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)

In a significant percentage of examined cases of fulminant hepatitis, subacute hepatitis, chronic aggressive hepatitis, liver cirrhosis and chronic persistent hepatitis, Australia (hepatitis-associated) antigen (Au HAA) was identified in the liver and in extrahepatic locations. The several immunofluorescent patterns of Au HAA localization in hepatocytes strongly suggested various stages of Au HAA accumulation and release. Deposits of a mixture of immunoglobulins G and M and occasionally beta1C-globulin were found in the cytoplasm of Au HAA containing hepatocytes, on their plasma membranes, on or in the nuclei, in the cytoplasm of Kupffer cells and, rarely, in the sinusoids. The accompanying tissue changes were hepatocellular degeneration and necrosis. These intra- and extracellular complexes of Au HAA and immunoglobulins displayed strong affinity for guinea pig complement in the immunohistochemical complement fixation reaction. When tested by immunodiffusion in agar, IgG dissociated from these complexes by potassium thiocyanate (KSCN) treatment showed anti-Au HAA specificity. In fulminant hepatitis neither Au HAA nor immunoglobulins and complement were found in the liver. In chronic aggressive hepatitis and subacute hepatitis the amount of the Au HAA immune complexes identified in the liver was approximately inversely proportional to the extent and severity of the parenchymal lesions. In liver cirrhosis and chronic persistent hepatitis there was a positive correlation between the amount of the Au HAA immune complexes found in the liver and the degree of hepatocellular damage. The deposits of Au HAA, identified in extrahepatic locations including germinal centers of lymph nodes and spleen, kidney glomeruli and blood vessel walls, were as a rule accompanied by deposits of IgG, IgM, beta1C-globulin and fibrin. All these deposits showed strong affinity for guinea pig complement in the immunohistochemical reaction of complement fixation. Germinal center activation, chronic membraneous glomerulonephritis, panarteritis and simple arteriolar hyalinosis were found at sites of localization of these deposits.
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PMID:Tissue localization of Australia antigen immune complexes in acute and chronic hepatitis and liver cirrhosis. 462 11

Using enzyme-linked immunosorbent assay technique (Boehring Institute Laboratory), eighty-one adult patients were studied for hepatitis Bs antigenaemia. Nine of the patients had asymptomatic persistent proteinuria, thirty-nine, nephrotic syndrome, and thirty-three had profuse proteinuria, azotoaemia and hypertension. The histopathology obtained in forty showed twenty-two with MCGN, four with focal glomerulosclerosis, three with proliferative glomerulonephritis, one with minimal change glomerulonephritis and ten with end-stage kidney disease. None of the patients had apparent clinical evidence of liver disease nor a past history of jaundice. One hundred and eighty apparently normal adults served as controls; 33.3% of the patients had positive hepatitis Bs antigenaemia, in contrast to 6% (P less than 0.001) in the normal controls. Hepatitis Bs antigenaemia was more prevalent in the groups with nephrotic syndrome and persistent asymptomatic proteinuria than in the group with advanced renal failure. Hepatitis Bs antigenaemia was detected in all histopathologic forms but was most prevalent in the MCGN (P less than 0.001) which is also the more commonly encountered lesion. The implications of these findings are discussed.
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PMID:Role of hepatitis Bs antigen in chronic glomerulonephritides in Nigerians. 608 37

Evidence has accumulated which indicates that several of the extrahepatic syndromes associated with HBV infection--the prodromal arthritis-dermatitis syndrome, systemic necrotizing vasculitis, and glomerulonephritis--result from immune complex-mediated injury; however, our understanding of their pathogenesis remains incomplete. Other disorders--essential mixed cryoglobulinemia and polymyalgia rheumatica--have also been linked to HBV, but these associations are more controversial. In most patients with HBV infection, circulating immune complexes are of no pathogenetic importance, but may reflect normal mechanisms for immune clearance of viral antigens. Little insight has been gained into the factors which predispose to immune complex-mediated tissue injury in only a small proportion of patients with type B hepatitis, and few options are available for the management of patients with these extrahepatic disorders. Finally, circulating immune complexes do not appear to contribute to the pathogenesis of liver disease associated with HBV infection.
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PMID:Hepatitis B as an immune complex disease. 612 7

21 patients with periarteritis nodosa (PN) were examined for evidence of viral hepatitis-B infection. Histologic evidence of PN was present in 11 patients, whereas in 10 patients the diagnosis of PN was based on the clinical presentation only. In the sera of 9 of the 21 patients (42%) HBsAg (4 patients) or anti-HBs (5 patients) was detected, while findings were present in 4-8% of blood donors. Hypertension, glomerulonephritis and renal failure developed more frequently in patients with hepatitis-B associated PN. The detection of immune complexes in the sera of hepatitis-B negative patients tends to suggest immune complex mediated mechanisms not related to hepatitis-B virus.
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PMID:[Significance of hepatitis B serology in periarteritis nodosa]. 613 34

Therapeutic drugs are well-recognized as a cause of the nephrotic syndrome in humans. However, documentation of the renal histopathologic features is lacking or incomplete in many cases. Even when accurate histopathologic information is available, there is little evidence to support a specific pathogenetic mechanism of renal injury in the vast majority of cases. We describe a patient with diabetes who had hepatitis and dermatitis in association with the use of chlorpropamide. In addition to these well-described toxic reactions to this drug, the nephrotic syndrome developed. Renal biopsy revealed the presence of a proliferative glomerulonephritis that was shown to be of an immune complex nature on immunofluorescence and electronmicroscopic study. Serial serum complement levels and circulating immune complex levels were consistent with an immunologically mediated reaction. Repeated renal biopsy documented resolution of the renal changes. Thus, in this patient, a drug-induced nephrotic syndrome was associated with a proliferative glomerulonephritis, probably due to the formation of immune complexes.
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PMID:Nephrotic syndrome and immune complex glomerulonephritis associated with chlorpropamide therapy. 621 54

In a survey the present possibilities are outlined to get knowledge about diseases of inner organs with the help of enzyme determinations in the urine. Here it is remarkable that changes of the enzyme excretion appear not only in renal disease with acute renal failure, pyelonephritis, glomerulonephritis, renal infarction and nephroptosis but are also to be observed in primarily extrarenal diseases such as diabetes mellitus, hyperthyroidism, thesaurismoses, myocardial infarction, hypertension, acute pancreatitis, epidemic hepatitis, liver cirrhosis, obstructive jaundice and rheumatoid arthritis. The causes of the changes of enzyme excretions are various. Since enzymes of different origin and localisation behave themselves variably, the simultaneous determination of a brush border marker (e.g. alanine aminopeptidase), a lysosomal enzyme (e.g. beta-glucuronidase or N-acetyl glucosaminidase) and a low molecular enzyme (e.g. lysozyme) is of use for the recognition of renal alterations. By the control of activities of urinary enzymes it is possible to get without risk informations about pathobiochemical processes in the kidney which are not to be gained by means of other methods.
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PMID:[Urinary enzyme excretion in diseases of the internal organs]. 636 87

Viruses have been demonstrated or suspected as the causative agents of various types of uveitis. Hepatitis B virus (HBV), apart from causing hepatitis, has also been implicated in the pathogenesis of systemic vasculitis, for example in glomerulonephritis and polyarteritis nodosa. It is therefore possible to postulate that a similar vasculitic process might occur in the eye leading to intraocular inflammation. A recent report from Switzerland suggests that HBV may be implicated in the aetiology of uveitis, as hepatitis B surface antigen (HBsAg) was found in the serum of 13% of cases of uveitis. Since the status of HBV in the aetiology of uveitis in Great Britain has not been investigated, we have examined serum from 200 cases of uveitis of various clinical types for the presence of circulating HBsAg. Only 4 cases (2%) were found to be HBsAg positive. This study failed, therefore, to confirm HBV as an important cause of uveitis in this country, but one cannot exclude the possibility that it may play a pathogenetic role in a small proportion of such cases.
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PMID:Status of hepatitis B virus in the aetiology of uveitis in Great Britain. 661 55

Primary liver diseases are often associated with disturbance of the renal function, but only two hepatic lesions are due to glomerular changes: hepatitis B and alcoholic liver disease. Hepatitis B associated with immune complex glomerulonephritis seems to be a rare condition in adults, however children are more often involved. Glomerular changes consist of membranous deposition of immune complexes, mainly corresponding to membranous glomerulonephritis, seldom to the membranoproliferative type. Because membranous glomerulonephritis develops due to deposition of small size soluble complexes, and the hepatitis B antigens alone are estimated to be greater than soluble nephritogenic complexes, most probably low molecular weight antigenic components of the hepatitis antigens are involved in the formation of glomerulonephritis. Alcoholic liver disease is often combined with glomerulosclerosis and mesangial IgA deposition resembling the morphological pattern of IgA mesangial glomerulonephritis. These common features implicate a similar pathogenesis of both diseases. Furthermore, experimental and clinical data indicate raised serum levels of IgA and IgA deposition within glomerula and other organs in the same manner, but the cause of high serum levels of IgA remains still obscure, and may be different in both diseases.
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PMID:[Kidney involvement in liver diseases: morphology]. 664 5

Two cases of nephrotoxicity associated with piroxicam therapy are reported. In the first case, severe reversible azotemia with hyperkalemia resolved after discontinuation of the medication. In the second case, biopsy-proved acute interstitial nephritis with immune complex glomerulonephritis and hepatitis improved after steroid therapy. The mechanism for such toxicity may be altered hemodynamics, cellular immunity, or humoral immunity related to prostaglandin inhibition.
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PMID:Piroxicam-induced renal disease. 669 75

Reports of cases of primary and secondary syphilis are increasing in the United States, particularly in urban areas and among homosexual men. While primary syphilis poses little diagnostic difficulty, many physicians are unfamiliar with the multisystem nature of secondary lues. Patients who have secondary syphilis commonly present with systemic signs, skin rash, mucous membrane lesions and generalized adenopathy. Less commonly, secondary syphilis may occur as acute meningitis, sensorineural hearing loss, iritis, anterior uveitis, optic neuritis, Bell's palsy, gastropathy, proctitis, hepatitis, pulmonary infiltration, nephrotic syndrome, glomerulonephritis, periostitis, tenosynovitis and polyarthritis. The diagnosis of secondary syphilis is easily confirmed. Its various manifestations are readily treated with penicillin and, if treated early, are entirely reversible. Two recent cases of secondary syphilis, one presenting as nephrotic syndrome and one as chorioretinitis and ptosis, illustrate the usual and unusual features of this common infection.
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PMID:Secondary syphilis: uncommon manifestations of a common disease. 670 90


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