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PubMed1978

ABO hemolytic disease of the newborn: evaluation of management and identification of racial and antigenic factors.

Data from 16,320 deliveries from two time periods were examined to compare the incidence of positive direct Coombs' tests and the number of exchange transfusions performed, using different methods of screening and treatment in each time period. Early routine screening revealed an eightfold increase in the number of Coombs-positive infants, while the combined effect of instituting early screening and the change from white light to special blue light phototherapy greatly diminihsed the number of exchange transfusions. In addition, data concerning racial and blood antigen factors in ABO hemolytic disease of the newborn (HDN) are compared, showing an increase in incidence but no increase in severity for black infants and infants with blood type B. Also, use of cord blood parameters in management of ABO HDN is discussed.

ABO Blood-Group System↗
PubMed1993

[Minor erythrocyte antigens: their sensitizing activity and rating in the practice of transfusion science].

A general situation in transfusiology influencing sensitization probability greatly differs from that in a panmictic population as blood transfusions are strictly controlled by ABO group and Factor D rhesus. However, with increasing hemotransfusion scope, clinical significance shifts to other factors, "minor" antigens of erythrocytes, which are not given due attention in hemotransfusions. Besides ABO factors and antigen D rhesus in practical transfusiology of importance are antigens C, c, E, e, K allosensitization to which is mainly observed in rhesus-positive subjects.

ABO Blood-Group System↗
PubMed2005

Relationship between ABO and Secretor genotype with plasma levels of factor VIII and von Willebrand factor in thrombosis patients and control individuals.

In contrast to earlier reports, this study examined the relationship between plasma levels of factor VIII (FVIII) and von Willebrand factor (VWF) and ABO blood group and secretor status at the genetic level in 355 patients with venous thrombosis as well as in 236 controls. ABO glycosyl transferase alleles A(1) and B were more frequent in the thrombosis collective and alleles O(1), O(2) and A(2) were more frequent in the controls. A low-risk group for venous thrombosis of individuals with genotypes O(1)O(1), O(1)O(2) and O(1)A(2) (H-antigen rich) could be distinguished from a high-risk group with genotypes A(1)A(1), A(1)B, O(1)A(1) and O(1)B (H-antigen poor). In both the thrombosis and control groups, the H-antigen rich group showed significantly lower levels of FVIII coagulant activity (FVIII:C) and VWF antigen (VWF:Ag) than the H-antigen poor group. The frequency of the different secretor genotypes in the thrombosis group was not different from that in the control group. No significant differences of FVIII:C and VWF:Ag levels were seen between SeSe, Sese and sese individuals in the thrombosis and in the control group. Thus the risk of venous thrombosis is associated with the ABO blood group genotype but not with secretor status.

ABO Blood-Group System↗
PubMed2002

von Willebrand disease: still an intriguing disorder in the era of molecular medicine.

von Willebrand disease (vWD) is a single-locus disorder resulting from a deficiency of von Willebrand factor (vWF): a multimeric multifunctional protein involved in platelet adhesion and platelet-to-platelet cohesion in high shear stress vessels, and in protecting from proteolysis and directing circulating factor VIII (FVIII) to the site of injury. vWD is the most frequent bleeding disorder, with an estimated prevalence in the general population of 1%. Almost all these cases are represented by a partial quantitative deficiency of von Willebrand factor (vWF) (type 1 vWD). Type 1 is transmitted as an autosomal dominant trait with an extremely variable penetrance and expressivity. A consensus figure for the prevalence of cases with significant bleeding symptoms, requiring some form of treatment, is approximately 100 cases million-1. Among these cases, more than 70-80% are represented by type 1 and respond to deamino-D-arginine vasopressin (DDAVP; desmopressin) administration. The remaining cases are represented by type 2 vWD (qualitative), some of which require substitutive treatment. Only 3-5 cases million-1 result from a total deficiency of vWF in plasma and platelets because of the recessive inheritance of two defective alleles. These cases may have severe bleeding episodes and may require frequent substitutive treatment. The molecular basis of type 2 (missense mutation in the functional domains of the vWF subunit) and type 3 (nonsense or large deletions) is quite well understood. On the contrary the molecular basis for most type 1 cases remains largely unknown, and many genetic factors (e.g. ABO blood group) and environmental or circumstantial factors (e.g. age, stress, drugs, pregnancy, and inflammation) are superimposed on to the genetic background determined by the vWF gene to produce a continuous spectrum from normality to mild type 1 cases. It is extremely difficult to make a clear distinction between mild type 1 cases and normal people because of the wide 'normal' range of laboratory measurements (e.g. length of bleeding time, and levels of vWF and FVIII) and of bleeding symptoms. Molecular testing is useless in this situation, and only good history-taking and repeated laboratory testing of vWF-related measurements in the propositus and his/her family members can help in clinical diagnosis, albeit imprecisely. This difficult task is the main focus of this review which is aimed at alerting the physician toward a balanced approach that should take into consideration both the risk of over- and under-diagnosis of this frequent disorder and the unavoidable production of a number of false positive and false negative cases.

Algorithms↗