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Background: Diego[sup b] (Di[sup b]) is a high frequency red cell antigen. The formation of corresponding antibodies has been observed in Asian and American/ Mexican Indians, but rarely has caused transfusion related hemolysis or hemolytic disease of the newborn. Case report: A 50 year-old Mexican American female was admitted to the hospital for anemia and respiratory failure secondary to congestive heart failure and infection. Her past medical history was significant for multiple transfusions during prior major surgeries and she had previously produced antibodies to c, E, Jk[sup a], K, and C[sup w]. During this admission she received the first transfusion of 2 RBC units that were c, E-, Jk[sup 8]-, K-, C[sup w]-, Di[sup b]+ . The AHG cross match and antibody screen were negative. A second transfusion of 2 RBC units was given 11 days later using c-, E-, Jk[sup a]-, K-, C[sup w]-, Di[sup b]+ units when the recipient had a positive RBC antibody screen which was later shown to be due anti-Di[sup b] and C[sup w]. Her own RBC were typed as Di[sup a]- Di[sup b]+. At that time, the DAT had become positive and IgG that was eluted from circulating red cells demonstrated specificity for Di[sup b]. There was no clinical reaction or laboratory evidence of acute hemolysis. However, the hemoglobin level gradually declined from 10.8 g/dl to the pretransfusion level of 6.7 g/dl in 10 days with increased bilirubin and LDH, decreased haptoglobin, and spherocytes on the peripheral smear, but without clinical bleeding. Subsequently, and after transfusion with Di[sup b] negative blood, her DAT again became negative while the bilirubin and haptoglobin returned to normal. Conclusion: We report mild delayed hemolysis of Di[sup b]+ red cell transfusion in a patient with anti Di[sup b]. [ABSTRACT FROM AUTHOR]

Background: Red blood cells (RBCs) with the Holley-negative phenotype are historically known to be Do(a-b+[sup w]), Gy+[sup w] and Hy- but also Jo(a-) and to have a single amino acid substitution in the Dombrock glycoprotein. Joseph-negative phenotype RBCs are Do(a+[sup w]b-), Gy+, Hy+[sup w] and Jo(a-) and also have a single amino acid substitution in the Dombrock glycoprotein. The paucity of anti-Jo[sup a] has precluded extensive study of the Jo[sup a] antigen. Case study: We report an unusual anti-Jo[sup a] in a 71-year-old black female (LB) who had received multiple RBC transfusions in 1994. Her plasma reacted with a routine RBC panel by albumin IAT (2+), addition of LISS or PEG did not enhance the reaction, but with papain or ficin-treated RBCs the reaction was 2+[sup s]. LB's plasma was non reactive with 3 of 3 Hy+[sup w], Jo(a-) RBC samples and, reacted microscopically with 5 of 5 Hy- RBC samples. Adsorption/elution studies were performed using HyRBCs: the eluate was reactive (1+[sup w]) with 6 of 6 control RBCs regardless of the Do[sup a]/Do[sup b] type (making the presence of anti-Do[sup b] unlikely), it was nonreactive with 4 of 5 Hy- RBCs and with 3 of 3 Jo(a-) RBCs. One Hy- sample was microscopically reactive. The patient's RBCs typed Hy+[sup w] with two examples of anti-Hy, and Jo(a-) with the only group A anti-Jo[sup a] available. DNA analysis showed the patient to be homozygous for the JO allele, which confirmed the serologically determined Jo(a-) status. Conclusion: We conclude that the antibody made by LB is anti-Jo[sup a], even though RBCs previously considered to lack Jo[sup a] antigen reacted. We postulate that the weak reactivity detected in tests with Hy- RBCs is most likely due to low levels of Jo[sup a] antigen on these RBCs that is being detected by this anti-Jo[sup a]. This finding contradicts previously published data concerning the Jo[sup a] phenotype of Hy- RBCs but it is consistent with the predicted single amino acid changes associated with the two antigens that are only eight amino acid residues apart. [ABSTRACT FROM AUTHOR]

Background: Recently, there has been a marked increase in the use of in vitro fertilization (IVF) to treat couples for infertility. In cases where donor gametes are required, special consideration should be given to women with preexisting red cell antibodies to select donors that decrease the incidence of hemolytic disease of the newborn (HDN). Case Report: A 39 year old (G3P0) A Rh Positive (most likely R R genotype as her red cells were negative for c and E) female with a history of anti-K and anti-c became pregnant via IVF with twin embryos comprised of her spouse's sperm and anonymously donated oocytes (red cell phenotype unknown). Throughout the entire pregnancy the anti-K titer ranged between 512 and 1024 but the anti-c titer never exceeded 4. One fetus expired in utero at 12 weeks gestation. At 32 weeks gestation, the mother prematurely delivered a stillborn fetus and a viable male infant (group B Rh negative and negative for C, E, and K) with a 1+ positive direct antiglobulin test, and hemoglobin (Hb) of 12.8 gm/dL with a total bilirubin (TB) of 11.7 gm/dL. Anti-c and anti-B were detected in the eluate. One-week postpartum, his bilirubin increased to 15.0 mg/dL, and his Hb was 8.6 gm/dL with a reticulocyte count of 4.6%. A request for compatible blood was sent to a reference laboratory that confirmed the previous serologic findings on the maternal and infant samples, but upon red cell phenotyping excluded the mother as being the genetic parent. Subsequently, the referring transfusion service learned for the first time about the donation of maternal ova. The baby was transfused successfully and discharged to home but twenty-two days later required another transfusion for a Hb of 7.5 gm/dL (reticulocyte count 7.1%). His Hb increased to 11.9 gm/dL and no additional therapy was needed. Conclusions: This donor egg was selected without consulting the blood bank about potential incompatibilities between the selected donor's phenotype and the patient's antibodies. Furthermore, the blood bank was not prepared to obtain rare group O Rho negative (r'r') had it been needed urgently for intrauterine transfusion. As gamete transplantation becomes more commonplace, careful planning involving all members of the healthcare team is needed to prevent complications of HDN in these pregnancies. [ABSTRACT FROM AUTHOR]

The Combat Wound Initiative (CWI) program is a collaborative, multidisciplinary, and interservice public-private partnership that provides personalized, state-of-the-art, and complex wound care via targeted clinical and translational research. The CWI uses a bench-to-bedside approach to translational research, including the rapid development of a human extracorporeal shock wave therapy (ESWT) study in complex wounds after establishing the potential efficacy, biologic mechanisms, and safety of this treatment modality in a murine model. Additional clinical trials include the prospective use of clinical data, serum and wound biomarkers, and wound gene expression profiles to predict wound healing/failure and additional clinical patient outcomes following combat-related trauma. These clinical research data are analyzed using machine-based learning algorithms to develop predictive treatment models to guide clinical decision-making. Future CWI directions include additional clinical trials and study centers and the refinement and deployment of our genetically driven, personalized medicine initiative to provide patient-specific care across multiple medical disciplines, with an emphasis on combat casualty care.

Background: The Kell blood group system consists of 25 antigens that result from single-nucleotide polymorphisms. Most polymorphic Kell antigens reside on the N-terminal domain of Kell before the zinc-binding catalytic motif, which is the major site for endothelin-3-converting enzyme activity. Kell antigens are important in transfusion medicine owing to their strong immunogenicity, and the corresponding antibodies are clinically significant. Two probands were studied whose serum samples contained antibodies to different high-prevalence Kell antigens., Study Design and Methods: Standard hemagglutination methods were used for serologic testing of Proband 1 and Proband 2. DNA was prepared from both probands and family members. The 19 exons and the intron-exon regions of KEL from both probands were amplified by polymerase chain reaction, and the sequences were compared with that of common KEL. The identified substitutions were located on a three-dimensional model of Kell generated based on the crystal structure of neutral endopeptidase, a homolog of Kell., Results: In Proband 1, a homozygous 1988G>A mutation (Arg623Lys) in Exon 17 was present. One sibling of Proband 1 was homozygous for 1988G>A. In Proband 2, a homozygous 1033G>A mutation (Asp305Asn) in Exon 8 was present. Three siblings of Proband 2 were heterozygous for 1033G>A., Conclusion: The identified KEL mutations of the two probands are novel and inherited. The antigen absent from the red blood cells (RBCs) of Probands 1 and 2 are named KALT and KTIM, respectively. KALT is unique in that it is the only Kell antigen sensitive to treatment of RBCs by trypsin.