Erythrocytapheresis for chronic transfusion therapy in sickle cell disease: survey of current practices and review of the literature.
Transfusion. 2016 Oct 19;:
Authors: Kelly S, Quirolo K, Marsh A, Neumayr L, Garcia A, Custer B
BACKGROUND: Chronic red blood cell (RBC) transfusion therapy (CTT) is an integral component of the management of severe sickle cell disease (SCD) and can prevent complications, such as stroke. RBC units can be administered via simple transfusion or exchange transfusion, and erythrocytapheresis (automated RBC exchange transfusion [aRBX]), is increasingly used for CTT. Comparisons of simple and aRBX transfusions are limited, and the current scope of aRBX use is not known.
STUDY DESIGN AND METHODS: We administered a survey to define current transfusion practices for CTT and performed a review of the erythrocytapheresis literature. The survey was disseminated to 62 SCD centers, and 31 institutions responded.
RESULTS: Collectively, 1274 of 12,644 patients (10.1%) received CCT, including 929 of 9324 children (10.0%) and 345 of 3320 adults (10.4%). The most common indication for CTT in children was a risk of stroke (86.8%), defined by abnormal transcranial Doppler, previous stroke, or abnormal brain imaging; whereas the most common indications in adults were previous stroke (37.5%) and recurrent/severe pain (29.0%). Simple transfusion was the most common method for children (480 of 919 children; 52.2%) followed by aRBX (344 of 919 children; 37.4%); whereas, in adults, aRBX was more common (180 of 345 adults; 52.2%) than simple transfusion (102 of 345 adults; 29.6%). A smaller percentage of patients received transfusion via manual exchange (7.2% of children and 16.5% of adults) or a combination of methods.
CONCLUSIONS: The current literature review was conducted to summarize reported methods, outcomes, and adverse effects with aRBX. Comparisons between chronic simple and aRBX transfusions were included when possible, and areas warranting further study are highlighted.
PMID: 27759170 [PubMed - as supplied by publisher]
Hepatitis E virus RNA in Australian blood donations.
Transfusion. 2016 Sep 25;:
Authors: Shrestha AC, Flower RL, Seed CR, Keller AJ, Harley R, Chan HT, Hoad V, Warrilow D, Northill J, Holmberg JA, Faddy HM
BACKGROUND: Hepatitis E virus (HEV) poses a risk to transfusion safety. In Australia, locally acquired HEV is rare and cases are mainly reported in travelers returning from countries endemic for HEV. The risk posed by HEV to transfusion safety in Australia is unknown; therefore, we aimed to measure the rate of current HEV infection in Australian blood donations.
STUDY DESIGN AND METHODS: A total of 14,799 blood donations were tested for HEV RNA by transcription-mediated amplification, with confirmatory testing by reverse transcription-polymerase chain reaction. Viral load quantification and phylogenetic analysis was performed on HEV RNA-positive samples.
RESULTS: One (0.0068%; 95% confidence interval [CI], 0.0002%-0.0376%) sample was confirmed positive for HEV RNA, resulting in a risk of collecting a HEV-viremic donation of 1 in 14,799 (95% CI, 1 in 584,530 to 1 in 2,657). The viral load in this sample was approximately 15,000 IU/mL, and it was determined to be Genotype 3.
DISCUSSION: Our finding of 1 in 14,799 Australian donations positive for HEV RNA is lower than that from many other developed countries; this is consistent with the relatively low seroprevalence in Australia. As this HEV RNA-positive sample was Genotype 3, it seems likely that this infection was acquired through zoonotic transmission, either within Australia or overseas in a developed nation. HEV has the potential to pose a risk to transfusion safety in Australia; however, additional, larger studies are required to quantify the magnitude of this risk.
PMID: 27667133 [PubMed - as supplied by publisher]
In a digital age, a relic of manual transfusion records.
Transfusion. 2016 Oct;56(10):2405
Authors: Allen ES, Klein HG
PMID: 27739156 [PubMed - in process]
Amotosalen and ultraviolet-A treated platelets and plasma are safe and efficacious in active hemorrhage.
Transfusion. 2016 Oct;56(10):2649-2650
Authors: Benjamin RJ, Carter KL, Corash L
PMID: 27739155 [PubMed - in process]
Immune destruction of human platelets in the NOD/scid mouse.
Transfusion. 2016 Oct;56(10):2648-2649
Authors: Bougie DW, Nayak D, Aster RH
PMID: 27739154 [PubMed - in process]
Syncope prevention in blood donors: when to do what?
Transfusion. 2016 Oct;56(10):2399-2402
Authors: Fu Q, Levine BD
PMID: 27739153 [PubMed - in process]
Red blood cell transfusion: 2016 clinical practice guidelines from AABB.
Transfusion. 2016 Oct;56(10):2627-2630
Authors: Tobian AA, Heddle NM, Wiegmann TL, Carson JL
PMID: 27739152 [PubMed - in process]
Feasibility of routine ferritin testing for donor management: validation of delayed processing and demonstration of within donor reproducibility over time.
Transfusion. 2016 Oct;56(10):2422-2425
Authors: Stone M, Brambilla D, Murcia K, Dimapasoc M, Cyrus S, Cable RG, Kiss JE, Busch MP, NHLBI Recipient Epidemiology and Donor Evaluation Study-III (REDS-III)
BACKGROUND: Understanding the effect of delayed processing of whole blood on plasma ferritin will inform the feasibility of both routine ferritin testing in donors and clinical research study design.
STUDY DESIGN AND METHODS: Whole blood tubes drawn from 16 donors were held at 4°C and centrifuged at 24-hour intervals to assess plasma ferritin concentration up to 5 days after draw. Intraindividual variation over time was measured in 21 healthy donors in blood samples collected weekly for 4 weeks and then at 12 weeks.
RESULTS: No significant variation in plasma ferritin concentration was observed in blood stored at 4°C for up to 5 days after draw (p = 0.32). The estimated loss of 4.75% ferritin over 5 days was within the reported 5% variation of the assay. Moderate intraindividual variation occurs over time in both sexes, with variability increasing with the mean. No difference was detected between men and women in the regression of standard deviation on mean ferritin (p = 0.43).
CONCLUSIONS: Ferritin is stable in whole blood up to 5 days, demonstrating operational feasibility of its use in monitoring donor iron stores. Moderate fluctuations over time occur, but ferritin measurements are sufficiently reliable to determine donor iron status on the day of donation.
PMID: 27739151 [PubMed - in process]
Autologous cryopreserved platelets to overcome immune platelet refractoriness.
Transfusion. 2016 Oct;56(10):2403-2404
Authors: Cid J
PMID: 27739150 [PubMed - in process]
Transfusion. 2016 Oct;56(10):2651
Authors: Hess JR
PMID: 27739149 [PubMed - in process]
Continuing Medical Education Program in Transfusion.
Transfusion. 2016 Oct;56(10):2477
PMID: 27739148 [PubMed - in process]
Bortezomib decreases the magnitude of a primary humoral immune response to transfused red blood cells in a murine model.
Transfusion. 2016 Oct 13;:
Authors: Natarajan P, Liu J, Santhanakrishnan M, Gibb DR, Slater LM, Hendrickson JE
BACKGROUND: Few therapeutic options currently exist to prevent or to mitigate transfusion-associated red blood cell (RBC) alloimmunization. We hypothesized that bortezomib, a proteasome inhibitor currently being utilized for HLA alloantibody and ADAMTS13 autoantibody reduction, may be beneficial in a transfusion setting. Herein, we utilized a reductionist murine model to test our hypothesis that bortezomib would decrease RBC alloimmune responses.
STUDY DESIGN AND METHODS: Wild-type mice were treated with bortezomib or saline and transfused with murine RBCs expressing the human KEL glycoprotein. Levels of anti-KEL immunoglobulins in transfusion recipients were measured by flow cytometry. The impact of bortezomib treatment on recipient plasma cells (PCs) and other immune cells was also assessed by flow cytometry and immunofluorescence.
RESULTS: After bortezomib treatment, mice had a 50% reduction in splenic white blood cells and a targeted reduction in marrow PCs. Mice treated with bortezomib before the transfusion of KEL RBCs became alloimmunized in three of three experiments, although their serum anti-KEL IgG levels were 2.6-fold lower than those in untreated mice. Once a primary antibody response was established, bortezomib treatment did not prevent an anamnestic response from occurring.
CONCLUSION: To the extent that these findings are generalizable to other RBC antigens and to humans, bortezomib monotherapy is unlikely to be of significant clinical benefit in a transfusion setting where complete prevention of alloimmunization is desirable. Given the impact on PCs, however, it remains plausible that bortezomib therapy may be beneficial for RBC alloimmunization prevention or mitigation if used in combination with other immunomodulatory therapies.
PMID: 27734515 [PubMed - as supplied by publisher]
How do we mobilize and collect autologous peripheral blood stem cells?
Transfusion. 2016 Oct 12;:
Authors: Yuan S, Wang S
Autologous stem cell transplantation (ASCT) with mobilized peripheral blood stem cells (PBSCs) has become a widely applied therapeutic approach for many hematologic and nonhematologic diseases. Adequate PBSC mobilization is critical to the success of ASCT. However, many factors can contribute to poor mobilization. Plerixafor is an effective yet costly adjunct agent that has been increasingly used to improve mobilization in a variety of diagnoses and clinical settings. However, to achieve both optimal cell collection yields and cost-effectiveness, the role of plerixafor in PBSC mobilization needs to be well defined in terms of triggers for initiating its use and criteria for monitoring response. As one of the largest hematopoietic transplant centers in the country, we have developed an approach to PBSC mobilization and collection that incorporates patient laboratory assessments, monitoring of the collection yields, and judicious use of plerixafor as well as various patient support and education programs. These measures have resulted in an increase in our collection success rate and a decrease in the mean number of collection days. In this article we describe our approach to autologous PBSC mobilization and collection. Pertinent reports in the literature are also reviewed and discussed.
PMID: 27731496 [PubMed - as supplied by publisher]
Inactivation and removal of Zika virus during manufacture of plasma-derived medicinal products.
Transfusion. 2016 Oct 12;:
Authors: Blümel J, Musso D, Teitz S, Miyabayashi T, Boller K, Schnierle BS, Baylis SA
BACKGROUND: Zika virus (ZIKV) is an emerging mosquito-borne Flavivirus of major public health concern. The potential for ZIKV transmission by blood transfusion has been demonstrated; however, inactivation or removal of ZIKV during the manufacture of plasma-derived medicinal products has not been specifically investigated.
STUDY DESIGN AND METHODS: Inactivation of ZIKV by pasteurization and solvent/detergent (S/D) treatment was investigated by spiking high-titer ZIKV stocks into human serum albumin and applying either heat or adding different mixtures of S/D reagents and assaying for infectious virus particles. Removal of ZIKV was evaluated using filters of differing pore sizes (75, 40, 35, and 19 nm), assaying for infectious virus and RNA. Electron microscopy was performed to determine the size of ZIKV particles. Neutralization of virus infectivity by immunoglobulins was investigated.
RESULTS: ZIKV was effectively and rapidly inactivated by liquid heat treatment as well as by various mixtures of S/D reagents with reduction factors more than 4 log, in each case. Effective reduction of ZIKV infectivity was demonstrated for virus filtration for filters with average pore sizes of not more than 40 nm, although a significant proportion of virus RNA was detected in the 40- to 35-nm filtrates likely due to the presence of subviral particles observed by electron microscopy. None of the immunoglobulin preparations investigated neutralized ZIKV infectivity.
CONCLUSIONS: Pasteurization and S/D treatment very rapidly inactivated ZIKV and filters with a pore size of not more than 40 nm removed all infectious ZIKV, demonstrating the effectiveness of these virus reduction strategies used during the manufacture of plasma-derived medicinal products.
PMID: 27731495 [PubMed - as supplied by publisher]