Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 EP1313 | DOI: 10.1530/endoabs.37.EP1313

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

Fainting matters: a case of an autoimmune polyglandular syndrome with an atypical involvement of the parathyroid gland

Ieva Ruza 1, , Sabine Upmale 2 , Justine Malina 2 & Inta Leitane 1


1Riga Eastern Clinical University Hospital, Riga, Latvia; 2Riga Stradins University, Riga, Latvia.


Introduction: The autoimmune polyglandular syndrome (APS) is characterised by the coexistence of at least two glandular autoimmune mediated diseases. We report a combination of an autoimmune thyroid disease, Addison’s disease and an atypical involvement of the parathyroid gland.

Case report: A 73-year-old white woman was admitted to our clinic for evaluation due to recurrent syncopes during last 3 years, along with vertigo, cold sweats, and general fatigue, associated with prolonged standing. Three months ago she was diagnosed with chronic autoimmune thyroiditis and primary hypothyroidism, as well as a parathyroid gland adenoma. Head CT scan revealed basal ganglia calcinosis. The patient had lost 15 kg within the past year, during investigation orthostatic hypotensia was detected, no skin colour changes. Biochemical tests revealed low aldosterone, renin, calcium, free T4 and mildly elevated creatinine serum levels. TSH was elevated, ACTH was high normal. She had low cortisol in 24 h urine and also in serum after insulin stress test. PTH level was normal, but coexisting hypocalcaemia and parathyroid gland adenoma must be taken into consideration. Antibody screen (ANA, thyroid peroxidase, and tranglutaminase) was negative. No substantial changes in other tests. No data on diabetes mellitus or malignancy was found. Diagnosis of primary adrenal insufficiency with glucocorticoid and mineralocorticoid deficiency, chronic autoimmune thyroiditis with primary hypothyroidism, hypocalcaemia, calcinosis of basal ganglia (possible Fahr’s syndrome), parathyroid gland adenoma, secondary osteoporosis due to malabsorption, chronic kidney disease was made. Based on these findings we suggest the final diagnosis of type 2 autoimmune polyglandular syndrome. Treatment was continued with L-thyroxine and oral calcium, started with alphacalcidol, hydrocortisone, fludrocortisone. A substantial improvement of symptoms was seen in a control visit after 3 months.

Conclusion: We would like to stress the importance of investigation for autoimmune glandular diseases and electrolyte level in case of unexplained syncope.

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