The short answer, in my opinion, is no. Pyoderma gangrenosum is not associated with drug allergy in general or NSAID or indomethacin in particular. Pyoderma gangrenosum is associated with a variety of diseases such as inflammatory bowel disease, autoinflammatory syndrome, pyogenic arthritis and acne, inflammatory arthritis, malignancy, myelodysplasia and polycythemia and monoclonal gammopathies. The differential diagnosis includes lymphoma, halogen induced rash, fungal skin infection, necrobiosis lipoidica with ulceration, factitous ulcer, ischemic ulcer, cutaneous vasculitis and brown recluse spider bite. Anti-inflammatory therapy is utilized for pyoderma gangrenosum but I am unaware of any data that NSAIDs or indomethacin will improve pyoderma gangrenosum.
I hope this information is of some help to you and your practice.
All my best.
Dennis K. Ledford, MD, FAAAAI
Etiology and management of pyoderma gangrenosum: a comprehensive review.
Ahronowitz I, Harp J, Shinkai K
Am J Clin Dermatol. 2012;13(3):191.
Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis characterized by painful, necrotic ulceration. It typically affects patients in the third to sixth decades of life, with almost equal incidence in men and women. PG occurs most frequently on the lower extremities. Five clinical variants are currently recognized: classic, bullous, pustular, vegetative, and peristomal types. Half of PG cases are seen in association with systemic disease. Mimickers include infection, vascular insufficiency ulcers, systemic vasculitides, autoimmune disease, cancer, and exogenous tissue injury, among others. PG is often a diagnosis of exclusion, as there are no specific laboratory or histopathologic findings to confirm the diagnosis. PG thus presents many clinical challenges: it is difficult to diagnose, is frequently misdiagnosed, and often requires a work-up for underlying systemic disease. Successful management of PG typically requires multiple modalities to reduce inflammation and optimize wound healing, in addition to treatment of any underlying diseases. Prednisone and cyclosporine have been mainstays of systemic treatment for PG, although increasing evidence supports the use of biologic therapies, such as tumor necrosis factor-αinhibitors, for refractory cases of PG. Here, we review the clinical presentation and pathophysiology of PG, as well as its associated conditions, diagnostic work-up, and management.