Endocrine Abstracts

Introduction: Autoimmune polyglandular syndrome type 2 (APS2) is the most common form of the polyglandular failure syndromes. Seventy-five percent of cases occur in women. Adrenal insufficiency is the principal manifestation occurs with autoimmune thyroid disease or type I diabetes mellitus. The incidence of autoimmune thyroid diseases in APS2 is 70%; 30% Hashimoto’s thyroiditis, 20% non toxic goiter, 20% hypertyroidism is seen. We will discuss about a patient with APS2, who previously had hypothyroidism, but now presenting with adrenal crisis and hyperthyroidism.

Case: A 25-year-old male patient admitted to out-patient clinic for nausea, vomiting and non specific abdominal pain. Biochemical results were as follow; sodium 130 mmol/l (135–146), potassium 5.13 mmol/l (3.5–5.1), free T4 2.8 ng/dl (0.9–1.7), free T3 3.97 pg/ml (2.5–3.9), TSH 0.02 μIU/ml (0.34–5.6). In his medical history, he has been diagnosed APS2 with adrenal insufficiency and hypothyroidism for 8 years. At the time of diagnosis TSH, ACTH were 21.8 μIU/ml, and 2000 pg/ml respectively and anti TPO was positive. He was on prednisolone 5 mg/day, fludrocortisone 0.1 mg/day and levothyroxin (LT4) 150 mcg/day treatment. We thought thyrotoxicosis factitia, so we stopped LT4 and increased prednisolone dose. After 2 weeks, despite cessation of L-thyroxin treatment, thyrotoxicosis was persisted, anti TPO antibody and anti thyroglobulin antibody were negative, but TSH receptor antibody (TRAbs) was high (315 U/l (0-14)) and thyroglobulin was 90.4 ng/ml (0–80). Thyroid ultrasonography revealed heterogeneous parenchyma with minimal increase in vascularity. Thyroid scintigraphy with Technetium showed non homogeneous increase uptake. The patient diagnosed as Graves disease.

Conclusion: TRAbs is responsible for two distinct clinical syndromes. Stimulating antibodies (TSAb) cause thyrotoxicosis where as blocking antibodies (TBAb) cause hypothyroidism. Antibody switch can occur. The etiology of this process remains unknown but hemodilution of TRAb titer can be one of the possible mechanisms. Also LT4 treatment in unusual patients can induces or enhances thyroid autoantibody levels. The occurrence of ‘switching’ emphasizes the need for careful patient monitoring and management.