Wiebe Nicole, Stueck Ashley, McLeod Magnus
Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
Department of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
Can Liver J. 2024 Dec 19;7(4):511-516. doi: 10.3138/canlivj-2024-0030. eCollection 2024 Dec.
Steatotic liver disease (SLD) may be caused by cardiometabolic risk factors, drugs/toxins, viral hepatitis, genetic diseases, malnutrition, or panhypopituitarism. SLD can advance to steatohepatitis with resulting lipid accumulation, inflammation, and hepatocellular damage. SLD is associated with pituitary dysfunction, in particular growth hormone deficiency, as insulin resistance leads to lipid buildup and oxidative stress. Growth hormone replacement may improve liver steatosis and fibrosis in patients with hypopituitarism.
We report a case of a 20-year-old man who was referred to Hepatology with abnormal liver enzymes. He had panhypopituitarism from a resected pituitary mass, for which he was treated with levothyroxine, hydrocortisone, growth hormone, and testosterone. He presented with elevated liver enzymes, normal liver function, obesity, dyslipidemia, and had no extrahepatic manifestations of chronic liver disease. Work-up for secondary causes of liver disease, including infectious, autoimmune, drug-induced, and genetic causes, were negative. An abdominal ultrasound revealed moderate hepatic steatosis with mild hepatomegaly and splenomegaly. His liver enzymes remained elevated, and his biochemical liver function remained normal despite withdrawal of hepatotoxic medications. Liver biopsy showed grade II/III steatohepatitis with stage III-IV fibrosis. The biopsy results suggested that panhypopituitarism, with growth hormone deficiency and related metabolic dysfunction, caused his liver disease.
This is a unique case of an aggressive form of SLD due to panhypopituitarism, and treating growth hormone deficiency with hormone replacement did not improve liver enzymes or liver damage. Physicians should recognize SLD as a serious complication of panhypopituitarism and resulting growth hormone deficiency and follow patients closely given the risk of disease progression.
脂肪性肝病（SLD）可能由心脏代谢危险因素、药物/毒素、病毒性肝炎、遗传疾病、营养不良或全垂体功能减退引起。SLD可进展为脂肪性肝炎，导致脂质蓄积、炎症和肝细胞损伤。SLD与垂体功能障碍有关，尤其是生长激素缺乏，因为胰岛素抵抗会导致脂质堆积和氧化应激。生长激素替代治疗可能改善垂体功能减退患者的肝脏脂肪变性和纤维化。
我们报告一例20岁男性，因肝酶异常转诊至肝病科。他因垂体肿物切除导致全垂体功能减退，接受左甲状腺素、氢化可的松、生长激素和睾酮治疗。他表现为肝酶升高、肝功能正常、肥胖、血脂异常，且无慢性肝病的肝外表现。对肝病的继发原因进行检查，包括感染性、自身免疫性、药物性和遗传性原因，结果均为阴性。腹部超声显示中度肝脂肪变性，伴有轻度肝肿大和脾肿大。尽管停用了肝毒性药物，他的肝酶仍持续升高，生化肝功能仍正常。肝活检显示为II/III级脂肪性肝炎伴III-IV期纤维化。活检结果提示全垂体功能减退伴生长激素缺乏及相关代谢功能障碍导致了他的肝病。
这是一例因全垂体功能减退导致的侵袭性SLD的独特病例，用激素替代治疗生长激素缺乏并未改善肝酶或肝损伤。医生应认识到SLD是全垂体功能减退及由此导致的生长激素缺乏的严重并发症，并鉴于疾病进展风险对患者进行密切随访。
