Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2017) 49 EP1261 | DOI: 10.1530/endoabs.49.EP1261

1Clinic of Endocrinology, Diabetes and Metabolic diseases, Clinical Center of Serbia, Belgrade, Serbia; 2School of Medicine, University of Belgrade, Belgrade, Serbia.


Abstract: A 55-year-old woman was admitted to our hospital due to severe hyperthyreosis. She started to feel symptoms of hyper-metabolism four months prior to hospitalization. At that time she was admitted in regional hospital and had gastroenterological examination because of diarrhea. Crohn’s disease was diagnosed and therapy started. At the same time, thyrosupressive therapy started. She had a history of hyperthyreosis thirteen years ago, duodenal hemorrhage ulcer, hypertension, cerebral vascular insult and myopericarditis. Despite maximal dose of thiamazole, on admission she was highly hyper-metabolic. Hormonal analysis revealed severe thyrotoxicosis (fT4 >100.0 pmol/l; T4>320.0 nmol/l; TSH<0.005 mIU/l) with increased TRAb (13.9 IU/l), and negative TPOAb (<28.0 U/ml) and TgAb (<15.0 IU/ml). Stool analysis was positive for muscle fibers, fat and carbohydrates indicating maldigestion and malabsorption. Because of multiple comorbidities, we decided to prepare a patient for radioactive iodine treatment (RAI). We concluded that at this hyper-metabolic state, it could lead her in thyroid storm and that her thyroid hormones should be decreased at safer levels prior to RAI. After admission, we started with intrathyroidal dexamethasone injections with initial decreasing of thyroid hormones. The procedure wasn’t continued because of gastric pain she started to feel (history of ulcer). We replaced thiamazole for PTU, and started with therapeutic plasma exchange (TPE). After TPE, we observed a significant decrease in fT4 (54.5 pmol/l), T4 (139.0 nmol/l) fT3 (8.5 pmol/l) T3 (2.27 nmol/l) levels. Clinical improvement was achieved. Patient underwent RAI treatment safely, and after two months, her thyroid hormones were in the normal referent range with TSH still suppressed (fT4 13.7 pmol/l; fT3 4.71 pmol/l; TSH 0.01 mIU/l). We concluded that severe thyrotoxicosis in our patient was due to malabsorption of thyrosupressive drugs caused by Crohn’s disease and thyrotoxicosis itself. In such cases alternative therapy options should be considered.

Volume 49

19th European Congress of Endocrinology

Lisbon, Portugal
20 May 2017 - 23 May 2017

European Society of Endocrinology 

Browse other volumes

Article tools

My recent searches

No recent searches.

My recently viewed abstracts