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Endocrine Abstracts (2015) 37 EP1264 | DOI: 10.1530/endoabs.37.EP1264

ECE2015 Eposter Presentations Clinical Cases–Thyroid/Other (101 abstracts)

Severe hyponatremia in the course of autoimmune polyglandular syndrome type 2 of atypical clinical picture

Maria Kurowska , Joanna Malicka , Jerzy & Stanisław Tarach


Department of Endocrinology, Medical University, Lublin, Poland.

Introduction: Severe hyponatremia defined as the blood sodium concentration below 115 mmol/l is rarely recognised in the course of autoimmune polyglandular syndrome type 2 (APS t.2). The aim of the paper is to present the female patient with severe hyponatremia preceding the diagnosis of APS t.2 of atypical clinical picture.

Case report: A 54-year-old woman with the diagnosis of psoriasis established 10 years earlier and treated for psoriatic arthritis from 7 years. She was admitted to the emergency ward because of persistent vomiting, hyponatremia=111 mmol/l and hyperkaliemia=5.4 mmol/l. For several months she observed increasing fatigue, hypotension, recurrent abdominal pain, loose stools, increased appetite for salt, progressive darkening of the skin and weight loss of 12 kg/6 months. Her ACTH level was 857.3 pg/ml; blood cortisol in the morning was: 3.7; 1.6 μg/dl and in the evening: 2.7, 1.7 μg/dl. Lack of adrenal response after stimulation with Synacthen and normal adrenal CT image were confirmed. 21-hydroxylase autoantibodies were negative (1: <10). FT4-32.2 pmol/l; FT3-16.2 pmol/l; TSH<0.004 mIU/l. Antibodies antiTPO-4659 U/ml; antiTG-391 U/ml, TRAb-1.8 U/ml. USG revealed 12 ml thyroid gland with numerous, hypoechogenic, small (4 mm) areas in both lobes. The diagnosis of primary adrenal insufficiency with concomitant autoimmune thyroid disease with hyperthyroidism in a patient with psoriatic arthritis was established. Summary. Psoriatic arthritis and thyroid disease with thyrotoxicosis are rare components of APS type 2 and hyponatremia occurs more frequently in patients with concomitant hypothyroidism.

Conclusion: Severe hyponatremia in our patient could be the result of a significant increase in demand for cortisol caused by thyrotoxicosis and the lack of opportunity to increase its production by the adrenal cortex.

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