ODP314 Gynecomastia as the Initial Presentation of Acromegaly.
Authors: Lim Frederick , Rao Ambika 
Published: November 2022

Abstract
Acromegaly is caused by persistent hypersecretion of growth hormone. In the US, its prevalence is less 20,000 per year. It is noted that co-secretion of growth hormone and prolactin from a single pituitary adenoma is common. Prolactin is co-secreted in about 25% of patients with acromegaly. We present a case of middle-age man who initially presented to our clinic for evaluation of bilateral gynecomastia with hypogonadism and found to have growth hormone secreting pituitary macroadenoma with co-secretion of prolactin. A 50 year-old Caucasian male veteran with past medical history of hypertension, hyperlipidemia, pre-diabetes, carpal tunnel syndrome, obstructive sleep apnea was referred to our clinic for evaluation and management of 5 months history of bilateral gynecomastia. He also reported chronic fatigue and erectile dysfunction. He denied headache, vision changes, change in shoes or ring size. He had gynecomastia with a larger left breast with some tenderness to palpation with no nipple discharge. He has short stature with large hands and feet. Some skin tags were also noted on physical examination. He was found to have elevated prolactin of 49.3 ng/ml (2.64-13.13ng/ml) with normal thyroid function test. His morning total testosterone was also low at 186 ng/dl (250-1100 ng/dl) with LH of 2.81 mIU/ml (1.24-8.26 mIU/ml), FSH of 5.98 mIU/ml (1.27-19.26 mIU/ml). Since his prolactin was elevated, MRI brain was done that showed 2.3 cm pituitary macroadenoma close to cavernous sinuses with no optic chiasm compression. Other pituitary function tests showed an elevated IGF-1 of 585 ng/ml (52-328 ng/ml). His morning cortisol and ACTH were normal. Oral glucose tolerance test revealed that growth hormone was not suppressed (GH &gt; 2.4ng/ml post OGGT) confirming growth hormone excess/Acromegaly. He was given a trial of octreotide but did not tolerate the medication. He underwent transsphenoidal hypophysectomy and developed transient post-operative diabetes insipidus requiring Desmopressin. His prolactin, IGF-1 and testosterone level had returned to normal after surgery and gynecomastia completely resolved. Repeat MRI in 6 months after surgery showed postoperative changes and OGTT showed that GH suppressed appropriately (GH &lt; 0.1 ng/ml post OGTT) and IGF-1 was149 ng/ml. Prolactin and testosterone had remained in the normal range. Acromegaly presents organomegaly with coarse physical features, enlarged hands and feet but some early symptoms are hyperhidrosis and extremity swelling with arthritis. We describe a case of acromegaly that initially presented with gynecomastia and secondary hypogonadism with hyperprolactinemia that lead to the diagnosis of acromegaly. The gynecomastia resolved completely with treatment. We hope that our case report is for the clinicians to be aware that acromegaly can present with metabolic syndrome, hypogonadism with gynecomastia and hyperprolactinemia and include screening tests to help diagnose and treat these patients at the early stages of the disease.
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