Polyglandular syndromes in internal medicine are characterized by a combination of lesions of endocrine and non-endocrine tissues. Autoimmune polyglandular syndrome type 2 (APS-2) is manifested by a combination of primary hypocorticism – adrenal insufficiency, autoimmune thyroid disease – Graves’ disease or hypothyroidism as the outcome of autoimmune thyroiditis. This pathology is the most common variant of polyglandular endocrinopathies. To diagnose APS at the current level, it is necessary to detect such a specific serological marker as antibodies to 21-hydroxylase in blood serum. The author observed a 57-year-old female patient with type 2 autoimmune polyglandular syndrome, manifested by hypothyroidism and hypocorticism. There is a history of thyroid resection for nodular form of chronic autoimmune thyroiditis 20 years ago with the outcome of hypothyroidism, later in 6 years with hypocorticism. She complained about postural vertigo, weakness. The condition deteriorated a month ago when the patient felt sore throat, symptoms of rhinitis. The autoimmune hemolytic anemia (AIHA) developed during the treatment of ARI with ergoferon. Over the past 5 years the patient has been admitted to the hematology department three times, whereas there was no necessity in admitting to the endocrinology department. While treating AIHA no other tissue damage was reported (hormonal or non hormonal) which is probably related to the unique antigenic structure of the red blood cell membrane. The membrane structure found in red blood cells does not occur in other tissues. The author believes that this form of anemia should be considered as an independent diagnosis, not as a part of APS-2. APS-2 and AIHA are two distinct, pathogenically independent diseases.
hypothyroidism, hypercortisolism, hemolysis, defect of immune regulation, polyglandular lesions, ergoferon, rituximab
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