SAT-027 - Growth Hormone Deficiency and Cirrhosis: Implications for MASLD Screening Beyond Metabolic Risk

Background: Growth hormone deficiency (GHD) is associated with hepatic steatosis and fibrosis through both metabolic and direct hepatic mechanisms. However, current metabolic dysfunction–associated steatotic liver disease (MASLD) screening recommendations rely on traditional metabolic risk factors and do not account for GHD as a potential independent risk factor.

Case: A 61-year-old man with panhypopituitarism following transsphenoidal surgery (TSS) for pituitary macroadenoma in 1992, with repeat TSS in 2020 for recurrence, presented with abdominal pain. CT abdomen obtained for suspected colitis incidentally revealed findings concerning for cirrhosis, subsequently confirmed on ultrasound. Pituitary deficiencies were identified immediately following the initial surgery, including central hypothyroidism (managed on levothyroxine), secondary adrenal insufficiency (managed on hydrocortisone), and secondary hypogonadism (untreated per patient preference). GHD was documented by 2004 (IGF-1 10 ng/mL; reference range 50–317) though was likely present earlier; it was also untreated. Other than class I obesity, he lacked traditional metabolic risk factors of hypertension, dyslipidemia, insulin resistance, or alcohol use.

Laboratory evaluation showed mild transaminitis (AST 62 U/L, ALT 54 U/L) and thrombocytopenia (109 ×10³/µL) with preserved synthetic function. Extensive evaluation excluded viral, autoimmune, and genetic liver disease. Liver biopsy demonstrated established cirrhosis with mild macrovesicular steatosis, consistent with MASLD despite the absence of significant metabolic risk factors. Growth hormone replacement was initiated after diagnosis but discontinued by the patient. He remains under hepatology surveillance.

Conclusion: This case demonstrates advanced MASLD presenting as cirrhosis in a patient with over two decades of untreated GHD despite absence of metabolic syndrome. GHD promotes hepatic steatosis and fibrosis through direct effects on hepatocyte lipid metabolism, mitochondrial dysfunction, oxidative stress, and stellate cell activation, independent of obesity or insulin resistance. Importantly, this represents a potential missed preventive opportunity, as earlier recognition of GHD-associated MASLD and initiation of GH replacement may have mitigated progression to cirrhosis. These findings suggest that GHD should warrant heightened vigilance for MASLD and support reconsideration of current screening guidelines to include patients with GHD even in the absence of traditional metabolic risk factors.

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