RESUMEN
Abrikossoff tumor, also called granular cell tumor (GCT), is a neoplasm of the soft tissues which is most commonly a solitary, painless, and benign tumor. However, 2% of Abrikossoff tumors can be malignant. We report here the case of a 75-year-old male who presented a local recurrence of Abrikossoff tumor of the left thigh. The anatomopathological analysis concluded to a malignant GCT, and the F-18 fluorodeoxyglucose positron emission tomography showed multiple lesions in the lymph nodes and bones. The potential conversion to malignancy should alert practitioners because of the extremely poor prognosis. The diagnosis of malignant granular cell tumor should be based on a bundle of clinical and histological features and not solely on histologic features because of the challenging distinction between malignant and benign tumors due to the lack of well-defined criteria for the diagnosis of malignancy. Large size and recurrence are the most important clinical features predicting malignant behavior. Patients with a history of Abrikossoff tumor should be followed closely to monitor recurrence and malignant transformation. The apparent originality of our observation - which could lie in the evolution of a GCT tumor, initially considered as benign, to a malignant form - has to be challenged regarding the issue of classifying some cases according to the classical "benign" and "malignant" dichotomy.
RESUMEN
BACKGROUND Antithyroid drugs, namely methimazole, are well-known causes of drug-induced lupus erythematosus. This is, however, an infrequent adverse effect. Selective Immunoglobulin A (IgA) deficiency, in contrast, is the most common primary immunodeficiency. Patients with IgA deficiency are at risk of developing infectious diseases, but also autoimmune diseases such as Grave's disease or systemic lupus erythematosus. CASE REPORT We report a case of methimazole-induced lupus erythematosus in a 32-year-old man with renal involvement and concomitant selective IgA deficiency. Symptoms promptly resolved after treatment with hydroxychloroquine and corticosteroids after discontinuation of methimazole. Lupus nephritis required treatment with cyclophosphamide followed by maintenance therapy with mycophenolate mofetil. CONCLUSIONS Drug-induced lupus erythematosus usually develops after a few months or years of exposure to the causative agent. No specific symptoms exist. The diagnosis is not based on particular specific tests, but relies on a set of arguments evoking the role of the medication inducing the condition. The first step in treatment is to stop the causative drug. The therapeutic management of the various manifestations does not differ from that of idiopathic systemic lupus erythematosus. We briefly discuss the relationship between drug-induced lupus erythematosus, Grave's disease, and IgA deficiency, and suggest that IgA deficiency may act as a potential risk factor. Testing for IgA deficiency could be helpful in patients being treated with drugs known to be associated with drug-induced lupus erythematosus.
