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PubMed2002

Acute haemolytic transfusion reactions due to weak antibodies that in vitro did not seem to be clinically significant.

BACKGROUND AND OBJECTIVES: In the present article, we report on two patients with acute haemolytic transfusion reactions (AHTRs), and whom we were unable to transfuse, owing to alloantibodies that in vitro did not seem to be clinically significant. MATERIALS AND METHODS: The patients were a 67-year-old male and a 64-year-old female, both of whom developed antibodies to red blood cells (RBCs) after repeat blood transfusions. Serological analyses were carried out using standard techniques. RESULTS: Both patients developed an AHTR of the intravascular type following blood transfusions. Serological re-examination revealed weakly reactive alloantibodies with anti-JMH specificity in one patient, and with unclear specificity in the second. Rechallenging the patients with 15-30 ml of packed RBCs caused AHTRs, and blood transfusion became impossible in both cases. CONCLUSION: Weak alloantibodies that in vitro do not seem to be clinically significant may cause severe AHTRs.

Acute Disease↗
PubMed1996

Delayed hemolytic transfusion reaction due to anti-Go(a), an antibody against the low-prevalence Gonzales antigen.

Go(a) (D(Cor)) is a low-frequency antigen in the Rh system found on red cells lacking part of the D mosaic (category IVa). Anti-Go(a) has not been previously reported to cause hemolytic transfusion reactions. A 27-year-old African American male with sickle-cell disease, maintained on chronic transfusion, was noted to have dark plasma during an erythrocytapheresis, procedure, and the pretransfusion hemoglobin was noted to be 1 g/dl lower than 4 weeks before (with hyperbilirubinemia and a significantly increased LDH). Polyspecific direct antiglobulin test (DAT) was weakly positive (C3-weak, IgG-weak), and indirect antiglobulin tests (IATs) performed on the serum (pre- and posttransfusion reaction) and a red blood cell (RBC) eluate from the postreaction sample were negative. A segment from one of the four implicated units from the prior month's transfusion was strongly reactive at 37 degrees C and using anti-human globulin (AHG) when crossmatched with the postreaction serum and the eluate. The postreaction serum, screened with a panel of red cells positive for low-prevalence antigens, reacted with three Go(a+) cells. The implicated unit was reactive with a previously identified anti-Go(a) serum.

Adult↗
PubMed1997

Are cytokines in platelet concentrates responsible for febrile transfusion reactions?

In recent years, several studies have identified the leukocyte content and the age of the blood components as dominant factors in febrile transfusion reactions (FTRs). At present, extensive efforts are being made to reduce adverse effects by implementation and/or introduction of new methods for leuko-depletion of blood components and by studying the mechanisms responsible for these phenomena. A recent approach has been the evaluation of cytokines in platelet concentrates and this issue has been addressed with some detail in this review. Comparative data currently available on levels of cytokines in the different platelet concentrates is provided along with the functional role of the detected cytokines in including adverse reactions.

Cytokines↗
PubMed1999

Delayed hemolytic transfusion reaction presenting as a painful crisis in a patient with sickle cell anemia.

CONTEXT: Patients with sickle cell anemia (SCA) are frequently transfused with red blood cells (RBC). Recently we reported that the calculated risk of RBC alloimmunization per transfussed unit in Brazilian patients with SCA is 1.15%. We describe a delayed hemolytic transfusion reaction (DHTR) presenting as a painful crisis in a patient with SCA. CASE REPORT: A 35-year-old Brazilian female with homozygous SCA was admitted for a program of partial exchange transfusion prior to cholecystectomy. Her blood group was O RhD positive and no atypical RBC alloantibody was detected using the indirect antiglobulin technique. Pre-transfusional hemoglobin (Hb) was 8.7 g/dL and isovolumic partial exchange transfusion was performed using 4 units of ABO compatible packed RBC. Five days after the last transfusion she developed generalized joint pain and fever of 39 degrees C. Her Hb level dropped from 12.0 g/dL to 9.3 g/dL and the unconjugated bilirrubin level rose to 27 mmol/L. She was jaundiced and had hemoglobinuria. Hemoglobin electrophoresis showed 48.7% HbS, 46.6% HbA1, 2.7% HbA2, and 2.0% HbF. The patient's extended RBC phenotype was CDe, K-k+, Kp(a-b+), Fy(a-b-), M+N+s+, Le(a+b-), Di(a-). An RBC alloantibody with specificity to the Rh system (anti-c, titer 1:16.384) was identified by the indirect antiglobulin test. The Rh phenotype of the RBC used in the last packed RBC transfusion was CcDEe. The patient was discharged, asymptomatic, 7 days after admission.

ABO Blood-Group System↗
PubMed2005

Delayed hemolytic transfusion reaction due to anti-Jk(a).

BACKGROUND: Kidd antibodies are very heterogeneous and difficult to detect. They have been frequently implicated in delayed hemolytic transfusion reactions (DHTRs). CASE REPORT: A 64 year old female (6 pregnancies, 2 deliveries, 4 abortions) with none red cell (RBC) transfusions in the history was admitted to hospital due to pneumonia and severe anemia. On admittance hemoglobin (Hb) level was 63g/L and hematocrit (Ht) 0.21 L/L. The blood sample of the patient was sent to laboratory for serologic testing since RBC transfusions were required. Patient appeared to beO Rh(D)+ with negative both direct antiglobulin (DAT) and routine antibody screen (ID-DiaCell I+II+III-P). Three units of packed RBCs with negative crossmatch (tube method) were prepared. Patient received two units on Day 2 and one more on Day 3 without any discomfort. Hematological values after the third unit were: Hb 116g/L and Ht 0.37 L/L. On Day 6 she started to feel week, tired, with nausea and mild jaundice. Her Hb and Ht had dropped to 99 g/L and 0.33 L/L respectively, with tendency of dropping further (Day 7: Hb 83 g/L, Ht 0.26 L/L). Total serum bilirubin was 58.9 umol/L (normal range 20.5 umol/L) and direct fraction was 14.9 umol/L (normal range 7 umol/L). DTHR was suspected. Antibody identification performed by ID-DiaMed Gel Techique (GT) showed the presence of anti-Jk(a) with dosage phenomenon. All three previously transfused units were typed Jk(a) and the patient s RBCs were Jk(a-b+). She received two units of Jk(a) negative packed RBCs and was well enough to be discharged on Day 14. CONCLUSION: It is important to monitor clinical effect of transfusion regularly and to provide good team work between specialists of transfusion medicine and related medical staff. The policy of transfusion practice is to keep pretransfusion sample for three weeks and to perform cross-match tests on the samples no older then 24h and 48h respectively.

Blood Group Incompatibility↗
PubMed1989

Investigation of transfusion reactions through microcomputer education software.

The purpose of this study was to develop educational software to simulate laboratory investigation of transfusion reactions. An interactive, branching-style program was developed using a 256K Personal Computer (International Business Machines, Boca Raton, FL). Over 75 institutions in the United States and Canada are currently using the software in preprofessional and continuing professional education programs.

Journal Article↗
PubMed1993

Reactive lysis--a phenomenon of delayed hemolytic transfusion reactions.

A 62-year-old female with Gaucher's disease demonstrated alloanti-c on pretransfusion testing. She was transfused with five units of c-negative red blood cells (RBCs) preoperatively and intraoperatively. The hemoglobin (Hb) level was slightly lower initially, hut was markedly lower on day 10 posttransfusion. Serologic results indicated a delayed hemolytic transfusion reaction (DHTR) due to alloanti-s, -Fya, and -Jkb, present both on the RBCs and in the serum. As late as day 35 posttransfusion, a mixed-field anti-IgG direct antiglobulin test (DAT) indicated that there were two cell populations present. The DAT remained positive with anti-C3b, -C3d throughout the course of the reaction. Because of the substantially lower Hb and the severity of symptoms, immunologic clearance of the antigen-positive donor RBCs was expected. However, we demonstrated their persistence. Our data corroborates the observation that complement activation occurring during DHTRs can result in the hemolysis of innocent bystander (autologous) cells.

Journal Article↗
PubMedDate not supplied

A delayed transfusion reaction caused by anti-K6.

This case report documents the demonstration of anti-K6 as the single antibody responsible for a delayed transfusion reaction. A 42-year-old white woman received three units of red blood cells for an episode of gastrointestinal bleeding from a duodenal ulcer. Twenty-three days following transfusion, laboratory and clinical evidence of hemolysis was noted. An anti-K6 was identified in the serum and in an eluate prepared from the patient's red blood cells. One of the three units transfused was positive for the K:6 antigen.

Adult↗
PubMed1997

Leukocyte phenotypic changes in an in vitro model of ABO hemolytic transfusion reaction.

BACKGROUND: ABO antigen-antibody interaction in the presence of peripheral blood leukocytes (white cells) results in the production of a variety of proinflammatory cytokines. However, although tumor necrosis factor alpha has been shown to be derived at least primarily from monocytes, the range of cells activated by this process has not previously been reported. Therefore, changes in mononuclear cell surface antigen expression were studied, to determine which subsets of white cells appeared to be activated in the setting of ABO incompatibility. STUDY DESIGN AND METHODS: Group O peripheral blood mononuclear cells (PBMCs) were incubated in autologous plasma with group A or O red cells (RBCs) for up to 24 hours. White cell expression of activation and adhesion markers was measured at 2 and 24 hours by flow cytometry, using direct or indirect fluorescein or phycoerythrin labeling. RESULTS: Expression of lymphocyte activation markers CD25, CDw108, and CD109 was equivalent when PBMCs incubated with group A and O RBCs were compared. However, after 2 hours, mean fluorescence of CD14 on PBMCs incubated with group A RBCs was 65 percent of that on PBMCs incubated with group O RBCs and remained similarly decreased at 24 hours. CD44 expression was upregulated on PBMCs exposed to both group A and O RBCs, but it was increased significantly more on monocytes exposed to group A RBCs. The ability to bind hyaluronic acid was induced in approximately 42 percent of CD14+ monocytes exposed to group A RBCs but in no cells exposed to group O RBCs. CONCLUSION: Downregulation of CD14 and increased binding of hyaluronic acid reflects monocyte activation in this model. No evidence of lymphocyte activation was found, supporting the hypothesis that ABO transfusion reactions primarily activate monocytes.

ABO Blood-Group System↗
PubMed1998

A delayed hemolytic transfusion reaction (DHTR) with multiple alloantibodies (Anti-E, Jka, Dia, Fyb, and S) induced by E-antigen-negative, crossmatch-compatible blood.

We describe the case of a 44-year-old woman with a delayed hemolytic transfusion reaction (DHTR). She had a history of two pregnancies and a blood transfusion, the details of which were unknown. At the time of her first vascular surgery on November 15, 1989, she received 1200 ml of crossmatch-compatible concentrated red blood cells (CRC). Before the first operation, screening for anti-RBC antibodies (Ab) was negative. At the time of the second admission on Feburary 15, 1996, anti-E Abs were detected by indirect antiglobulin test. She received 560 ml of E-antigen-negative, crossmatch-compatible, CRC for treatment of anemia on March 1 and 2, 1996. After this transfusion, total bilirubin (1.6 mg/dl) and lactate dehydrogenase (1355 IU/ml) were elevated on March 12, 1996. She had no evidence of clinical hemolysis. We suspected DHTR from these data, and therefore screened for anti-RBC Abs. Anti-E, Jka, Dia, Fyb, and S Abs were detected in blood samples obtained from the patient on March 12, 1996. Anti-E, Jka Dia, and S Abs were present more than 1 month and anti-Fyb Ab was disappeared at 18 days after transfusion.

Adult↗
PubMed1996

Leukocyte reduction of red cells when transfusing patients with autoimmune hemolytic anemia: a strategy to decrease the incidence of confounding transfusion reactions.

Autoimmune hemolytic anemia (AIHA) presents a difficult challenge to clinicians and blood bankers alike. Autoantibodies in the serum significantly complicate serologic evaluation, and necessitate performing procedures such as adsorptions to eliminate the possibility of underlying alloantibodies. In many instances the blood that is issued may be phenotypically similar but remains crossmatch incompatible, generating a considerable degree of anxiety among the clinical staff who are responsible for transfusing the patient. We report a case of warm autoimmune hemolytic anemia (WAIHA) in which the transfusion of red cells was complicated by a febrile transfusion reaction. Evaluation of the reaction resulted in a significant delay in transfusion therapy. Subsequent administration of leukocyte-poor red cells resulted in uneventful transfusions with a good therapeutic response. Retrospective analysis of the pretransfusion sample demonstrated significant levels of anti-neutrophil antibodies. This case resulted in the establishment of our policy to administer all red cell transfusions to patients with autoantibodies (warm or cold) as leukocyte- poor red cells.

Journal Article↗
PubMed2006

Repeat ABO-incompatible platelet transfusions leading to haemolytic transfusion reaction.

A 65-year-old woman, blood group A RhD positive, who had completed her first course of induction chemotherapy for acute myeloid leukaemia was transfused with apheresis platelets over a number of days. On three occasions she received group O RhD positive units, which had been screened and found not to contain high-titre anti-A,B isoagglutinins. Following the third unit, she developed a haemolytic transfusion reaction and died soon thereafter. This has led to change in policy of the supplying centre in testing for high-titre anti-A,B isoagglutinins. Blood group O apheresis platelets and fresh-frozen plasma units are now labelled as high titre with a cut-off of 1/50 as compared to the previous cut-off of 1/100 for anti-A,B isoagglutinins. A universal approach to testing donations for high-titre anti-A,B isoagglutinins, better compliance of guidelines and monitoring of patients is necessary.

ABO Blood-Group System↗
PubMed1983

Blood transfusion reaction in a patient with immunoglobulin A deficiency.

Selective deficiency of serum IgA is the most common immunodeficiency in humans; when immunodeficient individuals receive blood transfusions a severe anaphylactoid reaction can develop. The present report describes such a patient. After the transfusion reaction a hemagglutination inhibition assay revealed that her blood contained less than 1.0 micrograms/ml of IgA and an anti-IgA antibody that reacted with the 2 IgA proteins, isotypes IgA1 and IgA2. Immediately after the reaction the patient's serum anti-IgA antibody titer was 1:16,384, and when reevaluated 5 weeks later it was 1:8000. All 3 of her children were shown to be IgA deficient, and 2 of them had antibodies against IgA2. This type of anaphylactoid reaction can be avoided by transfusing blood from IgA-deficient donors, frozen deglycerolized red cells, or red cells that have been washed several times to extract all IgA proteins.

Adult↗