Global Journal of Health Science; Vol. 13, No.

5; 2021
ISSN 1916-9736 E-ISSN 1916-9744
Published by Canadian Center of Science and Education

Etiologies of Liver Cirrhosis and Their Clinical Presentation among

Inpatients in Medical City Complex - Baghdad Teaching Hospital
Khalid Abdulla Al-Khazraji1, Mohammed Kamal Hashim2, Mahmood Kamal Hashim3,
Mohammed Khalid Abdulla4, Issam Hadi Khudhair5 & Wissam Khudhair Abbas6
1
Professor of Gastroenterology, College of Medicine, Baghdad University, Iraq
2
Department of Surgery, Al-Noman Teaching hospital, Al-Iraqia Medical College, Iraq
3
Department of Dermatology, Baghdad Teaching hospital, Iraq
4
Medical student 4th grade, Baghdad Medical College, Iraq
5
Medical student 6th grade, Pleven Medical University, Iraq
6
Al-Mustansiriya University, College of Medicine, Iraq
Correspondence: Khalid Abdulla Al-Khazraji, MBCHB, MD, CAMB, FRCP, FACP, Professor of
Gastroenterology, College of Medicine, Baghdad University, Iraq.

Received: January 18, 2021 Accepted: February 28, 2021 Online Published: April 13, 2021
doi:10.5539/gjhs.v13n5p64 URL: https://doi.org/10.5539/gjhs.v13n5p64

Abstract
Background: Liver cirrhosis is one of common diseases that doctors deal with during working days, so it is
important for all doctors to have a basic knowledge about its etiologies, clinical presentations, complications and
prognosis.
Aim of the study: 1) To detect the most common causes of liver cirrhosis among Iraqi patients. 2) To Find the
most common clinical presentations and look for any association between them and a particular etiology. 3) To
make recommendations regarding screening for the most common etiology among population and deal with it and
treat it early prior to development of liver fibrosis and cirrhosis.
Patient and methods: A cross-sectional study was conducted from January 2016 to January 2019. 1000 patients
were enrolled in the current study and followed at medical wards at Baghdad teaching hospital, taking detailed
history from them including history of alcohol intake, drug history, etc... and sending them for complete work up
including Abdominal US, virology screening, autoimmune, Wilson, iron study etc... and calculating Child - Pugh
score for each patient.
Results: 1) The most common causes of liver cirrhosis are alcoholic liver disease (20%) and HCV (20%) followed
by HBV (18%), NAFLD (14%), cryptogenic (14%), AIH (6%), Wilson (4%), PBC (4%). 2) the most common
presentation of liver cirrhosis from all causes are ascites (38%) and encephalopathy (38%). followed by bleeding
varices (21%), jaundice (11%). 3) HCV was associated significantly with Encephalopathy, NAFLD significantly
associated with bleeding varices, Cryptogenic significantly associated with ascites, Wilson disease and PBC
significantly associated with jaundice.
Conclusions: HCV and alcoholism are so common among Iraqi patients with liver cirrhosis, while NAFLD cases
are commonly related to diabetes mellitus and obesity. Ascites and encephalopathy are the most common
presentation at medical wards from all causes of liver cirrhosis. Most cases of liver cirrhosis due to HCV are within
middle and elderly. While Wilson disease should be kept at the top of differential diagnosis of liver cirrhosis
among young individuals as it is significantly related to young age group. Cryptogenic cases of liver cirrhosis need
aggressive work up and screening for uncommon causes.
Keywords: hepatic cirrhosis, etiology, presentation
1. Introduction
1.1 Definition of Liver Cirrhosis
Cirrhosis, which can be the final stage of any chronic liver disease, is a diffuse process characterized by fibrosis
and conversion of normal architecture to structurally abnormal nodules. These “regenerative” nodules lack normal
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lobular organization and are surrounded by fibrous tissue. The process involves the whole liver and generally is
considered irreversible. Although cirrhosis is histologically an “all-or-nothing” diagnosis, clinically it can be
classified by its status as compensated or decompensated. Decompensated cirrhosis is defined by the presence of
ascites, variceal bleeding, encephalopathy, or jaundice, which are complications that result from the main
consequences of cirrhosis: portal hypertension and liver insufficiency (Lee Goldman, Andrew I. Schafer. 2016).
1.2 Diagnosis of Liver Cirrhosis
Although cirrhosis is strictly speaking a histologic diagnosis, a combination of clinical, laboratory, and imaging
features can help confirm a diagnosis of cirrhosis.
A clinical stigmata of liver cirrhosis includes palmar erythema, Terry’s nails, Clubbing of the fingernails,
Gynecomastia, Spider telangiectasias (or angiomata), Dilated abdominal veins (caput medusae) with flow away
from the umbilicus, toward the inferior vena cava in the infraumbilical area and toward the superior vena cava in
the supraumbilical area, suggest intrahepatic portal hypertension. On the other hand, dilatation of veins in the flank
with blood draining toward the superior vena cava suggests inferior vena caval obstruction. Parotid enlargement is
also a feature of cirrhosis, especially alcoholic cirrhosis.
Patients with a history of chronic liver disease with gastroesophageal varices, ascites, or hepatic encephalopathy
are likely to have cirrhosis, and liver biopsy is not essential in such cases for confirming cirrhosis. In patients with
a diagnosis of chronic liver disease without these complications, physical findings of an enlarged left hepatic lobe
with splenomegaly, along with the cutaneous stigmata of liver disease described earlier, suggest cirrhosis,
especially in the setting of thrombocytopenia and impaired hepatic synthetic function (e.g., hypoalbuminemia,
prolongation of the prothrombin time). If physical and laboratory findings are not suggestive of cirrhosis, imaging
studies can help make a diagnosis of cirrhosis. A small nodular liver with splenomegaly and intra-abdominal
collaterals and the presence of ascites on abdominal US (or other cross-sectional imaging study) suggests cirrhosis.
Liver biopsy has long been the gold standard for diagnosing cirrhosis but may be associated with costs and
procedure related risks, albeit infrequently the major concerns regarding the use of a liver biopsy to diagnose
cirrhosis includes sampling error and interobserver disagreement in the estimation of the extent of fibrosis. The
ideal combination of clinical findings and routine laboratory tests to determine whether a patient has cirrhosis
without the need for a liver biopsy has been addressed in a systematic fashion (Mark Feldman, Lawrence S.
Friedman, Lawrence J. Brandt. 2016).
1.3 Etiologies of Liver Cirrhosis and Their Epidemiological Studies Worldwide
1) Alcoholism
2) Chronic viral hepatitis: hepatitis B, Hepatitis C
3) Autoimmune hepatitis
4) Nonalcoholic steatohepatitis
5) Biliary cirrhosis: Primary biliary cirrhosis, Primary sclerosing cholangitis. Autoimmune cholangiopathy
6) Cardiac cirrhosis
7) Inherited metabolic liver disease: Hemochromatosis, Wilson's disease, Alpha 1 antitrypsin deficiency, Cystic
fibrosis
8) Cryptogenic cirrhosis
HCV infection:
The worldwide seroprevalence of HCV infection, based on detection of antibody to HCV (anti-HCV), is estimated
to be 3%, with more than 170 million people infected chronically. The overall worldwide prevalence increased
from 1990 to 2010.1 marked geographic variation exists, with infection rates ranging from 1.3% to 1.6% in the
United States to 15% in Egypt. In 2002, between 3.2 and 5 million persons were infected with HCV in the United
States, (3) but the incidence of HCV has declined continually since 1994. The highest prevalence in different age
groups shifted from 35 to 44 years (2.5%) to 55 to 64 years in 2005 (2.7%). It has therefore been recommended that
all persons born between 1945 and 1965 be tested for anti-HCV (Smith BD, Morgan RL, Beckett GA, et al. 2012).
HBV infection:
The sequelae of chronic HBV infection vary from an inactive carrier state to the development of cirrhosis, hepatic
decompensation, hepatocellular carcinoma (HCC), extrahepatic manifestations, and death. The prognosis appears
to vary with the clinical setting. Long-term follow-up studies of HBsAg positive blood donors have shown that the
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majority remain asymptomatic with a very low risk of cirrhosis or HCC (Villeneuve JP, Desrochers M,
Infante-Rivard C, et al. 1994), (Manno M, Cammà C, Schepis F, et al. 2004).
The prognosis is worse in HBV-infected patients from endemic areas and in patients with chronic hepatitis B
(Fattovich G, Brollo L, Giustina G, et al. ), (Liaw YF, Lin DY, Chen TJ, Chu CM. 1989).
Alcoholic liver disease:
Excessive alcohol consumption is associated with a range of hepatic manifestations, including alcoholic fatty liver
disease (with or without steatohepatitis), alcoholic hepatitis, and cirrhosis. Patients with an alcohol intake of 30 or
more grams per day are at increased risk of cirrhosis, although the majority of patients will not develop cirrhosis
despite heavy alcohol intake (point prevalence of 1 percent for those who drink 30 to 60 g/day and 6 percent for
those who drink 120 g/day). Unfortunately, among those who do develop liver disease, symptoms often develop
only after severe, life-threatening liver disease has already developed (Bellentani S, Saccoccio G, Costa G, et al.
1997)
NAFLD:
Nonalcoholic fatty liver disease (NAFLD) refers to the presence of hepatic steatosis when no other causes for
secondary hepatic fat accumulation (eg, heavy alcohol consumption) are present. NAFLD may progress to
cirrhosis and is likely an important cause of cryptogenic cirrhosis (Caldwell SH, Oelsner DH, Iezzoni JC, et al.
1999), (Poonawala A, Nair SP, Thuluvath PJ. 2000 ).
Nonalcoholic fatty liver disease (NAFLD) is subdivided into nonalcoholic fatty liver (NAFL) and nonalcoholic
steatohepatitis (NASH). In NAFL, hepatic steatosis is present without evidence of inflammation, whereas in
NASH, hepatic steatosis is associated with hepatic inflammation that histologically is indistinguishable from
alcoholic steatohepatitis (Ludwig J, Viggiano TR, McGill DB, Oh BJ. 1980), (Sheth SG, Gordon FD, Chopra S.
1997).
Autoimmune hepatitis:
Autoimmune hepatitis is a chronic hepatitis that occurs in children and adults of all ages. It is characterized by
immunologic and autoimmunologic features, generally including the presence of circulating autoantibodies and
high serum globulin concentrations (Krawitt EL. 2006).
Autoimmune hepatitis has a heterogeneous and fluctuating nature, leading to marked variability in its clinical
manifestations. The spectrum includes asymptomatic patients, those with considerable and sometimes debilitating
symptoms, and those with acute liver failure. Furthermore, long periods of subclinical disease may occur before or
after presentation. Physical findings range from a normal physical examination to the presence of hepatomegaly,
splenomegaly, stigmata of chronic liver disease, and jaundice (Muratori P, Granito A, Quarneti C, et al. 2009).
Primary biliary cirrhosis:
Primary biliary cirrhosis (PBC) is characterized by a T-lymphocyte-mediated attack on small intralobular bile
ducts. A continuous assault on the bile duct epithelial cells leads to their gradual destruction and eventual
disappearance. The sustained loss of intralobular bile ducts causes the signs and symptoms of cholestasis and
eventually results in cirrhosis and liver failure (Kaplan MM. 1996), (Moebius U, Manns M, Hess G, et al. 1990).
PBC occurs worldwide and predominantly in women, with a female-to-male ratio of 9: 1.
The diagnosis of PBC usually is made between the ages of 30 and 60 years, with a range of 21 to 93 years. The
disease has been documented in even younger patients-2 teenagers 15 and 16 years of age, respectively (Dahlan Y,
Smith L, Simmonds D, et al. 2003).
Hemochromatosis:
Hereditary hemochromatosis is an autosomal recessive disorder in which mutations in the HFE gene cause
increased intestinal iron absorption. The clinical manifestations of this disorder, and of other forms of iron
overload, are related to excessive iron deposition in tissues, especially the liver, heart, pancreas, and pituitary
(Bacon BR, Adams PC, Kowdley KV, et al. 2011).
Progressive iron deposition is associated with hepatomegaly, elevated liver enzymes, and the eventual
development of increasing fibrosis and cirrhosis (Adams PC, Deugnier Y, Moirand R, Brissot P. 1997),
(Fracanzani AL, Fargion S, Romano R, et al. 1995).
Wilson disease:
Wilson disease (hepatolenticular degeneration) is due to a genetic abnormality inherited in an autosomal recessive
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manner that leads to impairment of cellular copper transport. Impaired biliary copper excretion leads to
accumulation of copper in several organs, most notably the liver, brain, and cornea. Over time, the liver is
progressively damaged and eventually becomes cirrhotic. In addition, patients may develop neurologic
complications, which can be severe (J Hepatol. 2012).
Budd – Chiari syndrome:
The Budd-Chiari syndrome can be defined as any pathophysiologic process that results in an interruption or
diminution of the normal flow of blood out of the liver. However, as commonly used, the Budd-Chiari syndrome
implies thrombosis of the hepatic veins and/or the intrahepatic or suprahepatic inferior vena cava (Valla DC. 2008).
(Menon KV, Shah V, Kamath PS. 2004).
BCS is a rare disease. In Sweden, prevalence rates in 1990 to 2001 were estimated to be 1.4 per million population
(Rajani R, Melin T, Bjornsson E, et al. 2009).
There is a slight female predominance. The median age at diagnosis was 37 in one case series (Darwish Murad S,
Plessier A, Hernandez-Guerra M, et al. 2009).
The incidence of BCS in Asia may be higher. BCS accounted for 17% of hospital admissions for liver-related
disease in Kathmandu, Nepal, from 1990 to 1992 (Shrestha SM, Okuda K, Uchida T, et al. 1996).
Cardiac cirrhosis:
Patients with long-standing right-sided congestive heart failure may develop chronic liver injury and cardiac
cirrhosis. This is an increasingly uncommon, if not rare, cause of chronic liver disease given the advances made in
the care of patients with heart failure. Patients typically have signs of congestive heart failure and will manifest an
enlarged firm liver on physical examination.
Primary sclerosing cholangitis:
As in PBC, the cause of PSC remains unknown. PSC is a chronic cholestatic syndrome that is characterized by
diffuse inflammation and fibrosis involving the entire biliary tree, resulting in chronic cholestasis. This pathologic
process ultimately results in obliteration of both the intra- and extrahepatic biliary tree, leading to biliary cirrhosis,
portal hypertension, and liver failure.
Other types of cirrhosis:
α1AT deficiency results from an inherited disorder that causes abnormal folding of the α1AT protein, resulting in
failure of secretion of that protein from the liver. It is unknown how the retained protein leads to liver disease.
Patients with α1AT deficiency at greatest risk for developing chronic liver disease have the ZZ phenotype, but only
about 10–20% of such individuals will develop chronic liver disease. Diagnosis is made by determining α1AT
levels and phenotype. Characteristic periodic acid–Schiff (PAS)-positive, diastase-resistant globules are seen on
liver biopsy.
Cryptogenic cirrhosis:
Cryptogenic cirrhosis (CC) is the end stage of a chronic liver disease in which its underlying etiology remains
unknown after extensive clinical, serological, and pathological evaluations have been performed.
1.4 Types of Decompensation
At this stage, there are signs of decompensation: ascites, variceal hemorrhage, jaundice, hepatic
encephalopathy, or any combination of these findings. Ascites, which is the most frequent sign of
decompensation, is present in 80% of patients with decompensated cirrhosis (Lee Goldman,Andrew I.Shafer.
2012).
Variceal Hemorrhage
Gastroesophageal varices are present in approximately 50% of patients with newly diagnosed cirrhosis. Large
varices, severe liver disease, and red wale markings on varices are independent predictors of variceal hemorrhage.
Bleeding from gastroesophageal varices can be manifested as overt hematemesis or melena, or both (Dennis
L.Kasper,Anthony S.Fauci,Stephen L.Hauser,Dan L.Longo,J,Larry Jameson,Joseph Loscalzo. 2015).
Ascites:
Ascites is the most common cause of decompensation in cirrhosis and occurs at a rate of 7 to 10% per year. The
most frequent symptoms associated with ascites are increased abdominal girth, which is often described by the
patient as tightness of the belt or garments around the waist, and recent weight gain. When present in small to
moderate amounts, ascites can be identified on examination by bulging flanks, flank dullness, and shifting dullness
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(Lee Goldman,Andrew I.Shafer. 2012).

Hepatic Encephalopathy
Hepatic encephalopathy, which is the neuropsychiatric manifestation of cirrhosis, occurs at a rate of approximately
2 to 3% per year. On physical examination, early stages may demonstrate only a distal tremor, but the hallmark of
hepatic encephalopathy is the presence of asterixis. Additionally, patients with hepatic encephalopathy may have
sweet-smelling breath, a characteristic termed fetor hepaticus ((Lee Goldman,Andrew I.Shafer. 2012).
Jaundice
In cirrhosis is a reflection of the inability of the liver to excrete bilirubin and is therefore the result of liver
insufficiency. However, in cholestatic diseases leading to cirrhosis (e.g., primary biliary cirrhosis, primary
sclerosing cholangitis, vanishing bile duct syndrome), jaundice is more likely due to biliary damage than liver
insufficiency ((Lee Goldman,Andrew I.Shafer. 2012).
Child-pugh score (Dennis L.Kasper,Anthony S.Fauci,Stephen L.Hauser,Dan L.Longo,J,Larry Jameson,Joseph
Loscalzo. 2015):

2. Patients and Methods

The current study is a cross sectional study, which was conducted from January 2016 to January 2019, 1000
patients were enrolled in the study from Medical wards at Baghdad teaching hospital.
2.1 Selection Criteria
1) Inpatient, admitted with a previous or new diagnosis of Liver cirrhosis.
2) All cases of Liver cirrhosis were taken, including known and unknown cause of cirrhosis
3) All cases that were selected having decompensated liver cirrhosis with different types of decompensation
(Encephalopathy, jaundice, Ascites, Bleeding varices)
4) All patients were above 14 years old, with both sexes males and females.
5) Patients that are selected previously diagnosed as liver cirrhosis with or without liver biopsy depending
upon clinical and radiological evidence.
The study was approved by Research Ethics Committee at Baghdad teaching hospital, all patients included singed
an informed consent form after receiving information about the study. After that the following data were collected
from each patient:
1) Age
2) Sex
3) Date of Diagnosis of cirrhosis
4) Clinical presentation (decompensation)
5) Etiology of liver cirrhosis
6) Calculate child – Pugh score for each patient.(Based upon Clinical and Lab data obtained from patient's
file ).
7) Regarding the diagnosis of NAFLD (without biopsy ) depending on:
a. Exclusion of other causes of liver cirrhosis
Patient fulfill the criteria of diagnosis of metabolic syndrome (BMI>30, waist circumference >102 cm for male

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and >88 cm for females, Triglyceride >150 mg/dl, HDL<40 mg/dl for male and <50 mg/dl for female, and all
patients were Diabetic) as a NAFLD is significantly associated with obesity DM type 2 and metabolic
syndrome.(Ruhl & Everhart, 2003; Miyazaki, Glass, Triplitt, Wajcberg, Mandarino, & DeFronzo, 2002; Clark,
Brancati, & Diehl, 2003; Williams et al., 2011).
8) Considering the diagnosis of cryptogenic cirrhosis (without biopsy ) depending on:
a. Exclusion of all other causes
b. All patients were not diabetic, not obese (normal BMI), no dyslipidemia.
c. Biopsy was not taken, because all patients taken were in decompensated state, with
coagulopathy, small liver. Or uncooperative patient or his relatives.
2.2 Statistical Study
Anderson darling test was done to asses if continuous variables follow normal distribution, if follow normal
distribution than mean and standard deviation used, if did not follow normal distribution than median and
interquartile range (25% to 75% percentile range) will be used to present the data.
Discrete variables presented using there number and percentage used to present the data, chi square test used to
analyze the discrete variable or Fisher exact test used to analyze the distribution between 2 groups (used instead of
chi square for 2x2 table, if total sample <20 and if 2 or more with expected frequency less than 5). One way
ANOVA used to analyze the differences between more than two groups (if they follow normal distribution with no
significant outlier).
Linear regression analysis performed to assess the relationship between different variables, if one or both of them
follow normal distribution person regression used but if both did not follow normal distribution spearman
correlation will used. Scatter plot used to present the regression analysis, r (correlation coefficient or standardized
beta is a representative of magnitude and direction of the relationship), r<0.25 weak, 0.25 – 0.5 mild, 0.5 – 0.75
moderate, >0.75 strong correlation. Negative sign indicate inverse relationship, but positive sign represent direct
relationship.
SPSS 20.0.0, Minitab 17.1.0 software package used to make the statistical analysis, p value considered when
appropriate to be significant if less than 0.05.
3. Results
1000 Patients were selected, Mean age of patients is 55.6 ± 15.6 years, about 57% of them were males and 43%
were females (male to female ratio was 1.3:1) median duration of cirrhosis since diagnosis 15 months (with
interquartile range 2.25 – 48 months) as illustrated in Table 1.

Table 1. Demographic data

Variables Value
Age (years), mean ± SD 55.6 ± 15.6
Sex
Female 43 (43.0%)
Male 57 (57.0%)
Cirrhosis duration (months), median (IQR) 15 (2.25 – 48)

The most common initial presentation was ascites and encephalopathy followed by bleeding varices and jaundice,
while during the course of decompensation 65% had ascites, 57% had jaundice, 38% had encephalopathy and 24%
had bleeding varices. The majority of patients presented with two of these symptoms 58% followed by 30% had
only one and 10% had three and only 2% presented with all of them, as illustrated in Table 2

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Table 2. Signs of liver cirrhosis

Variables Values
Initial presentation, number (%)
Ascites 340 (34.0%)
Bleeding varices 210 (21.0%)
Encephalopathy 340 (34.0%)
Jaundice 110 (11.0%)
Clinical signs of cirrhosis during admission
Ascites 650 (65.0%)
Jaundice 570 (57.0%)
Encephalopathy 380 (38.0%)
Bleeding varices 240 (24.0%)
Number of clinical signs in each patient
Single 30 (30.0%)
Two 58 (58.0%)
Three 10 (10.0%)
Four 2 (2.0%)

There was no significant difference in child – Pugh score for patients according to their initial presentation, as
illustrated in Table 3.

Table 3. Child - Pugh score in each initial presentation

Bleeding varices Jaundice Ascites Encephalopathy All p value
10.8 ± 2.0 10.1 ± 2.3 11.2 ± 1.6 9.9 ± 2.4 10.7 ± 2.0 0.108

The most common causes of liver cirrhosis are illustrated in Table 4.

Table 4. Etiology of cirrhosis

Variables Value
HCV 200 (20.0%)
Alcoholic 200 (20.0%)
HBV 173 (17.3%)
NAFLD 140 (14.0%)
Cryptogenic 130 (13.0%)
Autoimmune 55 (5.5%)
Wilson disease 37 (3.7%)
PBC 35 (3.5%)
Hemochromatosis 30 (3.0%)

HCV associated significantly with encephalopathy and bleeding varices, NASH associated significantly with
bleeding varices, cryptogenic associated significantly ascites, Wilson disease associated significantly with
jaundice, PBC associated significantly with jaundice Table 5.

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Table 5. Association between clinical presentation and etiology of cirrhosis

Ascites Bleeding varices Encephalopathy Jaundice P value
HCV
No HCV 310 (91.2%) 150 (71.4%) 230 (67.6%) 110 (100.0%) 0.022 [Sig.]
HCV 30 (8.8%) 6 0(28.6%) 110 (32.4%) 0 (0.0%)
HBV
No HBV 26 0 (76.5%) 19 0(91%) 280 (83%) 90 (82%) 0.630
HBV 80 (23.5%) 20 (9%) 570 (17%) 20 (18%)
Alcoholic
Not 260 (76.5%) 170 (81.0%) 28 0(82.4%) 90 (81.8%) 0.937
Alcoholic 8 0(23.5%) 40 (19.0%) 60 (17.6%) 2 0(18.2%)
NAFLD
Not 30 0(88.2%) 140 (66.7%) 33 0(97.1%) 90 (81.8%) 0.016 [Sig.]
NAFLD 400 (11.8%) 700 (33.3%) 100 (2.9%) 20 0(18.2%)
Cryptogenic
Not 24 0(70.6%) 210 (100.0%) 30 0(88.2%) 110 (100.0%) 0.007 [Sig.]
Cryptogenic 100 (29.4%) 0 (0.0%) 40 (11.8%) 0 (0.0%)
Wilson disease
Not 340 (100.0%) 210 (100.0%) 320 (94.1%) 90 (83%) 0.039 [Sig.]
WD 0 (0.0%) 0 (0.0%) 20 (5.9%) 20 (17%)
Autoimmune
Not 340(100.0%) 190 (90.5%) 300(88.2%) 110(100.0%) 0.149
Autoimmune 0 (0.0%) 20 (9.5%) 350(14.8%) 0 (0.0%)
PBC
Not 330 (97.1%) 210 (100.0%) 340 (100.0%) 80 (72.7%) <0.001 [Sig.]
PBC 10 (2.9%) 0 (0.0%) 0 (0.0%) 30 (27.3%)

HCV positive was more with age group > 45 years compared HCV negative as illustrate in Table 6.
Table 6. HCV
HCV
Variables P value
Negative Positive
≤45 years 220 (27.5%) 0 (0.0%)
Age 46 – 65 410 (51.3%) 90 (45.0%) 0.002 [Sig.]
>65 170 (21.3%) 110 (55.0%)
Female 370 (46.3%) 60 (30.0%)
Sex 0.189
Male 430 (53.8%) 140 (70.0%)
A 10 (1.3%) 10 (5.0%)
Child – Pugh score B 220 (27.5%) 10 (5.0%) 0.052
C 570 (71.3%) 180 (90.0%)
<1 year 310 (38.8%) 100 (50.0%)
Duration since Diagnosis 1 – 3 year 260 (32.5%) 60 (30.0%) 0.613
>3 year 230 (28.8%) 40 (20.0%)

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HBV positive associated more with male than female as illustrated in Table 7.

Table 7. HBV
HBV
Variables P value
Negative Positive
≤45 years 160 (19.5%) 60 (33.3%)
Age 46 – 65 420 (51.2%) 80 (44.4%) 0.432
>65 240 (29.3%) 40 (22.2%)
Female 390 (47.6%) 40 (22.2%)
Sex 0.049 [Sig.]
Male 430 (52.4%) 140 (77.8%)
A 20 (2.4%) 0 (0.0%)
Child – Pugh score B 210 (25.6%) 20 (11.1%) 0.414
C 590 (72.0%) 160 (88.9%)
<1 year 320 (39.0%) 90(50.0%)
Duration since Diagnosis 1 – 3 year 260 (31.7%) 60 (33.3%) 0.518
>3 year 240 (29.3%) 30 (16.7%)

Alcoholic etiology associated more with male compared with female, also alcoholic associated less with child –
Pugh group A and more with group B then Group C on comparison with non – alcoholic group as illustrated in
Table 8.

Table 8. Alcoholic
Alcoholic
Variables P value
Negative Positive
≤45 years 180 (22.5%) 40 (20.0%)
Age 46 – 65 380 (47.5%) 120 (60.0%) 0.572
>65 240 (30.0%) 40 (20.0%)
Female 430 (53.8%) 0 (0.0%)
Sex <0.001 [Sig.]
Male 370 (46.3%) 20 (100.0%)
A 20 (2.5%) 0 (0.0%)
Child – Pugh score B 130 (16.3%) 100 (50.0%) 0.008 [Sig.]
C 650 (81.3%) 100 (50.0%)
<1 year 340 (42.5%) 70 (35.0%)
Duration since Diagnosis 1 – 3 year 240 (30.0%) 80 (40.0%) 0.685
>3 year 220 (27.5%) 50 (25.0%)

NASH significantly associated more with female compared to male as illustrated in Table 9

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Table 9. NAFLD
NAFLD
Variables P value
Negative Positive
≤45 years 200 (23.3%) 20 (14.3%)
Age 46 – 65 430 (50.0%) 70(50.0%) 0.654
>65 230 (26.7%) 50 (35.7%)
Female 300 (34.9%) 130 (92.9%)
Sex <0.001 [Sig.]
Male 560 (65.1%) 10 (7.1%)
A 20 (2.3%) 0 (0.0%)
Child – Pugh score B 180 (20.9%) 50 (35.7%) 0.493
C 660 (76.7%) 90 (64.3%)
<1 year 370 (43.0%) 40 (28.6%)
Duration since Diagnosis 1 – 3 year 280 (32.6%) 40 (28.6%) 0.335
>3 year 210 (24.4%) 60 (42.9%)

Cryptogenic associated significantly with duration of cirrhosis less than 1 year compared to non – cryptogenic as
illustrated in Table 10.

Table 10. cryptogenic

Cryptogenic
Variables P value
Negative Positive
≤45 years 180 (20.9%) 40 (28.6%)
Age 46 – 65 440 (51.2%) 60 (42.9%) 0.709
>65 240 (27.9%) 40 (28.6%)
Female 350 (40.7%) 80 (57.1%)
Sex 0.249
Male 510 (59.3%) 60 (42.9%)
A 10 (1.2%) 10 (7.1%)
Child – Pugh score B 220 (25.6%) 10 (7.1%) 0.114
C 630 (73.3%) 110 (84%)
<1 year 310 (36.0%) 100 (71.4%)
Duration since Diagnosis 1 – 3 year 320 (37.2%) 0 (0.0%) 0.012 [Sig.]
>3 year 230 (26.7%) 30 (27%)

Wilson disease associated significantly with age group less than 45 years as illustrated in Table 11.

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Table 11. Wilson disease

Wilson disease
Variables P value
Negative Positive
≤45 years 180 (18.8%) 37 (100.0%)
Age 46 – 65 500 (52.1%) 0 (0.0%) 0.003
>65 280 (29.2%) 0 (0.0%)
Female 410 (42.7%) 20 (50.0%)
Sex 1.0
Male 550 (57.3%) 20 (50.0%)
A 200 (2.1%) 0 (0.0%)
Child – Pugh score B 210 (21.9%) 20 (52.0%) NA
C 730 (76.0%) 20 (50.0%)
<1 year 410 (42.7%) 0 (0.0%)
Duration since Diagnosis 1 – 3 year 300 (31.3%) 20 (52.0%) NA
>3 year 250 (26.0%) 17 (48.0%)

Autoimmune hepatitis associated significantly with age group 46 – 65 years, and also with female sex as illustrated
in Table 12.

Table 12. Autoimmune

Autoimmune
Variables P value
Negative Positive
≤45 years 220 (23.4%) 0 (0.0%)
Age 46 – 65 440 (46.8%) 60 (100.0%) 0.046 [Sig.]
>65 280 (29.8%) 0 (0.0%)
Female 370 (39.4%) 60 (55.0%)
Sex 0.005 [Sig.]
Male 570 (60.6%) 0 (0.0%)
A 20 (2.1%) 0 (0.0%)
Child – Pugh score B 230 (24.5%) 0 (0.0%) NA
C 690 (73.4%) 60 (55.0%)
<1 year 400 (42.6%) 10 (16.7%)
Duration since Diagnosis 1 – 3 year 30 (31.9%) 20 (33.3%) 0.337
>3 year 24 (25.5%) 15 (49.0%)

PBC associated significantly with female, and with duration of cirrhosis of 1 – 3 years as illustrated in Table 13.

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Table 13. Primary biliary cirrhosis

PBS
Variables P value
Negative Positive
≤45 years 20 (20.8%) 2 (50.0%)
Age 46 – 65 48 (50.0%) 2 (50.0%) 0.251
>65 28 (29.2%) 0 (0.0%)
Female 39 (40.6%) 4 (100.0%)
Sex 0.031 [Sig.]
Male 57 (59.4%) 0 (0.0%)
A 2 (2.1%) 0 (0.0%)
Child – Pugh score B 21 (21.9%) 2 (50.0%) NA
C 73 (76.0%) 2 (50.0%)
Duration since Diagnosis <1 year 41 (42.7%) 0 (0.0%) 0.012 [Sig.]

4. Discussion
In this current study, The most common causes of liver cirrhosis are alcoholic liver disease (20%) and HCV (20%)
followed by HBV (18%), NAFLD (14%), cryptogenic (14%), AIH (6%), wilson (4%), PBC (4%).
The most common presentation of liver cirrhosis from all causes are ascites (38%) and encephalopathy (38%).
followed by bleeding varices (21%), jaundice (11%). Comparing with results from national studies and
international studies, Dr. Ashraf et al, in his study published in December 2015, taking 41 patients, showed that the
most common cause of liver cirrhosis is alcoholic liver disease and cryptogenic, followed by Wilson, HCV, HBV
respectively.
Internationally, Michitaka, K., Nishiguchi, S., Aoyagi, Y. et al published at 2009, National survey study in Japan
taking 33,379 patients with liver cirrhosis, showed HCV (60.9%), HBV (13.9%), Alcoholism (13.6%), PBC
(2.4%), AIH (1.9%), NASH (2.1%) (Michitaka et al., 2010).
Sang Soo Lee, Young-Sang Byoun et al, At 2010, published a study in Korea showed most common cause of liver
cirrhosis is Viral (73.4%)(among them HBV 83.7%, HCV 15.5%, HBV+HCV 0.9%) followed by alcoholism
(18.1%), Cryptogenic (6.6%), Budd chiari (1%), AIH (0.9%).(Sang Soo Lee, Young-Sang Byoun, Sook-Hyang
Jeong, Yeo Myung Kim, Ho Gil, Bo-Young Min. 2012)
GONCALVES, Patricia Lofego et al., At 2011, published a study in Brazil, taking 1,516 patients with liver
cirrhosis, showed that the most common causes of liver cirrhosis are alcoholism (39.7%), Alcoholism with HBV or
HCV (16.1%), HCV alone (14.5%), HBV alone (13.1%), cryptogenic (9.8%).(GONCALVES, Patricia Lofego et
al. 2013)
Nwokediuko S C, Osuala P C et al. At 2013, published a study in Nigeria, showed the most common causes of liver
cirrhosis are Alcoholism followed by HBV, Herbs and lastly HCV (Nwokediuko et al., 2013).
The most common presentation of liver cirrhosis for all causes is Ascites (38%) and Encephalopathy (38%),
followed by bleeding varices (21%) and jaundice (11%) respectively. That means:
1) Chronic liver disease should be kept at the top of differential diagnosis of Ascites.
2) Decompensated liver cirrhosis should be kept in mind in differential diagnosis of encephalopathy.
For each individual cause of liver cirrhosis and clinical presentation, It was found the HCV was significantly
associated with encephalopathy and bleeding varices, comparing with international studies, Benvegnù L, Gios M,
Boccato S, et al published a study at 2004 in Italy showed that Hepatocellular carcinoma was the most frequent
complication in untreated cases of HCV (24.5%), followed by ascites (20.1%), bleeding (5.7%), and
encephalopathy (2.9%). In contrast, treated patients had the same incidence of HCC and ascites (15.6%), followed
by bleeding (3.4%) and encephalopathy (0.9%).(Benvegnù et al., 2004) Planas, Ramon et al. Published a study at
2004 in Journal of hepatology showed Ascites was the most frequent first decompensation in HCV(48%), followed
by portal hypertensive gastrointestinal bleeding (PHGB) (32.5%), severe bacterial infection (BI) (14.5%) and
hepatic encephalopathy (HE) (5%).(Planas, Ramon et al. 2002). Such difference in these results from current study
may occur because Our patients usually come late with life threatening situations, they don’t pay attention to
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abdominal distension that could developed earlier than encephalopathy or bleeding varices.
NAFLD associated significantly with bleeding varices, cryptogenic cirrhosis was associated significantly with
Ascites, while Wilson and PBC were significantly associated with Jaundice. No previous international study was
found studying specifically which signs of decompensation most likely to develop in these etiologies of liver
cirrhosis.
Regarding Age group the study found that HCV was significantly presented in middle age and elderly.That mean
still, we can screen for HCV and treat it prior to development of fibrosis and cirrhosis. Same results obtained from
other study, in which Pradat et al., noted in a study published at 2007, taking 247 patient with HCV, that most HCV
patients, if untreated, are expected to develop cirrhosis at about 65 years, irrespective of the age at infection.(Pradat,
Voirin, Tillmann, & Chevallier, 2007). Wilson disease significantly present in Young aged patients. Comparing
with other study, Merle, Schaefer, Ferenci, and Stremmel in a study published at 2005, showed that most common
age of diagnosis of Wilson is about 15 year old with no treatment developed cirrhosis within young age group
(Merle et al., 2007). Autoimmune hepatitis significantly present in middle aged patients. In comparison with an
international study, Feld, Dinh et al, published a study at 2005, taking 139 patients with AIH, mean age of
diagnosis 43.5 ± 16.6 years (Feld et al., 2005). All other etiologies had no significant relationship to specific age
group.
Regarding Sex group Current study shows that HBV significantly present in males Different international studies
showed that male gender is predominant in HBV cirrhosis worldwide. There was no substantial difference in the
percentage of male gender among different series from different parts of the world, ranging from 86 to 95%
(Realdi et al., 1994; de Jongh et al. 1992).
Previous cross-sectional studies have shown that the male-to-female ratio increased proportionally during the
course of chronic HBV infection: the ratio was 1.2:1 in the immune-tolerant phase (HBeAg-positive patients with
normal aminotransferase), 5-6:1 in chronic hepatitis, and 6-8:1 in cirrhosis (Chu, Liaw, Sheen, Lin, & Huang,
1983). These data suggest that male HBsAg carriers are more likely to have progressive liver disease than carriers
of female gender. One recent longitudinal study from Taiwan has confirmed that male patients are significantly
more likely to have high aminotransferase activities during the immune clearance phase and more relapse of
hepatitis B after HBeAg seroconversion than females (Chu, Hung, Lin, Tai, & Liaw, 2004). These findings may
explain the predominance of male gender in HBV cirrhosis.
1) The study also shows significant association between alcoholic cirrhosis and male gender. Comparing with
international studies, women are more susceptible than men to the toxic effects of alcohol on the liver for any
given dose of alcohol, even though men abuse or depend on alcohol more than women, at A 12-year
prospective study of alcohol use in over 13,000 participants in Denmark showed that the risk of development
of alcohol-related liver disease increased in women who consumed 7 to 13 beverages per week (84-156 g)
compared with men who consumed 14 to 27 beverages per week.(Becker, Deis, Sorensen et al., 1996),
Compared with their male counterparts, women with alcoholic liver disease have a more rapid progression to
fibrosis that persists even after abstinence from alcohol.(Pares et al., 1986; Poynard et al., 2003). However
among Iraqi patients no female cases were reported with alcoholic cirrhosis, most likely related to social and
religious reasons prevent women from drinking.
2) In the current study, NAFLD were significantly present in females. Comparing with other international studies,
most of the studies reported that NAFLD is significantly more prevalent in men than in women, Ruhl et al.
(Ruhl & Everhart, 2003). Reported that NAFLD was more prevalent in men than in women (4.3% vs 1.6%,
respectively), a finding essentially explained by the higher waist-to-hip circumference (WHR) ratio in men.
WHR is correlated with visceral adipose tissue (VAT) and visceral adiposity is associated with both peripheral
and hepatic Insulin resistance. (Falck-Ytter, Younossi, Marchesini, & McCullough, 2001; Miyazaki et al.,
2002).. In another study using the same database but different cohort size, Clark et al. (Clark, Brancati, &
Diehl, 2003), also reported that men have higher prevalence of NAFLD than women (5.7% vs 4.6%,
respectively), Moreover, in the Dallas Heart Study, non-Hispanic white men had an approximately 2-fold
higher prevalence of hepatic steatosis than white women. Factors, including lifestyle and sex hormone may
also influence the gender difference in the prevalence of NAFLD. In one study, individuals with NAFLD had
similar degrees of Insulin resistance and obesity to those without, but males with NAFLD consumed more
non-diet soda on a weekly basis (54.4% vs 34%, P = 0.037) (Williams et al., 2011).
Difference between these results and current study, may have many causes, could be related to obesity variations,
or due to small sample size. More studies are needed concerning this subject with larger sample and more details to
work on.
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The study also shows a significant association between AIH and female gender, resembling results from other
international studies, Feld et al., published a study at 2005, taking 135 patients with AIH, showed a female
predominance (75.4%). (Feld et al., 2005), Verma et al. published a study at 2007, taking 157 patient with AIH,
also showed female predominance (77.2%) (Verma, Torbenson, & Thuluvath, 2007).
Also the study shows significant association between PBC and female gender, comparing with international
studies, Fumio Sakauchi et al, published a study at 2005 in Japan, taking 5,805 patients, showed that PBC most
common in females (89%) while in males (11%). (Fumio et al., 2005).
Other etiologies had no significant relationship to specific sex.
Regarding the duration since diagnosis, All cases of different etiologies were presented with different durations
since diagnosis of liver cirrhosis ranging from below than 1 year, from 1 to 3 years and more than 3 years with no
significant association to specific etiology apart from cryptogenic cases that were significantly associated with less
than 1 year group, this can give an idea about rapidity of developing decompensation with cryptogenic liver
cirrhosis, and focuses on the importance of aggressive work up to diagnose unknown causes and proper
management of compensated cases. No previous study was found to compare with regarding this entity.
5. Conclusions
1) HCV and Alcoholic liver disease are the most common causes of liver cirrhosis.
2) Ascites and encephalopathy are the most common presentation at medical wards from all causes of liver
cirrhosis.
3) Most cases of liver cirrhosis due to HCV are within middle and elderly. While Wilson disease should be kept
at the top of differential diagnosis of liver cirrhosis among young individuals as it is significantly related to
young age group.
4) Alcoholic liver disease should be kept in mind at the top of differential diagnosis of liver cirrhosis in males.
While a differential diagnosis of NAFLD, AIH, PBC are significantly among females
Competing Interests Statement
The authors declare that there are no competing or potential conflicts of interest.
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