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The Incidence of H Deficient A<sub>2</sub> and A<sub>2</sub>B Bloods and Family Studies on the AH/ABH Status of an A<sub>int</sub>, and Some New Variant Blood Types (A<sub>int H↓</sub><sup>A</sup><sub>1</sub>, A<sub>2↑H</sub>w<sup>A</sup><sub>1</sub>, A.<sub>2↑</sub>B<sub>H</sub><sup>A</sup><sub>1</sub>B and A<sub>2↓</sub>B<sub>H</sub><sup>A</sup><sub>2</sub>B
25
Citations
12
References
1970
Year
ImmunohematologyBlood SamplesGeneticsNew Variant PhenotypesGenetic EpidemiologyImmunologyPathologyHuman PolymorphismGenetic MedicineClinical GeneticsFamily StudiesHematologyClinical ChemistryPublic HealthMolecular DiagnosticsLaboratory MedicineVariant InterpretationMonogenic DisordersHuman Leukocyte AntigenInherited Metabolic DiseaseStatistical GeneticsGenetic VariationHeme HomeostasisAh/abh StatusAllelic VariantGenetic DisorderPhysiologyH Precursor SubstanceMedicineChromosome 9
Abstract. The incidence of H deficient A 2 blood samples in the Sheffield area was found to be 1 in 169 and 1 in 13 of group A 2 and A 2 B blood samples respectively. Family studies are described on an A int and on examples of the new variant phenotypes, A intH↓ ., A 2↑H W , A 2↑ B H W and A 2 B H W . The sera of some of the variants contained cold anti‐H s /HI s /HI c /Le bH antibodies, but none contained the Bombay type of anti‐H s active at 37°C. The authors suggest that the modified A status of most of the variants is due to reduced expression of the A 1 genes as a result of insufficient production of H precursor substance by weak H alleles. In paternity testing, it is important that an exclusion should not be based on the occurrence of an A 1 child of a not A 1 group A mating until the A 2 /A 2 B parent(s) have been shown to have a normal H status.
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