title: Discontinuation of hormone replacement therapy in young GH-treated hypopituitary women increases liver enzymes.
abstract: OBJECTIVE
  Hypopituitarism, often characterized by hypogonadism, is associated with central obesity, increased cardiovascular and endocrine morbidity and mortality. In Turner syndrome, which is also characterized by hypogonadism liver enzymes are often elevated, but readily suppressed by a short course of hormone replacement therapy (HRT). We investigated the effect of HRT on liver enzymes, lipid levels and measures of insulin sensitivity 26 in hypopituitary women.
  
  
  METHODS
  We studied 26 hypopituitary women (age 38.8+/-11.0 (mean+/-SD years), BMI 27.4+/-5.1kg/m(2)) during HRT and 28days off therapy.
  
  
  METHODS
  We measured liver enzymes, fasting levels of lipids, insulin and glucose as well as adiponectin and leptin levels. Body composition was assessed by means of anthropometry and bioimpedance.
  
  
  RESULTS
  Alanine transaminase (ALT) and aspartate transaminase (AST) increased after discontinuation of HRT (ALT; treated: 22.3+/-11.5 vs. untreated: 27.1+/-11.1 (U/L) (P<0.02); AST; treated: 20.4+/-6.1 vs. untreated: 24.6+/-8.9 (U/L) (P<0.002)), whereas other liver function tests remained unchanged. Measures of insulin sensitivity and fasting lipids were also unaffected by HRT, whereas leptin levels decreased with cessation of HRT (leptin; treated: 23 (8-71) vs. untreated: 20 (8-64) (mug/L) (P<0.0005)).
  
  
  CONCLUSIONS
  Short time discontinuation of HRT in young hypopituitary women increased liver enzymes, whereas measures of insulin sensitivity and lipid levels remained unchanged. We speculate that the estrogen component of HRT has beneficial effects on hepatic metabolism through various pathways. Further studies including liver imaging and with a time-dependent design are needed to clarify the role of HRT on liver enzyme levels, metabolic variables and liver fat content.
authors: Medical Department M, Diabetes and Endocrinology and the Medical Research Laboratories, Clinical Institute, Aarhus University Hospital, DK-8000 Aarhus C, Denmark. christian.host@ki.au.dk
authors: Christian
authors: C
authors: Høst
authors: Jens J
authors: JJ
authors: Christiansen
authors: Jens S
authors: JS
authors: Christiansen
authors: Jens O L
authors: JO
authors: Jorgensen
authors: Claus H
authors: CH
authors: Gravholt
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D000410:Alanine Transaminase / Q000097:blood / Q000187:drug effects; D001219:Aspartate Aminotransferases / Q000097:blood / Q000187:drug effects; D001786:Blood Glucose; D015992:Body Mass Index; D005260:Female; D020249:Hormone Replacement Therapy; D019382:Human Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D007006:Hypogonadism / Q000188:drug therapy* / Q000209:etiology; D007018:Hypopituitarism / Q000188:drug therapy* / Q000209:etiology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000201:enzymology*; D009765:Obesity / Q000150:complications; D028761:Withholding Treatment
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D008055:Lipids; D019382:Human Growth Hormone; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase