Frontiers in endocrinology · 2026
Liver transplantation for decompensated cirrhosis of uncertain etiology in a woman with long-standing untreated panhypopituitarism: a case report.
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Wang Lu, Ye Xiaojuan, Luo Wenwen, Zhang Wei, Qian Longliu, Huang Jiahuang
Аннотация
BACKGROUND: Hypopituitarism is associated with adverse body composition and steatotic liver disease, particularly when the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis is disturbed. Progression to decompensated cirrhosis is uncommon, and published reports do not establish a direct causal relationship.
CASE PRESENTATION: A 37-year-old woman presented with jaundice, massive ascites, splenomegaly, thrombocytopenia, hypoalbuminemia, coagulopathy, and hyponatremia. She had undergone pituitary adenoma surgery at approximately 12 years of age, followed by amenorrhea and more than two decades without regular endocrine follow-up or hormone replacement. The clinical and biochemical profile supported long-standing panhypopituitarism. Possible central HPA-axis dysfunction was present; secondary adrenal insufficiency was clinically probable but not dynamically confirmed. Other features included central hypothyroidism, hypogonadotropic hypogonadism, low prolactin, central diabetes insipidus, and severe GH/IGF-1 axis disturbance. GH stimulation testing was not performed, and interpretation of the GH/IGF-1 axis was confounded by advanced liver disease. Common viral, autoimmune, alcohol-related, drug-related, and overt cardiac causes were not supported. However, transferrin saturation was 94.6%, and iron overload, Wilson disease, alpha-1 antitrypsin deficiency, and histological metabolic steatohepatitis were not fully excluded. Liver biopsy supported advanced fibrosis/cirrhosis, and explant pathology showed micronodular cirrhosis with hepatocellular cholestasis. She underwent liver transplantation in May 2026. Aminotransferase levels subsequently declined, but persistent thrombocytopenia, pulmonary infection, and acute kidney injury requiring hemodialysis developed. She progressed to septic shock and died more than 20 days after transplantation.
CONCLUSION: Long-standing untreated panhypopituitarism may have contributed to metabolic and fibrogenic risk in this patient, but incomplete etiological evaluation precluded a definitive causal link. Lifelong endocrine follow-up and attention to liver health are warranted after pituitary surgery.
CASE PRESENTATION: A 37-year-old woman presented with jaundice, massive ascites, splenomegaly, thrombocytopenia, hypoalbuminemia, coagulopathy, and hyponatremia. She had undergone pituitary adenoma surgery at approximately 12 years of age, followed by amenorrhea and more than two decades without regular endocrine follow-up or hormone replacement. The clinical and biochemical profile supported long-standing panhypopituitarism. Possible central HPA-axis dysfunction was present; secondary adrenal insufficiency was clinically probable but not dynamically confirmed. Other features included central hypothyroidism, hypogonadotropic hypogonadism, low prolactin, central diabetes insipidus, and severe GH/IGF-1 axis disturbance. GH stimulation testing was not performed, and interpretation of the GH/IGF-1 axis was confounded by advanced liver disease. Common viral, autoimmune, alcohol-related, drug-related, and overt cardiac causes were not supported. However, transferrin saturation was 94.6%, and iron overload, Wilson disease, alpha-1 antitrypsin deficiency, and histological metabolic steatohepatitis were not fully excluded. Liver biopsy supported advanced fibrosis/cirrhosis, and explant pathology showed micronodular cirrhosis with hepatocellular cholestasis. She underwent liver transplantation in May 2026. Aminotransferase levels subsequently declined, but persistent thrombocytopenia, pulmonary infection, and acute kidney injury requiring hemodialysis developed. She progressed to septic shock and died more than 20 days after transplantation.
CONCLUSION: Long-standing untreated panhypopituitarism may have contributed to metabolic and fibrogenic risk in this patient, but incomplete etiological evaluation precluded a definitive causal link. Lifelong endocrine follow-up and attention to liver health are warranted after pituitary surgery.