Abstract
Background/Aims
In the recent years, the outlook of management of chronic inflammatory conditions have been promising with the introduction of biological therapies. With the patent protection of original biological drugs expires, biosimilar agents are introduced in replacement of the originators, though true clinical effectiveness remains debatable. As the rare side effect profiles of the originators are slowly emerging, these occurrences are yet to be observed in the biosimilars. We present the first case reported in the literature of pyoderma gangrenosum(PG) induced by Amgevita in a seropositive rheumatoid arthritis patient.
Methods
A 48-year-old gentleman had a long-standing history of seropositive rheumatoid arthritis, was commenced on Amgevita 40mg every other day in addition to his current regime of methotrexate and hydroxychloroquine in order to have better control of his disease acitivity. After 2 doses of Amgevita, he developed multiple blisters and ulcers on both of hands and the back of his neck. He denied any systemic illness and no new medication except Amgevita was initiated. He was referred urgently to the dermatologist which revealed on the dorsal aspect of hands several ulcers with fresh granulation and asymmetric border. Repeat immunology tests including vasculitis screen and bullous pemphigoid antibodies were negative. Blood and urine porphyrin screen came back negative. As skin biopsy’s findings were non-specific and inconclusive, treatment with Amgevita was reintroduced. Unfortunately, after a single dose of Amgevita, this patient developed similar ulcerations in the same distribution as previous. Amgevita was ceased immediately and patient was started a short course of steroid, which has led to complete resolution of the ulcers.
Results
Following his second presentation, it was concluded that the cause for his dermatological manifestation was Amgevita. Second opinion from the dermatologists and pathologist was sought and a diagnosis of pyoderma gangrenosum induced by Amgevita was finally made. Though patient’s skin lesions recovered after the withdrawal of Amgevita, he experienced severe flares of his joints. It was clear that he required another agent to help with his disease activity. The decision to initiate Benepali, another anti-TNF agent was made and the patient had managed to tolerate it well without any side effect.
Conclusion
Several recent studies have shown good therapeutic outcomes in patients with pyoderma gangrenosum treated with anti-TNF α antagonists, particularly in refractory cases. As our case proves that Amgevita can precipitate the manifestation of PG, this is suggestive that the anti-TNF α antagonist may have double-edged properties. There were very few reported cases of pyoderma gangrenosum linked to Humira, but no case of pyoderma gangrenosum induced by adalimumab-atto was known. This case highlights the paradoxical effect of anti-TNF α antagonists in PG and recognition of this association will allow the clinicians to withdraw the causative drugs promptly.
Disclosure
Y. Tan: None. S. Kavaklieva: None. F. Wood: None.
Sweet’s Syndrome in a Patient With Seropositive Rheumatoid Arthritis After Starting Adalimumab: Is Sweet’s Syndrome Related to Rheumatoid Arthritis or Is It the Paradoxical Effect of Adalimumab?
