[Acute Liver Failure in patient with liver amyloidosis associated to multiple myeloma].

We report a 67 years old woman admitted to the hospital for the study of a cholestatic jaundice and massive hepatomegaly. On admission, the patient did not have liver failure. During hospital stay, the patient experienced a progressive deterioration of liver function and a monoclonal gammopathy was detected.

[Hepatitis C virus and resulting diseases].

In 1989, the main agent causing non A non B hepatitis was identified as a RNA virus of the flavivirus family, with several serotypes, and was denominated virus C. At the present moment, the knowledge about the infection features and diseases that it causes has expanded thanks to the availability of reliable laboratory techniques to detect the antibody and the virus. The prevalence of infection and the frequency of serotypes varies in different regions of the world.

[Porphyric crisis: experience of 30 episodes].

The experience of 30 porphyric crisis is reviewed in 25 patients attended since 1967: 21 patients had 1 crisis, 3 had 2, and 1 had 3 of these episodes. In all patients, porphyria was diagnosed in relation to one crisis, even though many of them had family histories and/or previous clinical symptoms of this disease. There was clear predominance (80%) of women, but they are also a majority among acute porphyrias.

[Porphyrin excretion in patients with chronic hepatitis C virus infection].

Background: The high prevalence of chronic hepatitis C virus infection in patients with porphyria cutanea tarda, specially in those without family history of the disease, suggests that this could be an acquired disease and one of the most frequent extra hepatic manifestations of hepatitis C virus infection.

Aim: To study the excretion of porphyrins and its precursors in cirrhotic patients with and without hepatitis C virus infection.

Patients And Methods: Eighteen patients with cirrhosis Child-Pough A, eight infected with hepatitis C virus, were studied.

Hepato-splenic distribution of 99Tcm-phytate and hepato-enteric distribution of 99Tcm-DISIDA in mice with carbon tetrachloride-induced acute liver damage.

The hepato-enteric distribution of 99Tcm-labelled DISIDA and the hepato-splenic distribution of 99Tcm-labelled phytate were studied in controls and in mice with carbon tetrachloride-induced acute liver damage. The test group animals showed a diminished excretion of DISIDA to intestine with retention of this tracer in the liver and an increased splenic uptake of phytate. No changes in the hepatic uptake of phytate were found.