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

Swine have been used in biomedical research for many years, but have generally been limited to those locations with personnel familiar with this species and with specially designed facilities and equipment. There is currently a growing trend in the United States for more swine, both miniature and domestic to be used as research models. Commercial availability, education through workshops and symposia, and specific research applicability in the areas such as: organ transplantation, cardiovascular surgery, nutrition, diabetes, dermatology, and renal physiology have all contributed to the increased usage of swine. Additionally, increasing costs and public concern about the use of random source dogs and cats have also resulted in a refocus on swine as a laboratory animal model. The woodchuck (Marmota monax) has recently gained a role as a laboratory animal model when it was discovered that woodchuck hepatitis virus (WHV) is closely related to hepatitis B virus in humans (HBV). Chronic infections in woodchucks with WHV have shown protein particles in their blood which are similar to the Australian antigen found on the surface of HBV. There is also immunologic response similarities by the respective host to these viruses. These findings have resulted in a number of laboratories using the woodchuck in infectious disease comparative research studies. A euthymic hairless guinea pig has been described in Canada and recently been produced on a limited basis commercially in the United States. For dermatologic studies requiring an immunocompetent animal model the hairless guinea pig may prove useful. time to have the ability to add
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PMID:Emerging models in the U.S.A.: swine, woodchucks, and the hairless guinea pig. 360 91

Nonhuman primates are excellent animal models for human diseases because of their close relationship to humans. Indeed, comparisons of the chromosomes and DNA homologies between primates and humans testify to the commonality of the genetic material between these phylogenetically related species. Not surprisingly, this close relationship at the genotypic level extends to the phenotypic level. Thus, the patho-physiological responses of humans and nonhuman primates to internal and external insults are remarkably similar. Two types of human diseases for which nonhuman primates are paramount animal models are discussed. One type includes diseases with defined, single agent etiologies and to which all members of the species are genetically susceptible. Examples of these are leprosy, AIDS, hepatitis and Parkinson's disease. A second type represents diseases that have a substantial genetic component, but are multifactorial and are greatly influenced by the environment. Examples of these are diabetes, lymphoma, atherosclerosis, alcoholic cirrhosis and anxiety disorders. Nonhuman primates are also ideally suited to the role of animal models in the new area of human gene therapy. In the future, biomedical research will focus increasingly on genetic manipulations such as the transfer of genes from one individual to another to correct genetic diseases, particularly those diseases caused by single recessive gene defects. Before gene transfers are attempted in humans, they should be done in nonhuman primates. In a real sense, nonhuman primates, as animal models, represent the "step to man."
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PMID:Genetic significance of some common primate models in biomedical research. 360 96

Sixty-five patients with histologically proven chronic active hepatitis of unknown cause but associated with the antiliver/kidney microsome antibody type 1, confirmed by immunofluorescence and immunoprecipitation, were selected as forming a special entity. This disease was found to be rare with a prevalence of 5/1,000,000. The female to male ratio was 8:1. The condition occurred at all ages but was most common between the ages of 2 and 14 years. In 22 of the 65 cases, the hepatitis was associated with an autoimmune disease, most commonly insulin-dependent diabetes, autoimmune thyroid disease and vitiligo. The same autoimmune diseases were present in first-degree relatives from seven families. In 36 cases, the onset of disease resembled acute viral hepatitis. Serum biochemical tests showed marked elevation in aminotransaminases and hypergammaglobulinemia. Paradoxically, serum and salivary IgA levels were often normal or low. Histologic findings were multifocal hepatic necrosis with bridging in the acute stage, and aggressive hepatitis with mononuclear cell infiltration or macronodular cirrhosis in the late stages. Serologically, apart from the presence of antiliver/kidney microsome antibody type 1, the disease was characterized by the absence of antiactin, antimitochondria and antinucleus antibodies; however, organ-specific autoantibodies were often present. The clinical course was usually severe: six patients in the acute stage presented with fulminant hepatitis, and all, except two, other patients progressed to cirrhosis. Prolonged treatment with corticosteroids and immunosuppressants was usually effective in rendering the cirrhosis inactive. The cumulative survival rate was 51% at 14 years. We propose to call this entity "anti-LKM1 chronic active hepatitis" or "autoimmune hepatitis type II" to differentiate it from classical "lupoid hepatitis" or autoimmune hepatitis type I.
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PMID:Chronic active hepatitis associated with antiliver/kidney microsome antibody type 1: a second type of "autoimmune" hepatitis. 367 93

A 50-year-old man suffering from cholestatic hepatitis and diabetes mellitus with hyperlipoproteinaemia had small, painful, slightly elevated, reddish, firm indurated plaques on his soles. Histologically, the lesions were composed of a centrally located cutaneous nerve surrounded by concentric layers of xanthoma cells. Electron microscopy showed the cutaneous nerves to be unmyelinated, their axons were vacuolated and contained dense bodies. The xanthoma cells had the same ultrastructural features as those observed in usual xanthomatous lesions. We suggest that this entity be named perineural xanthoma.
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PMID:Perineural xanthoma. 380 10

In 1814, George Maton, first recognized that a mild illness characterized by rash, adenopathy, and little or no fever was a discrete entity. Henry Veale, in 1866, named the disease rubella. The illness attracted little attention until 1942, when Norman Gregg noticed that first-trimester maternal rubella caused serious birth defects. The full spectrum and impact of rubella embryopathy remained unclarified until rubella virus was isolated in tissue culture in 1962 by two independent groups: Parkman, Buescher, and Artenstein; and Neva and Weller. Using the new tools of the virus laboratory, many investigators concentrated on the consequences of a severe rubella epidemic in 1964, which affected approximately 1% of pregnancies. Newly recognized transient manifestations of congenital rubella infection (CRI) include neonatal thrombocytopenic purpura, hepatitis, bone lesions, and meningoencephalitis and late-emerging sequelae such as diabetes mellitus and progressive rubella panencephalitis added to the cataract, heart disease, mental retardation, and deafness previously defined as due to CRI. Sharp contrasts were documented between the patterns of virus excretion and immune response of postnatal vs. congenital rubella. Licensure and widespread distribution of attenuated rubella virus vaccines in 1969 have prevented epidemic rubella. Pockets of illness remain, even in the United States. Continued effort will be required to eliminate the rubella problem.
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PMID:The history and medical consequences of rubella. 389 Jan 5

To determine the outcome of chronic hepatitis in ESRD we studied all 358 renal transplant recipients and 295 hemodialysis patients treated for greater than 1 year since 1970. The incidence of chronic hepatitis (elevated SGOT for greater than 1 year) was 15% (N = 54) in transplanted and 3.4% (N = 10) in dialysis patients. Forty-eight percent (26) of transplanted and 50% (5) of dialysis patients were HBsAg positive. In the transplanted group, the clinical outcome of chronic hepatitis was significantly better in HBsAg-negative compared to HBsAg-positive patients; 11% died, none from liver disease, and 32% remitted after a mean follow-up from start of liver disease of 77.3 +/- 8.2 months, whereas in the HBsAg-positive group 54% (14) died, nine from liver disease, and one remitted after a follow-up of 90.2 +/- 8.9 months. Adverse prognostic factors (age, duration of diabetes, and heart disease) present before ESRD treatment began were similar in both groups, as was duration of follow-up. Only 14% (2/14) of HBsAg-negative patients progressed to chronic active hepatitis on liver biopsy compared to 71% (15/21) of HBsAg-positive patients. Histological stability in those with serial biopsies occurred in 66% (4/6) of HBsAg-negative patients, but in only 18% (13/16) of HBsAg-positive patients with a similar duration of follow-up. No dialysis patients died from liver disease. We conclude that chronic hepatitis occurs more frequently in transplanted than dialyzed patients, and that HBsAg-negative chronic hepatitis has a more benign, clinical, and histological outcome than chronic HBsAg-positive hepatitis in renal transplant recipients.
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PMID:Chronic hepatitis in end-stage renal disease: comparison of HBsAg-negative and HBsAg-positive patients. 393 66

The accidental finding of raised levels of serum aminotransferase levels may lead to extensive investigations of the liver in apparently healthy people. To identify diagnostic groups and their need for investigations, we have evaluated the results of all investigative procedures carried out in 149 asymptomatic patients with persistently raised serum levels of aminotransferases. Fatty liver was found in 64%. These patients often had a high body weight. A high alcohol intake and diabetes mellitus were also noted. Chronic active or persistent hepatitis was found in 20% of the patients. Six per cent had cirrhosis, 4% had alpha 1-antitrypsin deficiency, and 3.5% had hemochromatosis. Apart from ferritin, alpha 1-antitrypsin, and markers for hepatitis B, blood tests were of little value for distinguishing among different diagnostic groups. This was the case also for the imaging procedures, and neither liver scintigraphy nor ultrasonography was a reliable source of diagnostic information. The results of our study indicate that diagnosis in this group of patients cannot be made without liver biopsy.
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PMID:Liver investigation in 149 asymptomatic patients with moderately elevated activities of serum aminotransferases. 395 45

We report on clinical, nutritional, and hepatic histological findings in 50 non-selected obese subjects (mean overweight +74%; range +21-138%). The pathogenesis of the liver damage was assessed with the help of multidimensional analysis of a number of clinical variables. According to the severity of the hepatic lesions, the patients have been ranged in five groups: O (normal liver) 10%; I (fatty liver) 48%; II (fatty hepatitis) 26%; III (fatty fibrosis) 8%; IV (fatty cirrhosis) 8%. The more severe changes (groups III and IV) were constantly associated with excessive alcohol intake. The multidimensional analysis was unable to find a relationship between obesity and the development of fibrosis and cirrhosis whereas it showed that: (a) there was a highly significant correlation between the daily ethanol intake and the degree of overweight, (b) severe fatty metamorphosis was significantly associated with the degree of overweight, the existence of diabetes mellitus, and the amount of alcohol and fat intake, (c) nutritional factors, in particular deficient protein intake, have only an accessory effect in the development of mild inflammation and fibrosis, (d) the consumption of potentially hepatotoxic drugs, very high in the obese (about five drugs per day) could have a role in the development of cirrhosis. In conclusion in our study, there was no evidence that obesity per se could result in severe liver damage.
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PMID:Liver in obesity. 396 30

A patient who abstained from alcohol consumption but who had asymptomatic chronic progressive hepatomegaly, mild disturbance of liver function tests and hepatitis resembling alcoholic hepatitis (nonalcoholic steatohepatitis) developed glucose intolerance several years after the hepatitis was diagnosed. The patient had a family history of both diabetes and chronic liver disease. A lesion resembling alcoholic hepatitis in a patient who denies alcohol consumption, may be diabetic or pre-diabetic in aetiology and such a patient should be followed up with glucose tolerance tests.
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PMID:Diabetic hepatitis preceding the onset of glucose intolerance. 398 46

Serum markers for hepatitis B virus (HBV) were studied in 395 healthy control subjects and in 100 diabetic patients. Of the patients, 28 had type I diabetes, 31 had type II diabetes requiring insulin, and 41 had type II diabetes treated with oral agents or diet alone. None gave history of previous icterus or other signs of hepatitis, had received blood transfusions, or had been on hemodialysis. There was a significant difference in the prevalence of HBV markers (mainly HB surface antibody) between the diabetic group and the controls (51% versus 25%, P less than 0.001). The control subjects included hospital personnel and, hence, their risk of HBV exposure was already relatively high. The increased occurrence of HBV markers did not seem to be related to diabetes duration, patient age, intake of insulin injections, or presence of microvascular complications. This study reveals a high degree of exposure to HBV in a moderately controlled diabetic group and possibly a high degree of proneness to subclinical hepatitis B.
Diabetes Care
PMID:Hepatitis B virus markers in diabetes mellitus. 400 59


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