Mitochondrial alterations in children with chronic liver disease

Abstract EN

Background : Over recent years it has become apparent that the hepatocyte mitochondrion functions both as a cause and as a target of liver injury.

Resultant dysfunction of mitochondria yields deficient oxidative phosphorylation, increased generation of reactive oxygen species, impairment of other metabolic pathways and activation of both necrotic and apoptotic pathways of cellular death.

Methods : This study was conducted on 26 children and adolescents with chronic liver disease who presented to or were following up in the Pediatric Hepatology Clinic, Children’s Hospital, Ain-Shams University.

They were divided into three groups according to the aetiology of liver disease (GI = patients with Wilson’s disease (WD), GII = patients with chronic hepatitis C, GIII = patients with chronic liver disease other than Wilson’s and chronic hepatitis C).

Ultrasound-guided gun liver biopsies were performed, under local anaesthesia for all the 26 patients, using a modified 18-gauge truecut needle.

Two liver biopsy cores were taken from each patient.

One for light and electron microscopic examinations and the other was immediately immersed in liquid nitrogen to be frozen and used for studying mitochondrial DNA deletions by PCR.