other mechanisms of action to support treat to target," he added.

Dr. Kavanaugh disclosed research and grant support from Abbott, Amgen, Janssen, and UCB. His coauthors on the study disclosed financial support from additional manufacturers, and three were employees of Janssen.

Thanks to anti–tumor necrosis factor inhibitors and other highly effective biologic therapies, rheumatologists are increasingly embracing treat to target, a strategy in which patients are closely monitored and medications adjusted until a patient has the least disease activity possible.

Ample evidence from randomized, controlled trials has shown treat to target – sometimes referred to as tight control – to result in better outcomes than standard therapy in rheumatoid arthritis patients.

But in psoriatic arthritis (PsA), a more heterogeneous disorder with skin and nail manifestations as well as joint and connective tissue involvement, remission has historically been less well defined. Only in recent years have endpoints been developed and validated for minimal disease activity in PsA, and evidence in support of a treat-to-target approach is now slowly trickling in.

Mary Jo M. Dales/Frontline Medical News

At the annual European Congress of Rheumatology, Dr. Arthur Kavanaugh of the University of California, San Diego, presented results from a 5-year extension of a randomized, controlled trial of golimumab in patients with PsA that showed better long-term outcomes in those able to achieve minimal disease activity (MDA) through a treat-to-target strategy.

"I think [the study] does provide some evidence suggesting that treat to target could well be a valuable goal for PsA, Dr. Kavanaugh said. "Right now, RA has the advantage of more studies showing this."

Dr. Kavanaugh and his colleagues’ study used data from an open-label extension of a clinical trial in which about 400 patients were randomized to receive golimumab at 50 mg or 100 mg, or placebo; all placebo patients were crossed over to golimumab treatment at 24 weeks and during the long-term, open-label extension of the trial, were followed for as long as 252 weeks. Patients were assessed at 14, 24, and 52 weeks, then yearly until week 252. The investigators used a validated composite endpoint that included measures of skin, joint, and enthesis involvement.

About half of the patients (44.2% of those randomized to placebo and 51.7% of those randomized to active treatment) achieved persistent MDA over three or more consecutive time points during follow-up, and investigators saw significantly better clinically meaningful Health Assessment Questionnaire improvement and less radiographic progression in patients who had achieved MDA, regardless of treatment allocation.

Patients who achieved MDA after crossing over had improvements that were similar to those who started on golimumab at baseline, suggesting that delayed treatment initiation does not result in a worsening of physical function or radiographic progression.

"When it comes to patients, we cannot always control when we will see them in the course of disease," Dr. Kavanaugh said. "These data suggest that even though a patient may show up with months of uncontrolled disease, it is still a viable goal to treat them to try to get MDA."

Dr. Kavanaugh said that further studies in PsA patients were needed to confirm that treat-to-target strategies resulted in better long-term disease outcomes. "As always in medicine, it is important to have verification from multiple studies. It would be helpful to have data from studies using medications with other mechanisms of action to support treat to target," he added.

Dr. Kavanaugh disclosed research and grant support from Abbott, Amgen, Janssen, and UCB. His coauthors on the study disclosed financial support from additional manufacturers, and three were employees of Janssen.

Thanks to anti–tumor necrosis factor inhibitors and other highly effective biologic therapies, rheumatologists are increasingly embracing treat to target, a strategy in which patients are closely monitored and medications adjusted until a patient has the least disease activity possible.

Ample evidence from randomized, controlled trials has shown treat to target – sometimes referred to as tight control – to result in better outcomes than standard therapy in rheumatoid arthritis patients.

But in psoriatic arthritis (PsA), a more heterogeneous disorder with skin and nail manifestations as well as joint and connective tissue involvement, remission has historically been less well defined. Only in recent years have endpoints been developed and validated for minimal disease activity in PsA, and evidence in support of a treat-to-target approach is now slowly trickling in.

Mary Jo M. Dales/Frontline Medical News

At the annual European Congress of Rheumatology, Dr. Arthur Kavanaugh of the University of California, San Diego, presented results from a 5-year extension of a randomized, controlled trial of golimumab in patients with PsA that showed better long-term outcomes in those able to achieve minimal disease activity (MDA) through a treat-to-target strategy.

"I think [the study] does provide some evidence suggesting that treat to target could well be a valuable goal for PsA, Dr. Kavanaugh said. "Right now, RA has the advantage of more studies showing this."

Dr. Kavanaugh and his colleagues’ study used data from an open-label extension of a clinical trial in which about 400 patients were randomized to receive golimumab at 50 mg or 100 mg, or placebo; all placebo patients were crossed over to golimumab treatment at 24 weeks and during the long-term, open-label extension of the trial, were followed for as long as 252 weeks. Patients were assessed at 14, 24, and 52 weeks, then yearly until week 252. The investigators used a validated composite endpoint that included measures of skin, joint, and enthesis involvement.

About half of the patients (44.2% of those randomized to placebo and 51.7% of those randomized to active treatment) achieved persistent MDA over three or more consecutive time points during follow-up, and investigators saw significantly better clinically meaningful Health Assessment Questionnaire improvement and less radiographic progression in patients who had achieved MDA, regardless of treatment allocation.

Patients who achieved MDA after crossing over had improvements that were similar to those who started on golimumab at baseline, suggesting that delayed treatment initiation does not result in a worsening of physical function or radiographic progression.

"When it comes to patients, we cannot always control when we will see them in the course of disease," Dr. Kavanaugh said. "These data suggest that even though a patient may show up with months of uncontrolled disease, it is still a viable goal to treat them to try to get MDA."

Dr. Kavanaugh said that further studies in PsA patients were needed to confirm that treat-to-target strategies resulted in better long-term disease outcomes. "As always in medicine, it is important to have verification from multiple studies. It would be helpful to have data from studies using medications with other mechanisms of action to support treat to target," he added.

Dr. Kavanaugh disclosed research and grant support from Abbott, Amgen, Janssen, and UCB. His coauthors on the study disclosed financial support from additional manufacturers, and three were employees of Janssen.

Psoriatic arthritis patients treated with brodalumab improved by approximately 20%, compared with those on placebo, achieving the primary endpoint in a phase II trial, investigators reported online June 11 in the New England Journal of Medicine.

Brodalumab is a human monoclonal antibody targeting the interleukin-17 receptor A (IL-17RA). At week 12 of the 40-week randomized trial, 37%-39% of brodalumab patients had improved by at least 20% based on the American College of Rheumatology response criteria (ACR 20), compared with only 18% of the placebo patients (P = .03 and .02, respectively), reported Dr. Philip J. Mease of the Swedish Medical Center and the University of Washington, both in Seattle, and his associates.

Rates of 50% improvement in response criteria, or ACR 50, also exceeded placebo in both treatment arms (14%, compared with 4% for placebo; P = .05).

The researchers randomized 168 adults with psoriatic arthritis, of whom 159 finished the double-blind phase and 134 completed 40 weeks of the open-label extension (N. Engl. J. Med. 2014;370:2295-306 [doi: 10.1056/NEJMoa1315231]). By week 24, ACR 20 response rates were 51% for the 140-mg group, 64% for the 280-mg group, and 44% in placebo patients who switched to open-label brodalumab, said the researchers. Patients improved similarly whether they were treatment naive or had received previous biologic therapy, the investigators added.

Adverse events were comparable between the treatment and placebo groups, with no opportunistic infections or deaths, the investigators reported. Two patients tested positive for antibodies to brodalumab. "No significant neutropenic events were reported – an important safety outcome, since interleukin-17 is involved in neutrophil homeostasis," the researchers said. They noted, however, that larger trials would be needed to detect rare adverse events.

Amgen, a maker of brodalumab, funded the study. Dr. Mease and his coauthors reported employment with or receiving grants from Amgen.

The study findings also were scheduled for presentation in a poster at EULAR 2014.

Psoriatic arthritis patients treated with brodalumab improved by approximately 20%, compared with those on placebo, achieving the primary endpoint in a phase II trial, investigators reported online June 11 in the New England Journal of Medicine.

Brodalumab is a human monoclonal antibody targeting the interleukin-17 receptor A (IL-17RA). At week 12 of the 40-week randomized trial, 37%-39% of brodalumab patients had improved by at least 20% based on the American College of Rheumatology response criteria (ACR 20), compared with only 18% of the placebo patients (P = .03 and .02, respectively), reported Dr. Philip J. Mease of the Swedish Medical Center and the University of Washington, both in Seattle, and his associates.

Rates of 50% improvement in response criteria, or ACR 50, also exceeded placebo in both treatment arms (14%, compared with 4% for placebo; P = .05).

The researchers randomized 168 adults with psoriatic arthritis, of whom 159 finished the double-blind phase and 134 completed 40 weeks of the open-label extension (N. Engl. J. Med. 2014;370:2295-306 [doi: 10.1056/NEJMoa1315231]). By week 24, ACR 20 response rates were 51% for the 140-mg group, 64% for the 280-mg group, and 44% in placebo patients who switched to open-label brodalumab, said the researchers. Patients improved similarly whether they were treatment naive or had received previous biologic therapy, the investigators added.

Adverse events were comparable between the treatment and placebo groups, with no opportunistic infections or deaths, the investigators reported. Two patients tested positive for antibodies to brodalumab. "No significant neutropenic events were reported – an important safety outcome, since interleukin-17 is involved in neutrophil homeostasis," the researchers said. They noted, however, that larger trials would be needed to detect rare adverse events.

Amgen, a maker of brodalumab, funded the study. Dr. Mease and his coauthors reported employment with or receiving grants from Amgen.

The study findings also were scheduled for presentation in a poster at EULAR 2014.

Psoriatic arthritis patients treated with brodalumab improved by approximately 20%, compared with those on placebo, achieving the primary endpoint in a phase II trial, investigators reported online June 11 in the New England Journal of Medicine.

Brodalumab is a human monoclonal antibody targeting the interleukin-17 receptor A (IL-17RA). At week 12 of the 40-week randomized trial, 37%-39% of brodalumab patients had improved by at least 20% based on the American College of Rheumatology response criteria (ACR 20), compared with only 18% of the placebo patients (P = .03 and .02, respectively), reported Dr. Philip J. Mease of the Swedish Medical Center and the University of Washington, both in Seattle, and his associates.

Rates of 50% improvement in response criteria, or ACR 50, also exceeded placebo in both treatment arms (14%, compared with 4% for placebo; P = .05).

The researchers randomized 168 adults with psoriatic arthritis, of whom 159 finished the double-blind phase and 134 completed 40 weeks of the open-label extension (N. Engl. J. Med. 2014;370:2295-306 [doi: 10.1056/NEJMoa1315231]). By week 24, ACR 20 response rates were 51% for the 140-mg group, 64% for the 280-mg group, and 44% in placebo patients who switched to open-label brodalumab, said the researchers. Patients improved similarly whether they were treatment naive or had received previous biologic therapy, the investigators added.

Adverse events were comparable between the treatment and placebo groups, with no opportunistic infections or deaths, the investigators reported. Two patients tested positive for antibodies to brodalumab. "No significant neutropenic events were reported – an important safety outcome, since interleukin-17 is involved in neutrophil homeostasis," the researchers said. They noted, however, that larger trials would be needed to detect rare adverse events.

Amgen, a maker of brodalumab, funded the study. Dr. Mease and his coauthors reported employment with or receiving grants from Amgen.

The study findings also were scheduled for presentation in a poster at EULAR 2014.