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"Conventional exchange transfusion"—that delivers nondescript "standard issue" units of red blood cells (RBCs)—is used worldwide to rescue dying Plasmodium falciparum (Pf) malaria patients. Recently, exchanging special malaria‐resistant RBCs (T‐REX) has been recommended to prevent random delivery of malaria‐susceptible RBCs that promote Pf infection. Fortunately, Papua New Guinea (PNG) is well positioned to help optimize exchange as "a rescue adjunct" because (a) Gerbich‐negative (GN) RBCs that resist Pf invasion are prevalent in PNG; (b) with international support, PNG has conducted outstanding malaria research; (c) PNG's scientists feel studies of GN RBCs can advance malaria therapeutics; and (d) with blood‐bank support, evaluating exchange of GN RBCs is feasible in PNG. An exchange‐transfusion study of GN RBCs might attract international sponsorship given the threat of expanding drug‐resistance as well as growing recognition that advancing transfusion medicine and expanding blood donation could especially help Pf‐infected children—immediately. [ABSTRACT FROM AUTHOR]

In kidney transplantation acute allograft rejection is the most common cause of late allograft loss. Changes in indoleamine 2,3 dioxygenase (IDO) activity, which catabolizes the degradation of tryptophan to kynurenine, may predict rejection. However, exogenous IDO is immunosuppressive in rodent kidney transplantation. Thus, the increase in IDO activity observed in acute allograft rejection is insufficient to prevent rejection. To address this question, we assessed the regulation of IDO and its role in acute rejection in a porcine model of kidney transplant. In tissue samples from rejecting kidney allografts, we showed a 13-fold increase in IDO gene transcription and 20-fold increase in IDO enzyme activity when compared with autotransplanted kidneys. Allografts also demonstrated an over fourfold increase in tissue interferon (IFN)-γ, with marked increases in tumor necrosis factor (TNF)-α, TNF-β and interleukin 1β. Gene transcription and protein levels of kynurenine 3-monooxygenase (KMO) were decreased. KMO generates the immunosuppressive kynurenine, 3-hydroxykynurenine. The results of these studies demonstrate a clear association between rejection and increased allograft IDO expression, likely driven in part by IFN-γ and facilitated by other cytokines of the allogeneic response. Moreover, the loss of downstream enzymatic activity in the IDO metabolic pathway may suggest novel mechanisms for the perpetuation of rejection. [ABSTRACT FROM AUTHOR]

Background: Acute myeloid leukemia (AML) is a malignancy characterized by rapid clonal proliferation of myeloid precursors, which can result in hyperleukocytosis. Leukapheresis can be used to rapidly reduce the white blood cell count (WBC). However, the only FDA cleared device for WBC depletion, the COBE Spectra, will no longer be supported by the manufacturer in 2017, and there are few studies comparing different methods of leukapheresis. Case report: A 68‐year‐old African American female was admitted to the hospital for relapse of her AML. Laboratory data demonstrated a WBC count of 291 600/μL and flow cytometry of the peripheral blood demonstrated 85% myeloid blasts. Leukapheresis was ordered to help treat the leukostasis. Methods: Three different apheresis protocols were used to achieve cytoreduction: Spectra Optia mononuclear collection (MNC) protocol, Spectra Optia granulocyte collection (PMN) protocol, and Therakos CELLEX buffy coat collection without return. Due to different inlet flow rates, the procedures were evaluated based on the number of WBCs collected and volume of blood processed (VBP). Results: The Spectra Optia PMN collected the most WBCs and collected nearly as many WBCs per VBP as the Therakos CELLEX, which had the highest value. Conclusion: To our knowledge, we are reporting the first use of Therakos CELLEX and Spectra Optia PMN protocol for WBC depletion. While the Spectra Optia granulocyte protocol showed the best performance for this AML patient, further studies will be needed to compare the Spectra Optia PMN protocol to the MNC protocol for AML patients. [ABSTRACT FROM AUTHOR]

Conclusions: A 32-year-old African-American woman with a history of sickle cell disease presented for surgical evaluation of left total hip arthroplasty due to avascular necrosis of the femoral head. In anticipation of a complex orthopedic procedure, pre-surgical blood work was ordered. The patient's Fenwal blood sample typed as group O, D+. Although the patient had a history of anti-Fya, the antibody identification was inconclusive, so the workup was sent to a reference laboratory. The patient was last transfused with red blood cells (RBCs) 2 years earlier, but had no history of transfusion reactions. Due to surgery, the patient's hemoglobin (Hb) decreased from 10.2 g/dL (preoperative) to 8.6 g/dL (postoperative). One unit of weakly crossmatch-incompatible Fy(a-), C-, E-, K-, and sickle cell hemoglobin S (HbS)-negative RBCs was transfused without incident, and the patient was discharged. Several days later, the reference lab reported two new specificities, anti-Joa and anti-Jkb. Fortunately, the transfused RBC unit was Jk(b-). Therefore, the crossmatch incompatibility was attributed to anti-Joa, which targets a high-prevalence antigen found in 100 percent of most populations. Two weeks after discharge, the patient returned in sickle vaso-occlusive pain crisis. The patient was clinically stable, but her Hb was 6.7 g/dL. One unit of Fy(a-), Jk(b-), C-, E-, K-, HbS- RBCs, which was weakly crossmatch-incompatible, was transfused. The following day, her Hb was unchanged, lactic acid dehydrogenase increased from 951 to 2464 U/L, potassium increased from 3.7 to 4.6 mEq/L, creatinine increased from 0.60 to 0.98 mg/dL, and the patient developed a 38.4°C fever. These findings are consistent with a delayed hemolytic transfusion reaction (DHTR), mediated by anti-Joa, occurring 2 weeks after the first RBC transfusion. Further care could not be provided because the patient left the hospital against medical advice. The purpose of this case study is to report findings consistent with a DHTR attributed to anti-Joa, an antibody with relatively unknown clinical significance.

Conclusions: Polyagglutination is a rare and underdiagnosed condition, characterized by agglutination of red blood cells(RBCs) with almost all ABO-compatible adult sera. Polyagglutination can occur when a cryptantigen is exposed on RBCs via microbial enzyme activity. Becausenearly all adults naturally produce antibodies against cryptantigens, transfusion of plasma can cause unexpected hemolysis and hematologic complications, such as thrombocytopenia and disseminated intravascular coagulation, in patients whose cryptantigens are exposed. We report a case of Glycine soja polyagglutination occurring in a 60-year-old African-American man with disseminated methicillin-resistant Staphylococcus aureus (MRSA) infection. Prior to transfusion, the patient developed severe anemia of unknown etiology. Following transfusion of 3 units of fresh frozen plasma (FFP), his RBC count could not be determined for 24 days because of RBC agglutination in his blood sample. In addition, the FFP transfusion correlated with the rapid development of severe, transfusionrefractory thrombocytopenia and anemia. The perplexed clinical team consulted the blood bank. A direct antiglobulin test demonstrated 1+ mixed-field reactivity with both monoclonal anti-IgG and anti-C3d. Lectin panel testing showed reactivity with only Glycine soja, confirming the condition. Subsequently, plasma components were avoided, and RBC and platelet (PLT) components were washed prior to transfusion. After a 44-day hospitalization involving the transfusion of 22 units of RBCs and 13 units of PLTs, the patient was discharged to a long-term care facility. The patient's confounding hematologic complications can best be explained by polyagglutination, which developed secondary to the severe MRSA infection. The FFP transfusion likely passively transferred antibodies that bound to the patient's RBC cryptantigens, leading to RBC agglutination and anemia. The development of severe thrombocytopenia may be related to cryptantigen exposure on the patient's PLTs. Although difficult to identify, polyagglutination needs to be recognized to appropriately manage hemotherapy. The purpose of this case study is to report hematologic complications following FFP transfusion in a patient with Glycine soja polyagglutination, a rarely described condition.