A Caucasian JK*A/JK*B woman with Jk(a+b–) red blood cells, anti-Jkb, and a novel JK*B allele c.1038delG

Glenn Ramsey/ Ricardo D. Sumugod/ Paul F. Lindholm/ Jules G. Zinni/ Jessica A. Keller/ Trina Horn/ Margaret A. Keller

The Kidd blood group on the red blood cell (RBC) glycoprotein urea transporter-B has a growing number of weak and null alleles in its gene SLC14A1 that are emerging from more widespread genotyping of blood donors and patients. We investigated a 64-year-old Caucasian woman of Polish-Czech descent who developed anti-Jkb detected in solid-phase RBC adherence testing within 12 days after 7 units of RBCs were transfused. Her RBCs subsequently typed Jk(a+b–) by licensed reagents and human antisera. Ne(..)

DOI: 10.21307/immunohematology-2019-051

How to recognize and resolve reagentdependent reactivity: a review

Gavin C. Patch/ Charles F. Hutchinson/ Nancy A. Lang/ Ghada Khalife

Reagent-dependent reactivity can be described as agglutination of red blood cells (RBCs) in serologic testing that is not related to the interaction of RBC antigens and antibodies that the test system is intended to detect. In other words, reagent-dependent reactivity results in false-positive agglutination reactions in serologic testing. These false-positive reactions can cause confusion in antigen typing and RBC antibody detection and identification procedures, and may result in delays in pati(..)

DOI: 10.21307/immunohematology-2019-052

The Augustine blood group system, 48 years in the making

Geoffrey Daniels

The high-prevalence antigen, Ata, was first identified in 1967, but it was not until 2015 that Ata became AUG1 of a new blood group system, Augustine (AUG). The new system was established after the identification of the gene encoding Ata and the recognition of a null phenotype (AUG:–1,–2) in an At(a–) patient with an antibody (anti-AUG2) reactive with At(a–) red blood cells. The At(a–) phenotype is very rare and, with the exception of the one family with the null phenotype, has only been found i(..)

DOI: 10.21307/immunohematology-2019-053

Autoanti-C in a patient with primary sclerosing cholangitis and autoimmune hemolytic anemia: a rare presentation

Meenu Bajpai/ Ashish Maheshwari/ Shruti Gupta/ Chhagan Bihari

Primary sclerosing cholangitis (PSC) is rarely associated with autoimmune hemolytic anemia (AIHA), and the presence of  specific autoantibodies has not been reported previously. We present a unique case report of PSC associated with AIHA implicating autoanti-C. A 17-year-old girl was admitted to our hospital with PSC along with AIHA. Her blood sample demonstrated a positive direct antiglobulin test and a positive autocontrol in the antihuman globulin phase, confirming the patient had warm-reacti(..)

DOI: 10.21307/immunohematology-2019-054

Laboratory management of perinatal patients with apparently “new” anti-D

Judith L. Hannon/ Gwen Clarke

Despite the existence of long-standing, well-organized programs for Rh immune globulin (RhIG) prophylaxis, immune anti-D continues to be detected in the D– perinatal population. Between 2006 and 2008, 91 prenatal patients, found to have a previously unidentified anti-D, were followed up with a survey to their treating physician and with additional serologic testing where possible. The physician survey requested pregnancy and RhIG history information, including recent or distant potential alloimm(..)

DOI: 10.21307/immunohematology-2019-055

The H blood group system

Erwin Andreas Scharberg/ Coral Olsen/ Peter Bugert

The H blood group system, ISBT symbol H (018), consists of a single antigen (H) defined by a terminal fucose residue found on red blood cells and in secretions formed by the action of α-1,2-fucosyltransferases 1 (α2FucT1) and 2 (α2FucT2), respectively. Mutant alleles of the corresponding FUT1 and FUT2 genes result in either a H– phenotype (Bombay phenotype, Oh) or a weak H phenotype (para-Bombay, H+w). In addition, the FUT2 gene is the molecular basis of the secretor (Se) status, and homozygosit(..)

DOI: 10.21307/immunohematology-2019-056

Mary Harrell McGinniss, BB(ASCP), 1925–2016

DOI: 10.21307/immunohematology-2019-057