Impaired synthesis of taurine in a patient with tyrosinemia type I during the oral L-methionine loading test.
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Biomedical subjects
Publications and source records attributed to J Pintera.
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Blood donors' screening has been performed during the last twenty years and it has reached a considerable post-transfusion hepatitis prevention due to disqualifying hyperbilirubinemic donors. Since 1981, AST screening has been combined with the attention paid to bilirubin--conditioned plasma colour. In the following years a steep exponential increase of hyperbilirubinemic donors incidence has been observed from 1.3% in 1983 and 1984 to 4.0% in 1988. The possibilities of a relationship to hepatitis epidemic of the years 1979-80 or to other factors are discussed. The hyperbilirubinemias are suggested to be of a posthepatitic character, produced in the unrecognised hepatitis cases who had been subclinical at the time of the epidemic. More information is expected from the development of the trend in the next years.
Methods of post-transfusion hepatitis (PTH) prevention including voluntary donorship, search for the carriers of specific HBV markers, for donors having impaired liver function tests, i. e. AST screening, ALT quantitation, and AST + bilirubin screening are discussed on the basis of twenty years' development of their effect on regional PTH incidence. A combination of AST + bilirubin screening has been found to prevent 66% of PTH incidence in the year 1984 and on average 49% during the five years through 1988, disqualifying only 1-3% of donors, and avoiding wastage of blood through its performance before blood unit collection. A comparison with the data of Hollinger et al. about ALT quantitation suggests that the sources of PTH removed by either of the two preventive methods are different and that an improved effect could be therefore obtained by their combination.
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The lacking impact of various precautions on the incidence of post-transfusion hepatitis (PTH) in the last 15 years is presented. In 1984, however, PTH dropped from 0.12 to 0.04%. This PTH drop did not coincide with the disqualification of HBsAg carriers, nor with that of high ALT, nor with the introduction of complete voluntary donorship in 1982, but with the systematic exclusion of hyperbilirubinemic donors. Circulating immune complexes (CIC) were found in 28.9% of PTH compromised donors, and CIC are therefore supposed to be a marker of PTH risk even if HBsAg was not demonstrable. Re-examining donors compromised in 120 PTH found 12.4% HBsAg carriers who had not been detected by CIEP prior to the transfusions. Accumulation of more than one HBsAg positive transfusion in 56.5% of the PTH patients suggests a cumulative effect. The inability of specific tests to identify sources of infection in 50% of PTH suggests that doubts must be raised as to their post-transfusional origin. This thesis is also supported by the relative increase of this group after the considerable drop of PTH. The importance of viral sources non-B and B undetectable by sensitive specific methods must be emphasized. The latter is in accordance with the observed PTH drop due to a non-specific marker effect. The bilirubin level screening in each donor before stored blood collection is recommended by means of the described extended AST screening test and, besides HBsAg screening, this is supposed to be the most effective precaution for preventing PTH.
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The examination by means of counterimmunoelectrophoresis for protein incompatibility of the serum of 62 patients who developed an allergic or pyretic post-transfusion reaction revealed incompatibility in 23 cases (37.2%). It was due to the presence of antibodies in 8 recipients (34.8%) and in 15 blood donors (65.2%). The incidence was significantly higher than in a control group of transfused patients who did not develop a reaction. In this group protein incompatibility was found in only 14.7%, 80% of which was due to antibodies in the recipient. In 13 (56.5%) of the patients with reactions agglutinating, cytotoxic or complement fixing antibodies against cellular antigens or IgG were found in addition to protein incompatibility. In 10 cases (43.5%) protein incompatibility was the only explanation for the clinical symptoms. When, in the treatment of multiply transfused haemophiliacs who regularly developed adverse reactions, donors for the preparation of cryoprecipitate were selected by means of the described technique, the almost obligatory reactions were prevented.
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Evidence is presented for the new HBbrnoAg-Anti-HGbrno system association with the HBsAg. The association is displayed particularly in a prevalence of Ausria detectable HBsAg carriers among the anti-HBbrno carriers, suggesting the anti-HBbrno to be a marker of contact with hepatitis B or, possibly, an indicator of co-existing HBsAg antigenaemia, not detectable by radioimmunoassay. Identity of HBbrnoAg with HBsAg/a, d, y, w, is ruled out, the identity with the other HBV associated antigenic specificities remaining questionable.
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A quantitative method for the determination of blood group specific substances A and B on red blood cells was developed, using them to absorb isoprecipitating antisera anti-A and anti-B, followed by estimation of the residual antibody by means of a counterimmunoelectrophoretic technique with standard solutions of A and B substances prepared from saliva. The method was tested on a population of A2B donors. The mean amount of A substance in A2B RBC was 131 X 10(-12) +/- 217 X 10(-12) u/cell in the population of 95 donors. The A substance thus determined agreed significantly with values obtained by classical haemagglutinating titration. The mean amount of B substance in A2B RBC was 222 X 10(-12) +/- 178 X 10(-12) m/cell. The amounts of both the A and B substances were not correlated on the same RBC. Several peaks of the distribution curve of both substances confirmed the non-homogeneity of the populations, there being a wide standard deviation presumably due to differences in the antigen content of different subgroups.