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        <title>Immunohematology Feed</title>
        <link>https://reference-global.com/journal/IMMUNOHEMATOLOGY</link>
        <description>Reference Global RSS Feed for Immunohematology</description>
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        <copyright>All rights reserved 2026, American National Red Cross</copyright>
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            <title><![CDATA[Contents]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-012</link>
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            <pubDate>Sun, 11 Oct 2026 00:00:00 GMT</pubDate>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Artificial intelligence and machine learning in immunohematology: an expert overview of emerging tools for precision transfusion medicine]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-014</link>
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            <pubDate>Sun, 11 Oct 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Artificial intelligence (AI) and machine learning (ML) are transforming immunohematology, offering significant enhancements in precision, accuracy, and personalized transfusion care. This expert overview summarizes current applications of AI/ML in phenotypic and genotypic red blood cell (RBC) antigen determination, antibody detection, crossmatching, and quality control. Recent studies demonstrate the efficacy of image-based and deep learning methods, with accuracies reaching 99 percent for automated phenotyping and genotyping. AI-assisted models for antibody detection and compatibility assessment have also emerged, providing rapid, standardized decision-making that reduces human error and improves transf usion outcomes. Notably, AI-driven platforms like the Haem-Match Consortium’s bloodMatcher potentially reduce alloimmunization risks by as much as 80 percent, highlighting the technology’s clinical relevance. AI also bolsters hemovigilance and quality control by analyzing vast clinical data for early detection of adverse events. Challenges remain, however, including algorithmic bias, data privacy, and the need for extensive real-world validation to ensure safe and ethical adoption. Integration with existing hospital information systems and development of robust regulatory frameworks are crucial to fully harness these tools. Future research should prioritize validation in diverse populations and transparent AI development practices. Overall, AI and ML hold promise to revolutionize immunohematology by enhancing accuracy, minimizing adverse transfusion reactions, and supporting patient-centric transfusion care.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Isolating anti-D, anti-C, and anti-G in immunohematology: a method comparison]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-016</link>
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            <pubDate>Sun, 11 Oct 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[G is present on virtually all red blood cells expressing either D or C; thus, identification of anti-G, anti-D, and anti-C in a patient’s plasma can be challenging. While identification of anti-G is usually of little clinical significance, it becomes increasingly important in the context of prenatal care. Proper antibody differentiation is necessary to determine candidacy for Rh immune globulin administration to prevent anti-D immunization during pregnancy. We conducted an analytical experimental study of 18 plasma samples from donors and patients with apparent anti-D and anti-C upon initial antibody identification. Samples were tested in duplicate using two established anti-G differentiation methods. Method A consisted of sequential adsorption and elution techniques, and Method B consisted of double adsorption and elution techniques. Of the 18 samples obtained, 14 fit the criteria for inclusion in this study. Both methods successfully identified anti-G and anti-D when present. Method A failed to identify anti-C in one sample. Our results generated a percent positive agreement of 92.9 percent with a 95 percent confidence interval of 68.5–98.7. Our findings demonstrated that Method B detected more antibodies than Method A and allowed for a reduction in testing time, making it the preferred method in this study.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Rouleaux mimicking anti-H in molecularly confirmed para-Bombay siblings: a diagnostic pitfall]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-013</link>
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            <pubDate>Sun, 11 Oct 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[The para-Bombay phenotype is a rare H-deficient blood group variant characterized by markedly reduced or absent expression of H on red blood cells (RBCs) because of mutations in FUT1, with variable secretor status influenced by FUT2. The Bombay phenotype is relatively more common in the Indian population, but the para-Bombay phenotype remains exceedingly rare and is frequently underrecognized because of diagnostic challenges during routine serologic testing. We report molecularly confirmed para-Bombay siblings from India in whom rouleaux-induced pseudoagglutination mimicked anti-H reactiv ity. The index case demonstrated absent reactivity with anti-H lectin and weak reactivity with pooled group O RBCs during reverse grouping and thermal amplitude testing, initially raising suspicion of clinically significant anti-H. However, detailed serologic evaluation, including microscopic examination, saline replacement, adsor ption–elution studies, and saliva inhibition testing, favored rouleaux-induced pseudoagglutination over true anti-H–mediated agglutination. Molecular analysis identified homozygous FUT1 c.328G&gt;A and FUT2 c.357C&gt;T mutations in both affected siblings, consistent with para-Bombay secretor phenotype and similar to previously reported variants in the Telangana population. This case highlights rouleaux-induced pseudoagglutination as an impor tant diagnostic pitfall in para-Bombay phenotypes. Integration of conventional serologic methods with molecular characterization was essential for accurate diagnosis, appropriate transfusion planning, and avoidance of unnecessary restrictions on compatible blood components.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Antibodies to human leukocyte antigens and eplet patterns associated with platelet transfusion refractoriness in Hispanic patients]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-015</link>
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            <pubDate>Sun, 11 Oct 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Antibodies to Class I human leukocyte antigens (HLAs) are a major immunologic cause of platelet transfusion refractoriness (PTR). HLA inheritance is highly related to ethnicity. Because most platelet donors are White, Hispanic patients may be at an increased risk of developing HLA antibodies due to mismatch between donor and recipient. This retrospective study analyzed 16 Hispanic patients with PTR to evaluate HLA antibodies associated with PTR. Baseline mean fluorescent intensity (MFI) was used to measure HLA antibody detection. Additive MFI values and clinical cut points were evaluated for Class I HLAs. Additionally, eplet exposition scores for antibody-verified eplets were totaled and compared with corrected count increment (CCI). Significant negative correlations were found between CCI with total additive MFI (r = –0.656) and allele-specific MFI for HLA A*03:01 (r = –0.728), C*14:02 (r = –0.795), and C*01:02 (r = –0.727). Analysis of cut points yielded significance between negative and strong MFI for HLA B*07:02. Data reveal that antibodies against common HLA alleles, such as A*03:01, correlate with PTR, highlighting the potential impact on alloimmunization and PTR risks in Hispanic patients.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[D–– phenotype and anti-Rh17 alloimmunization: a comprehensive review of identification and clinical management]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-017</link>
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            <pubDate>Sun, 11 Oct 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[The D–– phenotype is an exceptionally rare Rh blood group phenotype characterized by expression of D in the complete absence of C, c, E, and e. Individuals with this phenotype are at risk of developing anti-Rh17 (anti-Hr0), a clinically significant alloantibody that can severely complicate transfusion support and pregnancy management because compatible blood is exceptionally difficult to obtain. This review critically synthesizes the available published evidence regarding the D–– phenotype and anti-Rh17 alloimmunization, integrating data from case reports, case series, family investigations, and molecular studies from different geographic regions. Current evidence regarding molecular mechanisms, immunohematologic character istics, serologic identification, transf usion management, pregnancy outcomes, and rare donor strategies is summarized, w ith emphasis on practical considerations relevant to transfusion medicine. Although the D–– phenotype is exceptionally rare, early recognition, comprehensive immunohematologic evaluation, and proactive transfusion planning, including collaboration with rare donor programs, are essential for optimizing patient outcomes.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Erratum]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-011</link>
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            <pubDate>Thu, 23 Jul 2026 00:00:00 GMT</pubDate>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Contents]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-006</link>
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            <pubDate>Thu, 23 Jul 2026 00:00:00 GMT</pubDate>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Rhnull phenotype: molecular basis, serologic features, clinical manifestations, and transfusion challenges—a scoping review of published cases]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-008</link>
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            <pubDate>Thu, 23 Jul 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[The Rhnull phenotype is the rarest of the Rh blood group system phenotypes and is characterized by the complete absence of all Rh antigens on red blood cells (RBCs). This phenotype carries major clinical relevance because of chronic hemolysis and profound transfusion incompatibility. We performed a scoping review to summarize the molecular basis, serologic features, clinical manifestations, and transfusion challenges associated with published Rhnull cases. A systematic literature search of PubMed/MEDLINE and Scopus was conducted from database inception to May 2025. Eligible reports included case reports, case series, or observational publications of individuals with the Rhnull phenotype. Data were extracted and synthesized narratively according to a scoping review method. Six eligible publications describing eight individuals with the Rhnull phenotype were identified. Common findings included chronic hemolytic anemia, stomatocy tosis or spherocytosis, and reticulocy tosis. Despite generally moderate intrinsic hematologic manifestations, the Rhnull phenotype imposes a disproportionate transfusion burden because of near-complete donor scarcity. Anti-Rh29 alloimmunization was reported after transfusion or pregnancy exposure, restricting patients to Rhnull RBC units from family members, frozen RBC inventories, or rare donor registries. Early recognition, molecular characterization, and proactive integration of eligible individuals with the Rhnull phenotype into rare donor programs are critical for access to compatible blood.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[First Vel-null alloimmunized blood donor identified in Uruguay]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-009</link>
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            <pubDate>Thu, 23 Jul 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[A 52-year-old, first-time blood donor presented with panreactivity during routine antibody screening. Current serologic evaluation showed uniform 2+ reactivity by the gel-indirect antiglobulin test and the conventional tube low-ionic-strength saline–indirect antiglobulin test. The molecular analyses revealed a homozygous 17–base pair deletion spanning nucleotides 64–80 in exon 3 of SMIM1 (VEL*01N.01/VEL*01N.01), confirming the Vel-null phenotype. The antibody was identified as anti-Vel IgG3, reacting in tube testing, exclusively in the anti-human globulin phase. We present the first case of a Vel-null alloimmunized donor identified in Uruguay and describe the serologic, molecular, and functional characteristics of the associated antibody.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[The Rh blood group system: RHCE update]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-010</link>
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            <pubDate>Thu, 23 Jul 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[While the previous review encompassed the Rh blood group system (Chou ST, Westhoff CM. The Rh and RhAG blood group systems. Immunohematology. 2010;26:178–86), this update focusses on the RHCE gene and its variants. Four new antigens— PARG, CEVF, CEWA, and CETW (RH60 to RH63)—were reported since the last update. RHCE*cEMI (RHCE*03.31) was amended from a null allele to an allele encoding very weak antigen expression. The following topics are discussed: cross-reactive alleles [such as RHCE*ceHAR (*01.22.01) and RHCE*ceCF (*01.20.06) which may type D+ with some monoclonal anti-D reagents], issues with hybrid alleles and allele dropout, common haplotypes (association between RHCE alleles and specific RHD alleles), and clinical considerations. While the detailed description of new Rh antigens has become rare, many RHCE alleles have been reported since the previous review, a result of increased adoption of DNAbased testing for red blood cell antigens in immunohematology laboratories. The Rh blood group system has fascinated generations of immunohematologists and is likely to continue to do so for decades to come.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[How slow can you be when performing a direct antiglobulin test?]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-007</link>
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            <pubDate>Thu, 23 Jul 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[While continuous performance is preferred for any assay, trans-fusion services are particularly susceptible to interruptions that may interfere with testing. If these interruptions occur after the red blood cell (RBC) suspension is made or after the last wash is decanted, direct antiglobulin test (DAT) results may be affected. This study aimed to assess if delays at these two procedural steps compromise DAT results. Samples with positive DATs (up to 2+) using anti-IgG (IgG-DAT) were included. RBC suspensions (2–5%) were prepared from unwashed RBCs or RBCs washed once. These suspensions were used to perform tube IgGDATs without delays to obtain baseline results. IgG-DATs were repeated with delays after preparation of the RBC suspension (1, 5, 15, 30, and 60 minutes) or after the last wash decant (1, 5, 15, or 30 minutes). Three anti-IgG reagents were used: Anti-IgG (Murine Monoclonal) Gamma-clone; Werfen, Barcelona, Spain; Anti-IgG (Rabbit); QuidelOrtho, Raritan, NJ; and AHG Anti-IgG; Bio-Rad, Hercules, CA. Samples were considered impacted if their IgG-DAT strength differed by two or more reaction grades from baseline. The analysis included 25 samples. Samples with baseline IgG-DAT results of 1+s and 2+ were determined to not be impacted. Three samples were weakened by delays after RBC suspension preparation. One sample was weakened when the addition of anti-IgG was delayed. While most samples with weakly positive baseline IgG-DAT results were not impacted, the samples with the weakest baseline IgG-DAT results were impacted more frequently than those with stronger baseline IgG-DAT results. Because it is impossible to predict which samples will not be impacted by delays in these testing steps, DAT procedures should be performed with minimal interruption.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Contents]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-001</link>
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            <pubDate>Fri, 10 Apr 2026 00:00:00 GMT</pubDate>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Novel JK*01 allele with c.299C&gt;T p.(Thr100Ile) single nucleotide variant associated with loss of Jka expression in two African American donors]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-004</link>
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            <pubDate>Fri, 10 Apr 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[The JK blood group system encodes the antithetical antigens Jka and Jkb as well as Jk3.1 SLC14A1 on chromosome 18 spans approximately 28 kb and has 10 exons. The diallelic single nucleotide variant (SNV) c.838G&gt;A p.(Asp280Asn) gives rise to the antithetical antigens Jka or Jkb, respectively. At the time of this publication and including this novel allele, there are 12 JK*01 alleles encoding Jk(a+w) and 29 JK*01 null alleles, and 6 JK*02 alleles encoding Jk(b+w) and 30 JK*02 null alleles.2We describe two African American donors whose red blood cells (RBCs) tested Jk(a–b+) with polyclonal and monoclonal antisera. The RBC genotyping panel HemoID DQS (Agena Bioscience, San Diego, CA) predicted the sample to type Jk(a+b+). This discrepancy was investigated using Sanger sequencing of the coding exons and exon/intron junctions of SLC14A1.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Investigation of a neonate with blocked D phenomenon: resolving D type using serologic and molecular methods]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-002</link>
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            <pubDate>Fri, 10 Apr 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[This article addresses the diagnostic challenges encountered and resolution of a neonate with blocked D phenomenon, where maternal anti-D had masked the D sites on the neonate’s red blood cells (RBCs), initially resulting in false-negative D typing. This article emphasizes the importance of integrating serologic and molecular methods for accurate blood type determination, which is crucial for managing hemolytic disease of the fetus and newborn. A mother, whose RBCs typed as D– and with a history of D isoimmunization, gave birth to a neonate who presented with anemia and jaundice. Initial D typing revealed the neonate had D– RBCs. The mother’s blood sample tested as group B, D– with a high anti-D titer (512). The neonate’s direct antiglobulin test (DAT) was strongly positive for IgG, and eluate testing confirmed anti-D specificity, indicating that maternal anti-D was coating the neonate’s RBCs. Treatment of the neonate’s RBCs with a commercial ZZAP reagent removed bound IgG antibodies, converting the DAT to negative and revealing the neonate’s RBCs to be group B, D+, thereby resolving the initial serologic dilemma. Further polymerase chain reaction–based molecular testing of the neonate’s RBCs confirmed the D+ phenotype (R1R1), demonstrating the utility of molecular methods in complex cases.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[An update on the GE (Gerbich) blood group system]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-005</link>
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            <pubDate>Fri, 10 Apr 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[Antibodies to antigens of the GE (Gerbich) blood group system are not encountered in transfusion center blood banks on a daily basis but are regular guests at reference laboratories. In this review, we present an update on the information on GE antigens and alleles that have been published since the release of the previous system review in 2010. Additionally, information on the clinical relevance of GE antibodies for both transfusion and hemolytic disease of the fetus and newborn and recent discoveries related to functional aspects of the glycophorin C and glycophorin D proteins have been included.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Effect of long-term frozen storage on antibodies in blood samples: immunoglobulin, tetanus toxin antibody, and ABO antibody]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2026-003</link>
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            <pubDate>Fri, 10 Apr 2026 00:00:00 GMT</pubDate>
            <description><![CDATA[The Japanese Red Cross Blood Services archives donor blood samples from all donations for look-back surveys. These samples, approximately 5 million per year, are stored frozen at –30°C for 11 years and are subsequently discarded. Because such samples may also be valuable for antibody-related research and other purposes after the mandated storage period, we evaluated their potential applicability, with a particular focus on the preservation of anti- body levels. Fresh samples were compared with frozen-stored samples (–30°C for 14 years: 11 years of mandatory good manufacturing practice storage period + 3 years until measurement) for immunoglobulin levels (IgM, IgG, IgA, and IgE) as a general indicator of humoral immunity, tetanus toxin antibody titers as a long-lived vaccine-induced antibody, and ABO antibody titers (saline-direct agglutination test and saline-indirect antiglobulin test [saline-IAT]), which are factors in blood group typing and hemolytic transfusion reactions. For immunoglobulin levels, comparisons of non-paired fresh and frozen-stored samples were made from a random donor population (IgM, IgG, IgA: 105 cases each, IgE: 32 cases). For tetanus toxin antibody and ABO antibody, comparisons were conducted from the same donors with fresh and frozen-stored samples (tetanus toxin antibody: 47 cases, ABO antibody: 12 cases). No significant differences were observed in immunoglobulin levels, tetanus toxin antibody titers, or ABO antibody titers measured by the saline-direct agglutination method. Saline-IAT–measured ABO antibody titers were significantly lower in frozen-stored samples. Detailed results were as follows: (1) Median immunoglobulin levels (fresh vs. frozen-stored): IgM, 78.5 mg/dL versus 86.7 mg/dL; IgG, 1240.2 mg/dL versus 1280.2 mg/dL; IgA, 241.0 mg/dL versus 245.3 mg/dL; and IgE, 0.24 μg/mL versus 0.12 μg/mL. (2) Tetanus toxin antibody titers—geometric mean titer (GMT) (95% confidence interval [CI]): fresh 0.23 (0.12–0.43) IU/mL versus frozen-stored 0.28 (0.17–0.46) IU/mL. (3) ABO antibody titers—GMT (95% CI): saline-direct agglutination, fresh 65.4 (33.3–128.5) versus frozen-stored 51.7 (24.9–107.4); saline-IAT, fresh 391.0 (160.3–953.6) versus frozen-stored 248.7 (107.8–573.6). The evaluated immunoglobulin levels were largely preserved, suggesting that archived blood samples retain sufficient stability for antibody research. However, careful study design is necessary to minimize potential sample deterioration.]]></description>
            <category>ARTICLE</category>
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        <item>
            <title><![CDATA[Contents]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2025-015</link>
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            <pubDate>Wed, 31 Dec 2025 00:00:00 GMT</pubDate>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Cephalosporin-induced hemolytic anemia: a case study]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2025-016</link>
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            <pubDate>Wed, 31 Dec 2025 00:00:00 GMT</pubDate>
            <description><![CDATA[Drug-induced immune hemolytic anemia (DIIHA) represents a rare but dangerous medical condition that more often affects children who are administered cephalosporins. A 10-year-old girl developed severe hemolysis after administration of cefuroxime and ceftriaxone for treating an infection linked to parotid lymphangioma. The patient had previously tolerated ceftriaxone and clindamycin but developed dizziness, pallor, and tachycardia, and her hemoglobin (Hb) levels decreased from 12.9 to 2.6 g/dL during her fourth day of treatment, which led to hypovolemic shock and transient renal dysfunction. Our objective is to establish cefuroxime and ceftriaxone as the responsible drugs for DIIHA through immunohematologic testing. The laboratory tests included the direct antiglobulin test (DAT) and the indirect antiglobulin test (IAT) along with drug-dependent antibody testing using the patient’s serum (1) to react against group O red blood cells (RBCs) treated with cefuroxime and (2) to react separately against group O RBCs not treated with, but in the presence of, ceftriaxone, with and without complement, at both room temperature and by the IAT. The DAT showed positivity for IgG and C3d. The patient’s serum reacted with cefuroxime-treated RBCs by the IAT and reacted with untreated RBCs when ceftriaxone and complement were present. The laboratory results showed that drug-dependent antibodies were present to target RBCs. The patient’s condition improved rapidly after stopping cephalosporins and starting ciprofloxacin/levofloxacin and clindamycin, which resulted in an Hb increase to 9.1 g/dL within 48 hours and the absence of hemoglobinuria. This case shows why health care professionals must identify DIIHA early through diagnostic testing even when patients have shown previous tolerance to antibiotics. This case report also shows that both cefuroxime and ceftriaxone were the drugs responsible for the DIIHA.]]></description>
            <category>ARTICLE</category>
        </item>
        <item>
            <title><![CDATA[Improving transfusion outcomes in sickle cell disease through extended red blood cell molecular matching]]></title>
            <link>https://reference-global.com/article/10.2478/immunohematology-2025-017</link>
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            <pubDate>Wed, 31 Dec 2025 00:00:00 GMT</pubDate>
            <description><![CDATA[We evaluated the impact of extended red blood cell (RBC) molecular matching on alloimmunization and transf usion-related outcomes in patients with sickle cell disease (SCD) and assessed the frequency and clinical significance of genotype– phenotype discrepancies. We conducted a retrospective analysis of 108 transfused patients with SCD who underwent phenotyping and molecular genotyping for clinically relevant RBC antigens. Patients were divided into two groups: those who received extended serologically matched RBC units (n = 55) and those who received extended molecularly matched RBC units (n = 53). Primary outcomes included the rate of alloimmunization, incidence of delayed hemolytic transfusion reactions (DHTRs), and the identification of antigen mismatches or discrepancies between genotype and phenotype. Molecular testing revealed clinically significant antigen mismatches in 42 percent of patients. Partial RH alleles were identified in 17 percent of patients. Discrepancies between genotype and phenotype were observed in 21.3 percent of patients. Alloimmunized patients were significantly more likely to have undetected mismatches. DHTRs after transfusion with RBC units that were serologically matched, but not molecularly compatible, were observed in two patients. In conclusion, extended RBC molecular matching improves the detection of clinically relevant antigen mismatches not identified by routine serologic methods and is associated with a lower risk of alloimmunization and transfusion-related complications.]]></description>
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