Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A dynamic estimation of the involvement of the complement system in various diseases was obtained by the direct quantitation of breakdown products of C3 and of properdin factor B. The methods used were based, first on the separation of native and fragmented molecules according to their molecular size through a precipitation with polyethylene glycol and, secondly, on an immunochemical quantitation, using specific antisera for the major antigens of C3 and factor B. The sensitivity and the specificity of these methods were demonstrated by activation of complement in vitro with generation of C3 and factor B fragments. A clinical investigation was carried out in 41 patients with systemic lupus erythematosus (SLE), 31 with membranoproliferative glomerulonephritis (MPGN), 26 with other types of glomerulonephritis, and 6 with severe alcoholic cirrhosis of the liver. The following observations were made: (a) an elevated plasma level of C3d fragment of C3 was found in 68% of SLE patients, in 87% of MPGN patients, in 62% of patients with other hypocomplementemic nephritis, and in 15% of those with normocomplementemic nephritis, but in only 33% of patients with liver cirrhosis and very low levels of C3; (b) a significant difference was observed between the levels of C3 obtained with either anti-"native" C3 or anti-C3c sera for immunochemical quantitation, in patients with SLE or MPGN, indicating the presence of "altered" or fragmented C3 in plasma; (c) an elevated plasma level of Ba fragment of properdin factor B was found in 46% of SLE patients, in 67% of MPGN patients, in 50% of patients with other hypocomplementemic nephritis, and in 9% of patients with normocomplementemic nephritis, while the level of properdin factor B was only slightly decreased in these diseases; (d) in SLE and MPGN there was an inverse correlation between the levels of C3d and Ba and the level of C3 in plasma. The level of these fragments was directly correlated with the clinical manifestations of SLE; (e) some patients with a normal C3 level exhibited an elevated plasma concentration of C3 and factor B fragments, suggesting the coexistence of an increased synthesis with a hypercatabolism of complement components. Therefore, the quantitation of complement breakdown products by simple immunochemical methods provides additional information concerning the involvement of complement in disease and new features for the evaluation of the intensity of immune reactions during immune complex diseases.
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PMID:Complement breakdown products in plasma from patients with systemic lupus erythematosus and patients with membranoproliferative or other glomerulonephritis. 114 31

Circulating immune complexes (CIC), complement and alpha-fetoprotein (AFP) were detected in 93 hepatitis B surface antigen (HBsAg)-positive patients with hepatocellular carcinoma (HCC), 16 patients with liver cirrhosis (LC) and 54 healthy controls. The CIC and complements were significantly higher in HCC patients than in LC patients. The complement and polyethylene glycol(PEG)-CIC in HCC patients with LC were higher than those in LC only (P less than 0.0001). The complement levels in LC patients were significantly lower than in controls. There was no difference in C3 and C4 between HCC patients and controls, while the C3 proactivator was higher in HCC patients (P less than 0.02). The C1q-CIC was higher in HCC and LC patients when compared to controls (P less than 0.0001). In patients with HCC, there was no difference in the CIC and complement levels between patients with cirrhosis and those without. There were inverse correlations between C1q-CIC and C3 (P less than 0.05), C1q-CIC and C4 (P less than 0.04). The mean level of 3% PEG-CIC and C1q-CIC increased significantly as AFP elevated, but decreased as AFP was higher than 1599 ng/ml (P less than 0.05). These results imply that CIC increase with tumor growth but further tumor burden may result in a fall in CIC, there was a shifting of CIC from complement-fixing to non-complement-fixing as AFP increased gradually.
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PMID:Relationship of serum alpha-fetoprotein to circulating immune complexes and complements in patients with hepatitis B surface antigen-positive hepatocellular carcinoma. 169 50

Sera from 54 children (mean age 5.8 years) with chronic hepatitis B virus (HBV) infection were investigated for the presence of immune complexes containing HBV proteins. Clinical diagnosis was established by histology and biochemical markers and included chronic persistent (36 cases) or chronic aggressive (seven) hepatitis, liver cirrhosis (six) and HBV-mediated membranous glomerulonephritis (five). Circulating immune complexes were precipitated with 2.5% polyethylene glycol and analysed by immune blot using monoclonal antibodies against S, pre-S2 glycopeptide, pre-S1 and HBe/c epitopes. All sera, including those from 11 healthy HBV-negative blood donors contained PEG-precipitable substances, but the amount of precipitate did not correlate with the presence or amount of HBV proteins. The great majority (36 out of 40) of HBeAg-positive patients contained HBs proteins in immune complexes, but no detectable HBe protein. The immune complexes usually contained more pre-S1 than the free HBsAg particles from the same patient. The precipitates of anti-HBe-positive patients rarely contained HBV proteins (two out of 14) and, if so, in low amounts. During follow up of six patients we found that high levels of HBs-containing immune complexes may be correlated with subsequent elimination of HBV. This elimination is possibly initiated by binding of anti-pre-S1 antibodies to HBV and HBs particles.
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PMID:Analysis of viral proteins in circulating immune complexes from chronic carriers of hepatitis B virus. 204 31

The effects of pretreatment with the hepatotoxin, thioacetamide, on the pharmacokinetics of praziquantel, a broad spectrum schistosomicidal agent with a high hepatic clearance, were studied in male Wistar rats. Animals were pretreated with either thioacetamide (25 mg in 100 ml of drinking water, n = 5) for 24 weeks or received plain drinking water (n = 5) over the same period. After the treatment period, praziquantel was administered orally (25 mg/kg as a 20 mg/ml solution in PEG 200) as a single dose. Blood samples (0.3 ml) were collected from the clipped tail at various times up to 4 h post administration. Plasma was analysed for praziquantel using an HPLC method. Mean peak plasma praziquantel concentrations were approximately 1.0 mg/l for both groups. The time to reach peak concentrations, and post-peak elimination half-life, were approximately 0.7 h and 1.0 h, respectively, for both groups. Similarly, mean AUC was approximately 2.0 mg.h/l for both groups. Statistical comparisons indicated that there were no significant differences in the pharmacokinetic parameters estimated in the two groups of animals. It was concluded that thioacetamide-induced hepatic cirrhosis has no effect on the pharmacokinetics of orally administered praziquantel in the rat, at the dose level studied.
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PMID:Effect of experimentally-induced hepatic cirrhosis on the pharmacokinetics of orally administered praziquantel in the rat. 225 49

Using immobilized anti-C3 antibody and an enzyme immunoassay, sera from 26 patients (eight with systemic lupus erythematosus (SLE), four with Hashimoto's thyroiditis, eight haemophiliacs and six with post-hepatitis cirrhosis) containing high levels of circulating immune complexes (IC) were selected. The IC were precipitated with 2.5% polyethylene glycol, washed, treated with acid buffer, neutralized and tested using an enzyme immunoassay in parallel with the original sera for antibody activity against a panel of antigens: human myosin and thyroglobulin, mouse actin and tubulin, calf thymus DNA and trinitrophenyl coupled to bovine serum albumin (TNP/BSA). It was found that all the isolated IC may contain IgG, IgA and IgM antibodies reacting with actin tubulin and TNP/BSA and also, depending upon the disease, antibodies reacting with some of the other antigens of the panel. By comparison to the antibodies present in the original sera, higher titers of antibodies were found in the isolated IC while some antibody specificities not detected in a given serum were occasionally noted in the isolated IC. The antibodies present in the IC seem to possess characteristics similar to those of polyreactive human natural autoantibodies. It is concluded that natural autoantibodies participate actively in the formation of IC found in pathological sera.
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PMID:Enzyme immunoassay analysis of antibody specificities present in the circulating immune complexes of selected pathological sera. 305 7

Alcoholic liver disease (ALD) is characterized by elevated serum IgA concentrations, the presence of circulating immune complexes containing IgA, and IgA deposits along sinusoids in the liver. When combined with the presupposed IgA-clearance function of the liver, a causal association between IgA abnormalities and the liver disease in ALD can be suggested. This prompted us to study the presence and concentration of circulating IgA-containing immune complexes (IgA-CIC) in 41 patients with ALD and 41 patients with other nonalcoholic liver diseases having comparable serum IgA levels. We searched for relationships among IgA-CIC and history of alcohol abuse, liver histopathology, and IgA deposits in the liver. Using an anti-IgA inhibition binding assay, 56% of the patients exhibited IgA-CIC in polyethylene glycol precipitate of serum and 38% showed IgA-CIC in whole serum. The prevalence and concentration of IgA-CIC was lowest in cases with nonspecific changes or steatosis in the liver biopsy and highest in cases with hepatitis or cirrhosis (P less than 0.01). The occurrence of IgA-CIC was not related to a history of alcohol abuse or to the presence of IgA deposits along hepatic sinusoids (which occurred in 78% of ALD and 20% of non-ALD cases). A skin biopsy was available from 34 patients (19 with ALD and 15 with non-ALD). In 68% of these biopsies, IgA deposits were observed in superficial blood capillaries.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating IgA immune complexes and skin IgA deposits in liver disease. Relation to liver histopathology. 337 Nov 40

This chapter reviews the disturbances of the serum sodium and potassium concentrations, acid-base imbalances, and acute renal dysfunction that are seen frequently in alcoholic patients. The hyponatremia common in decompensated cirrhotics is caused by an impairment of renal free water clearance and concomitant water ingestion. Excessive proximal renal tubular sodium reabsorption and nonosmotic vasopressin release underlie the defect in renal water excretion in cirrhosis. Restriction of water intake is the principal therapeutic measure for hyponatremia. Hypokalemia is common in alcoholics but when observed does not always represent true potassium depletion. Although most cirrhotics have a diminished total body potassium content, intracellular potassium concentration is usually normal. In some patients gastrointestinal and renal potassium losses and nutritional potassium deficiency may cause true potassium depletion. Respiratory and metabolic alkalosis are the acid-base disturbances seen most frequently in alcoholics. Acidosis is relatively uncommon and is usually due to renal insufficiency, lactic acid or keto-acid accumulation. Toxin ingestion (methanol, ethylene glycol, or isopropanol) may also cause severe acidosis. Rhabdomyolysis, common in severe alcoholism, may produce various electrolyte disturbances and acute renal failure. The prognosis for recovery is good although temporary dialysis may be necessary.
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PMID:Disorders of the serum electrolytes, acid-base balance, and renal function in alcoholism. 370 21

A method for detection and quantitation of circulating immune complexes using precipitation of the complexes by polyethylene glycol (PEG) has been reexamined to determine the influence of pH on the recovery and the reproducibility of the results. Results showed that the pH optimum for these determinations was 7.8. The recovery percentages range from 57.8-146.5% at lower immune complex concentrations, and from 73.9-101.3% at higher concentrations. The reproducibility of the method seems reasonably acceptable with a percent coefficient of variation ranging from 0.5-9.5. This method for quantitation of circulating immune complexes by polyethylene glycol precipitation is consistent and relatively reliable. Using this method, the levels of circulating immune complexes in sera in patients with hepatitis, liver cirrhosis, hepatoma, acute post-streptococcal glomerulonephritis (before and after treatment) and systemic lupus erythematosus have been examined. The results showed that except the patients with treated acute post-streptococcal glomerulonephritis who had a similar amount of immune complexes with normal controls, the level of immune complexes in patients with other types of diseases were all higher than the control. In addition, the composition of IgG, IgA, IgM, C3 and C4 of the precipitable complexes in sera of patients with three types of liver disease has been analyzed and demonstrated that the percentages of IgM were higher than the normal control. However, C3 and C4 in hepatitis and liver cirrhosis patients were lower than those of the control.
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PMID:Detection of circulating immune complexes in liver diseases, systemic lupus erythematosus and glomerulonephritis by polyethylene glycol precipitation. 377 14

The composition of immune complexes (IC) found in 28 patients with HBsAg positive and negative acute and chronic hepatitis was analysed. Components were defined in PEG-precipitated material isolated by preparative ultracentrifugation on linear sucrose density gradients and analysed by the Ouchterlony plate technique and by the radioimmunoassay of hepatitis B virus markers. Sedimentation rate ranged from 8 to 19s in the serum of patients with chronic hepatitis, whereas heavier IC (greater than 19s) were present in the active phase of the disease. The participation of hepatitis B virus in acute hepatitis was shown by the presence of its antigens. In contrast, a low incidence of vital components was seen in IC of chronic active hepatitis and liver cirrhosis. Thus, other causes must contribute to the formation of IC in chronic liver disease.
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PMID:Characterization of the circulating immune complexes in acute and chronic liver diseases. 686 64

Both the PEG-N technique and the PACIA were applied to determine ICLM in sera from patients with liver cirrhosis and gram-negative septicemia, that have been shown to yield positive reactions for endotoxemia with the LAL test. The precision of the PEG precipitation technique, with a stabilized fraction of human HAG of known molecular size used as a calibrator, was satisfactory. In liver cirrhosis, the detectable ICLM was mainly composed of IgG and C3, whereas in gram-negative septicemia IgM, IgG, and C3 were found. PACIA also measured significantly elevated levels of ICLM with rheumatoid factor-binding activity in both patient groups, although the two assay systems did not correlate. PEG precipitates from both patient groups analyzed by gel-chromatography and passive hemolysis test contained large immune aggregates and various amounts of immunoglobulins with specificity directed toward lipid A, the least variable portion of endotoxin. These compositional differences of detected substances may imply the presence of different types of ICLM in patients with liver cirrhosis and gram-negative septicemia.
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PMID:The polyethylene glycol precipitation technique and the particle-counting immunoassay for detection of circulating immune complex-like material in liver cirrhosis and septicemia. 707 26


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