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GH Treatment in Adults with Chronic Liver Disease: A Randomized, Double-Blind, Placebo-Controlled, Cross-Over Study

Metabolic Research Unit (J.D.W., R.C.C.), University of Queensland, Princess Alexandra Hospital, Brisbane 4102; Departments of Dietetics (W.J.A.-J.), Gastroenterology (D.H.G.C.) and Chemical Pathology (J.M.P.), Princess Alexandra Hospital, Brisbane 4102; and Department of Physiology and Pharmacology (R.B.), University of Queensland, Brisbane 4072, Australia

Address all correspondence and requests for reprints to: Jennifer D. Wallace, M.D., Metabolic Research Unit, Department of Medicine, University of Queensland, Princess Alexandra Hospital, Wooloongabba, Brisbane 4102, Australia. E-mail: . jwallace{at}medicine.pa.uq.edu.au

Abstract

Patients with chronic liver disease (CLD) are catabolic and GH-resistant. The effects of supraphysiological recombinant human GH (rhGH; 0.2 IU·kg^-1·d^-1) treatment in adults with CLD were assessed in a randomized, double-blind, placebo-controlled cross-over trial (4-wk dietary run-in, 4-wk treatment, and 2-wk wash-out phases). Nine adults with mild- to moderate-severity CLD participated (median age, 49 yr; three males and six females; Child’s classification A in six and B in three). Biopsy-proven etiologies were: alcohol (four patients), primary biliary cirrhosis (three patients), non-A, non-B, non-C hepatitis (one patient), and cryptogenic (one patient). Treatment with rhGH increased serum IGF-I (median increase over placebo, +93 µg·liter^-1; P = 0.004), IGF-binding protein-3 (+0.9 mg·liter^-1: P = 0.004), and acid labile subunit (+10.7 nM; P = 0.004). Total body potassium (+8.0 g; P = 0.023), body weight (+1.6 kg; P = 0.008), and total body water (by bioelectrical impedance; +4.9 kg; P = 0.004) increased. Resting metabolic rate (+313 ml·kg^-1·min^-1; P = 0.004) and lipid oxidation (+1072.0 kcal·d^-1; P = 0.032) increased. Metabolic changes included increased fasting plasma glucose (+1.2 mM; P = 0.008), insulin (+33.8 mU·liter^-1; P = 0.004), C-peptide (+0.7 nM; P = 0.004), and free-fatty acids (+0.1 mEq·liter^-1; P = 0.04). Clinical side effects included worsening edema and ascites. Hepatocellular function did not change. Therefore, rhGH treatment in CLD: 1) overcame hepatic GH resistance; 2) may have improved whole-body protein catabolism; 3) increased lipolysis and lipid oxidation; 4) increased insulin resistance; and 5) had potent antinatriuretic effects. Long-term safety and efficacy require further assessment.