RESUMEN
INTRODUCTION AND IMPORTANCE: Diabetic mastopathy is a rare entity affecting diabetic patients. It has been previously linked to type 1 diabetes mellitus; however, due to the several accompanying conditions, a theory of autoimmune factors contributing to the origin of this condition has been on the rise. In this paper, we report a case of diabetic mastopathy associated with several autoimmune diseases to highlight the immunological potential of this condition. CASE PRESENTATION: A 25-year-old female, known to have type 1 diabetes mellitus, hypertension, hypothyroidism, adrenal insufficiency, dilated cardiomyopathy and end-stage renal disease, was referred to our clinic for a breast lump. Radiological investigations showed a dense mass with irregular borders in the retroareolar area of the left breast. A core biopsy was obtained which revealed keloid-like fibrosis along with lymphocytes infiltrated, suggestive of lymphocytic mastopathy. CLINICAL DISCUSSION: Fibrous mastopathy has been merely attributed to a long-standing use of insulin therapy by diabetic patients; recent observations, however, proved the major contribution of immunity to etiopathogenesis. Even though human leukocyte antigen (HLA) association has not been supported in the literature, the histological changes of breast lymphocytic infiltrate are seen in patients who not only have T1DM, but also thyroiditis, systemic lupus erythematosus, Sjogren's syndrome, and Addison's disease. The frequent presence of several possible autoimmune conditions has promoted the theory of an autoimmune process affecting connective tissues, however, these claims are yet to be proven by future studies. CONCLUSION: Recent observations have proved the major contribution of immunity to etiopathogenesis of diabetic mastopathy. We shed light on the role of the immune system in triggering the disease process by reporting a case of diabetic mastopathy with a cluster of autoimmune diseases. Future studies should explore the genetic background of the condition as it would potentially have several clinical implications. The discussed pathophysiologic explanations raise the possibility of autoimmunity as a key driver in pathogenesis and indicate the need to change the nomenclature of this condition.
