[An important source of error in Rh(D) typing].
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Biomedical subjects
Publications and source records attributed to L Kornstad.
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Demonstration of chlamydial antibodies in patients with ankylosing spondylitis (AS) could show an etiological role of Chlamydia trachomatis in this condition. We studied serum specimens from 50 HLA-B27 positive patients with AS (Group I), 34 HLA-B27 positive patients with other rheumatic diseases (Group II), 67 HLA-B27 positive healthy blood donors (Group III) and 37 healthy untyped blood donors. (Group IV). Measured by an immunoperoxidase assay (IPA) chlamydial IgA (titre greater than or equal to 1:20) was more prevalent in the HLA-B27 positive persons than in the healthy controls not selected for HLA-group (Groups I + II + III vs IV : p less than 0.02). Chlamydia trachomatis IgA-IPA containing sera also had specific IgG-IPA antibodies (greater than or equal to 1:80) in 29 (96%) out of 30 sera from HLA-B27 positive individuals and controls. Conversely, 45% of specific IgG-positive (greater than or equal to 1:80) AS sera, 27.7% sera in Group II, 39.4% Group III sera vs. 11.1% of sera in Group IV had concomitant chlamydial IgA (greater than or equal to 1:20). The differences in the prevalence of specific IgA were statistically significant: Group I vs. IV : p less than 0.01; Group III vs. IV :p less than 0.05 and Gr. I + II + III vs. IV: p less than 0.05. Our data suggest an enhanced antibody production against Chlamydia trachomatis among the HLA-B27 positive individuals whether they have AS or are healthy.
The rare blood group antigen previously referred to as the 'Haakestad antigen' is shown to be identical with the Hov antigen (numerical designation: 700.038). Family studies add AB0 and HLA to the systems already known to segregate independently from Hov. Among 2,021 Danish blood donors, 4 Hov+ persons were found. Anti-Hov activity has been demonstrated in several 'multiple-antibody sera'.
The IgG subclass distribution of anti Rh antibodies (anti-D, 'anti-Du', anti-c, anti-E), anti-Kell and anti-Duffy (anti-Fya) antibodies was measured by two haemagglutination techniques on microtitre plates. The first technique involved rabbit subclass specific antisera which were used to agglutinate red cells previously reacted with the patients' antibodies at high concentration. The second, which was more sensitive, had an additional step by introducing sheep anti-rabbit antibodies (sandwich technique). By the sensitive sandwich technique we revealed, for anti-D antibodies: IgG1 8/19, IgG3 1/19, IgG1/IgG3 8/19, IgG1/IgG2/IgG3/IgG 41/19, IgG1/IgG4 1/19; for the Du reactive anti-D antibodies: IgG1 1/8, IgG1/IgG3 1/8, IgG1/IgG3/IgG4 6/8; for the anti-E antibodies: IgG1/IgG2/IgG4 2/3, IgG1/IgG2/IgG3/IgG4 1/3; for the anti-c antibodies: IgG1 2/5, IgG3 1/5, IgG1/IgG3 1/5; for the anti-Kell antibodies: IgG1 9/20, IgG1/IgG3 1/20, IgG1/IgG4 8/20, IgG1/IgG3/IgG4 2/20; and for anti-Duffy antibodies: IgG1 1/8, IgG1/IgG4 7/8. These results are partly at variance with previously published results.
The effect of the post-partum Rh prophylaxis in Norway was studied. From a preprophylaxis incidence of 47.4 new cases of Rh(D) immunization per 10,000 pregnant women the incidence fell to 8.9 per 10,000 in 1982-83, and further to 7.1 per 10,000 in 1986. In the period 1980-83 58 per cent of the new antibodies within the Rh system were anti-D, while 42 per cent had other Rh specificities occurring in Rh(D) positive women. The incidence of new immunizations within the Kell and Duffy systems was also studied. Fifty per cent of the antibodies detected within the three blood group systems occurred in Rh positive gravidae. It is known from other studies that at least 30 per cent of pregnant women who develop blood group antibodies do so after the first assay is performed. Therefore the number of antibodies found in Rh positive women would increase significantly if they too were retested towards the end of pregnancy.
A 'new', rare blood group antigen, Ola (Oldeide), is described. Only one Ol(a+) person was found among the 7,151 blood donors tested. Examination of the family of the proposita revealed 10 additional Ol(a+) persons. The study indicated that Ola is inherited as a Mendelian dominant character and segregates independently of the ABO, MNSs, P, Rh and Kidd blood group systems, of the ABH secretor genes, and of sex. Ol(a+) family members had depressed Rh antigens, while the Ol(a-) members had Rh antigens of normal strength. The depression was particularly pronounced for the C and E antigens, less marked for the D antigen. Individual antisera differed in their ability to demonstrate the presence of the antigens. Depression of the c and e antigens could not be demonstrated conclusively with the antisera available.
An Rh positive woman having the Rh(D) variant designated DVI formed a potent anti-D which caused a severe haemolytic disease in the infant. The infant received three exchange transfusions within the first 21 hours after delivery and, because of a 'late anaemia', three additional blood transfusions during the first 3 months of life. The authors point out the distinction between D variant antigens, where certain epitopes of the D antigen are lacking, and qualitatively normal D antigens with a reduced reactivity, Du. Women with D variant antigens should be subject to the same antenatal serological control as those who are Rh(D) negative, and if they form anti-D the infant should be controlled as in other cases where haemolytic disease of the newborn is suspected.
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In sera from 1643 randomly selected blood donors examined in 1979 thyroglobulin antibodies (TGA) were found in 3.4% and thyroid microsomal antibodies (TMA) in 7.0%. TMA, but not TGA, showed significant sex and age relationships. Eight-two donors with TMA titres greater than or equal to 1600 and/or TGA titres greater than or equal to 128 were available for a follow-up study in 1982. In 69 of these with TMA there was a significantly increased incidence of pathological thyroid function-test values (T4, T3 and TSH) as compared to age- and sexmatched donors without thyroid antibodies. In this group 9 individuals had overt and three latent hypothyroidism, two individuals were found with symptomless autoimmune thyroiditis and one with a non-toxic nodular goitre. Only 2 of these had been diagnosed before 1982, and none recognized before 1979. In addition, the group contained 9 individuals who had been treated because of hyperthyroidism, all except one before 1979. The likelihood of detecting a previously unrecognized hypothyroidism increased with increasing TMA titre. In contrast, the 24 donors with TGA did not show an increased frequency of pathological thyroid function-test-values in 1982.
The frequency of irregular blood group antibodies detected for the first time in pregnant women during the period 1975-80 has been examined. Whereas Rh(D)-negative gravidae in Norway are examined immuno-hematologically three times during pregnancy, Rh(D)-positive women are tested once only, usually early in pregnancy. Nevertheless, about one-third of the new cases of immunization within the Rh system were found in the Rh-positive women. In the latter, anti-E and anti-c were the Rh antibodies most frequently encountered. Among other irregular antibodies which can cause hemolytic disease of the newborn (HDN), those of the Kell and Duffy systems are the ones second in frequency and clinical significance to the Rh antibodies. In the present series about 40% of the new cases of immunization within the Rh, Kell and Duffy systems were found in Rh-positive women. This proportion would undoubtedly have been greater if also the Rh-positive women had been retested for the presence of irregular blood group antibodies towards the end of the gestation. Such a retesting of Rh-positive gravidae is desirable both for a better prediction and early diagnosis of HDN and to facilitate the procurement of compatible blood if the woman should need an emergency blood transfusion.
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An EDTA-containing, low ionic strength medium, pH 5.1, can be used for incubation of blood to obtain coating of red blood cells with C4 or C3. The coating achieved depends on incubation temperature (4 or 37 degrees C) and on whether or not CaCl2 or MgCl2 is added to the medium. The optimal concentration of EDTA appears to be 2 mM under the present conditions. This is equimolar to the final concentration of the added CaCl/MgCl2. The choice between CaCl and MgCl2 depends on whether blood without anticoagulant or ACD blood is employed. Coated cells keep satisfactorily for 5 weeks at 4 degrees C in Alsever's solution as well as after freezing and thawing. C3-coated cells can be converted to C3d-coated ones by incubation in normal, compatible, EDTA-containing serum at 37 degrees C.
A "new' rare blood group antigen Rla (Rosenlund) is reported. The antigen is present in about 1 in 900 Norwegians. Nine unrelated Rl(a+) people were found. Studies of seven families, leading to the discovery of 20 additional Rl(a+) people, indicated the antigen is inherited as a Mendelian dominant character. Independent segregation was demonstrated between Rla and the ABO, MNSs, Rh, Lutheran, Duffy and Kidd blood group systems, the ABH secretor genes, and sex. The Rla antigen is inactivated by papain treatment. The corresponding antibody, anti-Rla, has so far been found in three sera that also contain antibodies to other rare blood group antigens.
A female patient in her early sixties had for a period of at least 4 months a monoclonal IgG1 kappa protein in her serum and at the same time a very high level of anti-thyroglobulin antibodies. Different isolation procedures showed that the M component was responsible for the high anti-thyroglobulin activity. Anti-idiotypic antibodies raised in a rabbit against the monoclonal protein inhibited the M component's anti-thyroglobulin activity, and purified thyroglobulin blocked the reaction between the M component and the anti-idiotypic antiserum. After the M component had disappeared, no cross-idiotypic immunoglobulins could be detected in the patient's serum, nor could the anti-idiotypic antiserum inhibit the residual anti-thyroglobulin activity present in the serum at this time. No reaction could be detected between the antiserum and the anti-thyroglobulin antibodies of sera of other patients. Idiotypic autoantibodies against the M component, which might have caused its disappearance, could not be demonstrated.
A 'new rare blood group antigen R1a (Rosenlund) is reported. The antigen is present in about 1 in 900 Norwegians. Nine unrelated R1(a+) people were found. Studies of seven families, leading to the discovery of 20 additional R1(a+) people, indicated the antigen is inherited as a Mendelian dominant character. Independent segregation was demonstrated between Rla and the ABO, MNSs, Rh, Lutheran, Duffy and Kidd blood group systems, the ABH secretor genes, and sex. The R1a antigen is inactivated by papain treatment. The corresponding antibody, anti-R1a, has so far been found in three sera that also contain antibodies to other rare blood group antigens.
During routine ante-natal testing during the period 1953-73 anti-c was found in the serum of 63 women. Twenty-four of them had received blood transfusion previously and of these 22 were multigravidae. In 39 women pregnancies alone were responsible for the immunization. The anti-c titres of the 42 women giving birth to c positive babies showed that the probability of developing haemolytic disease increases with higher titres. But low titres by no means exclude the existence of such disease. Among the 42 c positive babies 32 had a positive direct antiglobulin test. Some of the affected infants had a serious degree of haemolytic disease.
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