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Nutritional Therapy in Liver Transplantation

Introduction to Alcoholic Liver Disease

Damage to the liver and damage to its functioning related to the use of alcohol is known as alcoholic liver disease (ALD) (Seitz et al. 2018). It constitutes a spectrum of clinico-histological conditions which develop in stages such as steatosis/fatty liver, alcoholic hepatitis followed by cirrhosis (Singal et al. 2018). The major cause of ALD is considered to be alcohol consumption. Looking at the pattern of alcohol consumption and its epidemiology worldwide will help get a better idea about alcoholic liver disease as well. A chronic consumption of alcohol ranging from 30-50g/day and 60-80g/day for men and women, respectively can increase the risk of development of alcoholic cirrhosis of liver (Mellinger 2019). ALD is the most prevalent type of chronic liver disease in the world. Around 21.5 million years of life were lost to ALD in the year 2016. Men are known to be more affected than women (Rehm & Shield 2019). This update discusses the aetiology, patho-physiology, clinical manifestations, diagnosis and management and treatment plan of alcoholic liver disease. In addition to the above, it also discusses the health promotion and preventive measures for alcoholic liver disease as well.

Aetiology and Pathogenesis

The major risk factor and also major cause responsible for the development of alcoholic liver disease (ALD) is excessive and chronic alcohol consumption. An excess of more than 40g/day of alcohol leads to the development of ALD and associated cirrhosis of liver consequently (Mellinger 2019). The liver bears the greatest tissue injury caused due to alcohol in the body because it is primarily responsible for the metabolism of ethanol. The two major pathways responsible for the metabolism of ethanol are- Alcohol dehydrogenase (ADH) and CYP 2E1(Cytochrome P450).

Cytochrome P450 is responsible for converting alcohol into acetaldehyde in the liver, whereas Alcohol dehydrogenase present in the hepatocytes as a cytosolic enzyme converts alcohol to acetaldehyde. The acetaldehyde thus produced is then metabolized into acetate through the enzyme- Acetaldehyde dehydrogenase (ADH2) present in the mitochondria. Both ADH and ADH2 cause the reduction of nicotinamide adenine dinucleotide (NAD+) to NADH (the reduced form of NAD). The increased production of NADH from NAD+ due to reactions catalysed by both the ADH and ADH2 enzymes leads to a decrease in the normal NAD+/NADH ratio in the hepatocyte known as the cellular redox potential. This leads to changes in the metabolic pathway from oxidative to reductive synthesis, which supports the formation of fatty acids in the hepatocytes leading to fatty liver (Osna et al. 2017). 

CYP 2E1 is an inducible enzyme, that means its production increases with increased consumption of ethanol, therefore, more the alcohol consumption, more is the release of this enzyme and formation of acetaldehyde and subsequent production of NAD+ and fatty acid formation. It also produces free radicals such as OH-, O2- etc. These free radicals need to be neutralized by the anti-oxidants present in the hepatocytes, but their continuous production due to chronic alcohol consumption causes oxidant stress which leads to enhanced lipogenesis. This chronic alcohol exposure also activates the macrophages present in the liver, which causes the production of TNF-alpha amongst others. This leads to mitochondrial production of reactive oxygen species, promoting oxidative stress associated with necrosis and cell death of hepatocytes in the liver. Acetaldehyde binds to proteins and DNA in the cell, thus, forming adducts which promote depletion if glutathione and peroxidation of lipid (Farooq 2016).

Further consumption of alcohol leads to development of end-stage liver disease, associated with greater production of acetaldehyde and subsequent fibrosis and cirrhosis of the liver. Acetaldehyde directly causes fibrogenesis by increasing the collagen production in the hepatic stellate cells of the liver. They are also activated by the damaged hepatocytes, activated Kupffer cells and neutrophils via the various pro-fibrogenic mediators such as TGF, growth factor, IL-8 and leptin. This fibrosis is also reactive and transient and can be reversed with abstinence, however if alcohol drinking continues, chronic inflammation and sustained fibrogenesis progress, resulting in the substitution of liver parenchyma by scar tissue that severely compromises the liver’s vascular architecture. The main pathological feature of cirrhosis is the formation of regenerative nodules of hepatic parenchyma surrounded by fibrous septa. Cirrhosis development begins from a compensated phase where the undamaged parts of the liver make up for the damaged parts to a state of decompensation where the entire liver parenchyma is scarred or beginning to convert into scar tissue (Osna et al. 2017).

Factors Modulating Progression of ALD

Apart from chronic alcohol abuse, other factors also modulate the progression of ALD such as the following-

Pattern of alcohol consumption and type- The type of beverage and the pattern and amount of drinking affect the development of ALD. More, specifically the problem of alcohol abuse amongst people. In the Australian context, around 17% of the population consumed alcohol at a risky level in the year 2019 and around 36% of the people taking drug treatment took it for alcohol addiction in the year 2018-19 making alcohol abuse and related disorders a problem in the country (AIHW, 2019).

Gender- Higher blood concentration levels of alcohol in women as compared to men after consumption of the same amount of alcohol makes them more susceptible to development of ALD. But, overall greater number of men indulging in chronic alcohol drinking behaviour puts men at a greater risk.

Nutritional factors such as high fat diet acts as a modifier for ALD and lifestyle associated changes such as obesity, smoking associated with alcohol and drug use also have a significant impact on the development and modulation of ALD(Sugimoto 2017).

Clinical Manifestations of ALD

Alcoholic liver disease does not show any specific manifestations unless in the later stages of disease. Initial symptoms are very vague and can include abdominal pain and nausea, associated with vomiting associated with continued alcohol consumption. More severe symptoms appearing only in the later stages might include – fever, jaundice, associated hepatomegaly, ascites, spider angiomas and encephalopathy. Symptoms of cirrhosis will include portal hypertension and associated hepatic failure and pruritis (Barve et al. 2017). Physical examination of patients with cirrhosis will show typical signs such as – spider angiomas, palmar erythema, smooth tongue and gynecomastia. Jaundice, ascites, pedal edema and hepatic encephalopathy are also observed in patients with end-stage liver disease (Stickel et al. 2017).

Diagnostic Process

The diagnosis of ALD is usually suspected when there is documentation of excessive alcohol use or alcohol abuse in the patient amounting to greater than 40-50g/day along with the presence of clinical signs and biological abnormalities described in the above section which are suggestive of liver injury. However, self-reporting of alcohol consumption is often under-reported while taking medical history of the patient. Previous history or complications of alcohol abuse and consumption such as drunkenness, ascites, GI bleeding etc. along with liver cirrhosis can be reported by the patient and his/her family and can be used for diagnosis as important information. Further, laboratory tests such as GGT(gamma-glutamyltransferase), AST(Aspartate amino-transferase), MCV of red blood cells and IgA are diagnostic of early ALD, whereas an increased international ratio and bilirubin level along with decreased albumin and platelet count are helpful in diagnosing advanced ALD. The AST/ALT ratio is typically >1 in patients of ALD and is > 2 in patients with alcoholic hepatitis. Liver biopsy is not usually performed to establish liver cirrhosis (Stickel et al. 2017). Noninvasive methods like measurement of liver stiffness and other serum markers are used to assess the level of liver fibrosis. Imaging techniques such as ultrasonography, computed tomography and magnetic resonance imaging are pretty useful for detecting steatosis, advanced fibrosis, cirrhosis along with portal hypertension (Pavlov et al. 2016).

Treatment and Intervention

The treatment and management protocol for ALD requires both pharmacological and non-pharmacological management. Non-pharmacological treatment includes management of alcohol abuse and abstinence of alcohol consumption in patients. Drinking cessation is the most important and effective method of controlling and preventing relapse of ALD and subsequent liver damage and failure. Lifestyle modification such as behavioural interventions and dietary alterations along with abstinence of alcohol consumption helps in improving the condition. Counselling and behavioural support can be provided by the nurses initially to promote alcohol abstinence. Abstinence from alcohol helps in resolving alcoholic steatosis and also helps in improving chances of survival in cirrhotic patients. Associated smoking, obesity and improper drug use should also be looked at (Pavlov et al.2016). Behavioural interventions such as cognitive therapy along with motivational enhancement therapy, supportive therapy and psychoeducation are useful methods of improving lifestyle and promoting alcohol abstinence (Singal et al. 2018). However, no psychosocial intervention has shown consistency in successfully maintaining abstinence in patients with ALD. Instead, a combined therapy including pharmacological intervention along with cognitive behavioral therapy appears to help better (Pavlov et al.2016). 

Nutritional therapy – ALD patients present with severe primary and secondary malnutrition, more specifically, protein energy malnutrition. Primary malnutrition occurs due to the presence of dietary imbalance because of alcohol intake and GI upset. Also alcohol associated mal-absorption and other complications like ascites are responsible for the same. Oral and enteral nutrition therapy will help in improving nutrition status of the patients. Patients of ALD with mild malnutrition showed improved outcomes in comparison to patients with severe malnutrition. A regular diet with approximately 1.5 g protein and 40 kcal/kg body weight is required for improved recovery of the ALD patient (Hammad et al.2017). Nursing intervention in terms of promoting rest and providing adequate nutrition to the patient along with close observation of the patient are beneficial.

Pharmacological interventions for the treatment of ALD include Silymarin which has been popularized as effective in chronic liver diseases (Stickel at al. 2017). However, a trial with 200 patients of cirrhosis of the liver due to alcohol when treated with 450 mg silymarin daily did not show any improvement, and a systematic review done by Cochrane including 13 randomized controlled trials did not find any benefit from the silymarin treatment (Rambaldi et al. 2005).

Corticosteroid therapy has also been promoted in cases of Alcoholic cirrhosis and hepatitis. The rationale behind this idea has been the possibility of the role of the immune system in beginning and promoting damage to the liver. 

Drug

Mechanism of action

Dosage

Duration

Side effects and interaction

Prednisolone

Suppresses the polymorphonuclear leukocyte migration and decreases capillary permeability. Suppresses immune system by reduction in volume and activity of immune system

40 mg p.o. once daily

28 days

Heartburn, nausea, vomiting along with headaches and dizziness.

Combined with alcohol can irritate the stomach and cause peptic ulcers as well.

Table 1: Corticosteroids used in alcoholic cirrhosis and hepatitis. (Louvet et al. 2015; Tkachenku et al. 2016)

Liver transplantation is considered the last option for treatment in cases of decompensated cases of liver cirrhosis and hepatic failure. Atleast 6 months alcohol abstinence pre-operatively, and continuous life-time monitoring is required post-operatively. Supportive alcohol de-addiction therapy and lifestyle modification is required to prevent transplant failure and relapse (Weinreib 2019).

Summary of Alcoholic Liver Disease

The clinical update has helped understand the alcoholic liver disease and its stages in a better way. The pathogenesis and aetiology was discussed along with the associated disorder of alcohol abuse. Also, the various treatment modalities including abstinence, liver transplant and associated lifestyle modifications were discussed. Alcohol abuse and chronic alcohol use needs to be looked at as a major problem and solved to help reduce the prevalence of liver disorder and liver disease in the population.

Reference for Alcoholic Liver Disease

Barve, A., Marsano, L. S., Parajuli, D., Cave, M., & McClain, C. J. (2017). Alcoholic liver disease. In Liver Disorders (pp. 173-197). Springer, Cham.

Farooq, M. O., & Bataller, R. (2016). Pathogenesis and management of alcoholic liver disease. Digestive Diseases34(4), 347-355.

Hammad, A., Kaido, T., Aliyev, V., Mandato, C., & Uemoto, S. (2017). Nutritional therapy in liver transplantation. Nutrients9(10), 1126.

Louvet, A., & Mathurin, P. (2015). Alcoholic liver disease: mechanisms of injury and targeted treatment. Nature Reviews Gastroenterology & Hepatology12(4), 231.

Mellinger, J. L. (2019). Epidemiology of alcohol use and alcoholic liver disease. Clinical Liver Disease13(5), 136.

Osna, N. A., Donohue Jr, T. M., & Kharbanda, K. K. (2017). Alcoholic liver disease: Pathogenesis and current management. Alcohol Research: Current Reviews38(2), 147

Pavlov, C. S., Casazza, G., Semenistaia, M., Nikolova, D., Tsochatzis, E., Liusina, E., & Gluud, C. (2016). Ultrasonography for diagnosis of alcoholic cirrhosis in people with alcoholic liver disease. Cochrane Database of Systematic Reviews, (3).

Rambaldi, A., Jacobs, B. P., Iaquinto, G., & Gluud, C. (2005). Milk thistle for alcoholic and/or hepatitis B or C liver diseases—a systematic cochrane hepato-biliary group review with meta-analyses of randomized clinical trials. American Journal of Gastroenterology100(11), 2583-2591.

Rehm, J., & Shield, K. D. (2019). Global burden of alcohol use disorders and alcohol liver disease. Biomedicines7(4), 99.

Seitz, H. K., Bataller, R., Cortez-Pinto, H., Gao, B., Gual, A., Lackner, C., & Tsukamoto, H. (2018). Alcoholic liver disease. Nature Reviews Disease Primers4(1), 1-22.

Singal, A. K., Bataller, R., Ahn, J., Kamath, P. S., & Shah, V. H. (2018). ACG clinical guideline: alcoholic liver disease. The American Journal of Gastroenterology113(2), 175.

Stickel, F., Datz, C., Hampe, J., & Bataller, R. (2017). Pathophysiology and management of alcoholic liver disease: update 2016. Gut and Liver11(2), 173.

Sugimoto, K., & Takei, Y. (2017). Pathogenesis of alcoholic liver disease. Hepatology Research47(1), 70-79.

Tkachenko, P., Maevskaya, M., Pavlov, A., Komkova, I., Pavlov, C., & Ivashkin, V. (2016). Prednisolone plus S-adenosil-L-methionine in severe alcoholic hepatitis. Hepatology International10(6), 983-987.

Weinrieb, R. M. (2019). New treatment models for alcohol use disorders and alcoholic liver disease. Clinical Liver Disease13(5), 118.

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