• Select Article Type
  • Abstract Supplements
  • Blood Group Review
  • Call to Arms
  • Hypothesis
  • In Memoriam
  • Interview
  • Introduction
  • Letter to the Editor
  • Short Report
  • abstract
  • Abstracts
  • Article
  • book-review
  • case-report
  • case-study
  • Clinical Practice
  • Commentary
  • Conference Presentation
  • conference-report
  • congress-report
  • Correction
  • critical-appraisal
  • Editorial
  • Editorial Comment
  • Erratum
  • Events
  • Letter
  • Letter to Editor
  • mini-review
  • minireview
  • News
  • non-scientific
  • Obituary
  • original-paper
  • original-report
  • Original Research
  • Pictorial Review
  • Position Paper
  • Practice Report
  • Preface
  • Preliminary report
  • Product Review
  • rapid-communication
  • Report
  • research-article
  • Research Communicate
  • research-paper
  • Research Report
  • Review
  • review -article
  • review-article
  • review-paper
  • Review Paper
  • Sampling Methods
  • Scientific Commentary
  • short-communication
  • short-report
  • Student Essay
  • Varia
  • Welome
  • Select Journal
  • Immunohematology


Article | 15-April-2020

Update on HDFN: new information on long-standing controversies

Hemolytic disease of the fetus and newborn (HDFN) results from maternal IgG antibodies that cross the placenta to the fetal circulation during gestation and cause RBC destruction and complications before birth (HDF), or anemia and hyperbilirubinemia after birth (HDN), or both. In its most severe form,HDF produces hydrops fetalis,which is characterized by total body edema,hepatosplenomegaly,and heart failure and can lead to intrauterine death. Before discovery of Rh immunoglobulin (RhIG), HDFN

Anne F. Eder

Immunohematology, Volume 22 , ISSUE 4, 188–195

original-report | 25-June-2021

Statistical model for prediction of ABO hemolytic disease of the fetus and newborn in India

In recent years, clinical and public health efforts, such as red blood cell antibody screening of all pregnant women and administration of Rh immune globulin (RhIG) in developed countries, have reduced the burden of Rh hemolytic disease of the fetus and newborn (HDFN), ultimately resulting in ABO HDFN as the most common cause of immune HDFN. Approximately 15–25 percent of feto-maternal pairs are ABO incompatible (blood group O mother with non–group O neonate), of which 10–15 percent of neonates

D.S. Patale, T.L. Lokhande, R.K. Chaudhary

Immunohematology, Volume 37 , ISSUE 2, 64–68

Case report | 26-October-2019

Severe hemolytic disease of the fetus and newborn due to anti-C+G

Anti-G is commonly present with anti-D and/or anti-C and can confuse serological investigations. In general, anti-G is not considered a likely cause of severe hemolytic disease of the fetus and newborn (HDFN), but it is important to differentiate it from anti-D in women who should be administered anti-D immunoglobulin prophylaxis. We report one woman with three pregnancies severely affected by anti-C+G requiring intrauterine treatment and a review of the literature. In our case, the

Riina Jernman, Vedran Stefanovic, Anu Korhonen, Katri Haimila, Inna Sareneva, Kati Sulin, Malla Kuosmanen, Susanna Sainio

Immunohematology, Volume 31 , ISSUE 3, 123–127

Article | 17-February-2021

Severe hemolytic disease of the fetus and newborn due to anti-E and anti-Jka

Red blood cell (RBC) alloimmunization to antigens other than D, such as C, c, E, e, and antigens in the Kell, MNS, and Duffy blood group systems, has emerged as an important cause of hemolytic disease of the fetus and newborn (HDFN).1 Antibody screening for these antibodies is not routinely practiced for all antenatal patients in developing countries, mainly because of financial constraints. We report a case of HDFN in a female baby due to maternal alloimmunization against Rh and Kidd blood

S. Mandal, S. Malhotra, G. Negi, A. Tiwari, S. Mitra, S. Basu, P. Singh

Immunohematology, Volume 36 , ISSUE 2, 60–63

Report | 01-December-2019

Prevalence of clinically significant red blood cell alloantibodies in pregnant women at a large tertiary-care facility

More than 50 red blood cell (RBC) alloantibodies are known to cause hemolytic disease of the fetus and newborn (HDFN). Although Rh immune globulin (RhIG) prophylaxis has significantly reduced the incidence of pregnancies complicated by anti-D, the need to detect and monitor maternal alloantibodies capable of causing HDFN is still a concern. The prevalence and specificity of these alloantibodies were determined. In this retrospective study, the prevalence and specificities of unexpected RBC

Heather M. Smith, Rosetta S. Shirey, Sandra K. Thoman, Jay B. Jackson

Immunohematology, Volume 29 , ISSUE 4, 127–130

Report | 14-March-2020

Absence of hemolytic disease of fetus and newborn despite maternal high-titer IgG anti-Ku

Anti-Ku seen in K0 (Kell-null) individuals has previously been shown to cause severe hemolytic transfusion reactions. Maternal anti-Ku can cause none or moderate to severe hemolytic disease of the fetus and newborn (HDFN). In two of four previously described HDFN cases, intrauterine transfusions were required because of severe anemia. We report a case in which maternal anti-Ku did not cause HDFN. Standard serologic methods were used for RBC antibody screening and identification, adsorption and

Ram M. Kakaiya, Angelica Whaley, Christine Howard-Menk, Jigna Rami, Mona Papari, Sally Campbell-Lee, Zbigniew Malecki

Immunohematology, Volume 26 , ISSUE 3, 119–122

Case report | 01-December-2019

Possible suppression of fetal erythropoiesis by the Kell blood group antibody anti-Kpa

Antibodies to antigens in the Kell blood group system are usually immunoglobulin G, and, notoriously, anti-K, anti-k, and anti-Kpa can cause severe hemolytic transfusion reactions, as well as severe hemolytic disease of the fetus and newborn (HDFN). It has been shown that the titer of anti-K does not correlate with the severity of HDFN because, in addition to immune destruction of red blood cells (RBCs), anti-K causes suppression of erythropoiesis in the fetus, which can result in severe anemia

Michelle Tuson, Kim Hue-Roye, Karen Koval, Sherwin Imlay, Rajendra Desai, Gayatri Garg, Esam Kazem, Diane Stockman, Janis S. Hamilton, Marion E. Reid

Immunohematology, Volume 27 , ISSUE 2, 58–60

Case report | 01-December-2019

Hemolytic disease of the fetus and newborn owing to anti-U, successfully treated with repeated intrauterine transfusions

Hemolytic disease of the fetus and newborn (HDFN) owing to anti-U has rarely been reported. U is part of the MNS system. M and N glycoproteins are located on glycophorin A (GPA); S and s antigens are on glycophorin B (GPB). Individuals who lack GPB are S– and s– and also lack U. The U– phenotype occurs almost exclusively in the African population and has a very low frequency (0.25%). Anti-U is of immunoglobulin G class and can cause hemolytic transfusion reaction and HDFN. In

Johanna Strindberg, Joachim Lundahl, Gunilla Ajne

Immunohematology, Volume 29 , ISSUE 2, 51–54

Article | 17-February-2021

K antigens on neonatal red blood cells blocked by anti-K with titer of 32

Hemolytic disease of the fetus and newborn (HDFN) is one of the serious causes of perinatal morbidity and mortality. It occurs because of a difference in red blood cell (RBC) antigens between the mother and fetus. The mother is alloimmunized during pregnancy or after blood transfusion. The mother’s antibodies, when of the IgG class, enter the placental circulation, bind to fetal antigens on the RBC surface, and cause hemolysis and/or anemia as a consequence of erythropoiesis suppression. The

J. Novoselac, M. Raos, G. Tomac, M. Lukić, B. Golubić Ćepulić

Immunohematology, Volume 36 , ISSUE 2, 54–57

Case report | 09-October-2019

Two cases of the variant RHD*DAU5 allele associated with maternal alloanti-D  

(HDFN) as D alloimmunization can occur with some D variants. Here, we describe two cases of the RHD*DAU5 allele associated with maternal alloanti-D in patients of African ancestry. Two obstetric patients were initially serologically classified as D+ with negative antibody detection tests on routine prenatal testing. Repeat testing at delivery identified anti-D in both patients with no history of RhIG administration or transfusion. DNA sequencing revealed that both patients possessed the RHD*DAU5

Jennifer A. Duncan, Susan Nahirniak, Rodrigo Onell, Gwen Clarke

Immunohematology, Volume 33 , ISSUE 2, 60–63

Case report | 16-October-2019

Management of pregnancy sensitized with anti-Inb with monocyte monolayer assay and maternal blood donation

Maternal red blood cell (RBC) alloantibodies can cause hemolytic disease of the fetus and newborn (HDFN). Although much is described about common antibodies associated with HDFN, management of a pregnancy complicated by a maternal rare antibody presents several challenges related to assessment of fetal anemia risk, availability of blood for transfusion to the mother and/or the fetus or newborn if needed, and planning for delivery in the case of maternal hemorrhage. Here we report the laboratory

Raj Shree, Kimberly K. Ma, Lay See Er, Meghan Delaney

Immunohematology, Volume 34 , ISSUE 1, 7–10

Review | 12-March-2020

The Gerbich blood group system: a review

]). GPC and GPD interact with protein 4.1R, contributing stability to the RBC membrane. Reduced levels of GPC and GPD are associated with hereditary elliptocytosis, and Gerbich antigens act as receptors for the malarial parasite Plasmodium falciparum. Anti-Ge2 and anti-Ge3 have caused hemolytic transfusion reactions, and anti-Ge3 has produced hemolytic disease of the fetus and newborn (HDFN).

Phyllis S. Walker, Marion E. Reid

Immunohematology, Volume 26 , ISSUE 2, 60–65

Article | 15-February-2021

Heat elution: a modification of the Landsteiner-Miller method

alloantibodies, due to drug-induced antibodies, or in the investigation of hemolytic disease of the fetus and newborn (HDFN).7 They may also be used in combination with in vitro adsorption studies to identify weakly expressed blood group antigens and for the identification of multiple alloantibodies. Indications for heat elution include: Investigation of ABO HDFN. Elution is rarely required, however, because the diagnosis is generally made from clinical findings consistent with HDFN in an ABO-incompatible

C. Dean-El, N. Quraishy

Immunohematology, Volume 35 , ISSUE 2, 45–47

Article | 16-February-2021


presence of high-titer ABO antibodies should be considered. Non-identical ABO group plasma components with high-titer anti-A and/or anti-B should only be given to group O recipients. Despite clinical significance in transfusion, hemolytic disease of the fetus and newborn (HDFN) due to ABO antibodies is rare. Most ABO antibodies cannot cross the placenta because they are IgM and IgG2. The ABO antigens are also present on tissues and within secretions of the fetus, preventing the antibodies from binding

N.M. Thornton, S.P. Grimsley

Immunohematology, Volume 35 , ISSUE 3, 95–101

Article | 17-February-2021

Identifying obstetrics patients in whom RHD genotyping can be used to assess risk of D alloimmunization

directed at RBCs expressing the D antigen containing the missing epitope. Alloimmunization can occur via blood transfusion or pregnancy. The significance of D in pregnant women and in women of childbearing potential is well appreciated in the obstetrics community.4,5 Maternal alloanti-D can cause mild to severe hemolytic disease of the fetus and newborn (HDFN).6–8 Importantly, some partial D phenotypes may present with a serologic weak D phenotype, a fact that causes confusion based on the terminology

T.N. Horn, J. Keller, M.A. Keller, L. Klinger

Immunohematology, Volume 36 , ISSUE 4, 146–151

case-report | 25-June-2021

Severe perinatal hemolytic disease due to anti-e

Hemolytic disease of the fetus and newborn (HDFN) is an alloimmune condition in which shortened survival of the red blood cells (RBCs) of the fetus or the newborn is caused by maternal antibodies passing through the placenta and binding to the corresponding antigen on the fetal RBCs. The pathogenesis of HDFN is based on a blood group incompatibility between the mother and fetus, where the fetal RBCs have antigens of paternal origin that are lacking on the mother’s RBCs. If the mother has an

G. Soler-Noda, Y. Romero-Díaz, L. Orbeal-Aldama, S. Aquino-Rojas

Immunohematology, Volume 37 , ISSUE 2, 72–77

No Record Found..
Page Actions