Identification of <i>RHCE</i> and <i>KEL</i> alleles in large cohorts of Afro‐Caribbean and Comorian donors by multiplex SNaPshot and fragment assays: a transfusion support for sickle cell disease patients

Silvy, Monique; Cristofaro, Julie Di; Beley, Sophie; Papa, Kassim; Rits, M.; Richard, Pascale; Chiaroni, Jacques; Bailly, Pascal

doi:10.1111/j.1365-2141.2011.08691.x

Cited by 25 publications

(26 citation statements)

References 48 publications

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“…Several studies have reported allele prevalences for other populations [18,19,44,45,46]. Partial RH2 antigens appear to be particularly prevalent in mainland France, whereas partial RH1 antigens are more prevalent in Guadeloupe and French Guiana.…”

Section: Discussionmentioning

confidence: 99%

Genotyping in Sickle Cell Disease Patients: The French Strategy

Floch

Tournamille

Chami

2018

Transfus Med Hemother

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This review presents the French strategy for blood group genotyping in high-responder and newly diagnosed sickle cell disease (SCD) patients. In addition to FY, JK, and MNS genotyping, the RH blood group system is now explored in SCD patients in France. Molecular typing has been used for the deduction of partial RH2 (C) antigens since 2010, and the gradual implementation of systematic RHD and RHCE genotyping nationwide was initiated in late 2014. In our laboratory, 962 RH:2 (C-positive) SCD patients have been tested since 2010, and 1,148 SCD patients of all RH phenotypes have been genotyped for clinically relevant alleles of RHD and RHCE since late 2014.

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Section: Discussionmentioning

confidence: 99%

Genotyping in Sickle Cell Disease Patients: The French Strategy

Floch

Tournamille

Chami

2018

Transfus Med Hemother

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“…In a study of 39 SCD patients with DIIIa, 18 had alloanti‐D (Westhoff et al , ). From over 1000 Afro‐Caribbeans living in Martinique, the allele frequencies of RHD*DIIIa and RHD*DAR were 0·88% and 0·39% respectively (Silvy et al , ). Although DAR gives a characteristic pattern of reactions with monoclonal anti‐D, DIIIa red cells react with all monoclonal anti‐D and so cannot easily be detected by serological methods.…”

Section: Variants and Sickle Cell Diseasementioning

confidence: 99%

Variants of RhD – current testing and clinical consequences

2013

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Anti-D (-RH1) of the Rh blood group system is clinically important as it causes haemolytic transfusion reactions and haemolytic disease of the fetus and newborn. Although most people are either D+ or DÀ, there is a plethora of D variants, often categorized as either weak D or partial D. These two types are inadequately defined and the dichotomy is potentially misleading. DVI is the D variant most commonly associated with anti-D production and UK guidelines recommend that patients are tested with anti-D reagents that do not react with DVI. Weak D types 1, 2, and 3 are seldom, if ever, associated with alloanti-D production, so a policy recommendation would be to treat patients with those D variants as D+, to preserve DÀ stocks, whereas patients with all other D variants would be treated as DÀ. All donors with D variant red cells, including DVI, should be treated as D+. The frequency of the D+ phenotype is about 85% in Caucasians, around 95% in sub-Saharan Africa, and greater than 99Á5% in eastern Asia (Daniels, 2013). Although most people are either D+ or DÀ, a grey area exists in the form of a plethora of D variants: the so-called weak D, partial D, and DEL phenotypes. These ill-defined terms are often a cause of consternation beyond their clinical relevance. Over its history of well over a century, blood group serology has been fraught with problems arising from nomenclature, and the terminology applied to D variants has led to confusion.In this review I will attempt to clarify the situation, recommend a testing and transfusion strategy that minimizes the risk of alloimmunization without undue waste of DÀ blood stocks, and describe the clinical issues relating to these aberrant forms of D.

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“…For instance, at least three studies have shown that alloimmunization to antigens within the Rh and Kell systems still occurs in patients with SCD despite serologic matching, even in cases when RBCs from minority donors were provided . One of the possible reasons for alloimmunization despite partial or extended matching is the existence of antigenic variants that cannot be reliably detected by serologic methods, but which nonetheless confer immunogenicity . If other large‐scale studies also demonstrate that antigen variants are culpable for alloimmunization despite serologic matching, then such findings may imply that DNA‐based approaches are superior for avoiding alloantibody development in SCD.…”

Section: The Efficacy Of Partial or Extended Blood Group Antigen Matcmentioning

confidence: 99%