Endocrine Abstracts

Introduction: Acromegaly is caused by growth hormone (GH) and insulin-like growth factor (IGF-1) excess and leads to various comorbidities. However, the association between acromegaly and thromboembolic diseases is unclear. Herein, we present a newly diagnosed acromegaly patient with massive pulmonary embolism.

Case report: A 61-year-old female was hospitalized with acromegaly pre-diagnosis. She complained about extensive arthralgia and snoring. She had hypertension, prediabetes, and vertigo in personal history. Her medications were amlodipine/valsartan and betahistidine. Her blood pressure was 130/80 mm/Hg and body mass index was 36.21 kg/m². The physical examination was unremarkable out of acral enlargements and macroglossia. Baseline serum IGF-1 was 538 ng/ml and GH was 2.85 ng/ml. Nadir GH level after glucose tolerance test was 1.68 ng/ml. Magnetic resonance imaging of the pituitary gland showed a 6-mm sized microadenoma. There was no pathological finding on the electrocardiogram and echocardiography. A sleep study confirmed sleep apnea syndrome. During hospitalization, she complained about a cough. Breathing sounds decreased while arterial oxygen saturation and chest radiography were normal. The patient consulted to pulmonary diseases department. The thorax tomography (CT) showed massive pulmonary embolism in bilateral main pulmonary arteries. 2 × 0.8 IU/day DMAH treatment was initiated in the acute period because she was clinically stable and followed by long-term anticoagulation therapy with warfarin. Lanreotide 90-mg was started instead of a pituitary surgery because of the high operation risk. Venous doppler ultrasonography, which was performed for excluding a deep vein thrombosis was unremarkable. Anti-nuclear antibody, protein C and S, fibrinogen, and anti-cardiolipin Ig-M and G were normal. Malignancy screening for breast, colon, and thyroid was also negative. Factor II was heterozygote and MTHFR (C677T) was homozygote in the thrombophilia screen. Bilateral pulmonary arteries were observed normally in the sixth month of warfarin therapy. We continue to follow up patient with normal GH and IGF-1 levels under lanreotide treatment.

Discussion: Although there are no clear data on whether acromegaly is a hypercoagulable condition or not, a few cases have been reported. Some studies demonstrated that serum coagulation markers altered in acromegaly. Besides active acromegaly, some comorbidities like sleep apnea syndrome and malignancies can contribute to hypercoagulability risk. Similar to our case, inherited hypercoagulability conditions accompanied by acromegaly in some of the reported cases. In conclusion, thromboembolism can be seen in acromegaly patients rarely, especially in those having additional risk factors.

Figure 1 CT showing filling defects in pulmonary arteries (A) and normal appearance after treatment (B).