[Analysis of the association of blood groups ABO and rhesus factor in children with myasthenia gravis].
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TITLE: ABO blood groups as risk factor in Helicobacter pylori infection.OBJECTIVE: To asses the relation between ABO blood groups and Helicobacter pylori (Hp) infection. METHODS: The present is a case and control study. A study population of dyspeptic patients who underwent upper gastrointestinal endoscopy was selected. Four biopsies were taken from the antrum and the body of the stomach and blood group was typified. Patients with gastrectomy, gastric cancer, treated for Hp infection in the previous six months or without blood group typification were excluded. The population sample was found using EPIINFO 5.1 program. We called case to every patient with Hp (+) biopsy and control all with Hp (-) biopsy. The risk of the infection was calculated with the OR (Odds ratio) and the study sample was compared with the blood bank control group using the Chi-square test (p<0.005).RESULTS: 367 patients were included (202 female). Age average was 45,06 years. 276 (75,2%) were Hp (+). There were not statistically significant differences in the distribution of ABO blood groups between the study population and the blood bank control. When we compared the ABO blood distribution between patients Hp (+) and Hp (-) we found significant differences for blood group O (p=0.004) and blood group A (p=0.03). Statistical analysis revealed an OR=2,22 for the blood group O and OR=0,5 for the blood group A.CONCLUSIONS: 1) The ABO blood group distribution is different in patients with Hp infection compared with those without Hp infection. 2) Blood group O would be a moderate risk factor for infection by Helicobacter pylori.
Factor VIII (FVIII), von Willebrand factor (vWF) and the ABO blood groups have been associated with thrombosis. The ABO locus has functional effects on vWF and FVIII levels and is genetically correlated with FVIII, vWF and thrombosis. We carried out a case-control study to assess the role of FVIII, vWF and ABO types on thrombotic risk. We analyzed 250 patients with venous thrombosis and 250 unrelated controls. FVIII, vWF and other factors related to thrombophilia were measured, ABO groups were analyzed by genotyping. FVIII and vWF were higher in non-O individuals. Group O was more frequent in the controls (44.3% v 23.3%; difference 21.1%; 95% CI: 13.0-29.3%) and Group A in patients (59.2% v. 41.5%; difference 17.7%, 95% CI: 9.1-26.4%). Individuals carrying the A1 allele had a higher risk of thrombosis (OR 2.6; 95% CI, 1.8-3.8). The risk attributed to vWF disappeared after adjusting for the ABO group. Patients with FVIII above the 90th percentile had a high thrombotic risk (adjusted OR 3.7; 95% CI, 2.1-6.5), and a high risk of recurrence (OR 2.3; 95% CI: 1.3-4.1). In conclusion, high FVIII levels and non-O blood groups, likely those with the A1 allele, are independent risk factors for venous thromboembolism and should be considered in evaluating of thrombophilia.
BACKGROUND: The aim of this study was to demonstrate an association between Helicobacter pylori infection, ABO blood groups and Rhesus factor; providing the association between duodenal ulcer and O group blood as well as the former and H. pylori infection. METHODS: Three-hundred and one healthy subjects were prospectively studied. In all of them ABO blood groups and Rhesus factor were determined by standard techniques. Systemic IgG antibodies against H. pylori were assayed using a quantitative enzyme-linked immunosorbent assay technique (Helico-G, Porton, Cambridge, UK). RESULTS: The overall seroprevalence was 52.2%. H. pylori infection distribution was similar among ABO blood groups and Rhesus factor. No statistically significant differences were observed in mean values of IgG antibodies among different blood groups. CONCLUSIONS: Distribution of H. pylori seroprevalence does not differ between different ABO or Rhesus factor blood groups. This excludes a possible link between this microorganism and the high ulcer prevalence in O blood group.
The distribution of ABO blood groups and rhesus factor was studied in patients with myasthenia as compared with the control. There was a statistically significant association of the diseases with the rhesus-negative phenotype and that of generalized myasthenia concurrent with thymoma with the B (III) blood group. The examination revealed no other determinants of the significant association with the disease. The values of a disease risk were obtained for persons having myasthenia-associated signs. It is concluded that the Rh-negative phenotype shows a 1.3-fold increase in the risk of the disease as compared with those having Rh-positive persons.
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Females homozygous for the maternal-effect mutation abo (2-44.0) produce a large fraction of eggs which arrest during embryogenesis. Increasing doses of defined heterochromatic regions inherited by offspring of abo mothers from their fathers function zygotically to bring about a partial rescue of the abo-induced embryonic lethality. Another property of the abo mutation is that the severity of the maternal effect decreases when an abo stock is maintained in homozygous condition for a number of generations. Here, we show that the factors which change in homozygous abo stocks to result in the decrease in maternally induced embryonic lethality, act zygotically, dominantly and additively. More importantly, we show that the X and second chromosomes, but not the Y and third chromosomes, derived from homozygous abo stocks are, when inherited from males, more effective in promoting zygotic rescue of the abo-induced lethality than are the equivalent chromosomes derived from an abo stock maintained in heterozygous condition. The chromosomal locations of the factors maintained in the homozygous condition. The chromosomal locations of the factors altered in homozygous stock, as well as their behavior, strongly suggest that the same heterochromatic elements that are responsible for rescuing embryos from the abo-induced maternal effect are altered in homozygous abo flies in such a way that the maternal effect itself is less severe.
Diagnosis of von Willebrand disease requires a combination of quantitative and qualitative tests including the von Willebrand factor ristocetin cofactor assay (vWF:RCo), the von Willebrand factor collagen binding assay (vWF:CB) and von Willebrand factor antigen quantification (vWF:Ag). Genetic factors, especially the ABO blood group, contribute significantly to the variation in vWF levels and function. Recent studies suggest that ethnicity may be another important modulator. We investigated the effect of the ABO blood group on these tests in 52 blood group O and 54 non-group O Chinese blood donors who were well-matched for sex and age distribution. Group O donors had significantly lower vWF:RCo, vWF:Ag and vWF:CB (P < 0.0001). Reduction in vWF:CB was greater than vWF:RCo in group O donors (53 versus 27%). This led to a lower vWF:CB/vWF:Ag ratio (P < 0.0001) in group O donors whereas the vWF:RCo/vWF:Ag ratio was unaffected (P = 0.97). These variations should be taken into consideration when interpreting these results in the Chinese.