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

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.
 ...
PMID:Membranoproliferative glomerulonephritis associated with hepatitis C virus infection. 751 May 33

Hepatitis C virus (HCV) infection is frequently found in autoimmune hepatitis and mixed cryoglobulinaemia. In these conditions HCV could be responsible for immuno-mediated organ alterations. The aim of this study was to evaluate the presence of immunological alterations in PCT patients, in which HCV infection has been frequently found. Twenty-three PCT patients were evaluated for clinical and serological alterations, including: chronic hepatitis, other systemic symptoms, serum cryoglobulins and rheumatoid factor (RF), haemolytic complement, serum immunoglobulins, anti-nuclear (ANA), anti-smooth muscle (ASMA), anti-liver-kidney-microsomal (anti-LKM1), anti-soluble-liver-antigen (SLA), anti-mitochondrial (AMA), anti-GOR antibodies, anti-HCV and HCV RNA. Abnormal serum ALT were present in the majority of cases (20/23, 87%), while liver biopsy revealed a chronic persistent hepatitis or chronic active hepatitis in 15/20 (75%) PCT patients. In a high percentage of subjects (91%) the presence of anti-HCV was detected by ELISA and RIBA II (Chiron, Emeryville CA, USA). In 17/22 (77%) cases the ongoing HCV replication in the serum was demonstrated by the detection of HCV genomes (polymerase chain reaction). The prevalence of both anti-HCV and HCV RNA in PCT was significantly higher if compared to 22 systemic immunological diseases (P < 0.001) and 47 healthy subjects (P < 0.001). A possible HCV-induced autoimmunity in PCT was suggested by the presence of the following immunological parameter alterations: anti-GOR in 13/23 (57%), ANA in 4/23 (17%), ASMA in 18/23 (78%), anti-LKM1 in 1/23 (4%), RF in 23/23 (100%), mixed cryoglobulins in 4/23 (17%), complement consumption in 10/23 (43%).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hepatitis C virus-related autoimmunity in patients with porphyria cutanea tarda. 751 37

The advent of specific antiviral therapy for chronic hepatitis C has increased the importance of establishing the correct etiology of chronic hepatitis in patients, especially because interferon alfa (IFN-alpha) has been reported to exacerbate autoimmune hepatitis (AIH), whereas corticosteroids increase viral replication in chronic hepatitis C. In our medical center, we have treated many patients with apparent chronic hepatitis C and serological or clinical evidence of autoimmunity. Our aim was to estimate the prevalence of this association and to learn whether demographic or clinical features distinguished between patients with or without autoimmune markers. We performed a retrospective review of the records of 244 unselected patients seen at the Clinics and Hospital of the University of Massachusetts between May 1991 and November 1993, who had elevated serum aminotransferases. One hundred seventeen patients had chronic hepatitis C defined by elevations of serum alanine transaminase (ALT) for at least 6 months, positive serum antibodies to hepatitis C virus (HCV; second-generation enzyme immunoassay [EIA2] or recombinant immunoblot assay [RIBA]), and absence of hepatitis B surface antigen in the serum. Records were reviewed for results of autoimmune markers in sera, including anti-nuclear antibodies (ANAs), anti-smooth muscle antibodies (SMAs), rheumatoid factor (RF), antimitochondrial antibodies (AMAs), anti-liver and kidney microsomal (LKM) antibodies, and cryoglobulins. We found a high prevalence of positivity, particularly for anti-SMAs (66%) and RF (76%) in both men and women. Forty of 41 patients tested negative for anti-LKM antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:High prevalence of serological markers of autoimmunity in patients with chronic hepatitis C. 753 20

Hepatitis C virus (HCV) infection has been found in the majority of patients with mixed cryoglobulinemia (MC) in studies conducted in different countries. In our series of 110 MC patients the frequency of HCV markers was significantly high (91%) compared with other rheumatic diseases (6.4%) and with healthy Italian controls (1.2%). Moreover, HCV RNA was detected in 81% of the peripheral lymphocytes from MC patients. Comparable percentages of HCV infection were detectable in other disorders, i.e. porphyria cutanea tarda (77%) and autoimmune hepatitis type 1 (77%). The HCV infection of peripheral lymphocytes suggests that this virus could be the triggering factor for the lymphoproliferation underlying MC. In a number of patients with MC the evolution from a benign lymphoproliferation to frank B-cell lymphoma was observed. In these subjects HCV RNA in the sera and in fresh and cultured peripheral lymphocytes was constantly detected. The same phenomenon has been observed in patients with long-lasting type C chronic hepatitis. Interestingly, HCV infection has also been recorded in 32% of idiopathic B-cell non-Hodgkin's lymphomas. Taken together, the above findings suggest that HCV can cause benign B-cell proliferation with the consequent production of various autoantibodies, including rheumatoid factor and mixed cryoglobulins. These serological abnormalities characterise different clinical disorders, including the appearance of lymphoma in a not negligible number of individuals.
 ...
PMID:Etiopathogenetic role of hepatitis C virus in mixed cryoglobulinemia, chronic liver diseases and lymphomas. 873 Apr 94

The aim of the study was to determine the role of peripancreatic lymph node swelling in systemic immunological alterations during chronic hepatitis C (HC). The prospective study was carried out as a clinical study in a university hospital. Clinical, haematochemical and ultrasonographic findings in 182 patients were studied. Ultrasonography was performed by the same operator and the findings were evaluated blind without the operator knowing the clinical and haematochemical parameters. Hepatitis B virus (HBV) markers, anti-HCV antibodies, LKM1, cryoglobulinaemia, rheumatoid factor and anti-tissue antibodies were determined. Liver biopsy was carried out in 43 of the 182 patients. One or two pathological peripancreatic lymph nodes (PLNs) were present in 30 of the 182 patients and, of the 30, 28 were anti-HC positive. Only one patient in the non-PLN group was positive for anti-HCV, there being statistical significance (P < 0.0001) between the PLN and non-PLN groups. In HCV-positive patients, extrahepatic immunological manifestations were observed (cryoglobulinaemia; positivity to anti-smooth muscle, antinuclear and antimitochondrial antibodies; positivity to rheumatoid factor and LKM1). In five patients the presence of focal lymphocytic aggregates was detected by biopsy, whereas one patient presented typical ocular lesion of Mikulicz's syndrome. Our results may confirm the marked lymphotropism shown by the HC virus and indicate more complex immune system involvement, especially in view of the coexisting signs of immune system involvement related to the presence of intrahepatic cellular aggregates detected in our study. We believe that the peripancreatic adenopathy in chronic HCV hepatitis is an important diagnostic sign and may indicate an involvement of the C virus in the still unexplained extrahepatic immunological disorders.
 ...
PMID:Peripancreatic lymphoadenopathy and extrahepatic immunological manifestations in chronic hepatitis C. 887 61

Several observations suggest that the evolution of schistosomal glomerulopathy into clinically overt and progressive disease may involve pathogenetic mechanisms other than simple glomerular deposition of parasitic antigens. In a previous study, IgA was suggested to be a mediator of late glomerular lesions in this disease. This issue is further addressed in this work. The study includes 32 patients with hepatosplenic schistosomiasis, of whom 16 had overt glomerular involvement, along with four control groups: (a) 15 healthy volunteers; (b) 15 patients with simple intestinal mansoniasis; (c) 17 patients with non-schistosomal chronic liver disease; and (d) 21 subjects with primary nephrotic syndrome not associated with schistosomiasis. Routine assessment was done for all subjects including confirmatory tests for schistosomal infection, liver and renal function tests, hepatitis viral markers and abdominal ultrasonography. The total serum concentrations of IgG, IgM, IgA were measured, as well as their respective circulating immune complexes, rheumatoid factors, anti-gliadin- and anti-DNA-antibodies. Liver and renal biopsies were obtained from the relevant groups and studied by light microscopy. Renal biopsies were also examined by immunofluorescence. Patients with simple intestinal schistosomiasis had a significant increase in IgM antigliadin antibodies. Those complicated with hepatosplenic involvement also had a significant increase in the mean IgG anti-gliadin antibodies, IgG rheumatoid factor and IgM anti-DNA activity. Cases further complicated by overt glomerular disease showed a distinct IgA predominance, mainly expressed in the serum anti-gliadin antibody pool and anti-DNA activity. This profile was essentially similar to that observed in control cirrhotics. There was a significant increase in the frequency of IgA glomerular deposits in renal biopsies obtained from patients with overt schistosomal glomerulopathy, in contrast to control nephrotics. The deposits were mainly mesangial, but were also encountered in subendothelial, subepithelial and peritubular locations. Their frequency was significantly higher with more advanced lesions as seen by light microscopy. The relevance of these data is discussed, leading to the following conclusions: (a) serum IgA-anti-gliadin and -anti-DNA antibodies, and glomerular IgA deposits are markers of significant renal involvement in patients with hepatosplenic schistosomiasis. (b) IgA may be involved in the pathogenesis of advanced glomerular pathology when superimposed on parasite-induced lesions. (c) There is a significant increase in serum auto-reactivity in hepatosplenic schistosomiasis, which may also have pathogentic implications. (d) Increased production by the inflammatory bowel lesions, impaired clearance by the fibrotic livers and probable switching of immunoglobulin synthesis are suggested to explain the observed IgA predominance in those who develop renal complications.
 ...
PMID:Immunoglobulin-A and the pathogenesis of schistosomal glomerulopathy. 887 67

Hepatitis C virus (HCV) infection has been associated with a plethora of immune and autoimmune perturbations. We review serological and clinical autoimmune manifestations associated with HCV infection, discuss treatment regimens for HCV-related autoimmune diseases, and present a framework for understanding HCV-associated autoimmune disease by performing a computerized literature search from which representative articles were used and referenced. The immune response to HCV may include the development of cryoglobulins, rheumatoid factor, antinuclear antibodies (ANA), anticardiolipin, antithyroid, anti-liver/kidney/microsomal antibodies (anti-LKM), as well as HCV/anti-HCV immune complex formation and deposition. HCV infection is a significant cause of mixed essential cryoglobulinemia, which may then be complicated by cryoglobulinemic glomerulonephritis, vasculitis, or neuropathy. It has also been associated with membranous and membranoproliferative glomerulonephritis. Subsets of autoimmune hepatitis patients are infected with HCV and evidence suggests that HCV is a causative agent of antithyroid antibodies and autoimmune thyroid disease. Although cause-and-effect remain to be proved, there are reports of HCV infection preceding or coincident with polyarthritis, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and polymyositis/dermatomyositis (PM/DM). HCV-infected patients also have a high incidence of sialoadenitis, and reports of low-grade lymphoproliferative malignancies have emerged. However, HCV is not a major causative factor for most autoimmune diseases. Optimal treatment for HCV-related autoimmune disease remains to be determined. Interferon alpha (IFN alpha) has successfully reduced viremia/transaminitis, cryoglobulins, proteinuria, and nephritis, but recurrent disease manifestations are frequent after discontinuation of therapy. Moreover, IFN alpha may precipitate or exacerbate autoimmune disease symptoms. HCV-related autoimmune disease also has been treated successfully with corticosteroids, azathioprine, and cyclophosphamide, although HCV viremia persists and may worsen.
 ...
PMID:Hepatitis C virus infection and autoimmunity. 906 50

Here we report an autopsy case with anti-neutrophil antibodies (ANCA) associated vasculitis accompanied by autoimmune hepatitis and hepatocellular carcinoma. A 69-year-old woman was admitted to Tokyo Metropolitan Ohtsuka Hospital in October 1995 because of leg edema. She had presented cough in 1990 and diagnosed as interstitial pneumonia, esophageal varices and liver chirosis. On admission, laboratory data showed mild anemia, hypoproteinemia, and marked gammagloblinemia. IgM-HA antibody, HBs antigen, HBs antibody, HCV antibody and HDV antibody were negative. Anti-nuclear antibody, anticentromere antibody, anti-neutrophil cytoplasmic antibody against myeloperoxidase and cathepsin G (MPO-ANCA and cathepsin G), rheumatoid factor and direct coombs test were positive. Serum level of AFP and CEA were elevated. Ultrasonography and computed tomography of abdomen scowed liver chirosis and tumor in left lobe of liver. The diagnosis of liver chirosis based on autoimmune hepatitis and Interstitial pneumonia was made with clinical course, laboratory findings and radiographic findings although liver biopsy was not performed. She complained of bloody stool due to ulcer of the large intestine, and died of liver failure which progressed rapidly. The autopsy findings detected that pulmonary fibrosis, liver fibrosis with multiple hepatocellular carcinoma, necrotizing crescentic glomerulonephritis, and vasculitis of small artery inn colon. This was the first report of MPO-ANCA associated vasuculitis complicated with autoimmune hepatitis and hepatocellular carcinoma. Clinical significance of ANCA and immunogenetic background of these diseases were discussed.
 ...
PMID:[An autopsy case of anti-neutrophil cytoplasmic antibodies associated vasculitis accompanied by autoimmune hepatitis and hepatocellular carcinoma]. 917 69

A 58-year-old man with subacute fulminant onset of autoimmune hepatitis (AIH) was treated by leukocytapheresis (LCAP) and bilirubin adsorption therapy (BAT), rather than by administration of high-dose corticosteroids as he had mild glucose intolerance, and a definitive diagnosis of AIH was not obtained on admission; further, there was a risk of viral infection. After initiation of the therapies, serum transaminases and bilirubin, immunoglobulins, anti-nuclear antibodies, and rheumatoid factor decreased rapidly, as did the initially high levels of activated cells and several pro-inflammatory cytokines. Liver inflammation observed on liver biopsy settled during the course of the therapies, with no adverse side effects. A pause in the therapies was associated with deterioration; however, restoration of apheresis was followed by normalization. Remission was sustained throughout the period monitored, except for a recurrence 14 months after discharge, which was successfully resolved by two additional LCAP sessions. These results suggest that LCAP influences the causal mechanism(s) of exacerbation of AIH.
 ...
PMID:Exacerbated autoimmune hepatitis successfully treated with leukocytapheresis and bilirubin adsorption therapy. 934 99

HCV-infection is an important infectious disease in rheumatology. It is the cause of mixed cryoglobulinemia and other rheumatic manifestations develop frequently during HCV-infection. These comprise: Sicca-syndrome, thromboembolic events associated with anti-cardiolipin antibodies and fibromyalgia. Also associated with HCV-infection is a non-erosive polyarthritis. This synovitis often fulfills the ACR-criteria for rheumatoid arthritis, but the disease course is different with frequent remissions and non-erosive joint involvement. The following autoantibodies are associated with HCV-infection: Cryoglobulins, rheumatoid factor, antinuclear antibodies (ANA), antismooth muscle antibodies (SMA), anti-phospholipid-antibodies and anti-thyroid-antibodies. In HCV-associated sicca-syndrom, antibodies against Ro (SSA) and La (SSB) are not detected. The course of HCV-infection is often occult, without elevation of liver enzymes. We summarize the clinical and serological signs and symptoms when HCV-infection should be suspected and when HCV-testing should be performed in a rheumatological setting. The identification of HCV-infection in rheumatic patients is important to minimize the risk of aggravating hepatitis by prescription of hepatotoxic drugs and because of the availability of alpha-interferon as a potential virus eradicating agent.
 ...
PMID:[Hepatitis C virus in rheumatic diseases]. 946 81


<< Previous 1 2 3 4 5 6 7 8 Next >>