Search PubMed⌕ Search

PubMed · 7433928

Liver function in some common rheumatic disorders.

Abstract

Liver function was studied primarily by determination of serum gamma glutamyl transferase and alkaline phosphatase. In subsamples of patients the investigation was extended by determination of serum amino-transferases, isoenzyme analysis of alkaline phosphatase, 99mtechnetium scintigraphy, and liver biopsy. In 183 in-patients with rheumatoid arthritis, the serum gamma glutamyl transferase level was elevated in 47% and serum alkaline phosphatase (of liver origin) in 24%. A concomitant increase in serum aminotransferases was found in 15% of patients with elevated gamma glutamyl transferase level. A closely similar pattern was found in 45 patients with non-rheumatoid arthritis (ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and undefined arthritis), and in 5 patients with polymyalgia rheumatica. In 23 patients with non-rheumatic inflammation (pneumonia), liver dysfunction was common, though the pattern of serum enzyme changes was different. In rheumatoid arthritis, liver scanning showed irregular or low uptake, but biopsy only indicated reactive hepatitis. Hepatotoxicity could not be traced to any single drug or combination of drugs given. On the contrary, chloroquine appeared to reduce serum gamma glutamyl transferase, and corticosteroids had a similar effect on serum alkaline phosphatase. In patients not treated with corticosteroids, both serum gamma glutamyl transferase and alkaline phosphatase were weakly to moderately correlated with laboratory indices of disease activity (ESR and serum orosomucoid). The frequently occurring isolated increase of serum gamma glutamyl transferase and/or serum alkaline phosphatase in arthritis may be an unspecific reaction to inflammation.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Akesson, K Berglund, M Karlsson. 1980. Liver function in some common rheumatic disorders.. https://doi.org/10.3109/03009748009098135

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Protective effect and mechanism of stronger neo-minophagen C against fulminant hepatic failure.

AIM: To investigate the protective effect of stronger neo-minophafen C (SNMC) on fulminant hepatic failure (FHF) and its underlying mechanism. METHODS: A mouse model of FHF was established by intraperitoneal injection of galactosamine (D-Gal N) and lipopolysaccharide (LPS). The survival rate, liver function, inflammatory factor and liver pathological change were obtained with and without SNMC treatment. Hepatocyte survival was estimated by observing the stained mitochondria structure with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate fluorescence nick end labeling (TUNEL) method and antibodies against cytochrome C (Cyt-C) and caspase-3. RESULTS: The levels of plasma tumor necrosis factor alpha (TNF-alpha), nitric oxide (NO), ET-1, interleukin-6 (IL-6), and the degree of hepatic tissue injury were decreased in the SNMC-treated groups compared with those in the model group (P < 0.01). However, there were no differences after different dosages administered at different time points. There was a significant difference in survival rates between the SNMC-treated groups and the model group (P < 0.01). The apoptosis index was 32.3% at 6 h after a low dose of SNMC, which was considerably decreased from 32.3% +/- 4.7% vs 5% +/- 2.83% (P < 0.05) to 5% on d 7. The expression of Cyt-C and caspase-3 decreased with the prolongation of therapeutic time. Typical hepatocyte apoptosis was obviously ameliorated under electron microscope with the prolongation of therapeutic time. CONCLUSION: SNMC can effectively protect liver against FHF induced by LPS/D-Gal N. SNMC can prevent hepatocyte apoptosis by inhibiting inflammatory reaction and stabilizing mitochondria membrane to suppress the release of Cyt-C and sequent activation of caspase-3.

Alanine Transaminase↗

Erdosteine treatment attenuates oxidative stress and fibrosis in experimental biliary obstruction.

Oxidative stress, in particular lipid peroxidation, induces collagen synthesis and causes fibrosis. The aim of this study was to assess the antioxidant and antifibrotic effects of erdosteine on liver fibrosis induced by biliary obstruction in rats. Liver fibrosis was induced in Wistar albino rats by bile duct ligation (BDL). Erdosteine (10 mg/kg, orally) or saline was administered for 28 days. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels were determined to assess liver functions and tissue damage, respectively. Pro-inflammatory cytokines, TNF-alpha, IL-1beta and IL-6 and antioxidant capacity (AOC) were assayed in plasma samples. Liver tissues were taken for determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Production of reactive oxidants was monitored by chemiluminescence assay. Serum AST, ALT, LDH, and plasma cytokines were elevated in the BDL group as compared to controls and were significantly decreased by erdosteine treatment. Hepatic GSH level and plasma AOC, depressed by BDL, were elevated back to control level with erdosteine treatment. Furthermore, hepatic luminol and lucigenin chemiluminescence (CL), MDA level, MPO activity and collagen content in BDL group increased dramatically compared to control and reduced by erdosteine treatment. Since erdosteine administration alleviated the BDL-induced oxidative injury of the liver and improved the hepatic functions, it seems likely that erdosteine with its antioxidant and antifibrotic properties, may be of potential therapeutic value in protecting the liver fibrosis and oxidative injury due to biliary obstruction.

Alanine Transaminase↗