A study on clinico-etiological
profile of chronic liver disease in children between 1year to 14 years
of age
Behera A.1, Murmu M.C.2
1Dr. Aarti Behera, Associate Professor, 2Dr Mangal Charan Murmu,
Associate Professor, both authors are affiliated with Department
of Paediatrics, S.C.B. Medical College Hospital, Cuttack,
Odisha, India
Corresponding Author:
Dr. Mangal Charan Murmu, Associate Professor, Department of Paediatrics,
S.C.B. Medical College & Hospital, Cuttack, Odisha,
India,Email: mangal74murmu@yahoo.co.in
Abstract
Introduction:
Chronic liver diseases(CLD) account for 1 to 5% of paediatric ward
admissions and upto 20% of ward mortality in our country. Now a day
Indian childhood cirrhosis is a rarity, whereas diseases likechronic
hepatitis, Wilsons disease and biliary atresia are diagnosed with
increasing frequency and therefore became relatively important forms of
paediatric liver disease. Methodology:
The study was done to determine the clinico-etiological profile of
chronic liver disease in children 1 year to 14 years. This is a
prospective case-controlled study done over a period of two years.
Various clinical, biochemical and radiographic parameters pertaining to
chronic liver disease were studied. Results:
About4 0 cases were studied. CLD was found to be prevalent in 5-10
years of age group. Male were more affected than female. Jaundice was
the most common presenting feature.Hepatomegaly, Ascitis, Splenomegaly
were thecommonest presenting signs. Conclusion:
CLD is not uncommon condition in children. It constitutes 18.34% of the
patients of the with liver disease in our region. Wilson’s
disease was the most common aetiology apart from idiopathic which
constitute 52.5% of the cause.
Keywords: Liver Diseases, Biliary Atresia, Non-alcoholic fatty liver
disease (NAFLD), Children
Manuscript received: 30th
December 2017, Reviewed:
9th January 2018
Author Corrected: 18th
January 2018, Accepted
for Publication: 24th January 2018
Introduction
Chronic liver disease refers to a wide spectrum of disorders
characterizedby ongoing liver damage with a potential for progression
to cirrhosis or end stage liver disease [1]. CLD implies long standing
disease (usually more than 3 to 6 months), leading to various
manifestations and complications of liver cell failure.Unlike in
adults, long duration of the disease should not be considered as a
mandatory aspect of definition of CLD in the children, as progressive
irreversible changes can occur in the children, even with symptoms as
short as one week [2]. There is emergence of relatively newer liver
disorders in children like NAFLD (non-alcoholic fatty liver disease)
that were rare in our subcontinent especially in children. There is
therefore a continuing need for studies on various aspects of liver
diseases in different communitiesand environments [3]. Acute and
Chronicliver disease constitute the majority of liver disorders in
children. The etiologic profile of CLD also shows geographical
variation. Hepatitis virus is leading cause of CLDin South East Asia,
Middle East and some of other Asian countries. It is predominantly due
to high prevalence of hepatitis in general population in these
countries. Some of the biliary disorders such as Biliary Artesia
present as CLD in regions where diagnosis is delayed beyond twelve
weeks. Such children often present with cirrhosis and portal
hypertension. Likewise,in some regions of world where oriental
cholangiohepatitis (OCH) is endemic can cause secondary biliary
cirrhosis, portal hypertension in children if left untreated [4]. The
profile of metabolic diseases producing chronic liver disease has not
been well documented from developing countries because of lack of
diagnostic facilitiesin these regions. Therefore,the metabolic diseases
causing chronic liver disease do not figure well in the studies
reported from these underdeveloped countries. The incidence of Indian
childhood cirrhosishas come down [5]. The parasitic liver diseases such
as hydatid cyst, schistosomiasis continue to form a part of liver
disease in endemic states [6]. In recent yearsnon-alcoholic
steatohepatitis (NASH) has been described as a commoncause of liver
disease in children which is related to obesity, hyperinsulinemia,
insulin resistance, and liver cell injury from free fatty acid toxicity
or oxidant stress. Overall prevalence of fatty liver in children is
2.6-12.5%[7].
In this study the pattern of CLD in children attending our hospital
were analysed as there is dearth of information on this.
Objectives
The aim of the study is to determine the etiological profile, clinical
manifestations, different haematological & biochemical
abnormalities and its complicationsof chronic liver disease in children
aged 1 year to 14 years.
Material
This is a direct observation study. The study was conducted in the
Department of Pediatrics, S C B Medical College and Hospital, Cuttack
from October 2015 to September2017 both in outpatient department and
indoor after getting Ethical committee clearance of the institution.
The total cases included in our study was forty. Detailed history and
clinical examination of all patients suffering from chronic liver
disease was taken and haematology and liver function test were
recorded. Other investigations like ultra sound, upper
gastro-intestinal (G I)endoscopy, viral and auto immune markers, liver
biopsy were done as and when indicated.
Inclusion Criteria:
The children age between 1 year to 14 years with features of chronic
liver disease which includes deranged liver functions test, enlarged or
shrunken liver,splenomegaly, edema, ascitis, bleeding from varices and
cutaneous features like spider angiomata /palmer erythema for more than
3 months.
Exclusion Criteria:
It includes a). Children below 1year and over 14 years, b). Children
with haemolytic anemia, c).children with neonatal hepatitis and
extrahepatic biliary atresia, d). Children suffering from HIV infection.
All cases were recorded in prescribed proforma and were subjected to
routine heamotological investigations and other ancillary
investigations as and when required.
Methods
1. SGOT (Serum Glutamic Oxaloacetic
Transaminase)/ (AST-Aspartate Aminotransferase): It is measured in
serum by the method of Reitman and Frankel.
2. SGPT (Serum Glutamic Pyruvic
Transaminase) (ALT - Alanine Aminotransferase): It is measured in serum
by the method of Reitman and Frankel.
3. Serum Alkaline Phosphatase: its
measured by King, Abdul Fade and Walker Method
4. Serum Bilirubin: It was done by Evelyn
and Malloy Method.
5. Serum Protein: It was done by Biuret
Method.
6. Serum Albumin: It was done by
principles based on the work of Doumas, modified by Spencer and Price.
7. Prothrombin Time: It was done by Quick
on stage method
8. Immunocombo HBsAg Test: it was done by
3rd generation Elisa Kit HBsAg one step.
9. Micro Elisa HCV: Done byThird
generation enzyme immune assay for determination of Antibodies to HCV.
10. Liver Biopsy: Done by using Tru-Cut Needle done
when indicated (with parental consent).
11. Upper GI Endoscopy: Done by gastroenterologist
for looking esophageal varices.
12. Slit Lamp Examination: To look for
Kayser-Fleischer Ring as an evidence of Wilson’sdisease.
The clinical, biochemical & etiological profile were noted and
analysed statistically.
Observation
Table-1: Incidence of CLD
in Patients with Liver Disease
|
Liver disease
|
Number of patients
|
Total
|
Percentage
|
|
1-5 years
|
6-10 years
|
11-14 years
|
|
Male
|
Female
|
Male
|
Female
|
Male
|
Female
|
|
Chronic liver disease
|
2
|
-
|
16
|
11
|
7
|
4
|
40
|
18.34
|
|
Non-CLD
|
5
|
4
|
71
|
45
|
38
|
15
|
178
|
82.56
|
|
Total
|
7
|
4
|
87
|
56
|
45
|
19
|
218
|
100
|
During the study period, 218 patients were diagnosed with liver
diseases, out of which 40 patients (18.34%) were diagnosed with chronic
liver disease and 178 (82.56%) were diagnosed with other forms of liver
disorders. The most common age group is between 5-10 years, males were
more affected than female.
Table-2: Clinical Symptoms
|
Clinical
Feature
|
Number
of Patients
|
Percentage
|
|
Fever
|
28
|
70
|
|
Jaundice
|
28
|
70
|
|
GI Bleeding
|
4
|
10
|
|
Altered Sensorium
|
2
|
5
|
Jaundice (70%) and fever (70%) were the most common presentation in our
study.
Table-3: Physical Findings
|
Features
|
Number
of Patients
|
Percentage
|
|
Pallor
|
34
|
85
|
|
Icterus
|
28
|
70
|
|
Hepatomegaly
|
28
|
70
|
|
Splenomegaly
|
19
|
47.5
|
|
Ascitis
|
26
|
65
|
|
Altered Sensorium
|
2
|
5
|
|
GI Bleeding
|
4
|
10
|
Pallor was present in 34 patients (85%). Icterus and Hepatomegalywere
present in 28 patients each (70%). Ascites wasnotedin 26 patients
(65%), splenomegaly was found in 19 patients (47.5%)
Table-4: Serum bilirubin
(total) at presentation (N=40)
|
Serum Bilirubin in mg %
|
Number of patients
|
Percentage
|
|
<1
|
2
|
5
|
|
1-5
|
15
|
37.5
|
|
6-10
|
18
|
45
|
|
11-15
|
4
|
10
|
|
16-20
|
1
|
2.5
|
The above table shows 15 patients (42.5%) had serum bilirubin level
between 1-5mg/dl, 18 patients (45%) had serum bilirubin between 6-10
mg/dl.
Table-5: Biochemical
Parameters
|
Level in IU/L
|
SGPT
|
SGOT
|
Serum albumin
|
|
<100
|
19
|
14
|
12
|
|
100-400
|
20
|
25
|
23
|
|
>400
|
1
|
1
|
5
|
Nineteen (47.5%) patients had SGPT value between 40-100IU/L. About 20
Patients (50%) patients had SGPT between 100-400 IU/L. One Patient
(2.5%) had SGPTvalue >400 IU/L. About 14 Patients (35%) patients
had SGOTvalue< 100 IU/L at the time of presentation. About 25
patients (62.5%) had SGOT value between 100-400 IU/L and 1 patient
(2.5%) had SGOT value > 400 IU/L.
Table-6: Upper GI
Endoscopy finding (N=35)
|
Endoscopic Finding
|
Number of patients
|
Percentage
|
|
Absence ofvarices
|
21
|
60
|
|
GradeI varices
|
3
|
8.57
|
|
GradeII Varices
|
8
|
22.85
|
|
GradeIII Varices
|
2
|
5.7
|
|
GradeI VVarices
|
1
|
2.85
|
In 60 % of patients the endoscopic finding was normal, 22.85 patients
show gradeII varices.
Table-7: Etiology of
chronic liver disease
|
Etiology
|
Number of Patients
|
Percentage
|
|
Wilson’s disease
|
11
|
27.5
|
|
Budd–Chiari syndrome
|
2
|
5
|
|
Auto immune hepatitis
|
2
|
5
|
|
Drug induced
|
2
|
5
|
|
Hepatitis –C
|
1
|
2.5
|
|
Choledochal cysts
|
1
|
2.5
|
|
Cryptogenic
|
21
|
52.5
|
|
Total
|
40
|
100
|
Eleven patients (27.5%) had Wilson’sdisease. In 21 patients
(52.5%) cause could not be established.
Table-8: Liver Biopsy
Findings
|
Liver biopsy finding
|
No of patients
|
Percentage
|
|
Chronic hepatitis
|
17
|
73.9
|
|
Cirrhosis
|
6
|
26.08
|
Around 23 patients (62.5%) out of a total of 40 patients underwent
liver biopsy. Around17 patients (73.9%) showed evidence of chronic
active hepatitis and in 6 patients (26.08%) cirrhosis was seen in the
liver biopsy specimens.
Discussion
A total of 218 patients with features of liver disease attending to our
hospital were thoroughly evaluated, out of which 40 patients (18.34%)
were diagnosed with chronic liver disease, these were included in our
study. The most of the patients were between 5-10 years of age group.
The mean age at presentation was 9.44±2.69 years. Our study
is similar tothe result reported by Ganie et al [5], 2014. About 25
patients (62.5%) were males and 15patients(37.5%) were females.The
males out numbered females by 1.67:1. The finding in our study is
similar that in studies by Akinbami et al and Hanif et al[9] but
contrary to study by Ganie et al[5].
Jaundice was found in 28 patients (70%) and fever in 28 patients (70%)
were most common presentations in our study. The other features in our
study were GI bleed in 4 patients (10%) and altered sensorium in 2
patients (5%). The finding in our study are similar to the study by
Dangwal et al. In their study they found jaundice in 70%of the cases
and fever in 67% of the cases.Pallor was present in 34 patients (85%)
and was most common clinical features. The other features were
hepatomegaly in 28 patients (70%) and icterus in 28 patients (70%). The
other features were ascitis in 26 patients (65%), splenomegalyin 19
patients, GI Bleeding in 4 patients(10%). This finding is similar to
study done by Hanif et al [9] in which they had reported pallor to be
present in 95% of the cases.
The percentage of patients presenting with jaundice /icterus in our
study is 70%, which correlates with the study conductedby Hanif et al
[9] and Ira Shah et al[12] who found jaundice in 67% & 70%
cases respectively.
Hepatomegaly was found in 70% of patients in our study which resembles
the finding in the study by Ira Shah et al [12] and Hanif et al [9] who
found hepatomegaly in 71%& 64% of the case respectively. This
differs from the study by Ganie et al [5]where hepatomegaly was found
in only 22% of cases.
Splenomegaly was found in 47.5% of our patients similar to the finding
by Ira Shah et al [12] and Dangwal et al [10]but differs from the
studyby Hanif et al [9] andGanie et al [5] who reported splenomegalyin
76%and 65% of the cases respectively.
In our study, 65% of the patients had Ascites. The finding resembles
the study by Dangwal et al but differs from the study by Hanif et al
who reported Ascites in 84% of the case in their study.
Altered sensorium was present in 2 patients (5%) in our study out of
which one patient died during course of study due to associated sepsis.
Ten percentage of the patients presented with GI bleeding resembling
the study by Ganie et al [5] but in a study by Hanif et al[9] GI Bleed
was present in 46% of patients.
According to Leuschner U [13], Serum bilirubin is normal except in
severe disease. In our study hyperbiliubinemia was seen in 95% of the
patients. These finding correlates with the study by Hanif et al [9] in
which hyperbilirubenimia was found in90% of the patients.
Directhyperbilirubemia was seen in 37patients (92.5%).
About 50% patients had moderate elevation in the SGPT levels. The
lowest SGPT value in the series was 43U /L and the highest value in the
series was 406U/L.
Moderately increased SGOT levels was seen most commonly. It was seen in
25 patients (62.5%). The lowest SGOT value in this series was 40 U/L
and the highestvalue was 412U/L.
Serum alkaline phosphatase was increased in 33 patients (72.5%). The
highest value of Serum Alkaline phosphatase in our study was 2029 U/L.
In our study 25patients (62.5%)had moderate anemia. About 3 patients
had hemoglobin less than 7 g/dl and 12 patients (30%) of the patients
had hemoglobin more than 10 g/dl.
Prothrombin time is prolonged in 70% patients and normal in 30% of the
patients. This finding is similar to the finding in the study by Hanif
et al [9].
Upper GI endoscopy was done in 35 patients (87.5%) of the patients. Out
of them 21 patients (60%) did not have any verices, whereas 14 patients
(40%) had esophageal varices suggestive of presence of portal
hypertension.
Seventeen patients (73.9%) who underwent liver biopsy had features of
chronic hepatitis in their liver biopsy specimen whereas 6 patients
(26.08%) had evidence of cirrhosis. This finding in our study is
similar to that of Hanif et al [9].
The most common etiology was to be found was Wilson’s disease
in 11 patients (27.5%) of patients .About2 patients (5%) were diagnosed
was Budd-Chiari syndrome and another 2 patients (5%) were diagnosed
with drug induced hepatitis. Chronic hepatitis C and Choledochal cyst
was diagnosed in 1 Patient (2.5%)each. No etiology was found in 52.5%
of the patients.
Wilson’s disease was diagnosed in 27.5% of the patients in
our study. This finding resembles the findings of the study by Yachha
et al [14] and Zhang et al [15]. This finding differs from the study by
Hanif et al [9]in which 16% of the patients were diagnosed with
Wilson’s disease. About 1 patient was diagnosed with Chronic
hepatitis C. No patient was diagnosed with hepatitis Binfection. This
finding is in contrast to the study by Yachha et al [14], Ganie et al
[5], Hanif et al[9] where hepatitis B was diagnosed in 12%. 18% and 24%
of the patients respectively.
In the present study autoimmune hepatitis was diagnosed in 5% of the
patients. This finding is similar to the finding by Yachha et al [14]
(4%), Rafeey et al [16](5.6%), Zhang et al [15](7%). Other authors
showed a higher incidence like Hanifetal [9] (16%).
No etiology could be found in 52.5% of our patients. Similar finding
were reported by Yachha et al [14], Rajeswariet al [17], Ganie et al
[5]. This finding differs from the study by Hanif et al [9].
Conclusion
Chronic liver disease is not uncommon condition in children. It
constitutes 18.34% of the patients with liver disease in our region.
Wilson’s disease was the most common etiology as it was found
in 27.5% of the patient. No case of hepatitis B infection was found
during the course of the study and ChronicHepatitis C was diagnosed in
2.5%of the patients. No etiology could be found in 52.5% of the
patient.
The high incidence of idiopathic chronic liver disease (Dar et al) [3]
indicates further research needs to be done to find out other cause of
liver disease. The low incidence of chronic liver disease due to
ChronicHepatitisB, wasmost probably due to good immunization coverage,
screening of blood products, usage of universal precautions.
Funding:
Nil, Conflict of
interest: None initiated
Permission from IRB:
Yes
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How to cite this article?
Behera A, Murmu M.C. A study on clinico-etiological profile of chronic
liver disease in children between 1year to 14 years of age. Int J
Pediatr Res. 2018;5(1):31-36. doi:10.17511/ijpr.2018.1.7.