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WASHINGTON —The use of anti-tumor necrosis factor-α (TNF-α) agents in patients with rheumatoid arthritis is associated with an increased risk for the development of palmoplantar psoriasis, Dr. Jacob A. Aelion reported at the annual meeting of the American College of Rheumatology.
There have been sporadic reports in the literature of psoriasiform skin lesions occurring after the initiation of anti-TNF-α therapy, but it has not been determined whether it is the therapy itself that increases the risk.
In a cohort of 1,195 patients with rheumatoid arthritis who were receiving methotrexate plus etanercept, adalimumab, or infliximab and 788 patients who were receiving methotrexate monotherapy between 1999 and 2005, seven cases of psoriasis developed, all in the group of patients receiving the anti-TNF-α agents, Dr. Aelion reported in a poster session.
None of these patients who developed psoriasis had a family history of the condition, and skin involvement was limited to the palms and/or soles in all seven patients.
The affected patients all were female. Two were receiving infliximab, two were receiving etanercept, and three were being treated with adalimumab.
Withdrawal of the anti-TNF-α therapy resulted in regression or resolution in three, and in two of these, relapse occurred when infliximab was restarted, wrote Dr. Aelion of the Arthritis Clinic, Jackson, Tenn.
The development of psoriasis was not limited to a single anti-TNF-α agent, but rather seemed to be a class effect of TNF blockade itself.
“This finding is surprising since TNF-α inhibitors have been used successfully in the treatment of psoriasis and psoriatic arthritis,” he wrote.
The pathogenic means by which this distinct adverse effect of TNF-α inhibition occurs in rheumatoid arthritis patients remain obscure.
“A possible explanation resides in the dual immunologic role of TNF-α. Besides its role as a proinflammatory cytokine, TNF-α is also known to exert an immunosuppressive effect by regulating antigen-presenting cell functions and apoptosis of potentially autoreactive T cells,” he continued.
Thus, blocking TNF-α may result in the unmasking of other autoimmune disorders in susceptible patients.
Nonetheless, these findings should not discourage the use of this class of drugs in patients with rheumatoid arthritis, in whom the overall benefits greatly outweigh the risks of the development of skin disorders, Dr. Aelion concluded at the meeting.
WASHINGTON —The use of anti-tumor necrosis factor-α (TNF-α) agents in patients with rheumatoid arthritis is associated with an increased risk for the development of palmoplantar psoriasis, Dr. Jacob A. Aelion reported at the annual meeting of the American College of Rheumatology.
There have been sporadic reports in the literature of psoriasiform skin lesions occurring after the initiation of anti-TNF-α therapy, but it has not been determined whether it is the therapy itself that increases the risk.
In a cohort of 1,195 patients with rheumatoid arthritis who were receiving methotrexate plus etanercept, adalimumab, or infliximab and 788 patients who were receiving methotrexate monotherapy between 1999 and 2005, seven cases of psoriasis developed, all in the group of patients receiving the anti-TNF-α agents, Dr. Aelion reported in a poster session.
None of these patients who developed psoriasis had a family history of the condition, and skin involvement was limited to the palms and/or soles in all seven patients.
The affected patients all were female. Two were receiving infliximab, two were receiving etanercept, and three were being treated with adalimumab.
Withdrawal of the anti-TNF-α therapy resulted in regression or resolution in three, and in two of these, relapse occurred when infliximab was restarted, wrote Dr. Aelion of the Arthritis Clinic, Jackson, Tenn.
The development of psoriasis was not limited to a single anti-TNF-α agent, but rather seemed to be a class effect of TNF blockade itself.
“This finding is surprising since TNF-α inhibitors have been used successfully in the treatment of psoriasis and psoriatic arthritis,” he wrote.
The pathogenic means by which this distinct adverse effect of TNF-α inhibition occurs in rheumatoid arthritis patients remain obscure.
“A possible explanation resides in the dual immunologic role of TNF-α. Besides its role as a proinflammatory cytokine, TNF-α is also known to exert an immunosuppressive effect by regulating antigen-presenting cell functions and apoptosis of potentially autoreactive T cells,” he continued.
Thus, blocking TNF-α may result in the unmasking of other autoimmune disorders in susceptible patients.
Nonetheless, these findings should not discourage the use of this class of drugs in patients with rheumatoid arthritis, in whom the overall benefits greatly outweigh the risks of the development of skin disorders, Dr. Aelion concluded at the meeting.
WASHINGTON —The use of anti-tumor necrosis factor-α (TNF-α) agents in patients with rheumatoid arthritis is associated with an increased risk for the development of palmoplantar psoriasis, Dr. Jacob A. Aelion reported at the annual meeting of the American College of Rheumatology.
There have been sporadic reports in the literature of psoriasiform skin lesions occurring after the initiation of anti-TNF-α therapy, but it has not been determined whether it is the therapy itself that increases the risk.
In a cohort of 1,195 patients with rheumatoid arthritis who were receiving methotrexate plus etanercept, adalimumab, or infliximab and 788 patients who were receiving methotrexate monotherapy between 1999 and 2005, seven cases of psoriasis developed, all in the group of patients receiving the anti-TNF-α agents, Dr. Aelion reported in a poster session.
None of these patients who developed psoriasis had a family history of the condition, and skin involvement was limited to the palms and/or soles in all seven patients.
The affected patients all were female. Two were receiving infliximab, two were receiving etanercept, and three were being treated with adalimumab.
Withdrawal of the anti-TNF-α therapy resulted in regression or resolution in three, and in two of these, relapse occurred when infliximab was restarted, wrote Dr. Aelion of the Arthritis Clinic, Jackson, Tenn.
The development of psoriasis was not limited to a single anti-TNF-α agent, but rather seemed to be a class effect of TNF blockade itself.
“This finding is surprising since TNF-α inhibitors have been used successfully in the treatment of psoriasis and psoriatic arthritis,” he wrote.
The pathogenic means by which this distinct adverse effect of TNF-α inhibition occurs in rheumatoid arthritis patients remain obscure.
“A possible explanation resides in the dual immunologic role of TNF-α. Besides its role as a proinflammatory cytokine, TNF-α is also known to exert an immunosuppressive effect by regulating antigen-presenting cell functions and apoptosis of potentially autoreactive T cells,” he continued.
Thus, blocking TNF-α may result in the unmasking of other autoimmune disorders in susceptible patients.
Nonetheless, these findings should not discourage the use of this class of drugs in patients with rheumatoid arthritis, in whom the overall benefits greatly outweigh the risks of the development of skin disorders, Dr. Aelion concluded at the meeting.