bstract one week before he was admitted to the

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Last updated: August 3, 2019

bstractAlcoholic liver disease is a chronic liver disease that caused byalcohol intake exceeding the safe limit of alcohol consumption. It may presentwith the same stigmata of chronic liver disease that are caused by otherrelated factors such as viral hepatitis, autoimmune hepatitis or hepatocellularcarcinoma. Besides of alcohol itself, there are other risk factors thatcontribute to the progression of liver cirrhosis in alcohol drinker such asgender, genetic factors, drinking pattern and also obesity or nutritional statusof that individual. This case report will depict the case of alcoholic liver disease inlight of its pathophysiology, risk factors, clinical presentation for all itsspectrum of disease, diagnostic evaluation, management and treatment. Keywords: liver disease;alcohol; cirrhosis IntroductionAlcohol is one of the most common causes of chronic liver disease.This is because of ethanol metabolism will take part in the liver whichdirectly will damage the hepatocytes in terms of fat accumulation and immune-mediatedreactions.

Liver damage that caused by alcohol will progress into threespectrum of disease including alcoholic fatty liver, alcoholic hepatitis andfinally develop into cirrhosis. Based on all those three stages of alcoholicliver disease, they have different clinical presentations, liver biochemistryand also prognosis. The investigations of alcoholic liver disease are mainly toestablish patient’s alcohol misuse, the severity of liver damage and to excludeother aetiologies that can cause chronic liver disease. The managements arefocussed on abstinence of the alcohol intake, dietary supplementation,prevention of the complication of chronic liver disease and also livertransplantation.

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 Case ReportA 55-year-old Indian Muslim gentleman, an ex-smoker, he stoppedsmoking for the past 1 year with 3 pack-year and a chronic alcohol drinker withunderlying of hypertension and dyslipidaemia diagnosed six months ago. He presented to the Emergency Department of Hospital Ampang withyellowish discolouration of his both eyes for three days prior to admissionassociated with passing tea-coloured urine. The yellowish discolouration of his eyes were noticed for threedays before he presented to the hospital by himself and also being told by hisfamily members and friends. Besides of having yellowish eye discolouration, heclaimed that he passed tea-coloured urine for one week before he was admittedto the hospital. He also complained of lethargic for one week with loss ofappetite and loss of weight for about two kilograms in three months.

On further questioning, he was an alcohol drinker for about 15years before he stopped for two months before he developed these complaints. Hetook beer for about a cup per day which equal to one unit per day and sevenunits per week. Otherwise, he had no pale coloured stool, fever, abdominal pain,itchiness, vomiting or vomit blood, passing blood per rectal, history ofintravenous drug user, history of blood transfusion, history of multiple sexualpartner, and history of hepatitis B or C and HIV. He also had no anaemicsymptoms such as palpitation, postural hypotension, pallor, no family historyof liver disease, history of thyroiditis or grave’s disease, rheumatoidarthritis, ulcerative colitis, diabetes mellitus type-1 or emphysema. He is having hypertension and dyslipidaemia since six months ago andstill on follow up at Hospital Ampang. He is on perindopril and amlodipine for hishypertension and simvastatin for dyslipidaemia and compliant to themedications. Patient had no past surgical history and no family historyrelated. For social history, he is a worker at a restaurant, married with sevenchildren, ex-smoker of 3 pack-year, ex-alcohol drinker and not a drug abuser.

At the Emergency Department, his blood pressure was 150/89 which ishypertensive, pulse rate was 102 beats per minute which is tachycardic,temperature was 37ºc, and spO2 was 99%. On physical examination in the ward, generally he was alert,conscious, well-nourished, jaundiced but not pale, not tachypnic withrespiratory rate of 20 breaths per minute and also not in respiratory distress.Hand examinations revealed no finger clubbing, no palmar erythema, noleuconychia, no dupuytren contracture, no flapping tremor, no stigmata ofinfective endocarditis, no koilonychia and no tar staining. No cervical lymphadenopathy,no spider naevi, no gynaecomastia, and no parotid swelling noted. The jugularvenous pulse was also not elevated but there were bilateral leg edema thatextend up to mid shin. On abdominal examination, there were dilated veins over the upperquadrant of abdomen, the umbilicus is centrally located, no scars, no caputmedusa noted and the abdomen was moving with respiration. On palpation, theabdomen was soft and non-tender, there was hepatomegaly noted with livermeasured for about 18 cm.

Otherwise, no splenomegaly or abnormal mass palpableand the kidneys were not ballotable.  Noinguinal lymphadenopathy and no inguinal hernia noted. There was shiftingdullness but no fluid thrill present and no hepatic or renal bruit noted andthe bowel sounds were present. On cardiovascular examination, the pericardium was normal with noscars or deformity seen. Apex beat was at 5th intercostal space inmid clavicular line and first and second heart sounds were heard. No murmur orany added sounds were heard. On respiratory examination, the breath sound was vesicular andequal on both lungs.

No rhonchi, crepitation or other abnormal sounds heard. On central nervous system, there was no abnormal movement, ptosis,dysphasia or dysarthria. All cranial nerves were grossly intact. Normal toneand reflex for both upper limbs and lower limbs with power of 5/5 and Babinskireflex were normal.Provisional diagnosis for this case is alcoholic liver disease andthe differential diagnosis are hepatocellular carcinoma, viral hepatitis,autoimmune hepatitis and non-alcoholic fatty liver disease. Few investigations have been done for this patient on the day ofadmission.

Based on his full blood count result, his white cell count showed leucocytosisof 12.8 x 109/L (n=4.1-11.4), haemoglobin level of 13.3 g/dL (n=13.

5-17.4)which is slightly anaemic, normal platelet count of 151 x 109/L(n=142-350), low haematocrit of 36.6% (n=40.1-50.6), high mean cell heamoglobinof 35.4 pg (n=26.9-32.

3), and high mean cell haemoglobin concentration 36.3g/dL (n=31.9-35.

3). Liver function test revealed hypoalbuminaemia of 30 g/L (n=35-52), highALP 302 U/L (n=40-129), high ALT 57 U/L, high AST 116, high total bilirubin119.4 umol/L (n=0-21), with high indirect 54.5 umol/L (n=0-13) and directbilirubin 144.

9 umol/L (n=0-5).For UFEME, his specific gravity was low of 1.015 (n=1.

016-1.022), nitritepositive, leucocytes 1+, bilirubin 3+, urobilinogen 4+, protein negative, glucosenegative.  For renal profile, urea was normal with 5.

00 mmol/L (n=2.76-8.07), hyponatremiaof 131 mmol/L (n=136-146), hypokalemia of 2.7 mmol/L (n=3.4-4.5), low chloride of96 mmol/L (n=98-107), low creatinine of 50 umol/L (n=62-106)His venous blood gas showed normal pH of 3.

797 (n=7.35-7.45), normalpartial carbon dioxide (paCO2) of 37.6 mmHg (n=35-48), low partialoxygen (paO2) of 47.1 mmHg (n=83-108), low oxygen saturation (spO2)of 76% (n=95-99), and normal serum bicarbonate (HCO3) of 22.8 mmol/L(21-28). His coagulation profile revealed normal activated partialthromboplastin time (APTT) of 33.5 s (n=31-43.

9), but high prothrombin time (PT)16.4 s (n=11.9-14.2), and INR of 1.31. Screening for Hep Bs Ag and Anti HCV have been done and both werenon-reactive.Chest radiography showed raised right hemidiaghram with clear lungsfiled and no cardiomegaly. Abdomen radiography was normal.

Ultrasound HBS showed features that suggestive of liver cirrhosis.A diagnosis of chronic alcoholic liver disease was made. DiscussionAlcohol is one of the most common aetiologies for developingchronic liver disease.1,2,3,4 Patient with alcoholic liver diseaseis commonly share risk factors for simultaneous injury from other liver insultssuch as coexisting non-alcoholic fatty liver disease or chronic viralhepatitis.3 Safe unit alcohol for men is only 21 units per week and14 units per week for women or they will have high risk for liver cirrhosis byexceeding those safe limits.1 However, it would be variable ondifferent individual but consumption of more than 30g per day of ethanol isbelieved to have high risk threshold for developing alcoholic liver disease.1Besides, there are a few risk factors that play their role in an individual todevelop alcoholic liver disease including dose, duration, type of alcohol,drinking patterns, sex, ethnicity and other associated factors such as ironoverload, viral hepatitis, genetic factors and obesity.1,2 The mostimportant risk factor to develop alcoholic liver disease is the amount ofalcohol consumption.

In men, ingestion of more than 60-80 g per day of alcoholfor 10 years or longer have high risk of developing cirrhosis and more than 20g per day in women. Drink beer and spirits are more likely to develop liverdisease than wine.2 People who take alcohol continuously have higherrisk compared to intermittent or “binge” drinker.1,6 Women havehigher susceptible to alcohol liver disease than men as they have higher bloodethanol levels.1 It is also believed due to pharmacokinetic reasonssuch as differences in the response of the liver between men and women toalcohol induced injury and ethanol absorption.6 Next, obesity peoplealso have higher risk towards alcoholic liver disease compared to those withnormal body size and genetic factors also predispose to the relation betweenalcohol and liver disease.

1,3,8 Ethanol is mainly metabolized in the liver by two pathways; 80% ofethanol will be converted into acetyldehyde and these acetyldehyde formsadducts with cellular protein in the hepatocytes that eventually activate theimmune system, contributing to cell injury.1,10,11 This pathway alsoresult in high NADH/NAD ration which will change the redox potential of thecells. Another 20% of ethanol is metabolised by the microsomalethanol-oxidising system (MEOS) pathway.

This pathway will release oxygen freeradicals, leading to lipid peroxidation and mitochondrial damage. Besides, pro-inflammatorycytokines also play a role in inducing hepatic damage in alcoholic hepatitis,where increased gut permeability will release endotoxin in the blood and thiswill subsequently release tumour necrosis factor alpha (TNF-a), interleukin(IL)-1, IL-2, and IL-8 from immune cells. All of these cytokines are believedto involve in the pathogenesis of liver fibrosis.1,10,11Alcoholic liver disease is divided into three main spectrum ofdisease. There are alcoholic fatty liver disease, alcoholic hepatitis, andalcoholic cirrhosis which they have different clinical presentations andhistological changes that may also overlap to each other.

7,9,12Alcoholic fatty liver disease is the first spectrum of liverdisease in alcohol drinker. It develops in about 90% of individuals who drinkmore than 60g per day of alcohol.3 In this stage, alcohol metabolismwill cause fat accumulation in the liver and it is corresponding to the amountof alcohol consumption. High alcohol consumption will produce swollenhepatocytes with fat or called as steatosis without liver cell damage yet.2At this stage, they normally have abnormal liver biochemistry but asymptomaticwith normal or enlarged liver.1,2,5 However, some cases may haveunspecific symptoms such as nausea, vomiting, and diarrhea due to alcoholeffect on gastrointestinal tract.

2 This stage of alcoholic liverdisease has a good prognosis and may disappear after three months ofabstinence. However, several studies stated that 5%-15% of patient willprogress to fibrosis and cirrhosis despite of abstinence.3Alcohol hepatitis occurs when there is infiltration ofpolymorphonuclear leucocytes hepatocytes necrosis. Mallory bodies (densecytoplasmic inclusion) and giant mitochondria are also usually can be seen inhepatocytes. However, Mallory bodies are only suggestive for alcohol liverdisease but it is not specific as it also may be found in Wilson’s disease andPrimary biliary cirrhosis.

2 At this stage, patient may present withjaundice, hepatomegaly and signs of portal hypertension; ascites andencephalopathy.Alcoholic cirrhosis is final stage of liver disease from alcoholuse and patient will have various stigmata of chronic liver disease, ascites,varices and encephalopathy. They also may have large, normal or small liver andhave risk to develop hepatocellular carcinoma.1,9  Investigations and diagnostic evaluation:The aims for investigations are mainly to establish alcohol misuse,to exclude other coexistent causes of liver disease and to assess the severityof liver damage. To establish the alcohol misuse, clinical history frompatient, relatives and friends is very important to know about the duration andthe exact portion of alcohol consumed because denial of alcohol misuse andunderreporting alcohol intake are common in patient with alcoholic liverdisease.

1,3 A few questionnaires have been widely used to assessalcohol abuse and its dependence. They are including CAGE, the MAST (MichiganAlcoholism Screening Test) and the Alcohol Use Disorder Identification Test(AUDIT).3Clinical examination also important to look for all the stigmata ofchronic liver disease especially parotid enlargement, Dupuytren’s contractureand signs of feminization. Besides, patient also may develop hepaticencephalopathy, presence of visible veins on the anterior abdominal wall,edema, ascites, spider naevi, weakness and hepatic bruit.1,3,9 Next,biological markers such as elevated mean cell volume (MCV), (macrocytosis) inthe absence of anaemia and raised gamma-glutamyltransferase (GGT) level maysuggest and support a history of  heavy alcoholmisuse.2,4 However, high GGT level is not specific as it may also beelevated in other conditions of liver disease, including NAFLD.

1 Liverbiochemistry also may show elevation of serum aminotransferase enzymes.2However, serum transaminase levels are often not so high in alcoholic liverdamage compared to viral or autoimmune hepatitis.4 Ultrasound and CTscan are beneficial to look for fatty infiltration and the degree of liverfibrosis can be estimated by doing elastrography. The main value of imaginginvestigation for patient with alcoholic liver disease are to exclude othercauses of abnormal liver test such as obstructive biliary pathology, orneoplastic disease of the liver. Specific features that suggestive foralcoholic liver damage are higher volume index of caudate lobe, smaller size ofregenerative nodules, and visualization of the right posterior hepatic notch.

Besides,ultrasound also beneficial to detect splenomegaly and ascites.3 Liverbiopsy is usually required to determine the extent of liver damage andhistological changes must be observed to establish the diagnosis. Thehistological changes in alcoholic liver disease include steatosis (fattychange), periportal fibrosis, Mallory bodies, lobular inflammation, bile ductalproliferation and fibrosis or cirrhosis.3In stage of alcoholic hepatitis, blood investigation usually showsleucocytosis and thrombocytopenia secondary to direct alcohol toxicity orhypersplenism effect in portal hypertension. Electrolyte abnormality alsocommon with hypokalaemia, hypernatremia, hypocalcaemia andhypomagnesaemia,  There will be also derangedliver biochemistry with elevation of serum bilirubin, serum AST and ALT, serumalkaline phosphatase, prothrombin time (PT).

2,4 Prothrombin time(PT) and bilirubin levels are important to calculate a ‘discriminant function'(DF) or Maddrey score which is useful to assess the prognosis of alcoholicliver disease. The formula of DF is DF = 4.6 x Increase in PT (sec) +Bilirubin (mg/dL) and the value of more than 32 implies severe liver diseasewith a poor prognosis. Other than Maddrey score, Glasgow score also being usedto assess the prognosis with components of age, white cell counts, PT,bilirubin in addition to renal function (urea level). A score of nine or moreis associated with a 40% 28-day survival, compared to 80% for patient with ascore less than nine.

1Besides, specific laboratory investigations also should be done toexclude other causes of liver disease. They are hepatitis B surface antigen,anti-hepatitis B core IgG, antibodies to hepatitis C virus to exclude viralhepatitis, serum ferritin and transferrin saturation for hemochromatosis, totalIgG  or gamma-globulin level,anti-nuclear antibody, anti-smooth muscle antibody, and anti-liver/kidneymicrosomal-1 antibodies for autoimmune hepatitis.4,5,7 Managements and treatments:Management for alcoholic liver disease are mainly to treat thecomplications of the cirrhosis including encephalopathy and signs of portalhypertension (ascites, variceal bleeding), and decrease progression tocirrhosis. The most important treatment and prognostic factor is life-longcessation of alcohol consumption. Abstinence is effective to preventprogression, hepatic decompensation and death once cirrhosis is present.1,2,3,4Several medications have been established in helping abstinence in patient withalcoholic liver disease. They include Disulfiram,3 Naltrexone,3Nalmefene,4 and Acamprosate.3 Diazepam should be given to patientwho have delirium tremens which is an alcohol withdrawal symptom.

2Since alcoholic patients are usually malnourished, so goodnutrition is crucial and enteral feeding via a fine-bore nasogastric tube maybe needed in severely ill patient. Patient should get high diet protein and  vitamin supplements and enough bed rest.Besides, to prevent Wernicke-Karsakoff encephalopathy, patient should beadministered empirically with intravenous thiamine.1,2For severe alcoholic hepatitis with Maddrey’s score >32 orGlasgow score of more than 9 steroid may be beneficial in 28-day survival from52% to 78% which we can give prednisolone 40 mg daily for 28 days.1,4However, steroid is strongly contraindicated in sepsis patient or those whohave variceal haemorrhage.

To reduce hepatorenal failure, patient may be givenpentoxifylline (anti-TNF). Liver transplantation is the best treatment for liver cirrhosis butit remains controversial in alcoholic liver disease patients since it isself-inflicted. A few programmes require a 6-months period of abstinence fromalcohol before a patient is considered for transplantation.1,2,3,4 Islamic input In Islam, every drinks or foods that can intoxicate human’s bodyand give bad effect to our brain are strictly forbidden because taking care ofour health is one of big responsibilities to every individuals in this world.In the Holy Quran, alcohol drinks were called as “Khamr” and its prohibitionwas mentioned three times by Allah and also being co-explained by Holy ProphetMuhammad in a few hadith. In one of the verses that tell us about alcoholprohibition had mentioned that there is greater harm in wine than its benefits.

Nowadays, there are many types and sources of alcoholic drinks which there arestill considered to be forbidden as long as it intoxicates people. Alcohol beverages is one of the things that Allah forbade and everyforbiddance is sin. Therefore, we as Muslim specifically should not drinkalcohol as it can affect many of our body functions mainly our liver that isone of important organ in our body. Besides, it also a bad habit that can driveus away from the remembrance of Allah. 

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