Site Loader
Rock Street, San Francisco

bstract

Alcoholic liver disease is a chronic liver disease that caused by
alcohol intake exceeding the safe limit of alcohol consumption. It may present
with the same stigmata of chronic liver disease that are caused by other
related factors such as viral hepatitis, autoimmune hepatitis or hepatocellular
carcinoma. Besides of alcohol itself, there are other risk factors that
contribute to the progression of liver cirrhosis in alcohol drinker such as
gender, genetic factors, drinking pattern and also obesity or nutritional status
of that individual.

We Will Write a Custom Essay Specifically
For You For Only $13.90/page!


order now

This case report will depict the case of alcoholic liver disease in
light of its pathophysiology, risk factors, clinical presentation for all its
spectrum of disease, diagnostic evaluation, management and treatment.

Keywords: liver disease;
alcohol; cirrhosis

 

Introduction

Alcohol is one of the most common causes of chronic liver disease.
This is because of ethanol metabolism will take part in the liver which
directly will damage the hepatocytes in terms of fat accumulation and immune-mediated
reactions. Liver damage that caused by alcohol will progress into three
spectrum of disease including alcoholic fatty liver, alcoholic hepatitis and
finally develop into cirrhosis. Based on all those three stages of alcoholic
liver disease, they have different clinical presentations, liver biochemistry
and also prognosis.

The investigations of alcoholic liver disease are mainly to
establish patient’s alcohol misuse, the severity of liver damage and to exclude
other aetiologies that can cause chronic liver disease. The managements are
focussed on abstinence of the alcohol intake, dietary supplementation,
prevention of the complication of chronic liver disease and also liver
transplantation.

 

Case Report

A 55-year-old Indian Muslim gentleman, an ex-smoker, he stopped
smoking for the past 1 year with 3 pack-year and a chronic alcohol drinker with
underlying of hypertension and dyslipidaemia diagnosed six months ago.

He presented to the Emergency Department of Hospital Ampang with
yellowish discolouration of his both eyes for three days prior to admission
associated with passing tea-coloured urine.

The yellowish discolouration of his eyes were noticed for three
days before he presented to the hospital by himself and also being told by his
family members and friends. Besides of having yellowish eye discolouration, he
claimed that he passed tea-coloured urine for one week before he was admitted
to the hospital. He also complained of lethargic for one week with loss of
appetite and loss of weight for about two kilograms in three months.

On further questioning, he was an alcohol drinker for about 15
years before he stopped for two months before he developed these complaints. He
took beer for about a cup per day which equal to one unit per day and seven
units per week.

Otherwise, he had no pale coloured stool, fever, abdominal pain,
itchiness, vomiting or vomit blood, passing blood per rectal, history of
intravenous drug user, history of blood transfusion, history of multiple sexual
partner, and history of hepatitis B or C and HIV. He also had no anaemic
symptoms such as palpitation, postural hypotension, pallor, no family history
of liver disease, history of thyroiditis or grave’s disease, rheumatoid
arthritis, ulcerative colitis, diabetes mellitus type-1 or emphysema.

He is having hypertension and dyslipidaemia since six months ago and
still on follow up at Hospital Ampang. He is on perindopril and amlodipine for his
hypertension and simvastatin for dyslipidaemia and compliant to the
medications. Patient had no past surgical history and no family history
related. For social history, he is a worker at a restaurant, married with seven
children, 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 is
hypertensive, 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 with
respiratory rate of 20 breaths per minute and also not in respiratory distress.
Hand examinations revealed no finger clubbing, no palmar erythema, no
leuconychia, no dupuytren contracture, no flapping tremor, no stigmata of
infective endocarditis, no koilonychia and no tar staining. No cervical lymphadenopathy,
no spider naevi, no gynaecomastia, and no parotid swelling noted. The jugular
venous pulse was also not elevated but there were bilateral leg edema that
extend up to mid shin.

On abdominal examination, there were dilated veins over the upper
quadrant of abdomen, the umbilicus is centrally located, no scars, no caput
medusa noted and the abdomen was moving with respiration. On palpation, the
abdomen was soft and non-tender, there was hepatomegaly noted with liver
measured for about 18 cm. Otherwise, no splenomegaly or abnormal mass palpable
and the kidneys were not ballotable.  No
inguinal lymphadenopathy and no inguinal hernia noted. There was shifting
dullness but no fluid thrill present and no hepatic or renal bruit noted and
the bowel sounds were present.

On cardiovascular examination, the pericardium was normal with no
scars or deformity seen. Apex beat was at 5th intercostal space in
mid clavicular line and first and second heart sounds were heard. No murmur or
any added sounds were heard.

On respiratory examination, the breath sound was vesicular and
equal 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 tone
and reflex for both upper limbs and lower limbs with power of 5/5 and Babinski
reflex were normal.

Provisional diagnosis for this case is alcoholic liver disease and
the 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 of
admission. Based on his full blood count result, his white cell count showed leucocytosis
of 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 heamoglobin
of 35.4 pg (n=26.9-32.3), and high mean cell haemoglobin concentration 36.3
g/dL (n=31.9-35.3).

Liver function test revealed hypoalbuminaemia of 30 g/L (n=35-52), high
ALP 302 U/L (n=40-129), high ALT 57 U/L, high AST 116, high total bilirubin
119.4 umol/L (n=0-21), with high indirect 54.5 umol/L (n=0-13) and direct
bilirubin 144.9 umol/L (n=0-5).

For UFEME, his specific gravity was low of 1.015 (n=1.016-1.022), nitrite
positive, leucocytes 1+, bilirubin 3+, urobilinogen 4+, protein negative, glucose
negative.  

For renal profile, urea was normal with 5.00 mmol/L (n=2.76-8.07), hyponatremia
of 131 mmol/L (n=136-146), hypokalemia of 2.7 mmol/L (n=3.4-4.5), low chloride of
96 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), normal
partial carbon dioxide (paCO2) of 37.6 mmHg (n=35-48), low partial
oxygen (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 partial
thromboplastin 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 were
non-reactive.

Chest radiography showed raised right hemidiaghram with clear lungs
filed 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.

 

Discussion

Alcohol is one of the most common aetiologies for developing
chronic liver disease.1,2,3,4 Patient with alcoholic liver disease
is commonly share risk factors for simultaneous injury from other liver insults
such as coexisting non-alcoholic fatty liver disease or chronic viral
hepatitis.3 Safe unit alcohol for men is only 21 units per week and
14 units per week for women or they will have high risk for liver cirrhosis by
exceeding those safe limits.1 However, it would be variable on
different individual but consumption of more than 30g per day of ethanol is
believed to have high risk threshold for developing alcoholic liver disease.1
Besides, there are a few risk factors that play their role in an individual to
develop alcoholic liver disease including dose, duration, type of alcohol,
drinking patterns, sex, ethnicity and other associated factors such as iron
overload, viral hepatitis, genetic factors and obesity.1,2 The most
important risk factor to develop alcoholic liver disease is the amount of
alcohol consumption. In men, ingestion of more than 60-80 g per day of alcohol
for 10 years or longer have high risk of developing cirrhosis and more than 20
g per day in women. Drink beer and spirits are more likely to develop liver
disease than wine.2 People who take alcohol continuously have higher
risk compared to intermittent or “binge” drinker.1,6 Women have
higher susceptible to alcohol liver disease than men as they have higher blood
ethanol levels.1 It is also believed due to pharmacokinetic reasons
such as differences in the response of the liver between men and women to
alcohol induced injury and ethanol absorption.6 Next, obesity people
also have higher risk towards alcoholic liver disease compared to those with
normal body size and genetic factors also predispose to the relation between
alcohol and liver disease.1,3,8

Ethanol is mainly metabolized in the liver by two pathways; 80% of
ethanol will be converted into acetyldehyde and these acetyldehyde forms
adducts with cellular protein in the hepatocytes that eventually activate the
immune system, contributing to cell injury.1,10,11 This pathway also
result in high NADH/NAD ration which will change the redox potential of the
cells. Another 20% of ethanol is metabolised by the microsomal
ethanol-oxidising system (MEOS) pathway. This pathway will release oxygen free
radicals, leading to lipid peroxidation and mitochondrial damage. Besides, pro-inflammatory
cytokines also play a role in inducing hepatic damage in alcoholic hepatitis,
where increased gut permeability will release endotoxin in the blood and this
will subsequently release tumour necrosis factor alpha (TNF-a), interleukin
(IL)-1, IL-2, and IL-8 from immune cells. All of these cytokines are believed
to involve in the pathogenesis of liver fibrosis.1,10,11

Alcoholic liver disease is divided into three main spectrum of
disease. There are alcoholic fatty liver disease, alcoholic hepatitis, and
alcoholic cirrhosis which they have different clinical presentations and
histological changes that may also overlap to each other.7,9,12

Alcoholic fatty liver disease is the first spectrum of liver
disease in alcohol drinker. It develops in about 90% of individuals who drink
more than 60g per day of alcohol.3 In this stage, alcohol metabolism
will cause fat accumulation in the liver and it is corresponding to the amount
of alcohol consumption. High alcohol consumption will produce swollen
hepatocytes with fat or called as steatosis without liver cell damage yet.2
At this stage, they normally have abnormal liver biochemistry but asymptomatic
with normal or enlarged liver.1,2,5 However, some cases may have
unspecific symptoms such as nausea, vomiting, and diarrhea due to alcohol
effect on gastrointestinal tract.2 This stage of alcoholic liver
disease has a good prognosis and may disappear after three months of
abstinence. However, several studies stated that 5%-15% of patient will
progress to fibrosis and cirrhosis despite of abstinence.3

Alcohol hepatitis occurs when there is infiltration of
polymorphonuclear leucocytes hepatocytes necrosis. Mallory bodies (dense
cytoplasmic inclusion) and giant mitochondria are also usually can be seen in
hepatocytes. However, Mallory bodies are only suggestive for alcohol liver
disease but it is not specific as it also may be found in Wilson’s disease and
Primary biliary cirrhosis.2 At this stage, patient may present with
jaundice, hepatomegaly and signs of portal hypertension; ascites and
encephalopathy.

Alcoholic cirrhosis is final stage of liver disease from alcohol
use and patient will have various stigmata of chronic liver disease, ascites,
varices and encephalopathy. They also may have large, normal or small liver and
have 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 severity
of liver damage. To establish the alcohol misuse, clinical history from
patient, relatives and friends is very important to know about the duration and
the exact portion of alcohol consumed because denial of alcohol misuse and
underreporting alcohol intake are common in patient with alcoholic liver
disease.1,3 A few questionnaires have been widely used to assess
alcohol abuse and its dependence. They are including CAGE, the MAST (Michigan
Alcoholism Screening Test) and the Alcohol Use Disorder Identification Test
(AUDIT).3

Clinical examination also important to look for all the stigmata of
chronic liver disease especially parotid enlargement, Dupuytren’s contracture
and signs of feminization. Besides, patient also may develop hepatic
encephalopathy, 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) in
the absence of anaemia and raised gamma-glutamyltransferase (GGT) level may
suggest and support a history of  heavy alcohol
misuse.2,4 However, high GGT level is not specific as it may also be
elevated in other conditions of liver disease, including NAFLD.1 Liver
biochemistry also may show elevation of serum aminotransferase enzymes.2
However, serum transaminase levels are often not so high in alcoholic liver
damage compared to viral or autoimmune hepatitis.4 Ultrasound and CT
scan are beneficial to look for fatty infiltration and the degree of liver
fibrosis can be estimated by doing elastrography. The main value of imaging
investigation for patient with alcoholic liver disease are to exclude other
causes of abnormal liver test such as obstructive biliary pathology, or
neoplastic disease of the liver. Specific features that suggestive for
alcoholic liver damage are higher volume index of caudate lobe, smaller size of
regenerative nodules, and visualization of the right posterior hepatic notch. Besides,
ultrasound also beneficial to detect splenomegaly and ascites.3 Liver
biopsy is usually required to determine the extent of liver damage and
histological changes must be observed to establish the diagnosis. The
histological changes in alcoholic liver disease include steatosis (fatty
change), periportal fibrosis, Mallory bodies, lobular inflammation, bile ductal
proliferation and fibrosis or cirrhosis.3

In stage of alcoholic hepatitis, blood investigation usually shows
leucocytosis and thrombocytopenia secondary to direct alcohol toxicity or
hypersplenism effect in portal hypertension. Electrolyte abnormality also
common with hypokalaemia, hypernatremia, hypocalcaemia and
hypomagnesaemia,  There will be also deranged
liver biochemistry with elevation of serum bilirubin, serum AST and ALT, serum
alkaline 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 alcoholic
liver 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 disease
with a poor prognosis. Other than Maddrey score, Glasgow score also being used
to assess the prognosis with components of age, white cell counts, PT,
bilirubin in addition to renal function (urea level). A score of nine or more
is associated with a 40% 28-day survival, compared to 80% for patient with a
score less than nine.1

Besides, specific laboratory investigations also should be done to
exclude other causes of liver disease. They are hepatitis B surface antigen,
anti-hepatitis B core IgG, antibodies to hepatitis C virus to exclude viral
hepatitis, serum ferritin and transferrin saturation for hemochromatosis, total
IgG  or gamma-globulin level,
anti-nuclear antibody, anti-smooth muscle antibody, and anti-liver/kidney
microsomal-1 antibodies for autoimmune hepatitis.4,5,7

 

Managements and treatments:

Management for alcoholic liver disease are mainly to treat the
complications of the cirrhosis including encephalopathy and signs of portal
hypertension (ascites, variceal bleeding), and decrease progression to
cirrhosis.

The most important treatment and prognostic factor is life-long
cessation of alcohol consumption. Abstinence is effective to prevent
progression, hepatic decompensation and death once cirrhosis is present.1,2,3,4
Several medications have been established in helping abstinence in patient with
alcoholic liver disease. They include Disulfiram,3 Naltrexone,3
Nalmefene,4 and Acamprosate.3 Diazepam should be given to patient
who have delirium tremens which is an alcohol withdrawal symptom.2

Since alcoholic patients are usually malnourished, so good
nutrition is crucial and enteral feeding via a fine-bore nasogastric tube may
be 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 be
administered empirically with intravenous thiamine.1,2

For severe alcoholic hepatitis with Maddrey’s score >32 or
Glasgow score of more than 9 steroid may be beneficial in 28-day survival from
52% to 78% which we can give prednisolone 40 mg daily for 28 days.1,4
However, steroid is strongly contraindicated in sepsis patient or those who
have variceal haemorrhage. To reduce hepatorenal failure, patient may be given
pentoxifylline (anti-TNF).

Liver transplantation is the best treatment for liver cirrhosis but
it remains controversial in alcoholic liver disease patients since it is
self-inflicted. A few programmes require a 6-months period of abstinence from
alcohol before a patient is considered for transplantation.1,2,3,4

 

Islamic input

In Islam, every drinks or foods that can intoxicate human’s body
and give bad effect to our brain are strictly forbidden because taking care of
our health is one of big responsibilities to every individuals in this world.
In the Holy Quran, alcohol drinks were called as “Khamr” and its prohibition
was mentioned three times by Allah and also being co-explained by Holy Prophet
Muhammad in a few hadith. In one of the verses that tell us about alcohol
prohibition had mentioned that there is greater harm in wine than its benefits.
Nowadays, there are many types and sources of alcoholic drinks which there are
still considered to be forbidden as long as it intoxicates people.

Alcohol beverages is one of the things that Allah forbade and every
forbiddance is sin. Therefore, we as Muslim specifically should not drink
alcohol as it can affect many of our body functions mainly our liver that is
one of important organ in our body. Besides, it also a bad habit that can drive
us away from the remembrance of Allah. 

Post Author: admin

x

Hi!
I'm Dora!

Would you like to get a custom essay? How about receiving a customized one?

Check it out