Chapter 4.3
Alcohol-related liver disease and nutrition
Regina Keenan1 and Barbara Davidson2
1St Vincent’s University Hospital, Dublin, Ireland
2Freeman Hospital, Newcastle upon Tyne, UK
4.3.1 Alcoholic hepatitis
Alcoholic hepatitis (AH) refers to acute decompensation of the liver function in an individual with a history of alcohol abuse [1]. Clinical presentation after abstinence for several weeks is not unusual. Clinical features include rapid onset of jaundice, fever, hepatomegaly, ascites, anorexia and encephalopathy. Typically presentation is between 40 and 60 years and female sex is an independent risk factor for AH [2].
Maddrey’s discriminant function provides risk stratification and a value more than 32 indicates severe AH. There is a significant mortality associated with severe AH: a 28-day mortality of higher than 40% compared to patients with mild AH [3].
Undernutrition: prevalence and effects on survival
Protein-energy malnutrition (PEM) is strongly associated with AH. Based on anthropometry and laboratory testing, protein malnutrition and/or PEM were found in all patients with AH [4]. The severity of PEM correlates with the severity of AH and mortality, with 2% at 30 days with mild PEM and up to 52% with severe PEM [5].
Pathogenesis of undernutrition
Contributing factors to developing undernutrition include anorexia, malabsorption and a diminished ability to utilise or store nutrients. The inflammation present in AH promotes a depletion of muscle and visceral proteins and therefore is associated with an increased catabolic state [6]. Patients with acute hepatitis can have an increased metabolic rate. AH is a hypermetabolic state and patients have a 55% higher energy expenditure compared to healthy controls [7].
Nutritional therapy
Alcohol
Alcohol abstinence is of paramount importance in the treatment of AH and has been shown to significantly improve long-term survival [8].
Oral and enteral nutrition
Nutritional status should be evaluated in patients with AH as adequate energy intake (>2500 kcal/day) was associated with 19% mortality, whereas patients with inadequate intake exhibited 51% mortality [9]. Increased intestinal bacterial translocation and endotoxaemia are frequent events in patients with AH with or without cirrhosis [10]. Enteral nutrition (EN) might exert its therapeutic action by improving the intestinal barrier function [11].
Nutrition support
Early trials assessing the benefit of oral, EN or parenteral nutrition (PN) in patients with AH suggested that nutritional support improves nitrogen balance and liver function but not survival. Interestingly, a randomised, controlled clinical trial comparing EN (2000 kcal/day) with prednisolone therapy (40 mg/day) for 28 days in 71 patients with severe AH found the survival rate to be similar between the two groups at 28 days and at 1 year, suggesting that nutrition support may be as effective as corticosteroids in some patients [11].
Vitamins
There are no published guidelines for vitamin or mineral supplementation in patients with AH [12]. As with alcoholic liver disease, consideration should be given to vitamins A, C, D, E, K, B1, B2, B6 and B12, nicotinic acid, folic acid and zinc.
Antioxidants
Alcohol ingestion increases the excretion of markers of oxidative stress, and the highest levels are observed in patients with AH [2]. Antioxidants are not currently recommended as research has failed to demonstrate a beneficial role in AH [13,14].
Nutritional assessment and goals
All patients with AH should be assessed for PEM, as well as vitamin and mineral deficiencies. Those with severe disease should be treated aggressively with EN [15].
As for cirrhosis, energy aims are 35–40 kcal/kg/day [16]. As a general consensus, a higher energy requirement of 45 kcal/kg/day is recommended for patients with AH given their greater prevalence of undernutrition and cachexia. A protein intake of 1.2–1.5g/kg/day is recommended [16].
4.3.2 Alcoholic liver disease
Alcoholic liver disease (ALD) encompasses a range of conditions from steatosis to cirrhosis with all the symptoms and nutritional challenges which these present posed. The association between alcohol and liver injury has been well known for centuries and liver disease caused by alcohol remains a major cause of morbidity and mortality worldwide. Although the incidence has always been high, patient demographics is changing with a pronounced trend towards younger people (<25 years) presenting with established cirrhosis. From the 1970s to 2000, deaths from liver cirrhosis steadily increased. In people aged 35–44 years, the death rate went up eight-fold in men and almost seven-fold in women, and in 25–34 year olds, a four-fold increase was seen [17]. The increasing incidence of non-alcoholic fatty liver disease (NAFLD) presents an additional stress to a liver already compromised by alcohol with patients presenting in a very poor nutritional state.
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