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)

A group of athymic nude mice developed an unusual chronic wasting disease within 1-3 months after their arrival into the laboratory. Affected nude mice had severe, acute-to-chronic, active hepatitis with multinucleated giant hepatocytes and fibrosis. Vascular and central nervous system lesions were frequently present, giant cell peritonitis, ascites, and multinucleated giant cells in the intestinal epithelial villi were less frequently observed. Mouse hepatitis virus was isolated from the livers of three mice with lesions. The virus, when inoculated into nude mice, produced lesions similar to those observed in the natural outbreak.
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PMID:Naturally occurring mouse hepatitis virus infection in the nude mouse. 19 36

The outbreak of wasting disease of nude mice occurred in the laboratory colony of a Pharmaceutical Company. The viruses producing cytopathic effect with syncytium formation were isolated from the wasted nude mice by DBT cells, and were identified as mouse coronavirus by direct immunofluorescence. The nude mouse colony was closed and all the nude mice (about 500) were killed by the reason of disease control. At autopsy about 60% of nude mice showed necrotic hepatitis. By the virus isolation to see the source of contamination, viruses were isolated from the feces of apparently healthy mice of ICR, CDF1, DBA/2 and C3H, and from human cancer cell line stocked in liquid nitrogen. In experimental infection, the isolates produced only mild hepatitis in ICR mice treated with cortisone. By cross-neutralization test, the nude isolate reacted closely with the virus from C3H mice but not with the virus from cancer cell line. The isolates from nude and C3H mice produced experimentally wasting disease with necrotic hepatitis in nude mice. These findings suggest that wasting disease in nude mice might be caused by low-virulent mouse coronavirus shed in feces from C3H mice introduced before the outbreak of disease.
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PMID:Natural infection of nude mice with low-virulent mouse coronavirus. 196 24

To characterize type and age distribution of malnutrition and to determine the usefulness of anthropometric indices in children with chronic liver disease (CLD), 56 children (aged 1 mo-10 y) with CLD underwent anthropometric evaluation when they were clinically stable. Mean-height Z score was depressed, whereas mean-weight Z score was closer to normal and mean-weight/height Z score was normal in patients with extrahepatic biliary atresia, idiopathic neonatal hepatitis, and other liver disorders. Patients with arteriohepatic dysplasia showed more severe depression of all three variables. In all patients, triceps skinfold (TSF) thickness Z scores were significantly more depressed than were weight/height Z scores. Depressions of midarm-circumference and midarm-muscle-area Z scores were intermediate. Mean-head-circumference Z score was depressed in children aged less than 24 mo. We conclude that acute (wasting) and chronic (stunting) malnutrition are common in childhood CLD and that weight/height values underestimate the degree of acute malnutrition compared with TSF thickness, most likely because of the inflated patient weight caused by organomegaly.
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PMID:Anthropometric evaluation of children with chronic liver disease. 237 85

Nutritional assessment factors (including dietary history, anthropometric and biochemical measurements, and evaluation of immunocompetence) were retrospectively reviewed in 74 patients undergoing an initial liver transplantation procedure. The patients were subdivided into four categories on the basis of type of liver disease: chronic active hepatitis (N = 24), primary sclerosing cholangitis (N = 22), primary biliary cirrhosis (N = 20), and acute or subacute hepatitis (N = 8). Our nutritional assessment data indicated that malnutrition was present preoperatively in all liver transplantation groups but that each group had distinct characteristics. The group with primary biliary cirrhosis seemed to have the best hepatic synthetic function despite extreme wasting of muscle and fat. On the basis of all criteria, the group with acute hepatitis was the most malnourished of the various disease groups. Aggressive nutritional support, which includes adequate intake of nutrients and supplementation of vitamins and trace minerals, should be encouraged for all potential liver transplant patients.
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PMID:Assessment of nutritional status of patients with end-stage liver disease undergoing liver transplantation. 249 64

Subacute fascioliasis was diagnosed by pathomorphological and parasitological investigations on 13 dead moufflons (Ovis ammon musimon) from a herd of 21 animals (mortality 62%) which had succumbed between January and April 1988. The flock had been kept on meadow in the so-called Leipziger Auenwald. The main findings like severe hepatitis traumatica fasciolosa, fibrinous and fibrous perihepatitis, chronic interstitial hepatitis (pseudocirrhosis), cholangitis fasciolosa (X 13), wasting (X 8), heart dilatation (X 10), lung oedema (X 12), anemia (X 5), ascites (X 3), gut oedema (X 3) and occasionally observed lesions are described in detail and discussed with regard to diagnosis and pathogenicity. Beside severe infection with Fasciola hepatica (juvenile and adult flukes) the parasitological investigation demonstrated, in some cases, various additional but unimportant infections with protostrongylids, gastro-intestinal nematodes, coccidia (X 2) and Moniezia expansa (X 1). The analysis of meteorological data (January 1987 till March 1988) established optimal conditions for F. hepatica development stages and Galba truncatula so that high multiplication and infection rates of the snails and long surviving of metacercariae must be assumed.
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PMID:[Fascioliasis in moufflons]. 278 70

The efficacy and safety of ganciclovir were evaluated for the treatment of 39 life-threatening or sight-threatening cytomegalovirus (CMV) infections in recipients of bone marrow transplants (15 patients), recipients of liver or renal transplants (8 patients), patients with AIDS (11 patients), and one patient each with lymphoma or systemic lupus erythematosus. Twenty-eight (72%) of 39 CMV infections improved during ganciclovir therapy, which was associated with elimination of CMV from cultures. Improvement occurred more frequently in patients with viremia, fever, and wasting (8 of 8), hepatitis (3 of 4), retinitis (5 of 5), or colitis (1 of 1), than in patients with pneumonia (11 of 21). Only two of nine marrow transplant recipients with CMV pneumonia survived, as compared with nine of 12 other immunosuppressed patients with pneumonia. However, all six marrow transplant recipients who were treated for CMV viremia, fever, and wasting without pneumonia survived. Neutropenia was the only adverse reaction associated with ganciclovir therapy and was more frequent in patients with AIDS (6 [55%] of 11) than in transplant recipients (5 [20%] of 25). These results suggest that ganciclovir is of clinical benefit for immunosuppressed patients with serious CMV infections. For bone marrow transplant recipients, ganciclovir may be more effective when used prophylactically or earlier in the course of CMV infection before the development of pneumonia.
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PMID:Ganciclovir therapy for cytomegalovirus infections in recipients of bone marrow transplants and other immunosuppressed patients. 284 92

The presence of maternal antibodies protected suckling C57BL/6 mice from the clinical manifestations of the acute encephalomyelitis caused by mouse hepatitis virus, strain JHM (MHV-JHM), a coronavirus, even though histological evidence of encephalomyelitis was found at early times after inoculation. 100% of infected suckling mice developed a fatal disease in the absence of maternal antibody. By 14 days after inoculation, the brains of all antibody-protected mice examined were nearly normal on histological examination. At 3-8 weeks post-inoculation, approximately 40% of the antibody-protected mice developed a neurological disease characterized by hindlimb paralysis and wasting. Evidence of inflammation and demyelination was apparent in the spinal cord and brainstem. The mice that remained asymptomatic at this time showed few signs of inflammation and none developed clinical disease over the following 9 months. Viral antigen could be detected in most of the mice examined at all times after inoculation, whether symptomatic or not, and was particularly evident in the animals with hindlimb paralysis. MHV-JHM could be consistently cultured from the mice with hindlimb paralysis. These results show that maternal immune factors can completely protect susceptible mice from the acute, fatal, clinical encephalomyelitis caused by MHV-JHM, but cannot prevent the establishment of a latent state and subsequent development of virus-induced, clinically evident, demyelinating disease. This model will be useful for studying the virus and host factors important for the development of MHV-JHM latency and subsequent virus-induced demyelination.
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PMID:Late onset, symptomatic, demyelinating encephalomyelitis in mice infected with MHV-JHM in the presence of maternal antibody. 285 74

"Wasting" or "fading" syndromes are common causes of puppy and kitten mortality. Numerous infectious and toxic, metabolic, or nutritional factors could potentially be responsible for wasting and death in young animals. Evidence has been presented that infectious canine hepatitis virus infection, beta-hemolytic streptococcus infection, and feline infectious peritonitis virus infection are responsible for a significant number of deaths due to wasting syndrome. However, many cases of wasting syndrome cannot be attributed to infectious agents or other specific etiologies. The thymus gland warrants special attention when one is evaluating an animal with a wasting syndrome because it is known that, in some species, neonatal thymectomy results in wasting and death. Unfortunately, most reports describing fading syndromes in puppies and kittens do not mention the gross or histologic appearance of the thymus gland at postmortem examination. When examining the thymus gland, one must keep in mind that the thymus may be hypoplastic owing to a congenital or genetic defect in its structure and function or it may be atrophic secondary to whatever is causing the fading syndrome. If a thorough history, clinical examination, and/or postmortem examination do not reveal a cause for the fading syndrome, then defective thymus function should be considered as a possible causative or contributing factor to the fading syndrome. In these cases, therapy designed to replace or improve the defective thymus function should be considered. At least one form of wasting syndrome in puppies (immunodeficient dwarfism) has been found to respond to short-term therapy with a thymus hormone (thymosin fraction 5) or with bovine growth hormone (which is thymotropic) in limited clinical trials. It is possible that other forms of wasting or fading syndromes would also respond to therapy with thymus hormone or growth hormone. Certain thymus hormones (thymopoietin pentapeptide, thymosin alpha 1, facteur thymique serique, and rabbit thymus acetone powder) and bovine growth hormone are commercially available. Before initiating therapy, one should consider that if the cause of the wasting syndrome is genetic, then successful treatment may perpetuate a genetic defect. More research (both basic and clinical) is needed to determine the role of thymus gland dysfunction in fading syndromes of puppies and kittens and if therapy with one or several of the thymus hormones or with growth hormone could reverse the symptoms of wasting.
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PMID:Possible association of thymus dysfunction with fading syndromes in puppies and kittens. 349 4

We studied the pathogenesis of hypertension in two patients with hepatitis-B surface antigen-positive systemic necrotizing vasculitis. Both presented with hypertension, hypokalemia, and renal potassium wasting. Plasma renin activity and urinary aldosterone levels were markedly elevated. Renal arteriograms showed widespread microaneurysms, and necrotizing vasculitis involving renal arteries was confirmed histologically. Hypertension was refractory to conventional treatment in both patients. In one patient, hypertension was easily controlled with the angiotension-converting enzyme inhibitor captopril. Diffuse renal vasculitis with secondary hyperreninemia and hyperaldosteronism appears to be an important cause of hypertension in patients with systemic necrotizing vasculitis.
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PMID:Hypertension, hyperreninemia, and secondary hyperaldosteronism in systemic necrotizing vasculitis. 610 32

Mild microcytic anemia (without changes in mean corpuscular hemoglobin concentration, MCHC) was discovered 6-14 weeks after a single s.c. administration of 4 mg of particulate glucan to C57BL/10ScSnPh mice serologically positive for murine hepatitis (MHV). The anemia was associated with granulocytosis, decreased body weight and spleen hypertrophy. The overall intensity of erythropoiesis was measured by 59Fe-incorporation into the heme of erythropoietic organs. The localization of erythropoiesis became markedly redistributed--heme production was suppressed in the bone marrow while a several-fold increase was recorded for the spleen. A new steady state was also discovered in ferrokinetics: an iron pool localized away from the blood, erythropoietic organs and the liver was significantly elevated, and hypoferremia was detected. Anemia and wasting of mice were not observed in the same mouse strain free of MHV. A single administration of particulate glucan resulted in late impairment of red blood cell formation in the C57BL/10ScSnPh mouse strain infected with the mouse hepatitis virus. The anemia shares a number of features with those observed for the anemia of chronic diseases.
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PMID:Microcytic anemia and changes in ferrokinetics as late after-effects of glucan administration in murine hepatitis virus-infected C57BL/10ScSnPh mice. 815 May 55


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