Steatotic liver disease arising in an asymptomatic 20-year-old man with panhypopituitarism and elevated transaminases.

IF 1.2 Q4 GASTROENTEROLOGY & HEPATOLOGY
Canadian liver journal Pub Date : 2024-12-19 eCollection Date: 2024-12-01 DOI:10.3138/canlivj-2024-0030
Nicole Wiebe, Ashley Stueck, Magnus McLeod
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引用次数: 0

Abstract

Background: 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.

Case: 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.

Conclusions: 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.

脂肪肝疾病发生于无症状的20岁男性,伴有全垂体功能低下和转氨酶升高。
背景:脂肪变性肝病(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低下引起。SLD可发展为脂肪性肝炎,导致脂质积累、炎症和肝细胞损伤。SLD与垂体功能障碍有关,特别是生长激素缺乏,因为胰岛素抵抗导致脂质积聚和氧化应激。生长激素替代可能改善垂体功能低下患者的肝脂肪变性和纤维化。病例:我们报告一例20岁的男子谁被转介到肝病异常肝酶。由于切除垂体肿块,他患有全垂体功能减退症,为此他接受左甲状腺素、氢化可的松、生长激素和睾酮治疗。患者表现为肝酶升高,肝功能正常,肥胖,血脂异常,无慢性肝病的肝外表现。继发性肝病的检查结果为阴性,包括感染性、自身免疫性、药物诱导和遗传原因。腹部超声显示中度肝脂肪变性伴轻度肝脾肿大。尽管停用了肝毒性药物,但他的肝酶仍然升高,生化肝功能仍然正常。肝活检显示II/III级脂肪性肝炎伴III- iv期纤维化。活检结果提示:全垂体功能低下伴生长激素缺乏及相关代谢功能障碍,导致他的肝脏疾病。结论:这是一个独特的由垂体功能减退引起的侵袭性SLD病例,用激素替代治疗生长激素缺乏症并不能改善肝酶或肝损伤。医生应该认识到SLD是全垂体功能低下和由此导致的生长激素缺乏的严重并发症,并密切关注患者的疾病进展风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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