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J Chiyende

Publications and source records attributed to J Chiyende.

5 recordsLinked to original sources

Fulminant hepatic failure resulting from coexistent Wilson's disease and hepatitis E.

Fulminant hepatic failure resulting from hepatitis E and coexistent Wilson's disease was diagnosed in a six year old girl six weeks after returning from a holiday in India. Wilson's disease was diagnosed on the basis of histological evidence of hepatocellular copper deposition, confirmed by biochemical estimation of liver copper concentration. Although severely damaged, the liver was non-cirrhotic. Hepatitis E virus (HEV) was diagnosed by nested polymerase chain reaction, the specificity of which was confirmed by direct sequencing of amplified DNA. Replication of HEV within the liver at the time of diagnosis was confirmed by selective amplification of the antigenomic strand of the virus obtained from total liver RNA. The patient had an orthotopic liver transplantation without recurrence of hepatitis and remains well at 19 months. Viral excretion, recorded by serial amplification of HEV RNA extracted from stool samples, persisted for 30 days after liver grafting. Severe vitiligo, present preoperatively, dramatically improved after liver grafting and institution of immunosuppressive treatment. This case suggests that viral infection may play a part in the acute decompensation seen in some cases of Wilson's disease.

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Orthotopic liver transplantation for hepatic complications of Wilson's disease.

Thirteen orthotopic liver transplantations were performed in 12 patients for hepatic complications of Wilson's disease between May 1988 and July 1992. Ten patients had fulminant hepatic failure and two chronic liver disease. One patient underwent retransplantation for liver abscess secondary to hepatic artery thrombosis. Nine patients survive at a median follow-up of 18 (range 6-31) months. Three patients have died: two from multiple organ failure and sepsis, one from B cell lymphoma. Postoperative complications included bleeding requiring laparotomy in two patients, renal impairment in five, bacterial septicaemia in three, fungal sepsis in two and acute cellular rejection in six. The nine surviving patients are well with normal liver function test results.

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Liver transplantation for fulminant hepatic failure and late-onset hepatic failure in children.

The mortality rate of fulminant hepatic failure (FHF) and late-onset hepatic failure (LOHF) in childhood has remained between 70 and 95 per cent despite recent improvements in medical therapy. Liver transplantation has become an important therapeutic option in adults with this condition but has been performed infrequently in children. Between March 1988 and August 1991, 12 children aged between 1 month and 14 years with FHF or LOHF received 13 liver transplants. The aetiology was viral hepatitis in eight children (non-A non-B in six, A in two), drug hepatotoxicity (carbamazepine) in two, autoimmune hepatitis in one and congenital haemochromatosis in one. Reduced-size livers were used for ten of the 13 transplants. Morbidity after operation included infective complications and abdominal bleeding. Two patients died from graft versus host disease, one from brain aspergillosis and another from graft infarction after portal vein thrombosis. Eight patients survive after a median follow-up of 18 months. Liver transplantation should be the therapeutic choice for children with FHF and LOHF for whom the chances of recovery are poor.

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