Issues of malnutrition and bone disease in patients with cirrhosis.
Malnutrition is a frequent complication of cirrhosis, and many studies have demonstrated the adverse influence of malnutrition on clinical outcomes in patients with cirrhosis. The coexisting complications of fluid overload and ascites may mask the severity of malnutrition, particularly in the early stages of its development. During periods of decompensation, protein and energy requirements are higher, and many patients have inadequate nutritional intake at these times. Further, protein supplementation should not be restricted ad hoc in cirrhotic patients, as for the vast majority of patients dietary protein does not precipitate hepatic encephalopathy. The impairment of hepatic glycogen storage in cirrhotic patients effects a state of accelerated starvation with catabolism of fat and protein to provide substrates for gluconeogenesis. Recent studies have demonstrated the efficacy of nocturnal nutritional supplements in improving nitrogen balance. Resistance to the actions of the anabolic growth factors insulin and growth hormone (GH) is common in cirrhosis, and recent studies have shown that GH resistance, in particular, may be overcome with exogenous GH therapy. Hypermetabolism may be observed in up to one-third of cirrhotic patients. The recent exciting observation that beta-blocker therapy can decrease energy expenditure and catecholamine levels in these patients indicates the need for further intervention studies of beta-blockers as metabolic therapy in cirrhosis.
Donaghy
Anthony
A
AW Morrow Gastroenterology and Liver Centre, Royal Prince Alfred Hospital, Camperdown, New South Wales 2050, Australia. tdonaghy@med.usyd.edu.au
D001851:Bone Diseases, Metabolic / Q000209:etiology*; D006801:Humans; D007165:Immunosuppression Therapy / Q000009:adverse effects; D008103:Liver Cirrhosis / Q000150:complications* / Q000601:surgery; D016031:Liver Transplantation; D015596:Nutrition Assessment; D009748:Nutrition Disorders / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy