Platelet-specific antibodies in HLA-immunized patients receiving chronic platelet support

BACKGROUND: In HLA-alloimmunized patients, the unexpected failure of HLA-matched platelet transfusions usually raises the suspicion about concomitant platelet-specific antibodies. As the reported frequency of platelet-specific antibodies in multitransfused patients varies widely, the aim of this study was to determine the prevalence of such antibodies in a population of chronic thrombocytopenic patients with HLA antibodies. STUDY DESIGN AND METHODS: From 1985 to 1997, 11,777 determinations of HLA antibodies were performed in 1330 hematologic patients receiving chronic platelet support. Fifty-two patients with HLA alloimmunization that lasted more than 1 month were selected. The search for platelet-specific antibodies was performed by using a monoclonal antibody immobilization of platelet antigens assay, thus allowing the identification of platelet-specific antibodies directed against the platelet glycoproteins (GP) Ib/IX, GPIIb/IIIa, and GPIa/IIa. Specificity of the platelet-specific antibodies was further investigated by using a solid-phase assay with chloroquine-treated platelets. RESULTS: Only 2 (3.8%) of the 52 patients had platelet-specific antibodies. One antibody reacted with an epitope of the GPIIb/IIIa that was present in all the panel platelets, and that probably was an autoantibody. The other was an anti-HPA-5b. CONCLUSIONS: The prevalence of platelet-specific antibodies in patients with HLA alloimmunization is very small. The search for concomitant platelet-specific antibodies would be indicated only when other causes of refractoriness to HLA-matched platelets are ruled out.     

Platelet transfusion refractoriness associated with HPA-1a (Pl(A1)) alloantibody without coexistent HLA antibodies successfully treated with antigen-negative platelet transfusions

BACKGROUND: Alloimmune-mediated refractoriness to platelet transfusion is most commonly due to antibody to HLA antigens in multiply transfused or multiparous patients. Published reports of poor transfusion response due to antibodies to platelet-specific antigens are rare and often confounded by the presence of coexistent antibodies against HLA antigens. CASE REPORT: A case is presented of a multiparous woman with acute myelogenous leukemia whose sole cause of transfusion refractoriness was antibody to platelet antigen HPA-1a. She responded dramatically to HPA-1a-negative platelet transfusion. CONCLUSION: This case provides strong serologic and clinical evidence that platelet transfusion refractoriness may result from antibodies to platelet-specific antigens.     

Optimizing pretransfusion antibody detection and identification: a parallel, blinded comparison of tube PEG, solid-phase, and automated methods

BACKGROUND: The ideal pretransfusion testing strategy identifies maximal significant antibodies at minimal cost. Objectives of this study were to compare the characteristics of three testing methods and determine their optimal incorporation into the following generic testing sequence: 1) screen, for antibodies 2) if results are positive, use primary identification method, 3) if results are inconclusive, use secondary identification method. STUDY DESIGN AND METHODS: A total of 2000 consecutive, unselected, coded specimens were tested with three screening methods-PEG IAT, manual and automated solid phase red cell adherence assay (SPRCA). Of 202 positive results, 187 were of sufficient volume and were tested with both PEG and manual SPRCA identification panels, yielding 82 with significant antibodies, plus one that was negative by both methods found on retrospective review of nonstudy results. Calculations were made on the 1985 volume-sufficient specimens, simulating the possible testing permutations. RESULTS: Manual SPRCA was the most sensitive antibody screen (67/83 = 81%) and the least specific (1840/1902 = 97%); automated SPRCA was the least sensitive (54/83 = 65%) and most specific (1883/1902 = 99%); and PEG was intermediate in both sensitivity (64/83 = 77%) and specificity (1860/1902 = 98%). Of the identification panels, manual SPRCA identified more antibodies than PEG (67 versus 66) but had more inconclusive results (41 versus 20). Of overall strategies, manual SPRCA screening with either sequence of identification methods identified the most antibodies (66). The combination of PEG screen, PEG identification, and manual SPRCA identification identified slightly fewer antibodies (63) but had the lowest reagent cost, total (reagent plus labor) cost, and cost per antibody identified. The sequence of automated SPRCA screening with manual SPRCA identification, and PEG identification had the lowest hands-on time. CONCLUSIONS: The most cost-effective pretransfusion strategy is PEG screen with PEG identification, plus manual SPRCA identification when PEG identification is inconclusive.     

Evaluation of a solid phase red cell adherence technique for platelet antibody screening

Summary. Solid-phase red-cell adherence (SPRCA) techniques in platelet serology are used mainly for crossmatching. A SPRCA method for general diagnostic application was evaluated in parallel with the platelet suspension immunofluorescence test (PIFT). Of 149 patient sera sent for investigation of thrombo-cytopaenia, 76 were negative and 59 positive when studied by both methods, eight positive by PIFT only and six positive by SPRCA only. The reactivity observed for 24 sera containing HLA antibodies tested with chloroquine-treated and untreated platelets was similar for both methods. All of 14 sera containing quinine-associated antibodies reacted strongly to both techniques in the presence of added quinine. In comparison, however, whereas all sera were non-reactive to SPRCA in the absence of added quinine, and with PIFT, seven of the sera reacted weakly. Titration studies with three examples of anti-Pl^A1 and five sera containing HLA antibodies generally showed a one doubling dilution lower titre with the SPRCA procedure. End-point interpretation, however, was more readily achieved with the SPRCA method. The SPRCA technique displays similar sensitivity and specificity to the PIFT and is recommended for use by routine hospital laboratories to screen platelet antibodies.     

Heterogeneity of antibody response to human platelet transfusion.

To study the antibody response to human platelet transfusions, nine thrombocytopenia patients with bone marrow failure were given 6 U (3X10(11)) of random platelet concentrates twice a week. Before transfusion, none of the patients had preexisting antibodies detectable with lymphocytotoxicity, platelet aggregation, or capillary leukoagglutination techniques. After receiving 18-78 U of platelets, they became refractory to further transfusions of random platelets and alloantibodies were detectable. Two patterns of antibody response could be identified. In three patients, the sera were not lymphocytotoxic with a panel of standard cells in which all the known HLA antigens in the first and second series were represented at least once. Yet, they caused platelet aggregation with 30, 24, and 60%, respectively, of a donor population studied. The aggregating activities were inhibited by antihuman IgG but not by antihuman IgA or antihuman IgM antiserum. The aggregating antibodies could be absorbed out with donor platelets but not lymphocytes or granulocytes. Antibodies from two of these patients aggregated platelets of their respective siblings matched for both HLA haplotypes. Transfusion of platelets from these two siblings did not increase the platelet count while platelets obtained from aggregation-negative donors did. The sera from the remaining six patients were lymphocytotoxic with 15-100% of the panel of standard cells. They also had aggregating antibodies, which could be absorbed out by both platelets and lymphocytes, suggesting that they were HLA antibodies. These data suggest that the development of platelet-specific antibodies may play an important role in the immunological rejection of isologous platelets, and should be considered in the selection of donors for patients who are refractory to platelets from random donors.     

A national survey of transfusion‐related acute lung injury risk reduction policies for platelets and plasma in the United States

BACKGROUND: Little information exists on the specific transfusion‐related acute lung injury (TRALI) risk reduction practices used by multiple blood collecting institutions in the United States. STUDY DESIGN AND METHODS: An AABB‐appointed TRALI working group designed a set of questions about TRALI risk reduction for platelets (PLTs) and plasma. AABB member institutions were asked to respond via an Internet‐based survey during a 3‐week period in August through September 2009. RESULTS: Valid responses were received from 47 US blood centers (accounting for 1.57 million apheresis PLT units and 3.15 million whole blood–derived transfusable plasma units) and 56 hospital blood collectors. Among the blood centers, 87 and 98% had initiated some PLT and plasma risk reduction, respectively. HLA antibody testing of plateletpheresis donors was performed by 20 (43%) blood centers. There was substantial variation in the number of pregnancies (from one to more than four) that triggered testing and most centers did not screen based on a transfusion history. Almost all centers had policies to redirect HLA antibody–positive donors to whole blood donation and to potentially retest HLA antibody–negative donors. There were no blood centers performing HNA antibody testing. Sex‐based risk reduction policies for plasma included all male, or predominantly male, and never‐pregnant females; these varied by blood center, blood group, and method of plasma collection. A majority of centers indicated increased production of plasma frozen within 24 hours after phlebotomy. CONCLUSIONS: Almost 3 years after the publication of the initial AABB bulletin on this issue, TRALI risk reduction strategies are commonly employed at most US blood centers. However, procedures are not uniform.     

HLA class I-eluted platelets as an alternative to HLA-matched platelets

BACKGROUND: Alloimmunized refractory thrombocytopenic patients often require HLA-matched platelet transfusions. As the HLA system is very polymorphic, sufficient HLA-matched donors are not available for every patient. STUDY DESIGN AND METHODS: In vitro elution techniques with citric acid incubation of platelets at pH 3.0 showed that platelets lose expression of HLA, whereas platelet-specific glycoproteins are preserved. This technique was modified for clinical use. Random-donor platelet concentrates were incubated with citric acid, subsequently washed, and transfused to two patients. RESULTS: Platelet-specific glycoproteins were unaffected, and HLA expression decreased generally to below 25 percent of the initial expression. One alloimmunized patient who was without compatible donors because of a rare HLA type underwent repeated transfusions with acid-treated platelets. In contrast to the results with random-donor platelet transfusions, posttransfusion increments up to 47 × 10(9) per L were obtained with acid-treated platelets, and profuse gastrointestinal bleeding was stopped, while multiple skin hemorrhages were resolved. No side effects were observed. A second patient developed a severe transfusion reaction without platelet increment after one transfusion with acid-treated platelets expressing 30 percent of the original HLA antigens. Further transfusions were not given. CONCLUSION: Standardization of the acid elution technique and validation of the technique in patients is necessary. The results suggest, however, that HLA-eluted platelets prepared under specified conditions may gain a place in platelet transfusion therapy.     

Acute and delayed hemolytic transfusion reactions secondary to HLA alloimmunization

BACKGROUND: HLA antibodies may be directed against HLA antigens on RBCs, but these antibodies are generally not considered to be clinically significant in transfusion practice. A case of a multiparous woman who had hemolytic transfusion reactions due to HLA-related Bg antibodies is reported. CASE REPORT: A 37-year-old woman was admitted with anemia. No unexpected RBC antibodies were identified. Two group O, D+ RBC units were transfused. Ten days later she returned with hemolysis and anemia. Two more RBC units were ordered, no unexpected RBC antibodies were identified, and two crossmatch-compatible units were issued. During the transfusion, the patient developed symptoms of an acute reaction, and the posttransfusion sample showed evidence of intravascular hemolysis. RESULTS: Repeat RBC antibody screen showed anti-Bg. HLA antibody screen identified anti-HLA-A2, A28, B7, B7 cross-reactive group (CREG). The two RBC units from the first transfusion episode and one RBC unit from the second transfusion episode were HLA incompatible with the patient. No other cause for the hemolytic reactions was identified. The patient was later successfully transfused with one RBC unit from an HLA-compatible donor. CONCLUSION: HLA antibodies should be considered in patients with hemolytic transfusion reactions when RBC-specific antibodies are not found to be the etiology.     

Platelet alloantibodies in transfused patients

BACKGROUND: Patients receiving cellular blood components may form HLA antibodies and platelet-specific alloantibodies. STUDY DESIGN AND METHODS: Serum samples from a cohort of 252 patients with hematologic or oncologic diseases who are receiving cellular blood components were studied for platelet-reactive antibodies. Specificity of platelet alloantibodies was determined with a panel of typed platelets RESULTS: Platelet-reactive antibodies were detected in the sera of 113 patients (44.8% of 252), HLA antibodies in the sera of 108 (42.9%), and platelet-specific antibodies in the sera of 20 (8%). The following platelet-specific antibodies were identified: anti-HPA-5b (n = 10), anti-HPA-1b (n = 4), anti-HPA-5a (n = 2), anti-HPA-1a (n = 1), anti-HPA-2b (n = 1), anti-HPA-1b+5b (n = 1), and anti-HPA-1b+2b (n = 1). Fifteen sera from the 108 patients with anti-HLA (13.9%) contained additional platelet-specific alloantibodies, while in 5 sera, platelet-specific alloantibodies only were detected: anti-HPA-5b (n = 4) and anti-HPA-1a (n = 1). Of the 108 sera with HLA antibodies, 29 (26.9%) showed discordant results when studied with the lymphocytotoxicity test and the glycoprotein-specific immunoassay. Ten sera contained panreactive antibodies against platelet glycoproteins (GP) IIb/IIIa, GPIa/IIa, and/or GPIb/IX. Alloimmunization occurred in 58.3 percent of female patients with previous pregnancies, but in only 23.3 percent of those without previous pregnancies (p = 0.0049). CONCLUSION: Platelet alloantibody specificities in transfused patients (predominantly anti-HPA-5b and -1b with antigen frequencies <30% among whites) differ significantly from those observed in patients with neonatal alloimmune thrombocytopenia or posttransfusion purpura, in whom anti-HPA-1a (antigen frequency >95%) is the most prevalent specificity. HLA antibody detection yields discordant results when the lymphocytotoxicity assay and a glycoprotein-specific immunoglobulin-binding assay are used.     

A fully automated blood typing system for hospital transfusion services. ABS2000 Study Group

BACKGROUND: The results of routine blood bank testing by a fully automated blood typing system (ABS2000) were compared with those obtained by standard manual methods in six hospital transfusion services. STUDY DESIGN AND METHODS: The ABS2000 system uses microtiter plates for determining ABO and D types, solid-phase red cell adherence (SPRCA) assays for antibody detection, and modified SPRCA plates for IgG crossmatches. The transfusion services used their standard manual test tube methods. RESULTS: Of 3779 donors' samples tested for ABO types (red cell typings only), 3.0 percent could not be interpreted by the ABS2000 system's neural network, because of clots, hemolysis, or lipemic samples. The results for ABO types were concordant for 99.8 percent of the remaining samples. Of 3779 donors' samples tested for D types, the results were concordant for 98.7 percent. Of 7580 patients' samples tested for ABO types (red cell and plasma typings), 5.8 percent could not be interpreted by the ABS2000 system. There was 100-percent concordance of ABO typing results for the remaining 7140 samples. There was 99. 7-percent concordance of results for patients' D types. The results of 96.7 percent of antibody detection tests and 98.8 percent of crossmatches were concordant. Neither method failed to detect a serologically incompatible crossmatch that was associated with a specific, clinically significant alloantibody. The ABS2000 system performed 45 confirmatory donor ABO and D types in 115 minutes, 22 antibody detection tests in 116 minutes, 16 patients' ABO/D types in 149 minutes, and 40 crossmatches in 140 minutes. CONCLUSION: The ABS2000 blood typing system automates routine blood bank tests with accuracy comparable to that of hospital transfusion services' standard manual methods.     

Prevalence of HLA antibodies in remotely transfused or alloexposed volunteer blood donors

BACKGROUND: HLA antibody testing of previously transfused or pregnant donors may help reduce the risk of transfusion‐related acute lung injury (TRALI). However, the prevalence of HLA antibodies in transfused donors has not been well characterized. STUDY DESIGN AND METHODS: Transfusion and pregnancy history was obtained from consenting donors. HLA Class I and II antibody testing was performed by multiantigen bead Luminex platform. Cutoff values for Class I and II antibodies used normalized background ratios of 10.8 and 6.9, respectively. Linear probability models were used to evaluate potential associations between HLA alloimmunization and donor characteristics. RESULTS: A total of 7920 donors (2086 males and 5834 females) were tested. HLA antibody prevalence did not significantly differ between 895 transfused (1.7%) and 1138 nontransfused males (1.0%; odds ratio [OR], 1.75; 95% confidence interval [CI], 0.80‐3.82]. Prevalence in 45 transfused nulliparous females (4.4%; 95% CI, 0.1%‐11.8%) was not different from the 1.6% prevalence in 1732 nontransfused nulliparous females (OR, 2.94; 95% CI, 0.68‐12.74). Transfused parous females had higher prevalence than nontransfused counterparts (p = 0.004; OR, 1.39; 95% CI, 1.07‐1.80). In a linear probability model, the estimated additive risk of transfusion‐induced alloimmunization was only 0.8% (95% CI, ?0.2% to 1.8%; p = 0.10). Donor transfusion history showed that 58% of transfusions occurred more than 10 years previously. CONCLUSION: Transfused volunteer blood donors do not appear to have a significantly higher prevalence of HLA antibodies than their nontransfused counterparts. Thus, in an effort to reduce TRALI risk, ascertaining past history of transfusion and testing these donors for HLA antibodies is not necessary.     

肿瘤患者血小板相关抗体分析

目的分析肿瘤患者血小板相关抗体产生规律及临床意义,探寻肿瘤患者临床血小板输注无效对策。方法先用ELISA方法QUIKSCREEN试剂筛查反复输注血小板3次以上肿瘤患者的HLA IgG抗体,再将初筛阳性样本用PAKPLUS试剂确定HLA、HPA抗体,同时观察抗体阳性患者临床症状并判断输注疗效。结果116份样本中筛查出HLA IgG抗体44例,抗体阳性率37.93%。初筛阳性样本经检测确认HLA抗体18例,HPA抗体8例,未能确认8例,其中HPA抗体及HLA抗体同时阳性10例。抗体阳性率与血小板输注次数成正相关(P<0.01),且与输注效果之间的相关性有统计学意义(P<0.01)。结论肿瘤患者血小板抗体阳性率与血小板输注次数相关,且与输注效果有关。     

Platelet transfusion refractoriness associated with two rare platelet- specific alloantibodies (anti-Baka and anti-PlA2) and multiple HLA antibodies

A 65-year-old patient with pancytopenia resulting from osteomyelosclerosis became refractory to platelet transfusions during long-time transfusion support. He developed two rare, platelet-specific antibodies (anti-PlA2 and -Baka) disguised by strong, multispecific HLA antibodies. The specificity of the platelet-specific antibodies was detected by a newly designed enzyme-linked immunosorbent assay using glycoprotein-specific monoclonal antibodies for immobilization of platelet antigens.     

Screening plateletpheresis donors for HLA antibodies on two high‐throughput platforms and correlation with recipient outcome

BACKGROUND: To determine the prevalence and impact of transfusing plasma containing white blood cell antibodies, we compared two high‐throughput HLA antibody screening assays and prospectively examined the medical records of all platelet (PLT) recipients to detect subtle manifestations of transfusion‐related acute lung injury and other transfusion reactions. STUDY DESIGN AND METHODS: Serum samples from 136 plateletpheresis donors were tested for HLA Class I and II antibodies using microbead (LABScreen PRA, One Lambda) and microchip (Dynachip, Invitrogen) assays. Electronic medical records of all recipients were reviewed for vital signs and nursing documentation before and after transfusion. RESULTS: In the microchip assay with a cutoff value of 0.25, 2.9% of samples were positive for Class I and 8.9% for Class II antibodies; with a cutoff value of 0.1, the results were 14.9 and 21.6%, respectively. In the microbead assay (normalized background ratio, 1.5), 15% were positive for Class I and 21% for Class II antibodies. The prevalence of HLA antibodies was 17% in donors without pregnancy or transfusion history and 47% in donors with such history. The PLTs were transfused in 265 episodes to 67 patients. There were no reported reactions; however, symptoms or vital sign changes were noted in seven transfusion episodes. The incidence of reactions was 2.7% (2/75) for antibody‐positive units and 2.6% (5/190) for antibody‐negative units. CONCLUSIONS: Microbead and microchip assays yielded similar results. The prevalence of HLA antibodies was greater in donors with a history of pregnancy or transfusion, but no increase in the incidence of transfusion reactions was noted in recipients of components from donors with HLA antibodies.     

Prevalence of HLA antibodies in transfused patients with and without red cell antibodies

BACKGROUND: Multiply transfused patients are at increased risk of developing red cell (RBC) antibodies, as well as antibodies to HLA. Although pretransfusion testing screens for RBC antibodies, no such testing is routinely performed for HLA antibodies. Determining which patients are more likely to make HLA antibodies may be important for patients undergoing elective surgery where platelets (PLTs) may be required. It is hypothesized that patients with RBC alloantibodies may be more likely to have HLA antibodies than previously transfused patients without RBC antibodies. STUDY DESIGN AND METHODS: Blood was collected from 53 adult male surgical patients with RBC alloantibodies and a control group of 69 similar male patients with a history of previous transfusions but no evidence of RBC alloimmunization. The samples were tested for the presence of immunoglobulin G Class I HLA antibodies by enzyme-linked immunosorbent assay. RESULTS: Of the 53 samples from patients with RBC alloantibodies, 12 (22.6%) also had HLA antibodies, whereas only 7 (10.1%) of the 69 patients in the control group had HLA antibodies (p < 0.03). CONCLUSIONS: There is a significant difference between the rates of HLA alloimmunization in male patients with RBC antibodies versus multiply transfused patients without RBC antibodies. Screening for HLA antibodies may be warranted in patients with RBC alloantibodies who might require PLT transfusion support for elective surgery.     

The effect of previous pregnancy and transfusion on HLA alloimmunization in blood donors: implications for a transfusion-related acute lung injury risk reduction strategy

BACKGROUND: Antibodies to human leukocyte antigens (HLA) in donated blood have been implicated as a cause of transfusion-related acute lung injury (TRALI). A potential measure to reduce the risk of TRALI includes screening plateletpheresis donors for HLA antibodies. The prevalence of HLA antibodies and their relationship to previous transfusion or pregnancy in blood donors was determined.
STUDY DESIGN AND METHODS: A total of 8171 volunteer blood donors were prospectively recruited by six US blood centers from December 2006 to May 2007. Donors provided a detailed history of pregnancy and transfusion and a sample for HLA Class I and II antibody testing by multiantigen bead flow analysis.
RESULTS: A total of 8171 donors were enrolled; 7920 (96.9%) had valid HLA antibody test results and 7841 (99%) of those had complete pregnancy and transfusion information. The prevalence of any HLA antibody was similar in nontransfused (n = 1138) and transfused (n = 895) men, 1.0% versus 1.7% (p = 0.16). HLA antibodies were detected in 17.3% of all female donors (n = 5834) and in 24.4% of those with a history of previous pregnancy (n = 3992). The prevalence of HLA antibodies increased in women with greater numbers of pregnancy: 1.7% (zero), 11.2% (one), 22.5% (two), 27.5% (three), and 32.2% (four or more pregnancies; p < 0.0001).
CONCLUSION: HLA Class I and Class II antibodies are detectable at low prevalence in male donors regardless of transfusion and in female donors without known immunizing events. The prevalence of HLA antibodies increases significantly with more pregnancies. These data will allow blood centers to estimate the impact of HLA antibody testing as a potential TRALI risk reduction measure.     

Post-transfusion alloimmunization to granulocytes and platelets in Japanese patients as determined by the MPHA method

The current occurrence of alloimmunization to granulocytes and platelets after blood transfusion is unclear due to the fact that antibody assays are cumbersome. Using the MPHA method with extracted granulocyte and platelet antigens, a randomized, blinded trial was conducted to investigate three types of alloantibodies in 431 Japanese patients receiving leukocyte-depleted blood transfusions prepared with or without our latest leukocyte-reduction filter. The frequency of granulocyte, platelet and HLA class I alloantibodies was 0.44%, 0.44% and 16.74%, respectively, in patients receiving non-filtered products and 0%, 0% and 0.49%, respectively, in patients receiving filtered products. The granulocyte antibody reacted with an antigen approximately of 51 KDa. The platelet-specific alloantibody was associated with GPIIb/IIIa and GPIa/IIa. The important factors affecting alloimmunization were the transfusion dose and the use of unfiltered platelet products.     

IMMUNOHEMATOLOGY: Identification and evaluation of false‐negative antibody screens

Background: Non‐ABO alloantibodies are frequently implicated in hemolytic transfusion reactions and are a leading cause of transfusion‐related mortality. Detection of clinically significant non‐ABO alloantibodies is reliant on an antibody screen, which is prone to clerical, technical, and reagent error. Data on the frequency of false‐negative antibody screens due to the occurrence of these errors are scarce, and the true incidence of false‐negative antibody screens in everyday practice is unknown. STUDY DESIGN AND METHODS: Monitoring for false‐negative antibody screens is routinely performed in our institution. All cases of false‐negative antibody screens involving clinically significant antibodies were identified through review of the blood bank quality assurance records from 2004 to 2007. The clinical impact was recorded in each case. RESULTS: Twenty‐one cases of false‐negative antibody screens due to clinically significant antibodies were detected. Sources of error included testing error (12 cases), reagent red blood cell (RBC) failure (one case), and reagent limitations (one case). The cause of error was inconclusive in seven cases. Nine patients were found to have received antigen‐incompatible blood as a consequence of these errors, resulting in a single nonfatal hemolytic transfusion reaction. CONCLUSIONS: The identification and investigation of false‐negative antibody screens is a valuable quality assurance measure which can serve to monitor staff performance, identify cases of reagent RBC failure, and identify patients who have received antigen‐incompatible blood at risk for hemolytic transfusion reactions.     

Transfusion-related acute lung injury caused by an NB2 granulocyte- specific antibody in a patient with thrombotic thrombocytopenic purpura

HLA and granulocyte-specific antibodies have been implicated in the production of transfusion-related acute lung injury (TRALI). Reported here is a case that suggests that the patient's preexisting condition may play an important role in determining whether TRALI develops upon transfusion of blood products containing anti-white cell (WBC) antibodies. A 29-year-old woman with thrombotic thrombocytopenic purpura (TTP) underwent an uneventful 1.5-volume plasma exchange, which was followed by the transfusion of 2 red cell (RBC) units. At the end of the second RBC transfusion, the patient developed clinical signs and symptoms of noncardiogenic pulmonary edema. Serologic studies demonstrated that the serum from the second RBC donor had no HLA antibodies but did have a granulocyte-specific antibody (anti-NB2) that caused the agglutination of the recipient's granulocytes, which were NB2 positive. Serum from the donor of the first RBC unit and serum from the donors of units used in the exchange had no HLA or granulocyte-specific antibodies that reacted with the recipient's WBCs. Because the donor implicated in this reaction had a history of 21 blood donations, none of which had been associated with a transfusion reaction, we suggest that the patient's preexisting condition played a significant role in this episode of TRALI, owing to the granulocyte-specific antibody.     

Nomifensine-induced immune hemolytic anemia and posttransfusion purpura in the same patient

A 53-year-old white woman had severe hemolytic anemia while taking nomifensine. A drop of hemoglobin to 61 g per I prompted the transfusion of two units of packed red cells. Nine days later, severe thrombocytopenia with multiple petechiae ensued. Both hemolysis and thrombocytopenia resolved promptly upon withdrawal of the drug and short-term prednisolone treatment. Serologic studies showed nomifensine-dependent, metabolite-specific red cell antibodies as the cause of immune-mediated hemolysis and, in serum samples obtained after purpura, strong platelet-specific PlA1 and weak HLA antibodies suggested a diagnosis of posttransfusion purpura.