AETIOLOGICAL FACTORS OF CHRONIC LIVER DISEASE IN CHILDREN
Abstract
Background: Chronicity of liver disease is determined either by duration of liver disease or byevidence of either severe liver disease or physical stigmata of chronic liver disease. Chronic liverdisease may be caused commonly by persistent viral infections, metabolic diseases, drugs, autoimmunehepatitis, or unknown factors. The objective of this study was to find out the aetiology of chronic liverdisease (CLD) in children. Methodology: It was a descriptive, prospective study which used astructured proforma designed to collect data of cases of CLD from both indoor and outdoor Paediatricsunits of Fauji Foundation Hospital, Rawalpindi, and Children Hospital, Pakistan Institute of MedicalSciences, Islamabad. All children under 12 years having either clinical or biochemical evidence of liverdisease and/or elevated liver enzymes for more than 3 months were included in this study. Results:Sixty cases of CLD were enrolled from indoor and outdoor units from January 2010 to July 2011.Thirty-nine (65%) cases were male and 21 (35%) were female. Eleven children were less than 1 year,18 were 1–5 years old and 31 were 5–12 years of age. Viral hepatitis was the most common causefound in 22 (36.7%) cases. Out of these 22 patients with viral aetiology 19 (31.66%) patients hadHepatitis C and 3 (5%) had Hepatitis B. Glycogen storage disease was seen in 8.3% cases, and biliaryatresia and Wilson disease in 6.7% each. Other less commonly found cases were autoimmune hepatitis,TORCH infections, hepatoma and drug induced hepatitis (1.7% each). Cause couldn’t be established in35% cases which remained idiopathic. Conclusion: Viral hepatitis is the leading cause of chronic liverdisease in children, with the highest incidence of chronic Hepatitis C followed by metabolic disorders(glycogen storage disease and Wilson disease) and biliary atresia. Chronic viral hepatitis was mostprevalent between 11 months to 12 years of age. Wilson disease was common in 3–7 years age group,and Biliary atresia in 4–7 months age group. Glycogen storage disease was prevalent between 5 monthsto 3 years.Keywords: Chronic liver disease, Chronic viral hepatitis, Wilson diseaseReferences
Benjamin L, Frederick J. Autoimmune and chronic hepatitis. In:
Kliegman R, Behrman R, Jensen H, Santon B, (editors). Nelson Text
Book of Paediatrics. Philadelphia:Saunders;2007. p.1698.
Hanif M, Raza J, Qureshi H, Issani Z. Etiology of Chronic Liver
Disease in Children. J Pak Med Assoc 2004;54:119–22.
Ordog K, Szendroi A, Szarka K. Perinatal and intrafamily
transmission of hepatitis B virus in three generations of a lowprevalence population. J Med Virol 2003;70:194.
Prevention of perinatal hepatitis B through enhanced case
management–Connecticut, 1994–95, and the United States, 1994.
Morb Mortal Wkly Rep 1996;45:584.
Resti M, Azzari C, Rossi ME. Hepatitis C virus antibodies in a longterm follow-up of beta-thalassaemic children with acute and chronic
non-A non-B hepatitis. Eur J Pediatr 2002;151:573.
Lai ME, De Virgilis S, Argiolu F. Evaluation of antibodies to hepatitis
C virus in a long-term prospective study of posttransfusion hepatitis
among thalassemic children: comparison between first- and secondgeneration assay. J Pediatr Gastroenterol Nutr 2003;16:458.
Blanchette VS, Vorstman E, Shore A. Hepatitis C infection in
children with hemophilia A and B. Blood 2007;78:285.
Locasciulli A, Gornati G, Tagger A. Hepatitis C virus infection and
chronic liver disease in children with leukemia in long-term
remission. Blood 2001;78:1619.
Rossetti F, Cesaro S, Pizzocchero P. Chronic hepatitis B surface
antigen-negative hepatitis after treatment of malignancy. J Pediatr
; 121:39.
Jonas MM, Zilleruelo GE, LaRue SI. Hepatitis C infection in a
pediatric dialysis population. Pediatrics 2004;89:707.
Greco M, Cristiano K, Leozappa G. Hepatitis C infection in children
and adolescents on haemodialysis and after renal transplant. Pediatr
Nephrol 1998;7:424.
Nelson SP, Jonas MM. Hepatitis C infection in children who received
extracorporeal membrane oxygenation. J Pediatr Surg 2006;31:644.
Ni YH, Chang MH, Lue HC. Posttransfusion hepatitis C virus
infection in children. J Pediatr 2004;124:709.
Arad M, Maron BJ, Gorham JM. Glycogen storage diseases
presenting as hypertrophic cardiomyopathy. N Engl J Med
;352:362.
Lang PA, Schenck M, Nicolay JP. Liver cell death and anemia in
Wilson disease involve acid sphingomyelinase and ceramide. Nat
Med 2007;13:164.
Hanif M, Raza J, Qureshi H, Issani Z. Etiology of Chronic Liver
Disease in Children. J Pak Med Assoc 2004;54:119–22.
Ray G, Ghoshal UC, Banerjee PK, Pal BB, Dhar K, Pal AK, Biswas
PK. Aetiological spectrum of chronic liver disease in eastern India.
Trop Gastroenterol 2000;21:60–2.
Pediatric Liver Study Group of India. Metabolic liver diseases in
childhood: Indian scenario. Indian J Pediatr 1999;66:97–103.
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