Sarcoidosis During Therapy With Adalimumab in a Crohn’s Disease Patient: Consequence of the Therapy or Association With the Disease Itself?

Biological therapy represented an advance in the management of granulomatous and rheumatologic conditions. Adalimumab (ADA) is approved for the management of Crohn’s disease (CD) since 2007, and the experience with its safety profile and possible adverse events is expanding over the last years. Induced sarcoidosis due to anti-TNF therapy is described in some patients with rheumatologic and skin conditions. There are only two reported CD patients who developed sarcoidosis after anti-TNF initiation, one with Infliximab and another one with Natalizumab. The aim of this report is to present one of the first described CD patients with the diagnosis of sarcoidosis during ADA therapy, with emphasis on the differential diagnosis with hepatosplenic T-cell lymphoma and on the obscure relation between CD and this condition. Short report with detailed clinical description of a young CD patient who developed sarcoidosis during therapy with ADA. This is the case of a 25 year-old female with diagnosis of ileocolic CD for 18 months (Montreal classification A2L3B3). She first came to our unit after 8 months of medical therapy with ADA, Azathioprine (AZA) and steroids, and presented with an abdominal abscess secondary to fistulizing abdominal CD. She was submitted to laparotomy, ileocolic resection and retroperitoneal abscess drainage, without further complications. Prevention of postoperative recurrence with ADA and AZA was maintained, and a colonoscopy 6 months after surgery revealed endoscopic recurrence. Ten months after surgery, she presented with subacute cough and respiratory symptoms. Further investigation with CT-scan revealed bilateral nodules on the mediastinum with perihilar infiltrate, as well as multiple nodules on the spleen. A hypothesis of hepatosplenic T-cell lymphoma was made. A mediastinoscopy with biopsy of the nodes was performed, and histology demonstrated clear pattern of sarcoidosis, with no lymphoproliferative characteristics. After discussion with the pneumology department, AZA therapy was interrupted and biological treatment with ADA was maintained under strict supervision. Oral prednisolone was initiated and the patient improved. She is still in monotherapy with ADA as steroids were withdrawn after 3 months, and persisted asymptomatic. The correct mechanism that explains the occurrence of sarcoidosis in CD patients is not clear. It can be related to anti-TNF therapy or even to an association between these two conditions that can be explained due to immunological basis (paradoxical effect). The resolution of the signs and symptoms of sarcoidosis after anti-TNF interruption could elucidate the causative factor of the drug. In the present report, the decision regarding the maintenance of ADA was difficult, and supported by the literature in some reported cases with other conditions. The risk of severe recurrence and further need for surgery in a young patient with worse prognostic features led to this treatment issues. Multidisciplinary and individualized decisions are advised in complex cases as this.

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