title: Growth hormone reverses nonalcoholic steatohepatitis in a patient with adult growth hormone deficiency.
abstract: OBJECTIVE
  Nonalcoholic steatohepatitis (NASH) is an emerging progressive hepatic disease and demonstrates steatosis, inflammation, and fibrosis. Insulin resistance is a common feature in the development of NASH. Molecular pathogenesis of NASH consists of 2 steps: triglyceride accumulation in hepatocytes with insulin resistance and an enhanced oxidative stress caused by reactive oxygen species. Interestingly, NASH demonstrates a striking similarity to the pathologic conditions observed in adult growth hormone deficiency (AGHD). AGHD is characterized by decreased lean body mass, increased visceral adiposity, abnormal lipid profile, and insulin resistance. Moreover, liver dysfunctions with hyperlipidemia and nonalcoholic fatty liver disease (NAFLD) are frequently observed in patients with AGHD, and it is accompanied by metabolic syndrome.
  
  
  METHODS
  We studied a case diagnosed as NASH with hyperlipidemia in AGHD. The effect of GH-replacement therapy on the patient was analyzed.
  
  
  RESULTS
  Six months of GH-replacement therapy in the patient drastically ameliorated NASH and the abnormal lipid profile concomitant with a marked reduction in oxidative stress.
  
  
  CONCLUSIONS
  These results suggest that GH plays an essential role in the metabolic and redox regulation in the liver.
authors.affiliation: Division of Endocrinology/Metabolism, Neurology, and Hematology/Oncology, Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, Kobe, Japan. takahash@med.kobe-u.ac.jp
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Keiji
authors.initials: K
authors.lastname: Iida
authors.forename: Kentaro
authors.initials: K
authors.lastname: Takahashi
authors.forename: Shiro
authors.initials: S
authors.lastname: Yoshioka
authors.forename: Hidenori
authors.initials: H
authors.lastname: Fukuoka
authors.forename: Ryoko
authors.initials: R
authors.lastname: Takeno
authors.forename: Mari
authors.initials: M
authors.lastname: Imanaka
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Nishizawa
authors.forename: Michiko
authors.initials: M
authors.lastname: Takahashi
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Seo
authors.forename: Yoshitake
authors.initials: Y
authors.lastname: Hayashi
authors.forename: Takuma
authors.initials: T
authors.lastname: Kondo
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Okimura
authors.forename: Hidesuke
authors.initials: H
authors.lastname: Kaji
authors.forename: Riko
authors.initials: R
authors.lastname: Kitazawa
authors.forename: Sohei
authors.initials: S
authors.lastname: Kitazawa
authors.forename: Kazuo
authors.initials: K
authors.lastname: Chihara
mesh_terms: D000328:Adult; D005234:Fatty Liver / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D006505:Hepatitis / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D019382:Human Growth Hormone / Q000008:administration & dosage* / Q000172:deficiency; D006801:Humans; D006949:Hyperlipidemias / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D007018:Hypopituitarism / Q000097:blood / Q000150:complications*; D007279:Injections, Subcutaneous; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008297:Male; D011994:Recombinant Proteins / Q000008:administration & dosage; D012720:Severity of Illness Index; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D011994:Recombinant Proteins; D019382:Human Growth Hormone