Biochemical Marker of Hepatic Injury in Sickle Cell Disease

Abstract

Background: Sickle cell anemia is an inherited blood disorder characterized primarily by chronic anemia and periodic episodes of pain. Evidence of liver disease in sickle cell disease is obtained either from abnormal biochemical tests or postmortem liver biopsy specimen rarely an antemortem liver specimen. Icterus and increased tendency to gall stones is the most common presentation. Materials and methods: To evaluate biochemically, the patients with sickle cell disease (n=100) from medicine and pediatrics wards/OPD were included in the study. 100 age matched healthy individuals were also selected as controls. An informed written consent was obtained from all the study subjects who were enrolled in the study. Results: The levels of serum AST, ALT, ALP and bilirubin is found to be significantly higher in sickle cell disease patients than in healthy subjects. Discussion: Intrahepatic cholestasis is one of the fatal complications of sickle cell anemia. Sickling of red blood cells in hepatic sinusoids and their stasis may also cause serious damage to hepatocytes and Kupffer cells. This can lead to frequent enlargement of liver making it sensitive so that a minor stimulus can lead to hepatic dysfunction which can cause frequent rise in liver enzyme levels in blood. Hepatic injury due to transfusional iron overload and staining of hepatocytes and Kupffer cell with iron leading to hepatic iron overload due to repeated blood transfusion may be a possible reason for hepatic dysfunction in those patients who have received multiple blood transfusions. Conclusion: Serum enzyme (ALP, ALT, and AST), bilirubin and uric acid parameters are significantly increased as compared with the controls. The liver function of the patients was significantly compromised as compared to controls. Increased serum bilirubn indicates the likelihood of continuous ongoing hemolysis.