Endocrine Abstracts

JOINT1153

A 39-year-old female patient with history of type 2 diabetes mellitus (DM 2) and pituitary macroadenoma was referred to endocrinologist for the follow-up examination. She had regular menstrual cycle on combined oral contraceptive pills (COCPs). Her physical, ophtalmological and neurological examinations were unremarkable except for BMI of 34 kg/m². Further testing demonstrated CBC, liver function tests fasting blood glucose, glycated hemoglobin, creatinine, serum electrolytes, TSH levels within the normal range, but decreased GH <0,05 (reference range 0,126-9,88) ng/ml, IGF-1–34,9 (135-449) ng/ml, PRL – 2,5 (6,0-29,9) ng/ml levels and signs of pituitary macroadenoma on MRI about the same size compared to previous examination. After the first delivery (at the age of 24 years) she had irregular menstrual cycle. During the second pregnancy (at the age of 28 years) gestational diabetes was diagnosed. After the second delivery she has received COCPs. At the age of 35 years DM 2 was established. Metformin and DPP-4 inhibitors were administered. At about the same time arterial hypertension and complaints of episodic headaches have appeared. Two years later (at the age of 37 years) pituitary macroadenoma with infra-laterocellar growth with maximal size of 16 mm was detected on MRI, and she was referred to endocrinologist. Patient denied any significant changes in her appearance. Laboratory testing showed normal PRL – 17,15 (6,0-29,9) ng/ml and TSH – 1,6 mIU/ml, but elevated GH–11,7 (0,126-9,88) ng/ml and IGF-1–678,7 (135-449) ng/ml. Somatotropinoma was diagnosed, but patient refused recommended surgery. 3 months later she was admitted to the neurology department with severe headache, resistant to NSAIDs, and vomiting. No visual impairment was detected. Stroke was ruled out on CT scan. Subsequent examination showed normal GH – 0,5 (0,126-9,88) ng/ml, IGF-1 – 154 (135-449) ng/ml, TSH – 2,0 mIU/ml, fT4 – 12 pmol/l, ACTH – 9,0 (6,3-46) pg/ml and depressed PRL – 0,79 (6,0-29,9) ng/ml. The diagnosis of non-active pituitary macroadenoma was established. At the follow-up examination, presented at the beginning of the abstract, further declines in GH and IFG-1 levels were observed. This case demonstrates spontaneous remission of somatotropinoma, gradually resulted in GH deficiency, most likely caused by pituitary adenoma apoplexy. It is remarkable to note that somatotropinoma was initially revealed in the absence of obvious typical features of acromegaly. Further monitoring is needed. Medical specialists should refine their knowledge about pituitary adenoma apoplexy.