Hepatitis B‐associated polyarteritis nodosa in alaskan eskimos: Clinical and epidemiologic features and long‐term follow‐up

Brian J. McMahon, William L. Heyward, David W. Templin, David Clement, Anne P. Lanier – 1 January 1989 – We analyzed the demographic, clinical, laboratory and histologic features of 13 patients who were diagnosed as having polyarteritis nodosa associated with hepatitis B virus infection over a 12‐year period, 1974 to 1985. All 13 patients were Yupik Eskimos and resided in southwest Alaska, an area hyperendemic for hepatitis B virus infection. The annual incidence of hepatitis B virus‐associated polyarteritis nodosa for this population is 7.7 cases per 100,000 population.

Dynamics of hepatic connective tissue matrix constituents during murine schistosoma mansoni infection

Safaa El Meneza, G. Richard Olds, Thomas F. Kresina, Adel A. F. Mahmoud – 1 January 1989 – Hepatic fibrosis is the major clinical sequela of infection with the helminth Schistosoma mansoni. However, little is known regarding its dynamics and regulation in schistosomiasis. The present study presents the dynamics of deposition and resorption of two major extracellular matrix components of fibrosis, glycosaminoglycans and collagens, during the course of experimental S. mansoni infection.

Acinar heterogeneity of fatty acid binding protein expression in the livers of male, female and clofibrate‐treated rats

Nathan M. Bass, Mary E. Barker, Joan A. Manning, Albert L. Jones, Robert K. Ockner – 1 January 1989 – Liver fatty acid binding protein may play a role in the intracellular transport and compartmentation of long‐chain fatty acid metabolism. The distribution of liver fatty acid binding protein in the hepatic acinus was determined by means of immunocytochemistry as well as by measurement of liver fatty acid binding protein in cellular protein selectively released from zone 1 and zone 3 cells by means of anterograde and retrograde liver perfusion with digitonin.

Regulation of the hepatic transferrin receptor in hereditary hemochromatosis

Martin Lombard, Adrian Bomford, Miriam Hynes, Nikolai V. Naoumov, Stephanie Roberts, John Crowe, Roger Williams – 1 January 1989 – The liver is the main site of iron accumulation and pathologic sequelae in hereditary hemochromatosis. Whether this is a result solely of inappropriately increased absorption of iron by the gastrointestinal tract or a more generalized regulatory failure of iron balance is unknown.

Alterations in the functional expression of receptors on cirrhotic rat hepatocytes

Carolyn N. d'Arville, Mysan Le, Thomas M. Kloppel, Francis R. Simon – 1 January 1989 – Reduced hepatic uptake and clearance of macromolecules in liver cirrhosis is due to two major factors: increased diffusional barriers, resulting primarily from the deposition of excessive connective tissue in the space of Disse, and hepatocellular dysfunction, manifested by receptor and/or postreceptor defects.

Treatment of post‐shunt portal‐systemic encephalopathy by embolization of the shunt

J. Michael Henderson – 1 January 1989 – Operative ligation of portosystemic shunts is effective in controlling chronic portosystemic encephalopathy (CPSE) but is associated with significant mortality. Review of the records of five paients with CPSE treated with radiologic occlusion procedures showed that these are suitable alternatives to surgery. Three patients had alcoholic cirrhosis, one had hepatic fibrosis from schistosomiasis, and one had post‐necrotic cirrhosis. All had CPSE with progressive, severe cerebral impairment refractory to clinical treatment.

HBsAg carrier infants with serum anti‐HBc negativity

Shou‐Dong Lee, Kwang‐Juei Lo, Yang‐Te Tsai, Jaw‐Ching Wu, Tzee‐Chung Wu – 1 January 1989 – A total of 128 HBsAg carrier infants born to HBeAg‐positive HBsAg carrier mothers were tested for serum HBsAg, HBeAg, hepatitis B virus DNA and anti‐HBc. Ninety‐three of them had received hepatitis B vaccination. Anti‐HBc had been found to be negative in sera of 12 infants who were HBsAg, HBeAg and hepatitis B virus DNA positive during the follow‐up period of 3 to 5 years.

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