Primary biliary cirrhosis in antimitochondrial antibody-negative patients: Chang Gung Memorial Hospital experience.

BACKGROUND: It is known that some patients with clinical, histological, and laboratory features of primary biliary cirrhosis (PBC) lack serum antimitochondrial antibodies (AMAs). In Asian countries, clinical information regarding AMA-negative PBC is still limited. In this report, we reviewed our patients with AMA-negative PBC in order to further understand this disease. METHODS: Clinical features of 36 patients with PBC diagnosed by the histopathologic characteristics of the liver at Chung Gung Memorial Hospital-Lin Kou Medical Center from 1985 to 2000 were reviewed. Of them, 15 were negative and 21 were positive for serum AMAs at presentation. Clinical, biochemical, immunological, and histological parameters were compared between these 2 groups. RESULTS: There were only a few differences between the AMA-negative and -positive groups. Significantly more asymptomatic patients (p=0.0017) and a higher positive rate of serum antinuclear antibodies (ANA) (p=0.0323) were observed in the AMA-negative group. Otherwise, there were no significant differences with regard to clinical, biochemical, immunological, or histological parameters. Interestingly, 4 of the 15 patients with AMA-negative PBC became AMA positive during 10, 23, 47, and 56 (mean, 34) months of follow-up. CONCLUSIONS: The results show that patients with AMA-negative PBC tend to be asymptomatic and ANA positive. Some patients may develop positive AMA during follow-up. Our data imply that AMA-negative PBC might be a variant of AMA-positive PBC, rather than a separate disease.

[Ultrastructural features of virus infected hepatocytes in patients with pathology of the hepatobiliary organs]. / Ul'trastrukturnye osobennosti virusinfitsirovannykh gepatotsitov u bol'nykh s patologiei organov gepatobilirnoi zony.

In electron-microscopic study of the puncture biopsy material in 52 patients with diseases of the hepatobiliary organs in 22% of cases, the liver contamination with the viruses was revealed. They caused destruction of hepatocytes and induced their appearance in the cytoplasma and mitochondria of the protein crystalline inclusions. This was of certain diagnostic and, perhaps, lithogenic importance.

[Relation of RNA-dependent DNA-polymerase from the rat liver with virus-like particles]. / Sviaz' RNK-zavisimoi DNK-polimerazy iz pecheni krys s virusopodobnymi chastitsami.

RNA-dependent DNA-polymerase activity was found in the 165 000 g supernatant and pellet of the postmitochondrial rat liver fraction. Further fractionation of the 165 000 g pellet in the linear sucrose gradient (20-50%) showed that RNA-dependent DNA-polymerase activity was distributed between fractions with densities 1.18-1.19 g/ml and 1.09-1.1 g/ml. In the fractions with 1.18-1.19 g/ml density the enzymic activity could be detected only after Triton X-100 treatment and disappeared after the incubation with pancreatic ribonuclease A. Triton X-100 treatment of the 165 000 g supernatant and the fractions with density 1.09-1.1 g/ml did not increase further the enzymic activity. Electron microscopy revealed in the 1.18 g/ml fraction virus-like particles resembling retroviruses of A and C type. In the light peak "non-mature" virus-like particles were found. The 165 000 g supernatant devoid of virus-like particles contained free RNA-dependent DNA-polymerase activity. The virus-like particles of both types seem to be endogenous rat retroviruses serving as a source of the particular and free reverse transcriptase in the rat liver.

Mechanisms of pathogenesis in Listeria monocytogenes infection. VI. Oxidative phosphorylation in mouse liver mitochondria during experimental listeriosis.

Previous reports have demonstrated early changes in hepatic carbohydrate and energy metabolism in mice infected with Listeria monocytogenes. This study was undertaken to further elucidate mechanisms of damage involved in these changes. Female CD-1 mice were injected intraperitoneally with 10(6)L. monocytogenes A4413. At 0, 10, and 20 hr after infection, groups of mice were sacrificed and the livers were removed and pooled. Oxidative phosphorylation was assayed immediately upon isolation of mitochondria from pooled liver homogenates. Appropriate metabolic inhibitors were employed to examine each of the three phosphorylation sites in mitochondrial electron transport. When pyruvate-malate (equimolar concentrations) and alpha-ketoglutarate were used as substrates, decreases in both phosphorylation and oxidation were noted as early as 10 hr after infection. With beta-hydroxybutyrate and citrate as substrates, alterations were not noted until 20 hr after infection, whereas no changes were seen when glutamate, succinate, or ascorbate were employed. These results suggest possible derangement of the first site in oxidative phosphorylation as well as lowered activity of nicotinamide adenine dinucleotide-linked dehydrogenases during experimental listeriosis in mice.