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)

Mice infected with Schistosoma mansoni were highly sensitive to the lethal effects of bacterial lipopolysaccharide (LPS). The hyper-reactive state of LPS coincided with the development around the parasite eggs of multiple granulomas in the liver. Elevated aspartate transaminase levels in blood and severe hypoglycaemia in LPS-challenged animals indicated extensive liver parenchymal cell damage. There was also a complete depletion of glycogen in hepatocytes of these animals. From this work and studies on other hepatitis models, it is suggested that individuals affected with granulomatous disorders may be at risk because of everyday exposure to LPS from the gut.
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PMID:Increased hepatotoxicity of bacterial lipopolysaccharide in mice infected with Schistosoma mansoni. 55 82

A model of acute schistosomiasis of the mouse was used to observe whether curative treatment would be followed by an enhancement of the hepatic and splenic lesions, as a consequence of the massive destruction of worms and eggs within the portal system. Mice infected with 50 cercariae of Schistosoma mansoni were treated with both oxamniquine and praziquantel on the 50th day of infection and submitted to a sequential histologic examination from the 2nd to the 45th day after treatment. Although severe focal lesions due to dead and disintegrating worms were present in the livers of the treated animals, no aggravation of the general changes (reactive hepatitis and splenitis, or periovular granulomas) was seen in comparison with a control non-treated group. Of 50 animals treated during the acute phase of schistosomiasis only one died spontaneously, while 16 out of 30 infected controls died before the end of the experiment. The present investigation indicates that curative treatment during the acute phase of schistosomiasis does not enhance previous lesions at first and results in progressive disappearance of the lesions starting six days following chemotherapy.
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PMID:Treatment of acute experimental schistosomiasis. 248 44

Three hundred twenty-four individuals in a farming village located in the Nile Delta of Egypt were serially tested for hepatitis markers and Schistosoma mansoni to determine whether there is an increased risk of hepatitis B in persons infected with schistosomiasis. One-half of the subjects had stools positive for S. mansoni. Thirty-seven percent of the individuals had been infected with hepatitis B, and 3% were chronic HBsAg carriers. No statistical association was found between S. mansoni infection and hepatitis B infection, including chronic hepatitis B. Although there was no evidence of an association between these 2 pathogens, larger nonhospital based studies are needed to resolve this question.
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PMID:Risk of hepatitis B infection among Egyptians infected with Schistosoma mansoni. 309 91

In order to evaluate the ELISA for schistosomiasis under the conditions of clinical practice, 1576 hospital patients were tested using a crude soluble Schistosoma mansoni egg antigen. Test sensitivity in detection of S. mansoni was found to be 96.2% and in S. haematobium 92.3%. The predictive value of positive results was high, reaching 88% at antibody levels three or more times the screening level. The test was considered by clinicians to be valuable for diagnosis and patient management, though it did not distinguish active from recently treated infections. Of 37 apparently false positive schistosome ELISA results only seven could be attributed to other helminth infections. Another nine patients had hepatitis. It is suggested that the antigens and antibodies of the two diseases are mutually cross-reactive, since reports have suggested a high increase of HBsAg patients with schistosomiasis.
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PMID:An evaluation of the ELISA for schistosomiasis in a hospital population. 309 36

In an attempt to establish an experimental model of acute schistosomiasis, sequential histological changes were investigated in the skin, lung, liver and spleen of mice infected with 30 or 100 cercariae of Schistosoma mansoni according to four sets of experiments: single infection, repeated infections, unisexual infection and infection in mice born from infected mothers. Animals were killed every other day from exposure up to 50 days after infection. Only mild, isolated, focal inflammatory changes were found before the appearance of mature eggs in the liver, even when repeated infections were made. Severe changes of reactive hepatitis and splenitis appeared suddenly when the first mature eggs were deposited, around the 37th to 42nd day after infection. The mature eggs induced lytic and coagulative necrosis of hepatocytes around them which was soon followed by dense infiltration of eosinophils. So, mature egg-induced lesions appeared as the major factors in the pathogenesis of acute schistosomiasis in mice. Mice born from infected mothers were apparently able to rapidly modulate the egg-lesions, forming early fibrotic granulomas. The murine model of acute schistosomiasis appeared adequate for the study of pathology and pathogenesis of acute schistosomiasis.
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PMID:A contribution to the study of acute schistosomiasis (an experimental trial). 314 21

Human infection with Schistosoma haematobium and/or Schistosoma mansoni is known to be widespread in central Liberia, but no information is available about its clinical manifestations or its significance for public health. Details of a cross-sectional morbidity study are reported. A sample from hospital out-patients and samples from 3 villages situated in areas with different transmission patterns (lack of transmission, transmission of only S. haematobium and transmission of both S. haematobium and S. mansoni) were examined. All 184 individuals were examined by standardized case history, clinical and parasitological investigations, including a skin snip for onchocerciasis and a count of schistosomal and other intestinal worm eggs from stool and urine. A complete blood count, urine analysis, urine cultures, hepatitis-B surface antigen determination and abdominal X-rays were also carried out. Schistosomal egg counts ranged from 1 to 6200/10 ml urine for S. haematobium and from 1 to 228/g stool for S. mansoni. Difficulties for the definition of accurate morbidity indices are discussed. Except for haematuria and dysuria, the overall morbidity in the study area was not striking, neither for S. haematobium nor for S. mansoni infection. No cumulative pathology was observed in patients with mixed infection. The frequency of hypertension, hepato- and splenomegaly, ascites and bacteriuria was low and no relationship to schistosomiasis could be established. Bladder calcifications were found in 10% of people living in an area of transmission of S. haematobium. Although the intensity of infection is low for both S. haematobium and S. mansoni, long-term follow-up studies are essential for a more accurate assessment of the public health importance of these parasites.
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PMID:The impact of schistosomiasis among rural populations in Liberia. 613 75

The purified Schistosoma mansoni adult microsomal antigen, MAMA, was used in the quantitative single-tube kinetic dependent enzyme-linked immunosorbent assay (k-ELISA) to measure antibody levels of various human patient sera. The 511 serum specimens tested were from patients with both homologous and heterologous infections. Sera from U.S., Egyptian, Brazilian, and Puerto Rican patients infected with S. mansoni reacted strongly with MAMA. Chinese patients infected with S. japonicum, and Nigerians or Egyptians infected with S. haematobium produced much lower responses to this antigen than those infected with S. mansoni. Sera from patients with echinococcosis, filariasis, paragonimiasis, clonorchiasis, trichinosis, amebiasis, and hepatitis and from healthy uninfected control individuals generally contained no detectable antibodies against this antigen. The S. mansoni adult microsomal antigen, MAMA, therefore, appears to be a highly potent and specific reagent for the serodiagnosis of S. mansoni infections.
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PMID:Schistosoma mansoni adult microsomal antigens, a serologic reagent. II. Specificity of antibody responses to the S. mansoni microsomal antigen (MAMA). 618 78

Histological features of chronic active and chronic persistent hepatitis were observed in mice, rabbits and non-human primates infected with either Schistosoma mansoni and Schistosoma japonicum. In early infection hepatitis appeared as a reactive change due to liver damage caused by the deposition of schistosome eggs, but portal and septal cellular infiltrations tended to remain long after parasite aggression had diminished or disappeared, either spontaneously with time or after chemotherapy. In rabbits, and to a lesser degree in monkeys, a picture of chronic active hepatitis was present, with evolution to cirrhosis in the former. The experimental findings indicate that schistosomiasis has the potential to induce chronic hepatitis and suggest that the current assumption that chronic hepatitis seen in humans with schistosomiasis is always due to concomitant viral infection should be reviewed.
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PMID:Chronic hepatitis in experimental schistosomiasis. 770 27

A patient with HbsAG positive chronic persistent hepatitis is demonstrated in whom a liver biopsy specimen showed a nonsuspected asymptomatic infection with Schistosoma mansoni. Further investigations showed no signs of liver fibrosis or portal hypertension. Rectal biopsy specimens also showed Schistosoma mansoni. The combination of Schistosomiasis and hepatitis is well known in the literature, the effect of recombinant interferon therapy in these cases, however, is not known. Attention is drawn to this combination.
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PMID:Liverbiopsy because of Hbs Ag positive hepatitis revealing a non-suspected hepatic schistosomiasis. Implication for future therapy with recombinant alpha interferon? 913 55

To investigate the possible involvement of autoimmune mechanisms in the development of hepatosplenic schistosomiasis (HSS), 234 patients with chronic Schistosoma mansoni infections were screened for a wide range of non-organ-specific autoantibodies as well as for antibodies reacting with the GOR peptide and with a liver-specific autoantigen, the hepatic asialoglycoprotein receptor (ASGP-R). Thirty-five (15.0%) were seropositive for antinuclear, smooth muscle or gastric parietal cell antibodies at low titres (< or = 1:80), and 15/176 (8.5%) had anti-GOR, all of whom had concomitant hepatitis C viral (HCV) infections. Anti-ASGP-R was found in 64 (27.4%) of the 234 patients at titres similar to those found in 18 untreated auto-immune hepatitis patients studied concurrently. Anti-ASGP-R seropositivity occurred significantly (P < 0.005) more frequently in patients with HSS (62/190, 32.6%) than in those with hepatointestinal schistosomiasis (2/44, 4.5%), but did not correlate with severity of liver disease or with the presence of the non-organ-specific autoantibodies. Anti-ASGP-R was found significantly (P < < 0.0005) less frequently in HSS patients who had had a splenectomy for portal hypertension (5/86, 5.8%) than in those who had not had a splenectomy (57/104, 54.8%). The findings suggest that liver-specific autoreactivity may play a role in the development of HSS.
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PMID:Specific liver autoreactivity in schistosomiasis mansoni. 923 Dec 5


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