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Results for “Liver Dysfunction”

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At least 379 records · Page 21Linked to original sources
PubMed1984

Polyclonal B cell activation in alcoholic patients with no evidence of liver dysfunction.

Unstimulated and pokeweed mitogen (PWM) stimulated immunoglobulin (Ig) synthesis by peripheral blood mononuclear cells (PBMC) in vitro and plasma Ig concentrations were measured in three groups of alcoholic patients: (i) with clinical or biochemical signs of liver disease, (ii) with evidence of an alcohol related disease but no overt signs of liver damage and (iii) with no evidence of any alcohol related disease. The concentrations of IgG and IgA were significantly raised in the supernatants of unstimulated cultures of PBMC from the patients, while the stimulation of Ig synthesis by PWM, measured as a stimulation index, was significantly reduced. The ratio of the concentration of IgG to IgA was reduced in the unstimulated cultures of PBMC from the alcoholics, indicating a greater relative increase in IgA synthesis compared to IgG synthesis. Comparing the alcoholics to the controls, it was found that the concentration of IgA in the plasma of the alcoholics was increased, but that the concentration of IgG was not altered. Comparing the different groups of patients, it was found that the concentration of IgG in the plasma was higher in the alcoholics with evidence of liver damage compared to alcoholics with alcohol related disease but no evidence of liver damage, and that the concentration of IgA in the plasma was higher in alcoholics with liver damage than those without. Otherwise there were no differences between the alcoholics with respect to the synthesis of IgG or IgA or the plasma Ig concentrations. These results indicate that IgG synthesis by PBMC in vitro, and serum Ig concentration in vivo, are abnormal in all alcoholics, not just those with overt clinical or biochemical signs of liver damage.

Alcoholism↗
PubMed1976

Liver dysfunction and polymyalgia rheumatica. A case report.

Hepatic dysfunction may be a manifestation of polymyalgia rheumatica. We present a second patient with the polymyalgia rheumatica syndrome and a significantly elevated alkaline phosphtase who, on liver biopsy, demonstrated granuloma formation and massive infiltration of the portal spaces with lymphocytes. The alkaline phosphatase elevation was favorably influenced by low dose steroid therapy.

Aged↗
PubMed1991

A case of erythropoietic protoporphyria with severe liver dysfunction suggesting a close relationship between erythrocyte protoporphyrin levels and those of gamma-GTP.

A case of erythropoietic protoporphyria (EPP) with severe acute abdominal pain and jaundice was reported. Erythrocyte protoporphyrin (PP) levels were constantly high, and liver histology showed a slight fibrosis with inflammatory infiltration. During the investigation period of 18 months, erythrocyte PP levels closely paralleled those of serum gamma-GTP.

Acute Disease↗
PubMed2006

Oxidative injury and hepatocyte apoptosis in total parenteral nutrition-associated liver dysfunction.

PURPOSE: The aim of this study was to investigate the impact of oxidative injury and apoptosis on total parenteral nutrition (TPN)-associated hepatic dysfunction. METHODS: Fifty-nine New Zealand rabbits (6-8 days old) were divided into 4 groups: 12 in the control group (maternal fed), 15 in the PN-3 group (TPN for 3 days), 14 in the PN-7 group (TPN for 7 days), and 18 in the PN-10 group (TPN for 10 days). At the end of the experiment, blood biochemistry analysis and histologic examination of the liver were performed; the malondialdehyde content of liver tissues was determined and hepatocyte apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated nick-end labeling assay. RESULTS: We found that the serum level of direct bilirubin became higher as PN duration was extended. The light microscopy features in the PN-3 and PN-7 groups included inflammatory cells infiltrated in portal areas and some degeneration changes, whereas in the PN-10 group, cholestasis (proliferation of bile ducts and bile pigments in hepatocytes) or diffuse steatosis was shown. Electron microscopic manifestation in PN groups included reduced numbers of microvilli and some preapoptosis changes. Both the malondialdehyde content and apoptosis index were the highest in the PN-10 group; there were more apoptotic hepatocytes in the groups with longer PN duration. CONCLUSIONS: The longer the TPN duration, the more severe the liver injury. Both oxidative injury and apoptosis may play important roles in the mechanism of TPN-associated hepatic dysfunction.

Animals↗
PubMed2006

Hypolipidaemia is not always indicating liver dysfunction. A review of primary and secondary high density lipoprotein and low density lipoprotein deficiencies.

Hypolipidaemias can be either primary due to several genetic defects altering the serum concentration of lipoproteins, or secondary resulting from various disorders such as liver disease, malabsorption, malnutrition, malignancy, hyperthyroidism and immunoglobulin disorders. We present a review of the current knowledge regarding the various causes of hypolipidaemias. Our aim is to emphasize on the different mechanisms, apart from deranged liver synthetic function, that are responsible for unusually low levels of cholesterol and on the disorders that need to be considered during the investigation of hypolipidaemia.

Cholesterol, HDL↗