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)

During the period between January 1975 and August 1976, 203 liver biopsies were received at the Singapore General Hospital from patients with a variety of liver diseases. A histological diagnosis of chronic hepatitis was made in 29 patients: 13 cases of Chronic Aggressive Hepatitis (C.A.H.). 10 cases Chronic Persistent Hepatitis (C.P.H.) and 6 of Chronic Lobular Hepatitis (C.L.H.). C.P.H. and C.L.H. were found mainly in the third and fourth decades. C.A.H. was more common in the fifth to seventh decades and occurred principally in females. Hepatitis B antigenaemia was detected in 48.3% of these cases using the immunoelectroosmophoresis (EOP) technique and showed an even scatter in all histological sub-types. Using the reverse passive haemagglutination (rPHA) method for detection by HBs antigen and the radioelectrocomplexing (REC) method for anti-HBs, an immune sub-group (HBs Ag+/anti-HBs+) was identified in greater proportions in C.A.H. and C.P.H. compared to normal controls. This was interpreted to mean that these patients suffered from a primary immunodeficiency characterized by failure of production of high avidity anti-HBs with resulting failure to clear HBsAg leading to perpetuation of liver damage due to circulating immune complexes. It is also suggested that patients with C.P.H. belonging to this immune sub-group may progress to C.A.H. with its more ominous prognosis.
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PMID:Hepatitis B surface antigen and antibody status in biopsy proven chronic hepatitis in Singapore. 52 86

We recently observed a increase in factor-VIII clot promoting activity as measured by a one-stage assay (VIII AHF) in a haemophiliac with hepatitis. However, VIII AHF as measured by a two-stage assay (VIII AHF) was 0.013 u/ml at a time when VIII AHF measured 0.38 u/ml. We then studied seven non-haemophiliacs with liver disease, and attempted to correlate the lvels of VIII AHF and VIII AHF with factor VIII-like antigen (VIII AGN) as measured by quantitative immunoelectrophoresis. In four of the seven patients, disproportionate elevations of VIII AHF compared to VIII AHF were found. Furthermore, VIII AHF values correlated well with VIII AGN vales . No such discrepancy was apparent in four normal control subjects. These findings emphasize the necessity for performing two-stage assays in haemophiliacs as well as non-haemophiliacs with liver disease to assess factor-VIII levels. In addition, they suggest that confirmation of the diagnosis of haemophilia may not be possible in the haemophiliac with hepatitis unless VIII AHF determinations are performed. The reason for the disparity between VIII ahf and VIII AHF levels is not apparent. However, the correlation of VIII AGN and VIII AHF levels in the non-haemophiliacs with liver disease provides further support for the concept that VIII AGN and VIII AHF are closely related or identical molecular entities.
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PMID:Relationship of factor VIII-like antigen (VIII AGN) and clot promoting acitivty (VIII AHF) as measured by one- and two-stage assays in patients with liver disease. 99 Jan 95

The authors applied a silver colloid technique to identify Argyrophilic Organiser Region (AgNOR) to 8 groups of hepatic lesions: alcoholic hepatitis with dysplasia (3 cases); chronic active hepatitis with dysplasia (4 cases); cirrhosis with dysplasia (5 cases); focal nodular hyperplasia (4 cases) and hepatocellular carcinomas (3 cases of grade I, 3 cases of grade II and 5 cases of grade III of Edmondson). Four cases of non-specific reactive hepatitis were used as control. This work suggests the simplicity and utility of simultaneous application of clumps per cell, AgNORs per clump and total AgNORs counts in the evaluation of neoplastic and preneoplastic lesions of the liver. The results show, in hepatocellular carcinomas, a relationship between the number of clumps, the AgNORs per clump, the total number of AgNORs and the grading of Edmondson. The nodular lesions that can be considered in the differential diagnosis with carcinoma are sufficiently well discriminated using the two parameters AgNORs per clump and total number of AgNORs.
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PMID:Hepatocellular carcinoma and preneoplastic lesions of the liver: evaluation of argyrophilic nucleolar organizer regions (AgNORs). 133 18

The course of infection of a pancreas-adapted isolate of coxsackievirus B4 was followed over a 10 month period in a murine model. Following intraperitoneal inoculation a typical acute infection was seen in nine of 10 inbred mouse strains. Virus rapidly infected the exocrine pancreas, titres peaking 3 to 4 days post-infection (p.i.). Lesions were almost exclusively confined to pancreatic acinar cells and varied in severity among the inbred strains. Virus shed into the blood-stream was not cell-associated. Evidence of persistent infection was found in nine mouse strains and infective virus was recovered from the pancreas of seven strains for up to 10 months p.i. Approximately 28% of pancreases examined beyond the acute phase showed focal inflammation and 22% showed focal necrosis (cell death). Virus was occasionally recovered from other organs (heart, liver and spleen), but lesions were rarely seen. Virus-specific antigen was localized to small groups of pancreatic acinar cells using an indirect immunogold silver staining technique. These observations suggested that the virus persists in pancreatic tissues because it seems unlikely that virus disseminated from distant sites would cause such localized infection. In three of these strains, the course of infection may have been influenced by superinfection with mouse hepatitis virus.
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PMID:Coxsackievirus B4 infection of the mouse pancreas: acute and persistent infection. 160 60

In the US and northern Europe, the prevalence of pregnant syphilitic women is estimated at .1-.6%, while in South Africa it was 7.6% in 1982. In 1978, there 108 cases in the US which increased to 268 reported cases in 1985. The increase of congenital syphilis (CS) by 25% from 1985 to 1988 was attributed to the spread of crack cocaine in the US. The rate was 10.5 cases/100,000 live births in the US during this period, a 21% increase. In contrast, in the Netherlands there were 2.5 cases/100,000 live births during 1982-85. Clinical symptoms appear 3 weeks after birth, but some are present at birth such as hepatosplenomegaly, bloated abdomen, cutaneous lesions, and nasal discharge turning into purulent rhinitis. Anemia occurs in 90% of children with CS. Generalized lymphadenopathy, splenomegaly with hepatomegaly, and syphilitic hepatitis may also occur. Syphilitic skeletal abnormalities include osteochondritis, periostitis, osteomyelitis, and osteitis. Meningovascular syphilis produces nervous system effects. CS complications include nephrotic syndrome and acute glomerulonephritis. Ocular abnormalities are caused by treponemes found in the cornea, sclera, uvea, retina and the optic nerve. Chorioretinitis and iridocyclitis are common ocular lesions. The pathogen Treponema pallidum can be diagnosed by dark field microscopy, by immunofluorescence, or by histopathological examination of silver-stained preparations. Pregnancy women with syphilis are treated with penicillin although failures have been reported after single or 2 or 3 in administrations of 2.4 MU benzathine penicillin and after giving tetracycline in 3rd trimester pregnancy. The CDC recommendation for treating infants with CS is iv 50,000 U/kg penicillin G every 8-12 hours for 10-14 days or im 50,000 U procaine penicillin once daily for 10-14 days. Single administration of 50,000 U/kg benzathine penicillin is recommended for newborn children whose mothers have been treated with erythromycin.
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PMID:Congenital syphilis. 161 61

High-resolution two-dimensional polyacrylamide gel electrophoresis in combination with silver staining was used to analyze between 800 and 1000 cytosolic and particulate polypeptides from age-matched livers of normal male Long-Evans rat with Agouti coat color (LEA) and Long-Evans rat with Cinnamon-like coat color (LEC) rats with hereditary trait of hepatitis at ages long before, immediately prior to, and just after the onset of hepatitis. Although the electrophoretic patterns of polypeptide expression were very similar with respect to the overall spot patterns, a number of polypeptides which differed either qualitatively or quantitatively were noted. Two constitutively expressed cytosolic polypeptides, P29.5 (Mr 29.5 kDa/pI 6.73) and P30 (30 kDa/6.70), were not detected in livers of LEC animals at any age. In the normal LEA rats both P29.5 and P30 were detected as early as one day after birth and both were expressed at similar concentrations at all ages. In the LEC rats P30-C (30 kDa/6.68) was constitutively expressed in close proximity to the expected position of P30, and P30-C was not detected in the LEA rats. By means of non-equilibrium pH gradient electrophoresis two relatively basic polypeptides were detected in the LEC rats. P18ne was detected immediately prior to and P27ne immediately after the clinical manifestation of hepatitis. Experiments in F1 backcross ([LEA x LEC] x LEC) animals, however, failed to demonstrate any genetic link between either the expression or lack of expression of P29.5, P30, P30-C, or P18ne and hepatitis development. P27ne was detected in all backcross animals exhibiting hepatitis, but was never observed in LEC rats prior to the onset of hepatitis. Although we were unable to identify any unique loss of expression of polypeptides which are genetically linked to hepatitis susceptibility in LEC rats, specific subsets of quantitatively modulated polypeptides were detected.
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PMID:Two-dimensional electrophoretic analysis of hepatitis-associated polypeptides in liver of LEC rats developing spontaneous hepatitis. 211 96

The raw carp bile has both nephrotoxic and hepatotoxic effects which are not well known. Recently, we studied 13 patients who had toxic acute renal failure and toxic hepatitis after ingestion of raw bile of carp in 3, grass carp in 8 and silver carp in 2 cases. The purpose of this report is to alert physicians to this very rare cause of toxic acute renal failure and hepatitis. All patients presented initially with gastrointestinal upset after eating. These symptoms were followed by oliguria in 7 patients (54%), hematuria was noted in 10 (77%) and jaundice in 8 patients (62%). Elevation of blood urea nitrogen, creatinine and transaminases lasted for about 3 weeks. The severity of the symptoms depended on the amount of bile ingested. All the patients recovered with conservative therapy and hemodialysis. Biopsy of the kidney revealed findings compatible with acute tubular necrosis similar to that produced by other nephrotoxins. Biopsy of the liver revealed findings consistent with acute toxic hepatitis. Both suggest toxic effects of carp bile as a cause of toxic acute renal failure and hepatitis.
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PMID:Toxic acute renal failure and hepatitis after ingestion of raw carp bile. 224 75

The morphologic evolution of hepatitis B virus (HBV) liver disease in 45 hepatic allograft recipients who were HBV surface-antigen positive (HBs-Ag+) at the time of liver replacement and who survived for more than 60 days was studied by routine histologic and immunocytochemical analysis of serial pathology specimens. The findings in these patients were compared to a control group of 30 individuals who were immune to the HBV (anti-HBs antibody positive), but required hepatic replacement for other reasons. Eight of the forty-five (18%) HBsAg-positive patients have no serologic evidence of HBV reinfection after transplantation. All 37 remaining patients are reinfected; 21 (47%) developed chronic active hepatitis and/or cirrhosis, 3 (7%) developed submassive necrosis, and 6 (14%) developed chronic lobular hepatitis. One patient lost her graft to chronic rejection, despite reinfection with the B virus. Four other patients (9%) developed a chronic carrier state. No long-term follow-up biopsies were available in the remaining two patients. The histologic features associated with dysfunction related to recurrent HBV infection evolved from an acute to chronic phase and were similar to hepatitis B seen in nonallografted livers. Furthermore HBV-related lesions could be separated from rejection using routine histology alone. The only exception to this conclusion was the occurrence of a peculiar HBV-related lesion in two recipients, described herein. Immunohistochemical analysis demonstrated the presence of viral antigens in almost all cases. Hepatic inflammation also was commonly present during HBV disease and consisted mostly of accessory cells and T lymphocytes. Analysis of the effect of major histocompatibility complex matching revealed no clear association between the number of class I or II matches or mismatches and the development, or pattern, of active hepatitis in the allograft. Peculiar pathologic alterations in several of the biopsies and failed allografts after HBV reinfection suggests that, under special circumstances, the B virus may be cytopathic.
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PMID:Evolution of hepatitis B virus liver disease after hepatic replacement. Practical and theoretical considerations. 239 36

Investigations were conducted to establish the optimal conditions for silver staining of polypeptides separated by polyacryle-amide gel electrophoresis. The thickness of the gel layer was of 1.5 mm. The experiments showed that the modified Hankeshover and Dernick's technique (4) (replacement of the fixative for the electrophoretically separated polypeptides and extension of the bleaching by Farmer's reagent time) had the best sensitivity and reproducibility. This technique can be performed also on polyacryle-amide gel preparations already stained by the Coomassie Brilliant Blue method. To check the efficiency of this silver staining technique, the authors used it to detect the Sendai virus and B hepatitis virus surface antigen polypeptides.
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PMID:[Demonstration of viral proteins by silver staining]. 243 53

A specific enzyme-linked immunosorbent assay (ELISA) was developed for the detection and characterisation of antibodies directed against amodiaquine (AQ), an anti-malarial drug associated with agranulocytosis and liver damage in man. The assay incorporated an antigen which was produced by the reaction of amodiaquine quinone imine (AQQI), a protein reactive product produced from AQ by silver oxide oxidation, and metallothionein. The protein-conjugate (AQ-MT) had a ratio of AQ to protein of 5.2:1. Specific anti-drug antibody was defined as the differential binding to AQ-MT and unconjugated MT which was inhibitable by AQ-mercapturate (5 microM). Following administration of AQ (0.27 mmol/kg; for 4 days) to male Wistar rats there was a significant increase in the IgG anti-AQ activity on day 18 (P less than 0.05, 0.596 +/- 0.410, N = 7) compared to pre-injection levels (0.111 +/- 0.074, N = 7). This activity was shown to be specific for the AQ determinant by hapten inhibition with AQ (IC50 250 nM) and AQ-mercapturate (IC50 310 nM). Following administration of AQQI (27 mumol/kg; i.m.; 4 days) there was a significant increase in IgG anti-AQ antibody activities on day 18 (0.584 +/- 0.161, N = 7) compared to pre-injection levels (0.078 +/- 0.048, N = 7). This activity was inhibited by AQ (IC50 150 nM) and AQ-mercapturate (IC50 180 nM). In addition IgG anti-AQ antibodies were detected in four patients who exhibited agranulocytosis and one patient who exhibited hepatitis (range 0.017-0.842) whilst receiving AQ at a dose of 400 mg weekly for several weeks, but not in individuals who had not received the drug (-0.014 +/- 0.022, N = 7). There was no increase in IgG anti-AQ antibody activities in patients who had not exhibited an adverse reaction whilst receiving the drug for the treatment of malaria (-0.059 +/- 0.074 on day 0 and -0.053 +/- 0.068 on day 7, N = 13). Thus, we have shown that AQ is immunogenic in the rat and that the formation of a chemically reactive metabolite (AQQI) is involved in the generation of the antibody response. Furthermore, drug-specific antibodies were detected in sera from five patients with severe adverse reactions to the drug.
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PMID:Drug-protein conjugates--XVIII. Detection of antibodies towards the antimalarial amodiaquine and its quinone imine metabolite in man and the rat. 247 Mar 78


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