Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the clinical features, immunopathology and the prognosis of hepatitis B virus-associated membranous nephropathy (HBVMN), 34 patients (25 boys and 9 girls) from April 1981 to November 1986 were studied. With Fab fragments of monoclonal antibodies, hepatitis B e antigen (HBeAg) was detected in the glomerular deposits from 30 cases (88.2%) and in the sera from 32 cases (94.1%). These results suggest that HBe Ag plays an important role in the development of HBVMN. In patients without corticosteroid treatment, HBV DNA was found as only episomal molecules with 3.2 kb in macrophage, T and B cells. The HBV cellular DNA disappeared within 12 months. In a HBVMN patient with corticosteroid treatment, even three years later, cellular HBV DNA was still detectable in T cells. They also had occasional proteinuria. From the in vitro study, we also demonstrated that corticosteroid stimulated endogenous HBsAg and HBeAg production from patient's mononuclear cells. Therefore, the use of corticosteroid could lead to a potential risk of enhancing viral replication. In addition, clinical trials of 32 cases demonstrate a relatively poor response to the steroid therapy with persistent heavy proteinuria (32.4%) or a high frequent relapse rate (38.2%); only one case (3.1%) had early response. Four cases received follow-up renal biopsy, progressive sclerosis with interstitial fibrosis being noted in each instance. The stage of membranous nephropathy in light microscope had progressed from stage I or II into III. One had impaired renal function. Therefore, HBVMN does not always take a benign course. Usage of corticosteroid in HBVMN patients should be avoided.
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PMID:Clinical features and natural course of HBV-related glomerulopathy in children. 177 Jul 10

Circulating immune complexes (CIC) containing HBsAg and HBeAg were identified in sera of 5 out of 6 children with hepatitis B mediated membranous glomerulonephritis. CIC were precipitated from sera by 3.5% PEG, washed and subsequently analysed after acid dissociation and trypsin digestion. HBsAg, anti-HBs and albumin; HBeAg, anti-HBe and anti-HBc were recovered from the isolated complexes and these findings are discussed. Analysis of 3.5% PEG mediated precipitate of human serum proteins showed the relatively high content of IgG classical pathway complement components: C1q, C4 and C3.
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PMID:Isolation and partial characterization of circulating immune complexes in sera of children with HBV-mediated glomerulonephritis. 184 49

Ninety-eight children with glomerulonephritis concomitant with hepatitis B surface HBs antigenemia were studied, the antigenemia being first documented at the clinical onset of glomerulopathy. Initial diagnoses, based on examination of the paraffin sections, varied, membrano-proliferative, mesangial, and membranous glomerulonephritis being most frequently considered. However, electron microscopic examination showed that 77 children had a uniform type of glomerulopathy, irrespective of the light microscopic appearance. This type was diagnosed as secondary membranous glomerulonephritis. The clinical course of this nephropathy was relatively indolent and short. Moreover, in many children, elimination of some hepatitis B virus (HBV) antigens from the circulation was also associated with clinical remission of glomerulopathy. The remaining 21 children with HBs antigenemia had various morphological forms of glomerulonephritis, these being similar to their idiopathic counterparts in both morphology and clinical course. The distinct clinical and morphological picture of secondary membranous glomerulonephritis with HBs antigenemia occurring in 77 of 98 children supports the hypothesis that HBsV-associated glomerulonephritis is of the secondary membranous type. Thus, we conclude that in children HBV antigenemia associated with glomerulonephritis other than secondary membranous is coincidental.
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PMID:Hepatitis B virus-associated glomerulonephritis: electron microscopic studies in 98 children. 188 21

Previously we found that corticosteroid treatment in the hepatitis B virus (HBV)-associated membranous nephropathy (HBVMN) was not associated with a favorable outcome. To distinguish the differences of the HBV DNA in macrophage, T and B cells among HBVMN patients with or without corticosteroid treatment, serial studies at different time points were investigated. HBV DNA appeared as an "episomal" molecule as with 3.2 kb in macrophage, T and B cells. This molecule disappeared after 12 months among HBVMN patients without corticosteroid treatment. HBV DNA, by contrast, appeared as episomal form even three years later in T cells, with frequent proteinuria among HBVMN patients with corticosteroid treatment. This finding indicates that the use of corticosteroids leads to a potential risk of enhancing HBV viral replication in T cells. We studied 24 HBVMN patients who had previously received corticosteroid treatment and had persistent proteinuria, who were administered combination therapy with adenine arabinoside for two weeks and thymic extract (Thymostimulin) for six months to decrease urine protein loss and obtain seroconversion. These 24 patients had heavy (22 of 24, 91.6%) or mild (2 of 24, 8.4%) proteinuria prior to adenine arabinoside and thymostimulin treatment. All 24 patients demonstrated HBV DNA in mononuclear cells and simultaneously exhibited sera positive with HBsAg and HBeAg. In contrast, after treatment only one case (4.2%) had heavy and two cases (8.4%) mild proteinuria; HBV DNA was demonstrated in macrophage (4 of 24, 16.7%), T cells (9 of 24, 37.5%), and B cells (6 of 24, 25%) as well as serum (24 of 24, 100%) prior to treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of hepatitis B virus-associated membranous nephropathy with adenine arabinoside and thymic extract. 200 43

Hepatitis B virus (HBV) infection has been associated with several renal diseases, the most common being membranous glomerulonephritis (MGN). The role of concurrent human immunodeficiency virus (HIV) infection in affecting the course of the renal involvement is largely unknown. We report the case of a HIV-infected adult male with chronic HBV-associated MGN who had complete remission of the nephrotic syndrome associated with spontaneous seroconversion from hepatitis B e antigen (HBeAg)-positive to HBeAg-negative. The present case illustrates that HIV infection does not preclude improvement of chronic HBV infection or an associated membranous nephropathy. Such improvement may be dependent on the ability of the host immune system to clear HBeAg.
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PMID:Remission of hepatitis B-associated membranous glomerulonephritis in human immunodeficiency virus infection. 204 56

Hepatitis B virus carriers, a 30-year-old man (case 1) and a 31-year-old man (case 2), associated with nephrotic syndrome were treated with interferon-beta. The nephrotic syndrome did not respond to corticosteroid therapy. Their HBs-Ag, HBe-Ag and HBc-Ab were positive. Renal biopsies revealed membranous glomerulonephritis in case 1 and mixed membranous and proliferative glomerulonephritis in case 2. Direct immunofluorescence studies showed strong granular staining of the GBM with IgG and using sandwich technique with anti-HBe antiserum, granular deposits were seen throughout the GBM. Patients were administrated mainly 3-6 x 10(6) IU/day interferon-beta intravenously for four weeks. After transitory elevation of serum transaminase, HBe-Ag and DNA-polymerase have disappeared with development of HBe-Ab (seroconversion) about six months after the end of interferon-beta administration. Then nephrotic syndrome has recovered in incomplete remission after a year and a half follow-up. The secondary renal biopsy in case 1 showed less intense deposits of HBe-Ag along GBM. These facts suggest that the improvement of proteinuria is associated with the decrease in HBV replication due to interferon therapy.
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PMID:[Clinical and histological observation of HBV glomerulonephritis treated with interferon-beta]. 208 50

By using immunohistochemical techniques the deposition of HBV associated immune complexes was studied in 845 consecutive cases of renal biopsy. In 665 cases of primary glomerulonephritis the frequencies of HBsAg, HBeAg and HBcAg detection in glomeruli were 11.9%, 8.3% and 3.2% respectively with a total HBV antigen positive frequency of 12.2%. High positive rates were found in membranous glomerulonephritis (MGN, 37.1%), mesangioproliferative GN (MPGN, 26%) and IgA nephropathy (IgA-NP, 18.9%). The detection of HBV infection markers in serum were simultaneously performed in 213 cases; 31.7% of the patients with primary GN were found to be positive. In patients with positive HBV infectious markers in the serum, deposits of HBV antigens in glomeruli were found in 49.1% of the cases. The incidence was significantly different in the serum negative group (10.6%). Meanwhile, about 68.3% of the cases with HBV antigen deposits in the kidney was found to have positive HBV markers in the serum. Also the incidence was significantly different in the group without HBV antigen deposits in the kidney (20.9%). It was again confirmed that the pathogenesis of hepatitis B virus associated glomerulonephritis (HBV-GN) was related to the deposition of HBV immune complexes in kidney tissue. It was noticed that the deposition of three different types of HBV antigens was somewhat associated with the development of specific forms of HBV GN. The diagnostic criteria of HBV-GN were discussed in detail.
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PMID:[Further study on the immunopathology of hepatitis B virus associated glomerulonephritis]. 208 24

Hepatitis-B-associated glomerulonephritis (HBGN) is a distinct entity occurring frequently in hepatitis-B-prevalent areas of the world. The disease affects both adults and children who are chronic hepatitis-B-virus (HBV) carriers with or without a history of overt liver disease. The diagnosis is established by serologic evidence of HBV antigens/antibodies, presence of an immune complex glomerulonephritis, immunohistochemical localization of 1 or more HBV antigens, and pertinent clinical history, when available. In this study we present clinicopathologic and follow-up findings in 12 patients (7 children, 5 adults) with hepatitis-B-associated glomerulonephritis. Twelve patients provided 15 renal biopsies and 1 specimen of kidney tissue, obtained at autopsy; these were examined by light microscopy, electron microscopy, and immunohistochemical methods. Membranous glomerulonephritis (MGN) with or without mesangial proliferation was noted in 7 biopsies, mesangiocapillary (membranoproliferative) glomerulonephritis (MCGN) in 5 biopsies, and proliferative glomerulonephritis with or without membranous changes in 2 biopsies. Tubulointerstitial changes were minimal except in 3 adults, in whom they were attributable to arterionephrosclerosis. Ultrastructural findings included the presence of considerable amounts of focal or diffuse granular electron-dense deposits in the glomeruli, in the subepithelial, subendothelial, and mesangial locations, occasionally destroying or replacing the lamina densa of the basement membrane. Variable mesangial proliferation was also observed, with interposition, with focal irregular reduplication of the basement membranes and rare clusters of spherical particles, probably representing viral particles in the deposits. In addition, granular deposits along tubular basement membranes were seen in 1 case. The glomerular deposits stained for 2 or more immunoglobulins, the predominant one being IgG, and variably also for complement components (C3, C4 and C1q). Hepatitis B viral antigens (HBsAg, HBcAg, HBeAg) were demonstrated using acid elution techniques in the deposits in all biopsies where frozen tissue was available, singly or in a variety of combinations and intensities. There were deposits of IgG, C3, C1q, and HBsAg along the tubular basement membranes in 1 case. Follow-up biopsies in 2 cases, 2 and 5 years apart, showed a transformation from a diffuse MGN to MCGN with segmental membranous features. Follow-up biopsy after 3 years in the third patient, who went into clinical remission, revealed partially resolving glomerular lesions. Renal lesions secondary to chronic liver disease, parasitic diseases, certain tropical nephropathies, and lupus nephritis are some of the diseases that may morphologically resemble HBGN. Recognition and differentiation of HBGN from other entities may have significant prognostic and therapeutic implications.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hepatitis-B-associated glomerulonephritis: pathology, pathogenesis, and clinical course. 214 48

The therapeutic benefits and risks of short-term corticosteroid were investigated in 8 patients with membranous nephropathy and hepatitis B surface antigenaemia. Seven patients presented with nephrotic syndrome, and the remaining patient had significant proteinuria. Their liver function tests were normal on repeated examination. Their sera demonstrated the persistent presence of hepatitis B virus surface antigen and high titres of antibody to hepatitis B virus core antigen. Hepatitis B virus e antigens were present in the sera of 4 patients at initial presentation. Their clinical responses were compared with 7 similar patients previously treated with diuretic therapy alone and acting as historic controls. Short-term corticosteroid (6 months) with stepwise reduction resulted in an early regression of the nephrotic syndrome in 3 patients. Five patients had persistent but reduced proteinuria. Transient liver impairment was observed in 3 patients. Corticosteroid therapy induced transient viral replication with increased serum concentration of hepatitis B virus e antigen and hepatitis B virus DNA. Two of the 7 patients receiving diuretics developed spontaneous remission though apparently later than those receiving corticosteroid. Yet complications such as liver dysfunction and hypertension were not observed in the patients treated with diuretics. Our findings suggest that corticosteroid therapy could be harmful in membranous nephropathy related to hepatitis B surface antigenaemia, as activation of viral replication could occur with corticosteroid therapy.
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PMID:The therapeutic dilemma of the usage of corticosteroid in patients with membranous nephropathy and persistent hepatitis B virus surface antigenaemia. 224 84

The incidence of atopic diseases in 206 children with nephrotic syndrome (NS) was studied. Boys with NS had three times higher incidence of bronchial asthma than the general population. There was no difference in the girls. Both boys and girls with NS had about three times more allergic rhinitis and ten times more atopic dermatitis than the general population. In NS patients with associated allergic disease, skin test and allergen-specific IgE antibodies by radioallergosorbent test (RAST) were performed. Most of the patients with dust mites (Dermatophagoides pteronyssinus, Dermatophagoides farinae), egg white, or cow's milk protein-specific antibodies had positive skin tests. One hundred of the 206 children with NS received renal biopsies and serum IgE levels were measured. During the acute nephrotic phase the geometric mean serum IgE levels in minimal change nephrotic syndrome (MCNS), IgM mesangial nephropathy (IgMN), hepatitis B virus-associated membranous nephropathy, and treatment-responsive focal segmental glomerular sclerosis patients were all significantly elevated, in descending order of significance. These high serum IgE levels decreased in remission of NS and elevated again during relapse. The relationship between high serum IgE levels in NS patients and the incidence of allergic diseases showed that one third to one fourth of either IgMN or MCNS patients developed allergic diseases. These results suggest that NS patients had a higher allergic disease incidence. Serum IgE level may serve as one of the prognostic factors. However, an increase in the IgE level may be a reflection of body immunoregulatory imbalance that plays a direct pathogenic role in the occurrence of NS and proteinuria.
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PMID:A study of the relationship between childhood nephrotic syndrome and allergic diseases. 234 27


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