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. Author manuscript; available in PMC: 2022 May 20.
Published in final edited form as: Transfusion. 2020 Mar 12;60(4):855–859. doi: 10.1111/trf.15741

It’s time to phase out “serologic weak D phenotype” and resolve D types with RHD genotyping including weak D type 4

Willy A Flegel 1,2, Gregory A Denomme 3, John T Queenan 4, Susan T Johnson 5, Margaret A Keller 6, Connie M Westhoff 7, Louis M Katz 8, Meghan Delaney 9, Ralph R Vassallo 10, Clayton D Simon 11, S Gerald Sandler 1
PMCID: PMC9121350  NIHMSID: NIHMS1802170  PMID: 32163599

In 2015, the AABB and the College of American Pathologists sponsored an Interorganizational Work Group on RHD Genotyping,1 inviting the American College of Obstetricians and Gynecologists (ACOG), American Red Cross, America’s Blood Centers, and Armed Services Blood Program to recommend organizational representatives. In addition, five scientific consultants were invited to be members of the Work Group.1 The Work Group developed and published recommendations2 for phasing-in RHD genotypings for individuals with a “serologic weak D phenotype,”3,4 focusing on pregnant women and potential recipients of a blood transfusion.1,2 During the subsequent 5 years, molecular immunohematology laboratories have observed an increase in the number of requests for RHD genotyping reflecting expanded implementation of RHD genotyping in clinical practice. The potential benefit if the Work Group’s recommendations2 were fully implemented, rather than treating all individuals with serologic weak D phenotype as D−, would be the elimination of an estimated 24,700 unnecessary ante- and postpartum injections of Rh immune globulin (RhIG) annually in the United States.2 Also, as many as 47,700 units of D− red blood cells (RBCs), always in short supply, would be made available for patients with definite need for such units.2

As members of the previously convened Work Group, we have observed several impediments to the integration of RHD genotyping in clinical practice, which are the subject of this Commentary. The Work Group’s recommendation could not require the hospitals to alter their D antigen typing practice, and did not specify whether the interpretation of RHD genotyping results should be included in the laboratory report or whether laboratories should report only RHD genotyping results, deferring the interpretation to clinical practitioners. We have observed that when the molecular report does not provide an interpretation and recommendation, clinical practictioners not experienced in blood group genetics hesitate to interpret RHD genotyping results as D+ or D−. For the purposes of RhIG adminstration and transfusion, interpretation of an RHD genotype requires not only pertinent experience but also knowledge of the history2,5 as well as the current evolving data6–22 and literature reports15,16,23–26 of the risks for alloimmunization associated with specific RHD genotypes.27 Hospital computer systems may require updating to accomodate new requirements, such as the ability to change a prior serologic D typing result, when it is overridden by a different D type based on RHD genotyping results.

We provide guidance on the interpretation and update our previous recommendation2 to include the management of weak D type 4.0 and 4.1 based on research published since 201515–18 (Table 17,28–34).

TABLE 1.

Guidance for managing transfusion or RhIG administration in individuals with a serologic weak D phenotype and the associated RHD genotype (alleles)*

Traditional designation28 Typical reactivity by immediate spin† Includes ISBT allele designation33 SNV (amino acid substitution) Manage as D type
Weak D type 1 0 to 2+ Weak D type 1.028 RHD * 01W.1
RHD * weak D type 1 		c.809T>G (p.Val270Gly) D+
Weak D type 1.130 RHD * 01W.1.1
RHD * weak D type 1.1 		c.809T>G (p.Val270Gly)
c.52C>G (p.Leu18Val)
Weak D type 1.27 RHD * 01W.1.2
RHD * weak D type 1.2 		c.809T>G (p.Val270Gly)
c.712G>A (p.Val238Met)
Weak D type 2 0 to 1+ Weak D type 2.028 RHD * 01W.2
RHD * weak D type 2 		c.1154G>C (p.Gly385Ala) D+
Weak D type 2.132 RHD * 01W.2.1
RHD * weak D type 2.1 		c.1154G>C (p.Gly385Ala)
c.301T>A (p.Phe101Ile)
Weak D type 2.27 RHD * 01W.2.2
RHD * weak D type 2.2 		c.1154G>C (p.Gly385Ala)
c.916G>A (p.Val306Ile)
c.932A>G (p.Tyr311Cys)
Weak D type 3 0 to 2+ Weak D type 3.028 RHD * 01W.3
RHD * weak D type 3 		c.8C>G (p.Ser3Cys) D+
Weak D type 3.17 RHD * 01W.3.1
RHD * weak D type 3.1 		c.8C>G (p.Ser3Cys)
c.178A>C (p.Ile60Leu)
Weak D type 4.0 ± to 2+s Weak D type 4.0.028 RHD * 09.03.01
RHD * DAR3.01 		c.602C>G (p.Thr201Arg)
c.667T>G (p.Phe223Val)
c.819G>A (p.Ala273Ala)		 D+‡
Weak D type 4.0.132 RHD*09.03
RHD*DAR3 		c.602C>G (p.Thr201Arg)
c.667T>G (p.Phe223Val)
Weak D type 4.1 ± to 3+ No known subtype29 RHD * 09.04
RHD * DAR4 		c.602C>G (p.Thr201Arg)
c.667T>G (p.Phe223Val)
c.48G>C (p.Trp16Cys)
c.819G>A (p.Ala273Ala)		 D+
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*

For the more than 150 other known weak D alleles, typically associated with a serologic weak D phenotype,32,33 not listed in this tabulation, the risk for anti-D is often unknown, but no clinically significant hemolytic disease of the fetus and newborn or transfusion reaction have been reported.

†

Strength of reactivity34 is variable and depends on technical details, such as test method, reagent, and RBC condition. Also, the reactivity is enhanced in gel matrix tests.

‡

D− transfusion and RhIG may be considered during pregnancy in an abundance of caution (see text).31

SNV = single-nucleotide variation.

LIMITATIONS OF THE CURRENT PRACTICE OF REPORTING A “SEROLOGIC WEAK D PHENOTYPE”

In August 2006, and reaffirmed in 2016, the ACOG Practice Bulletin on “Management of Alloimmunization During Pregnancy”35 stated that “patients who are weak D positive are not a risk for alloimmunization.” Authors of the August 2017 ACOG Practice Bulletin on “Prevention of Rh D Alloimmunization”36 reviewed the Work Group’s recommendation in detail and stated that an “attractive solution to this problem is to perform molecular genetic RHD typing in weak D phenotype individuals.”36 Nevertheless, the Committee on Practice Bulletins–Obstetrics concluded that “clinicians are advised to administer Rh D immune globulin to patients with weak D blood type in appropriate clinical situations, by the same rationale as that for Rh D typing blood donors, until further scientific and economic studies are available.”36 That is, the ACOG Committee did not recommend resolving serologic weak D phenotype results by RHD genotyping and reverted to the 50-year-old practice of administering RhIG according to serologic test results.37 This decision has the potential to increase the number of unnecessary doses of RhIG, while the implementation of RHD genotyping to resolve serologic weak D cases has the potential to significantly reduce RhIG doses.

Approximately 0.2% to 1% of a Caucasian population may react weakly with anti-D or react only when tested by a specific serologic method or with a specific anti-D reagent.38–40 Typically in the United States, serologic weak D phenotypes in blood donors are not resolved by molecular methods, unless presenting as a donor unit typing discrepancy. When serologic and molecular results are reported in patient testing, clinical practitioners who are not specialized in blood groups should not be expected to interpret molecular results.

We recommend that laboratories performing RHD genotyping do not defer interpretation of the RHD genotype result to nonspecialist practitioners. From ACOG’s 2017 recommendation,36 it is evident that optimal, up-to-date management of serologic weak D phenotypes and interpretation of RHD genotype results should be guided by subject matter experts in blood group genetics. There is observational indirect serologic evidence, with41–43 and without genotyping results,6 to support the premise that patients who have a serologic weak D phenotype and who were transfused with D-positive RBCs experienced a low or no risk of D alloimmunization.

To support effective phase-in of RHD genotyping in this era of precision medicine, we encourage relevant AABB program units to update the Standards for Blood Banks and Transfusion Services and the Standards for Immunohematology Reference Laboratories and require processes for managing a serologic weak D phenotype.3 Use of two different serologic methods or anti-D reagents have been shown to be an effective practice for identifying those patients who will benefit from RHD genotyping.28,29,39,40,44–48 Our interpretations of RHD genotype results are summarized in a crosswalk table of RHD allele assignments (Table 1) to standardize reporting and guidance to manage as D+, D−, or uncommonly as indeterminate risk. Indeed, AABB-accredited immunohematology reference laboratories are already required to provide recommendations for RhIG administration and selection of the most compatible RBCs for transfusion. We believe this responsibility should also include guidance for interpreting RHD genotyping results for the purpose of RhIG administration and transfusion. It is our opinion that laboratories should phase out reporting results for a D type as a serologic weak D phenotype and instead provide a report that includes guidance based on RHD genotyping.2,29,45,49

MOLECULAR WEAK D TYPES 4.0 AND 4.1

In 2015, the Work Group reviewed published and unpublished case reports to determine whether weak D types 4.0 and 4.1 should be recommended, along with weak D types 1, 2, and 3, as weak D types that can be managed safely as D+.2 The Work Group limited its recommendation to manage serologic weak D phenotypes as D+ to weak D types 1, 2 and 3 until more data were available.2 Additional data are now available.15–18 No allo- or auto-anti-D has been reported associated with weak D type 4.1,2,16,45 despite its being more common than weak D type 4.0 in Caucasians.29,50 Recipients carrying weak D type 4.1 are also more likely to be routinely transfused with D+ RBC units than recipients carrying weak D type 4.0.15,16,50 We recommend changing the classification of these two alleles from partial D to weak D in RHD allele tables.33 We also recommend continuing the collection and publication of clinical outcomes data in patients with weak D type 4.0 or type 4.1 and anti-D.2,17 In the African American population, weak D type 4.0 is not uncommon, with an allele frequency of 0.02. In the United States, 38 cases with anti-D have been reported17: While adsorption studies to differentiate allo- from auto-anti-D formation remain to be published, most importantly, no hemolytic transfusion reaction or hemolytic disease of the fetus and newborn have been associated.17

Indeed, supporting every patient with weak D types 4.0 or 4.1 with D− units to prevent anti-D puts a burden on the D− blood supply. Hospitals in France have begun to use D+ RBCs for patients and pregnant women with weak D types 4.0 and 4.1.16

These additional observations update our previously published recommendation.2 Patients with a serologic weak D phenotype, if not already tested, should be tested by a molecular method and those with weak D types 1, 2, 3, 4.0 and 4.1, including women of childbearing age, may be managed safely as D+ with regard to blood transfusion. However, for a pregnant woman with a weak D type 4.0, consideration may be given for D− transfusions and RhIG for D immunoprophylaxis in an abundance of caution.

PHASE-IN OF RHD GENOTYPING AND PHASE-OUT OF REPORTS FOR SEROLOGIC WEAK D PHENOTYPES

We reaffirm and update our 2015 recommendation for a transfusion strategy based on molecular testing whenever a serologic weak D phenotype is detected in patients.2 We also reaffirm that our primary goal is “to increase awareness of the available molecular science and promise of RHD genotyping and, thereby, to shorten the time for achieving the full benefits of … implementation of RHD genotyping.”2

Recognizing the financial and logistical complexity of this transition,25,51 we emphasize the concept of “phasing in” as a step-by-step, responsible integration of RHD genotyping. As cost-effective and quicker methods for managing serologic weak D phenotypes become available, the focus should turn to developing protocols for managing patients with RHD alleles, who do not have a serologic weak D phenotype, but who are at risk for developing anti-D, such as RHD*DIIIa and RHD*DIVa. Blood samples with a serologic weak D phenotype that do not have a prior RHD genotype result should be routinely reflexed for molecular testing to complete the determination of the D type. We encourage the AABB, through appropriate standard-setting program units to support this recommendation, with a particular focus on females of childbearing potential.

SUMMARY

We propose that hospital laboratories and immunohematology reference laboratories phase-out the practice of reporting a “serologic weak D phenotype”, when a request has been made for an RhD type. Interpreting serologic weak D results, especially for females of childbearing potential, is not straightforward. The clinically relevant distinction between various molecular weak D types cannot be made by serologic method. Laboratories offering RhD typing services should take responsibility for obtaining RHD molecular testing – whether in-house or by a molecular reference laboratory – and interpret the RHD genotyping result with a recommendation to manage the individual as either RhD-positive or RhD-negative. Unless historical red cell genotyping results are available, RHD genotyping should be performed to resolve a serologic weak D phenotype for women of childbearing potential or transfusion recipients. We also update our previous recommendation to include the management of weak D types 4.0 and 4.1. If a serologic weak D phenotype is detected by routine RhD antigen typing, the laboratory should consider the result to be incomplete and resolve the serologic result by RHD genotyping. Laboratories should report the serologic and molecular results and provide an interpretation that includes a recommendation to manage the patient as RhD-positive or RhD-negative, with the goal to limit alloimmunization while avoiding unnecessary use of RhD-negative blood and Rh immune globulin.

ACKNOWLEDGMENTS

GAD identified the approach in the AGOC Practice Bulletin; SGS conceived the proposal and wrote the first draft; SGS, CMW, and WAF revised manuscript versions. All authors edited and approved the final manuscript.

Supported by the Intramural Research Program (project ID Z99 CL999999) of the NIH Clinical Center at the National Institutes of Health; a Diagnostic Laboratories Strategic Initiative fund from Versiti Blood Center of Wisconsin.

CONFLICT OF INTEREST

CDS, JTQ, LMK, SGS and WAF have disclosed no conflicts of interest. CMW has received speaker honorarium from Grifols and Immucor and consulting honorarium from Quotient, Cerus, and ArchOncology with renumeration to New York Blood Center. GAD and MAK are on the Grifols Speakers Bureau. MD has received speaker honorarium from Grifols. RV receives financial support from bioMérieux, Cerus, Fresenius-Kabi, Hemanext, and Hemastrat. STJ receives speaker honorarium from Grifols and Immucor.

ABBREVIATIONS:

ACOG

American College of Obstetricians and Gynecologists

RhIG

Rh immune globulin

Footnotes

The views expressed do not necessarily represent the view of the National Institutes of Health, the Department of Health and Human Services, the Department of Defense, or the US federal government.

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