NEW YORK (Reuters Health)—Hidradenitis suppurativa can complicate biologic therapy of chronic inflammatory diseases, according to a retrospective study from France and Belgium.
Hidradenitis suppurativa (HS) often responds to treatment with biologic agents, but there have been scattered reports of patients developing HS while undergoing biologic therapy.
Dr. Coline Faivre from Hôpital Edouard Herriot in Lyon, France, and colleagues in the French Society of Dermatology and Club Rheumatisms and Inflammation describe the characteristics and outcomes of 25 patients who developed HS while receiving biologic agents.
These patients developed HS a median 12 months (range: 1–120 months) after initial exposure to a biologic agent, including adalimumab in 12 cases, infliximab in six cases, etanercept in four cases, rituximab in two cases, and tocilizumab in one case.
In most cases (19 of 25, 76%) the underlying inflammatory disordered was controlled at the time of HS onset, the researchers note in an article online on March 7 in the Journal of the American Academy of Dermatology.
Eleven patients, all of who where receiving anti-TNF-alfa therapy, developed additional inflammatory diseases simultaneously or within one year of HS onset.
HS improved partially or completely after discontinuing or switching the biologic agent in 54% of cases, and complete remission was more common when the agent was discontinued or switched than when it was maintained.
When a biologic agent had to be reintroduced because of the underlying inflammatory disease, HS worsening occurred in one of eight cases where an alternate agent from the same was used and in one of eight cases where an agent of a different class was used.
At last follow-up (median: 18 months), partial or complete remission had been achieved in 14 of 24 patients (58%).
“Most of our patients had HS risk factors (e.g., smoking, overweight), a family history or clinical features (e.g., pilonidal cyst) suggesting a predisposition to HS, or received a BA for an HS-associated inflammatory disease (e.g., Crohn’s disease, spondyloarthropathies),” the researchers note. “Therefore, HS may occur mainly in predisposed patients, or be coincidental and related to the underlying disease.”
For treatment, they say, “We propose the following strategy: 1) In all cases, add specific HS treatment. 2) For mild HS (Hurley I), consider continuing the same biologic agent (BA), namely if there are few alternate molecules, and switch only upon worsening or lack of improvement. 3) For moderate to severe disease (Hurley II or III), consider discontinuing the BA and switching to an alternate BA, including one of the same class. When needed, pursuing the same BA may still achieve partial remission or stable disease. 4) Refrain from reintroducing the culprit BA even after a long period of time. These suggestions should be considered cautiously because they rely on a rather small sample size.”