Antituberculous therapy–induced fulminant hepatic failure: Successful treatment with liver transplantation and nonstandard antituberculous therapy

Ramazan Idilman, Sadik Ersoz, Sahin Coban, Ozlem Kumbasar, Hakan Bozkaya – 24 August 2006 – Standard antituberculous therapy including isoniazid, rifampin, ethambutol, and pyrazinamide is widely used for the treatment of active tuberculosis. Its most important side effect is hepatotoxicity, ranging from asymptomatic transaminitis to fulminant hepatic failure. A 19‐year‐old woman was admitted to our unit due to jaundice and unconsciousness. According to her past medical history, she was diagnosed as having extrapulmonary tuberculosis and had been prescribed standard antituberculous therapy.

Nutrition for the liver transplant patient

Antonio J. Sanchez, Jaime Aranda‐Michel – 24 August 2006 – Patients with end‐stage liver disease (ESLD) frequently have diverse abnormalities of carbohydrate, lipid, and protein metabolism that cause progressive deterioration of their clinical condition and lead to malnutrition. Malnutrition is almost universally present in patients with ESLD undergoing liver transplantation and has been associated with increased morbidity and mortality.

Cryptogenic fulminant hepatic failure in infancy: Report of 2 cases with unique vascular obstructive changes in native livers

Naoki Shimojima, Rie Shibata, Ken Hoshino, Shigeyuki Kawachi, Minoru Tanabe, Go Wakabayashi, Motohide Shimazu, Michiie Sakamoto, Yasuhide Morikawa, Masaki Kitajima – 24 August 2006 – Although the causes of fulminant hepatic failure (FHF) remain cryptogenic in many cases, a few reports have reviewed the pathological findings of native livers to evaluate the etiology. We report 2 cases of infantile cryptogenic FHF with unique vascular obstructive changes in the native livers.

The amazing regenerative powers of the liver

James D. Perkins – 24 August 2006 – The liver can regenerate its volume after major tissue loss. In a mouse model of liver regeneration, thrombocytopenia, or impaired platelet activity resulted in the failure to initiate cellular proliferation in the liver. Platelets are major carriers of serotonin in the blood. In thrombocytopenic mice, a serotonin agonist reconstituted liver proliferation. The expression of 5‐HT2A and 2B subtype serotonin receptors in the liver increased after hepatectomy. Antagonists of 5‐HT2A and 2B receptors inhibited liver regeneration.

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