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Case Reports
. 2024 Dec 19;7(4):511-516.
doi: 10.3138/canlivj-2024-0030. eCollection 2024 Dec.

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

Nicole Wiebe  1 , Ashley Stueck  2 , Magnus McLeod  3
Affiliations
Case Reports

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

Nicole Wiebe et al. Can Liver J. .

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.

Keywords: Rathke cleft cyst; fibrosis; growth hormone deficiency; panhypopituitarism; steatohepatitis; steatotic liver disease.

Plain language summary

Lay Summary: Fatty liver disease, also known as steatotic liver disease, can develop as a result of metabolic factors, such as body weight and high blood sugar. After significant fat buildup occurs in liver cells, steatotic liver disease can progress to a condition called steatohepatitis with widespread liver inflammation and cell damage. A disorder in the pituitary gland can cause abnormalities in hormone signaling pathways, such as growth hormone, and has been found to lead to steatotic liver disease. One of the possible mechanisms for this association is that insulin resistance may cause further accumulation of fat and cell damage due to oxidative stress. Patients with a malfunctioning pituitary gland and growth hormone deficiency have shown improvements in liver damage after treatment with growth hormone replacement. Here, we report a case of a 20-year-old man who was referred to the Hepatology Clinic with abnormal liver enzymes. He previously had a pituitary mass removed, so he was treated with thyroid, steroid, growth, and sex hormone replacement. He presented with elevated liver enzymes, normal liver function, elevated cholesterol, obesity, and no findings of liver disease on physical examination. Investigations into causes of liver disease, including infectious, autoimmune, drug-induced, and genetic cause, were negative. An abdominal ultrasound showed liver inflammation and enlargement. Liver-toxic medications were withdrawn but laboratory findings remained the same. A liver biopsy showed inflammation and scarring of the liver tissue and determined that due to his inadequate production of pituitary hormones, he developed growth hormone deficiency, metabolic dysfunction, and ultimately liver disease. The patient's case is unique, as he was found to have severe liver damage, and long-term treatment with growth hormone therapy did not lead to any improvement. Physicians should consider fatty liver disease as a complication of pituitary dysfunction and follow patients closely given the high likelihood of disease progression.

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Conflict of interest statement

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Figures

Figure 1:
Figure 1:. (A) Liver parenchyma showing macrovesicular steatosis (*) and steatohepatitis including hepatocytes with ballooning degeneration and poorly formed Mallory-Denk bodies (arrows) and inflammation (arrowheads). Hematoxylin–eosin stain; original magnification, ×300. (B) The same area with extensive pericellular “chicken wire” fibrosis. Masson trichrome stain, original magnification, ×300
See this image and copyright information in PMC

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