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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve marmosets (Saguinus mystax) were inoculated intravenously (iv) with hepatitis A virus (HAV). One died early (day 12); seven were sacrificed at the time of elevation in level of alanine aminotransferase (serum glutamic-pyruvic transaminase), and four without elevation were not sacrificed but seroconverted. In the seven marmosets sacrificed during the acute stage of illness, hepatitis A antigen (HA Ag) was detected in the liver by immunofluorescence in all cases, by immune electron microscopy in four, and by enzyme-linked immunosorbent assay (ELISA) in three. The HA Ag appeared by immunofluorescence as very fine granules in the cytoplasm of hepatocytes and Kupffer cells. The HA Ag could not be detected by immunofluorescence in biopsy specimens taken from the duodenum, jejunum, ileum, or transverse colon in any of eight marmosets in which necropsy was performed during the acute or preacute stage of illness. These findings suggest that the gut is not involved during the acute phase of HAV infection following iv inoculation into marmosets. The ELISA results showed that only three of 12 marmoset livers obtained during the acute phase of HAV infection could be used as an antigen source in serologic testing for antibody to HA Ag. Thus, marmoset livers were no better as a source of HA Ag than acute-phase stools from patients with type A hepatitis.
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PMID:Localization of hepatitis A antigen in marmoset organs during acute infection with hepatitis A virus. 21 88

A new strain of mouse hepatitis virus (MHV) was isolated from pooled gut suspensions from an epizootic of lethal enteritis in newborn mice. Negative-contrast electron microscopy showed an abundance of coronavirus particles in the intestinal contents and intestinal epithelium of moribund mice. We found no other virus in the epizootic. Dams seroconverted to MHV polyvalent antigen and to the agent isolated, but did not develop antibodies to other known mouse pathogens. Virus propagated in NCTC-1469 tissue culture produced enteric disease in suckling mice but not fatal diarrhea; the dams of these mice also developed antibodies to MHV and to the isolates. By complement fixation, single radial hemolysis, and quantal neutralization tests, we found the isolates antigenically most closely related to MHV-S, unilaterally related to MHV-JHM, and more distantly related to MHV-1, MHV-3, MHV-A59, and human coronavirus OC-43. We also studied cross-reactions among the murine and human coronaviruses in detail. Tissues of infected newborn mice were examined by light microscopy, thin-section electron microscopy, and frozen-section indirect immunofluorescence, revealing that viral antigen, virus particles, and pathological changes were limited to the intestinal tract. We have designated our isolates as MHV-S/CDC.
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PMID:New strain of mouse hepatitis virus as the cause of lethal enteritis in infant mice. 22 87

An important adaptation of the gastrointestinal tract to the extrauterine environment is its development of a mucosal barrier against the penetration of harmful substances (bacteria, toxins and antigens) present within the intestinal lumen. At birth, the newborn infant must be prepared to deal with bacterial colonization of the gut, with formation of toxic byproducts of bacteria and viruses (enterotoxins and endotoxins) and with the ingestion of antigens (milk proteins). These potentially noxious substances if allowed to penetrate the mucosal epithelial barrier under pathological conditions can cause inflammatory and allergic reactions which may result in gastrointestinal and systemic disease states. To combat the potential danger of invasion across the mucosal barrier the infant must develop an elaborate system of defence mechanisms within the lumen and on the luminal mucosal surface which act to control and maintain the epithelium as an impermeable barrier to uptake of macromolecular antigens. These defences include a unique immunological system adapted to function in the complicated milieu of the intestine as well as other non-immunological processes such as a gastric barrier, intestinal surface secretions, peristaltic movement and natural antibacterial substances (lysozyme, bile salts) which also help to provide maximum protection for the intestinal surface. Unfortunately, during the immediate postpartum period, particularly for premature and small-for-dates infants, this elaborate local defence system is incompletely developed. As a result of the delay in the maturation of the mucosal barrier newborn infants are particularly vulnerable to pathological penetration by harmful intraluminal substances. The consequences of altered defence are susceptibility to infection and the potential for hypersensitivity reactions and for formation of immune complexes. With these reactions comes the potential for developing life-threatening diseases such as necrotizing enterocolitis, sepsis and hepatitis. Fortunately, 'nature' has provided a means for passively protecting the 'vulnerable' newborn against dangers of a deficient intestinal defence system, namely human milk. It is now increasingly apparent that human milk contains not only antibodies and viable leucocytes but many other substances which can interfere with bacterial colonization and prevent antigen penetration.
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PMID:Gastrointestinal host defence: importance of gut closure in control of macromolecular transport. 26 21

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

Metabolism of calcium and magnesium may be disturbed in hepatobiliary disease because of deficient or absent bile flow into the gut, since bile is important for the intestinal absorption of these elements. In the present paper the tubular reabsorption of phosphate (TRP), calcium (TRCa), and magnesium (TRMg) were determined in an attempt to evaluate the parathyroid function of infants and children with hepatobiliary disease. In unrepaired biliary atresia TRP was conspicuously reduced (mean 49.8%, SD 15.1). In successfully repaired biliary atresia the value was increased near the normal range (mean 80.7%, SD 8.1). In neonatal hepatitis the value was variable in individual cases, but significantly lower than the normal (mean 47.6%, SD 19.9). TRCa was reduced in one third of the patients with unrepaired biliary atresia and in one fifth of the cases of neonatal hepatitis. The value was within the normal range in repaired biliary atresia. TRMg was decreased in both unrepaired and repaired biliary atresia and in neonatal hepatitis. The effect of intravenous calcium infusion on TRP, TRCa and TRMg was evaluated in 3 patients with unrepaired biliary atresia. TRP was conspicuously enhanced after infusion. TRCa was decreased in 3 to a variable extent. TRMg was moderately increased in 2 and greatly decreased in 1. These results indicate that infants with hepatobiliary disease are in a state of secondary hyperparathyroidism because of deficient or absent bile flow into the intestines.
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PMID:Hyperparathyroidism in hepatobiliary disease in infancy. 81 5

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.
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PMID:[Therapy of hepatic insufficiency]. 91 52

In the course of a typhoid epidemic during the autumn of 1974 in the Heidelberg region 74 persons were treated in hospital. Chloramphenicol was give to 45, ampicillin to 19. The former, in daily doses of 2.0 g, gave worse results if given for only two instead of three weeks. In comparison, ampicillin was less effective. A second course of treatment became necessary in 13 patients, with trimethoprim-sulphamethoxazole (Bactrim) being succesful in all, although the follow-up period is still too short for definitive results. Three complications occurred: one case of massive bleeding from the gut requiring operation and followed some weeks later by a HBS-antigen-negative hepatitis; one case of typhoma (several weeks after the end of antibiotic treatment), requiring operative removal; a case of febrile abortion in the second month of pregnancy.
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PMID:[Clinical course of typhoid in the Heidelberg region (author's transl)]. 108 Jul 5

A premature neonate with severe Coxsackie B1 hepatitis acquired in utero developed disseminated intravascular coagulation a few days after birth. The neonate did not respond to conventional treatment. Eradication of aerobic gram-negative bacilli (Enterobacteriaceae) from the gut with oral nonabsorbable polymyxin E and tobramycin (selective decontamination of the digestive tract) was followed by clinical improvement; disseminated intravascular coagulation was controlled. After an unstable convalescence, the neonate recovered and was discharged in good general condition. A correlation between oral feeding, gut carriage of Enterobacteriaceae, fecal endotoxin pool, and platelet counts was observed. The eradication of gut carriage of aerobic gram-negative bacilli was associated with a significant decrease of the intestinal endotoxin pool and paralleled the recovery from thrombocytopenia. Selective decontamination is discussed as a method of possible value for controlling systemic endotoxin-induced symptoms in the critically ill with intestinal endotoxemia.
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PMID:Selective decontamination of the digestive tract contributes to the control of disseminated intravascular coagulation in severe liver impairment. 132 53

The epidemiology of infections associated with orthotopic liver transplantation is summarized herein, and approaches to prophylaxis are outlined. Infection is a major complication following orthotopic liver transplantation, and more than half of transplant recipients develop at least one infection. The risk of infection is highest in the first month after transplantation, and the most common pathogens are bacteria and cytomegalovirus (CMV). Bacterial infections usually occur in the first month, arise in the abdomen, and are caused by aerobes. The peak incidence of CMV infection is late in the first month and early in the second month after transplantation. CMV syndromes include fever and neutropenia, hepatitis, pneumonitis, gut ulceration, and disseminated infection. Other significant problems are Candida intraabdominal infection, Herpes simplex mucocutaneous infection or hepatitis, adenovirus hepatitis, and Pneumocystis carinii pneumonia. Prophylaxis of infection in liver transplant recipients has not been well-studied. Several different regimens of parenteral, oral absorbable, and/or oral non-absorbable antibiotics active against bacteria and yeast have been used at various centers, but no randomized controlled trials have been conducted. Selective bowel decontamination appears to be a promising approach to the prevention of bacterial and Candida infections, while oral acyclovir may be a relatively convenient and effective agent for CMV prophylaxis.
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PMID:Infections following orthotopic liver transplantation. 165 Feb 45

Forty to sixty percent of conventionally (CON) raised BALB/cAnPt (BALB/c) mice develop plasmacytomas (PCT) when injected with three 0.5 ml i.p. injections of pristane. When CON-BALB/c mice were converted to specific pathogen free (SPF) status by foster nursing caesarean delivered term mice on C3H/HeN SPF mothers and maintained under strict SPF conditions, less than 5% of the mice developed pristane-induced PCT. FACS analysis of the cellular composition of oil granulomatous tissue revealed a dramatic influx of CD4+ cells in CON mice that was significantly reduced in SPF mice. Moreover, while both CON and SPF mice had similar patterns of gut flora colonization, only CON-BALB/c mice had occasional circulating antibodies to mouse hepatitis virus and Sendai viruses. Maintenance in strict SPF conditions, therefore, results in a prolonged state of relative Ag deprivation and a failure to continuously activate new T and B cell populations. The results suggest that PCT formation depends on exogenous antigenic stimulation and that the presence of minimal gut flora is insufficient to render these mice susceptible to PCT induction.
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PMID:Specific pathogen-free BALB/cAn mice are refractory to plasmacytoma induction by pristane. 168 79


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