Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic alcoholism is accompanied by systemic involvement of the internal organs. Clinico-morphological forms of chronic alcoholism are distinguished on the basis of the prevailing organ pathology, Morphological data are presented, and pathogenesis of the lesions of the liver, heart, pancreas, and kidneys in patients with chronic alcoholism is analysed. The hepatic form may present alcoholic dystrophy, hepatitis or cirrhosis which are stages of progressing hepatopathy. The toxic and metabolic effect of ethanol is important in the pathogenesis of liver lesion. The cardiac form is characterized by the development of alcoholic myocardiodystrophy. In addition to the toxic influence of ethanol, hormonal and electrolyte changes and microcirculatory disorders play a role in its pathogenesis. Chronic calcifying pancreatitis in chronic alcoholism is associated with the effect of ethanol on the mediatory system. The renal form any present necronephrosis, hepatorenal syndrome, glomerulonephritis or pyelonephritis. Their pathogenesis is determined by toxicity of ethanol, circulation of immune complexes in the blood, or immunosuppression.
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PMID:[Morphology and pathogenesis of visceral manifestations of chronic alcoholism]. 711 39

Glomerular lesions associated with hepatic disease were evaluated. Among 752 consecutive patients with hepatitis and cirrhosis, nephritic urinary changes appeared in 1.0% of chronic hepatitis and 9.2% of cirrhotics, but none in patients with acute or subacute hepatitis. Kidney tissue was obtained from 141 cases, of which 59 underwent immunofluorescent studies. Except for a few with possibly coincidental glomerulonephritis, the main glomerular pathology was mesangial depositive or proliferative lesions with frequent circumferential mesangial interposition. The highest incidence (up to 69.2%) occurred in liver cirrhosis. The glomerular immunohistology was not necessarily homogeneous. In acute or subacute hepatitis, IgG or IgM, if present, was dominant. The more chronic the course the liver disease followed, the more frequently significant IgA deposition emerged, occurring in 60.5% of cirrhotics. The IgA positive cases often disclosed paramesangial dense deposits, which is one of the characteristics of primary IgA nephritis. Hepatic IgA nephritis exhibited a lower nephritogenicity and a proneness to show mesangial interposition when compared with primary or purpuric IgA nephritis. The possible origin of glomerular IgA associated with liver disease is discussed.
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PMID:Hepatic glomerulonephritis. Characteristics of hepatic IgA glomerulonephritis as the major part. 728 1

A 24-year old female patient developed extramembranous glomerulonephritis 8 months after acute hepatitis-B with virus antigen persisting in the serum. Two years later, the glomerular lesions were found to be clinically and histologically cured, with parallel disappearance of the antigen from the serum. Although the presence of HBsAg in the glomeruli could not be demonstrated, it is likely from the sequence of events that hepatitis-B virus was responsible for the renal disease.
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PMID:[Extramembranous glomerulonephritis following hepatitis-B. Simultaneous disappearance of serum virus antigen and glomerular lesions (author's transl)]. 742 18

The hepatitis C virus genome has been recently sequenced and cloned, allowing the identification of patients exposed to this virus, which is now felt to be the principal cause of "non-A, non-B" hepatitis. The hepatitis B virus has long been implicated in the pathogenesis of several glomerulopathies including membranoproliferative glomerulonephritis, mixed cryoglobulinemia, and membranous glomerulonephritis. Several authors have recently reported an association between hepatitis C virus infection and glomerular disease. The case of a patient with chronic hepatitis C virus infection who developed the nephrotic syndrome 3 months after liver transplantation is described. Serologic testing was significant for an elevated rheumatoid factor, circulating cryoglobulins, and a mildly depressed C4 level. Hepatitis C virus antibody and viral RNA (by polymerase chain reaction) were present in both the serum and cryoglobulin fraction. A renal biopsy demonstrated membranoproliferative glomerulonephritis. It is believed that persistent infection with the hepatitis C virus is responsible for an immune complex-mediated glomerulonephritis in this patient. Because hepatitis C has now been pathogenetically linked to several glomerulopathies, testing for this virus should be considered in the serologic work-up of the patient with glomerulonephritis.
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PMID:Membranoproliferative glomerulonephritis associated with hepatitis C virus infection. 751 May 33

Hepatitis C virus (HCV) infection is one of the important causes of chronic and severe hepatitis in China. In an attempt to understand if there is any relationship between HCV infection and glomerulonephritis (GN), serum samples from 570 GN patients and 100 normal volunteers were screened for anti-HCV antibody (HCV-Ab) with ELISA method. Among the cases with positive HCV-Ab, serum HCV-RNA was tested with nested RT-PCR method. The incidence of serum HCV-Ab was 2 in 100 normal volunteers (2%) and 34 in 570 GN patients (6%). The incidence of positive serum HCV-RNA was 0 in normal volunteers whereas 21 in GN patients. The main clinical manifestation of GN patients with serum positive HCV-Ab was an unique proteinuria with/without nephrotic syndrome or renal failure, whereas the pathologic lesions in GN patients with serum positive HCV-Ab or HCV-RNA consisted of different disease entities. There was no close link between MPGN and active HCV infection. From the data observed, it seems that there is a coincidence between glomerular diseases and HCV infection rather than a matter of cause and consequence.
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PMID:[Is there hepatitis C virus associated glomerulonephritis?]. 753 65

Typhoid fever is endemic in developing countries and may cause very different clinical findings. Although hepatic involvement and abnormal liver function tests may be seen in 50% of the patients, intravascular hemolysis and renal involvement are rare. In this report, a 10-year-old patient with enteric fever presenting with hepatitis, severe intravascular hemolysis and glomerulonephritis is presented. To see all of these findings together in a patient with typhoid fever is very rare and may cause diagnostic difficulties.
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PMID:Typhoid fever with very high transaminase levels. 759 69

The efficacy of therapy with reaferon (recombinant alpha 2-interferon) was studied in children with glomerulonephritis (GN) associated with hepatitis B virus infection as well as its effect on the interferon status (IFN), production of interleukins (IL) 1 and 2 and synthesis of active arachidonic acid (AA) metabolites by the blood cells in the course of treatment. The IFN status, IL-1, IL-2 production, and synthesis of AA active metabolites (LTB 4- and 5-HETE) by the blood cells, as well as markers of HBV-infection (HBsAg, anti-HBs, anti-HBc total and anti-HBc of the IgM class) were examined over time in 60 GN patients treated with reaferon alone and administered immunosuppression therapy (IST), with antioxidants, or IST alone. The employment of reaferon for treatment of GN patients was shown to increase the efficacy of GN treatment, especially in combination with immunosuppressive drugs, to prevent reactivation of hepatitis B virus when prednisolone and/or cytostatic drugs were used, and to reduce hepatitis activity. It way be assumed that the above effects were mainly due to the action of reaferon and antioxidants on the improvement of the condition of immunocompetent cells, primarily monocyte-macrophage system and leukocytes. During reaferon therapy, normalization of alpha-IFN and IL-1 production by the blood cells and inhibition of production of AA active metabolites were observed.
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PMID:[The dynamic production of interferons, interleukins and arachidonic acid metabolites by the blood cells of children with glomerulonephritis associated with HB virus infection while treated with reaferon]. 769 26

A variety of prodromal symptoms of viral hepatitis (urticaria, fever, arthralgias, headache, polyradiculonevritis) are attributed to A, B, C, D or E hepatitis only when jaundice appears, and because they disappear with it. Spectacular extrahepatic symptoms (polyarteritis nodosa, cryoglobulinemia, glomerulonephritis, marrow aplasia...) may be associated with B or C hepatitis without any liver symptom. Some of the extrahepatic symptoms observed during chronic hepatitis C therapy with interferon (thyroid dysfunctions, cutaneo-mucous lichen) may be related to the immunomodulatory effects of interferon rather than to virus C itself.
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PMID:[Extra-hepatic manifestations of viral hepatitis]. 772 20

The blood-borne hepatitis viruses, hepatitis B virus (HBV) and hepatitis C virus (HCV), have similar epidemiological features. The association of chronic HBV infection and glomerulonephritis is well established, particularly in children. Recent reports have shown an association between HCV infection and glomerulonephritis in adults. In order to assess the role of these hepatotropic viruses in membranoproliferative glomerulonephritis (MPGN) we screened 34 children with idiopathic MPGN for the presence of HBV and HCV infection using highly sensitive polymerase chain reaction techniques for the detection of HBV DNA and HCV RNA. Also, enzyme-linked immunosorbent assays were used to detect the presence of antibody to hepatitis B surface antigen and antibody to HCV. No evidence of HBV or HCV infection was demonstrated in any of the patients. We conclude that HBV and HCV are not significant causes of idiopathic MPGN in children in the United States.
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PMID:Absence of hepatitis B and C viruses in pediatric idiopathic membranoproliferative glomerulonephritis. 774 14

Several extrahepatic syndromes have been associated with chronic hepatitis C virus infection. In our patient (a 57-yr-old woman without risk factors for hepatitis), chronic active hepatitis C was diagnosed serologically and histologically. Three months later, membranoproliferative glomerulonephritis with compromised renal function and peripheral edema, cryoglobulinemia, and a vasculitis of the finger tips developed. During interferon treatment for 3 months, neither the clinical condition nor serological parameters improved significantly. Progressive dyspnea was due to bilobar pulmonary infiltration. Despite antibiotic, virostatic, and corticosteroid therapy, the patient died from respiratory failure. Autopsy revealed diffuse pulmonary vasculitis. Thus, this is the first description of chronic hepatitis C virus infection, glomerulonephritis, and cryoglobulinemia complicated by immunologically mediated pulmonary vasculitis. Because interferon therapy may be ineffective, immunosuppressive therapy should be considered.
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PMID:A lethal course of chronic hepatitis C, glomerulonephritis, and pulmonary vasculitis unresponsive to interferon treatment. 777 95


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