An epidemic outbreak of non-A, non-B hepatitis occurred in 1977/78 involving 30 donors at a plasmapheresis center. A chimpanzee inoculated with serum of one donor developed non-A, non-B hepatitis with characteristic tubular alterations in the endoplasmatic reticulum. Infections were detected over a period of several months, with two well defined peaks in December 1977 and between the end of January and the beginning of February 1978. Epidemiological data suggested a spread within the center. The most probable mode of transmission was contamination with serum from plastic bags used for reinfusing erythrocytes. The estimated mean incubation time was 41 days (range 27 to 59 days).

Adult↗

PubMedDate not supplied

Epidemic outbreak of non-A, non-B hepatitis in a plasmapheresis center. II: Clinical observations and a four-year follow-up of patients.

An epidemic outbreak of non-A, non-B hepatitis occurred in 1977/78 involving 30 donors at a plasmapheresis center. Of 27 hospitalized patients with peak ALT values between 334 and 1736 (mean 831) IU/l, only 16 had subjective symptoms like fatigue and lack of appetite, 11 had nausea, 11 were jaundiced and one developed transient arthritis. Patients with jaundice became chronically ill significantly less frequently than those without jaundice. Nineteen of 26 patients followed up had elevated ALT values after 12 months (73%) and 11 after 46 months (42%). Needle liver biopsies performed in 18 of the 19 patients with elevated ALT after 12 months revealed chronic persistent hepatitis in 14 and chronic active hepatitis in three. Follow-up biopsies always showed improvement (nine patients) or complete recovery (eight patients).

Adult↗

PubMedDate not supplied

Effect of body weight changes on plasma lipids in patients with primary hyperlipoproteinemia.

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Adult↗

PubMedDate not supplied

Association of DNA polymorphism at the apolipoprotein B gene locus with coronary heart disease and serum very low density lipoprotein levels.

The role of genetic variation at the 3' end of the apolipoprotein B gene locus in the development of coronary heart disease and the regulation of the serum levels of various lipoproteins was studied by using two common restriction fragment length polymorphisms detected with the enzymes Xba I and EcoR I. A group of 106 male patients with coronary heart disease and 118 matched controls of Austrian origin were investigated. The frequency of the R2 allele of the EcoR I polymorphism at cDNA position 12,669 defined by the absence of the polymorphic EcoR I cutting site was significantly higher among patients than among controls. The controls with the R2 allele had significantly higher levels of total triglycerides, very low density lipoprotein (VLDL) triglycerides, and VLDL cholesterol than did the controls without this allele. Among the patients, the R2 allele was associated with higher serum VLDL apolipoprotein B levels. The chemical composition of VLDL in individuals with different genotypes for the EcoR I polymorphism did not differ significantly. For the Xba I polymorphism at cDNA position 7673, no correlation with coronary risk could be demonstrated. Patients and controls homozygous for the X2 allele characterized by the presence of the polymorphic Xba I cutting site showed a higher total and low density lipoprotein cholesterol level than did subjects with the genotype X1X1 or X1X2. This difference, however, was not statistically significant. These findings indicate that the R2 allele of the EcoR I polymorphism is associated with the occurrence of coronary heart disease and that variation at the 3' end of the apo B gene is involved in the regulation of VLDL metabolism.

Alleles↗

PubMedDate not supplied

Apolipoprotein B gene mutations in Austrian subjects with heart disease and their kindred.

In a group of 110 subjects with severe coronary artery disease, two were heterozygous for the apolipoprotein (apo) B arginine3,500----glutamine mutation that characterizes familial defective apo B-100. Both affected subjects were moderately hypercholesterolemic, and their low density lipoproteins (LDLs) were deficient in binding to the LDL receptor. Pedigree analysis of the two probands' families established a correlation between the apo B mutation, defective LDL, and a particular apo B haplotype that was characterized by 10 apo B gene markers. In addition to having one allele carrying the arginine3,500----glutamine mutation, one family member may harbor a second mutant apo B allele that causes its gene product to be present in plasma at a lower than normal level, despite the fact that the affinity of the protein for the LDL receptor appears to be normal. The metabolic basis for the underrepresentation of this second allotype remains to be elucidated.

Antibodies, Monoclonal↗