Abstract
Abstract Disclosure: C.S. Botero Suarez: None. D. Broutin: None. H. Yau: None. Introduction: Glucagon-like peptide-1 receptor agonists (GLP1-RA) act by stimulating the GLP-1 receptor resulting in a reduction in food intake, increased energy expenditure, and improved glycemic control. The role of GLP1-RA in pituitary/suprasellar tumors causing hyperphagia and hypothalamic obesity is yet unknown. We present a case of a patient with a large non-functional pituitary mass resulting in severe hyperphagia and hypothalamic obesity. A trial of GLP-1RA showed significant improvement of hyperphagia. Case Description: A 30-year-old African American male is seen in the Endocrinology clinic. He was recently diagnosed with a non-functional pituitary mass 2 months prior, after a presentation of hyperphagia, significant weight gain, and altered personality changes causing significant social distress. He underwent transsphenoidal pituitary resection which resulted in postoperative hypopituitarism. His physical exam showed normal vital signs, a weight of 185 lbs, and a BMI of 25. His medications included hydrocortisone total of 15 mg daily, desmopressin 0.1mg daily, levothyroxine 137mcg daily, and risperidone 1mg daily. A brain MRI showed postoperative changes depicted by a T1 hyperintensity within the sella as well as T2 hyperintensity of the chiasm and hypothalamus indicating edema and a mass effect. Based on his presentation of marked hyperphagia and rapid weight gain with suggestive imaging, the clinical diagnosis of hypothalamic obesity was made. Further follow-up revealed a rapid weight gain of 45 lbs in 2 months, a worsening glycemic control, and a HbA1C of 7.2% compared to a HbA1C of 5.4% in his prior visit. Lab work showed a TSH of 0.017 mlU/mL, fT4 of 1.4ng/dL, prolactin 3.94 ng/mL, alpha subunit of 0.1 ng/mL (reference 0.1-0.5 ng/mL), ACTH of 15 pg/mL, morning cortisol of < 3 ug/dL. Given the significant metabolic consequences of his marked hyperphagia, related weight gain, and new onset of diabetes, the patient was started on semaglutide 0.5mg weekly and later up-titrated to 1mg weekly. There was marked improvement of hyperphagia, and his weight remained neutral at the 3-month follow-up. Discussion: Hyperphagia is a rare presentation of sellar and suprasellar tumors and can lead to hypothalamic obesity. Tumors can affect the arcuate nucleus of the hypothalamus, which is a key regulator of energy homeostasis and is regulated by orexigenic (AgRP/NPY) and anorexigenic neurons (POMC/CART). GLP-1R agonists, have shown to cause significant weight loss due to decreased gastric emptying and stimulating POMC/CART neurons, but they also inhibit neuropeptide Y (NPY) and agouti-related peptide (AgRP), leading to reduced hunger, energy intake, and food cravings. Although the clinical role of GLP1-RA in pituitary tumors with significant hyperphagia is unknown, we believe early initiation can help avoid a rapid progression of obesity and glycemic deterioration. Presentation: Friday, June 16, 2023
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