Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Transfusion Reaction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMedDate not supplied

Anti-Dob implicated as the cause of a delayed hemolytic transfusion reaction.

A 27-year-old, gravida 3, para 2 woman experienced a delayed hemolytic transfusion reaction. She had anti-Dob in both serum and eluate 8 days after infusion of 6 units of Do(b+) red cells. No antibody had been detected prior to transfusion. By the 15th day after transfusion, there was no evidence of survival of red cells from any of the 6 units. Anti-C and anti-M were demonstrated later, but 29 months after transfusion, no atypical antibodies were detectable. The evidence suggests anti-Dob should be considered an antibody of potential clinical significance until contrary evidence becomes available.

Adult↗
PubMed1987

Haemolytic transfusion reactions due to HLA antibodies. A prospective study combining red-cell serology with investigations of chromium-51-labelled red-cell kinetics.

In a prospective study to see whether HLA sensitisation is associated with increased red-blood-cell (RBC) destruction after HLA-incompatible transfusion, chromium-51-labelled RBC survival and site of sequestration were monitored in nine patients in whom HLA antibodies had developed after RBC transfusions. The donors selected were compatible in ABO and RBC-specific antigen systems but mismatched for the HLA antigen in question. Haemolytic transfusion reactions occurred in all four patients who received HLA-B7-incompatible RBC. A direct radioimmune anti-IgG test became positive, Cr51-RBC survival was very short (22.3, 36.9, 41.4, and 44.0 days), and excess sequestration in the spleen was measured. There was a rise in serum lactic dehydrogenase and a fall in haptoglobin. HLA-B7 antibody was detected in the eluate prepared from RBC collected after transfusion. A similar reaction was found in only one further patient, caused by an HLA-A2 incompatibility. No indications of immune-mediated RBC sequestration were discernible after transfusion of HLA-B7-compatible RBC in one of the patients who had shown a reaction with HLA-B7-incompatible blood, nor in any of the other patients who received HLA-B7-compatible RBC. The haemolytic transfusion reactions could not be anticipated by conventional crossmatch procedures, nor by the measurement of the Cr51-RBC survival 1 h after transfusion.

Aged↗
PubMedDate not supplied

Acute hemolytic transfusion reactions--a fresh look at pathogenesis and considerations regarding therapy.

A review of our knowledge of acute hemolytic transfusion reactions indicates that we have learned much in recent years about the pathogenetic mechanisms involved. An approach to effective therapy for patients suffering such reactions should be based on our latest understanding of the pathophysiology of this syndrome. However, changes in our therapeutic approach have not kept abreast of our increased awareness of the etiologic factors, and the patient, therefore, is not getting the benefit of our increased knowledge in this area. The primary pathogenetic mechanisms involved in these reactions appear to be disseminated intravascular coagulation and a series of hemodynamic alterations leading to ischemic necrosis of tissues. Therapy would best be aimed at interfering with these primary pathophysiologic pathways.

Acute Kidney Injury↗
PubMed1997

[A delayed hemolytic transfusion reaction due to irregular antibodies with an anti-Kidd(a) specificity].

HISTORY AND CLINICAL FINDINGS: A 56-year-old woman was admitted for replacement of a previously implanted right hip prosthesis which had become loose (no infection). She limped painfully on a shortened leg whose mobility was markedly impaired. At the site of the previous operation the pelvis was lower by about 2 cm; the scar looked well healed. INVESTIGATIONS: Routine laboratory tests were normal except for moderately raised erythrocyte sedimentation rate (18/ 27 mm). There was complete loosening of the prosthesis on X-ray. TREATMENT AND COURSE: Intraoperative bleeding from a branch of the inferior gluteal artery required blood transfusion and further erythrocyte infusions became necessary. Jaundice developed on the 4th postoperative day and 7 days later the direct Coombs test was positive with demonstrable agglutination. Free irregular erythrocytic anti-Kidd(a) (anti-jk[a]) antibodies were found in the serum. To counteract the delayed haemolytic transfusion reaction, exclusively jk(a)-negative erythrocytes were infused. The jaundice gradually disappeared and the bilirubin values became normal. CONCLUSION: Jaundice and signs of haemolysis after erythrocyte transfusion may be due to delayed transfusion reaction and should be investigated with the direct Coombs test.

Antibodies↗
PubMed2006

The association of cytokine gene polymorphisms with febrile non-hemolytic transfusion reaction in multitransfused patients.

Cytokines are associated with inflammatory responses including febrile non-hemolytic transfusion reactions (FNHTR). Moreover, there are some polymorphisms of these cytokine genes associated with different levels of gene expression. The aim of the present study was to investigate the association of inflammatory cytokine gene polymorphisms with the occurrence of FNHTR in multitransfused patients. We studied two groups of transfused patients: one presenting FNHTR before 20 transfusions of red blood cells concentrates and the other which never presented FNHTR even after 20 transfusions. The gene polymorphisms studied were IL1B-511C/T and +3953C/T, IL1RN (intron 2, variable number tandem repeat), IL6-174G/C, IL10-1082G/A and -819C/T, TNF-308G/A and LTA+253G/A using polymerase chain reaction and restriction digestion or sequencing methods. An association of IL1RN*2.2 genotype with the occurrence of precocious FNHTR (P < 0.025) was detected. This allele and this genotype have been related with higher serum levels of interleukin (IL)-1beta in vivo and higher promoter activity. No other association was demonstrated. The association of gene polymorphisms related with the increase of inflammatory cytokine gene expression may be a relevant factor in FNHTR and requires confirmation.

Adult↗
PubMed2003

Fatal hemolytic transfusion reaction due to anti-Ku in a Knull patient.

A fatal transfusion reaction due to anti-Ku in a Knull (Ko) patient is reported. The patient was transfused with 34 units of incompatible RBCs during 44 days of hospitalization. Apart from the first transfusion, all subsequent transfusions failed to raise the patient's Hb. No serum antibody was identified until he was transferred to another hospital for dialysis. A compatibility test demonstrated a weak antibody and autocontrol reacting at room temperature by a manual polybrene method. The antibody was considered to be a "cold agglutinin." A blood sample was sent to a reference laboratory where the patient was found to be Knull and the antibody was identified as anti-Ku.

Journal Article↗
PubMed1983

A study of the routine use of the Imugard IG500 Leukocyte Removal Filter illustrating a possible cause of transfusion reactions and a method of prevention.

The results of the use of the Imugard IG500 Leukocyte Removal Filter in the transfusion of 100 patients requiring leucocyte poor blood are presented. The patients were suffering from a variety of disorders. Many of them had previously received leucocyte poor blood prepared by other methods. Five patients developed non-haemolytic transfusion reactions. Subsequent investigations suggested that these were reactions to the plasma proteins present in the leucocyte poor blood prepared by filtration. A simple method of removal of these plasma proteins combined with filtration is described. The resultant product has been transfused, without incident, into the patients who previously reacted.

Anemia, Sideroblastic↗
PubMedDate not supplied

Anti-M causing delayed hemolytic transfusion reaction.

A 52-year-old gravida 1, para 1 woman with M- red cells experienced a delayed hemolytic transfusion reaction and exhibited an anti-M antibody following the infusion of four units of M+ red cells. Measurements of erythrocyte survival using 51Cr-labeled donor M+ and M- red cells and in vitro studies of monocyte-macrophage phagocytosis of sensitized reagent red cells implicate anti-M in the pathogenesis of hemolysis.

Chromium Radioisotopes↗
PubMedDate not supplied

TREACT. An expert system consultation program to aid in the diagnosis of transfusion reactions.

We have developed a rule-based, expert system consultation program, TREACT, to aid in the diagnosis of transfusion reactions. Given clinical signs, symptoms, and laboratory results, the program generates diagnoses, alerts the user when a medical director should be called, suggests follow-up actions, and makes recommendations for future transfusion. Diagnoses made by TREACT, including 121 reactions, were compared with those of the medical directors over a 6-month period. The overall diagnostic concordance between the medical directors and the program was 0.777. When this was corrected for chance association (kappa statistic), the concordance was 0.703 (p less than 0.0001), which can be interpreted on a qualitative scale as substantial agreement. The program has also been used successfully as a tool for training new technologists. Other advantages and possibilities that expert systems offer to transfusion medicine are discussed.

Diagnosis, Computer-Assisted↗
PubMed2005

Heterogeneity of platelet responsiveness to anti-CD36 in plasma associated with adverse transfusion reactions.

BACKGROUND AND OBJECTIVES: Antibodies to CD36 (anti-CD36) are clinically important. As some platelet immunoglobulins produced by transfusion or pregnancy have been shown to induce platelet activation and to play roles in non-haemolytic transfusion reactions (NHTRs), we investigated the in vitro response of platelets to plasma containing anti-CD36. MATERIALS AND METHODS: Plasma containing anti-CD36, implicated in the development of NHTRs and subsequent thrombocytopenia, was incubated with CD36-positive platelets. Plasma-induced platelet activation was examined by evaluating platelet aggregation and RANTES (regulated on activation, normal, T-cell expressed, and presumably secreted) release. RESULTS: Platelet activation was induced by plasma alone in four out of 20 CD36-positive subjects. In seven subjects, platelet activation was synergistically induced by the combination of epinephrine priming and the plasma. The platelets of the nine remaining subjects failed to respond to the plasma. Platelet activation induced by either the plasma alone or by synergy with epinephrine required the involvement of Fc gamma RIIa. The different responsiveness of the platelets was partially associated with the surface levels of CD36 and Fc gamma RIIa, but not with Fc gamma RIIa polymorphisms. CONCLUSIONS: Plasma containing anti-CD36, implicated in the development of NHTRs, exhibited a platelet-activating capability. Additionally, platelets from healthy human subjects exhibited a considerable degree of heterogeneity in their responsiveness to this plasma. The heterogeneity of these responses may determine the occurrence of anti-CD36-related NHTRs.

Antigens, CD↗
PubMed1998

An acute hemolytic transfusion reaction caused by an anti-P1 that reacted at 37 degrees C.

BACKGROUND: Hemolytic transfusion reactions (HTRs) due to anti-P1 have rarely been reported. There is only one report (from 1945) of an acute HTR due to anti-P1. CASE REPORT: A 74-year-old woman with anti-P1 was given blood that had been found to be compatible by the use of prewarmed serum and saline-suspended red cells (RBCs) and of an antiglobulin test with anti-IgG. The test mixtures were not centrifuged or inspected for agglutination after the 37 degrees C incubation phase. After transfusion of 50 mL of P1 + blood, the patient had an acute HTR (hemoglobinemia, hemoglobinuria, and increased blood pressure, temperature, and respiration). RESULTS: When studied by a reference laboratory, the anti-P1 was shown to be easily detectable (3+ agglutination) by a prewarming technique (saline or low-ionic-strength saline [LISS]), which included centrifugation at 37 degrees C, but only weak reactions were observed when centrifugation after 37 degrees C incubation was omitted. The indirect antiglobulin test was weakly positive (1+) with anti-IgG, but polyspecific anti-human globulin reacted 2+. The anti-P1 agglutinin was IgM, and its titer was 16 at 37 degrees C (prewarmed) and 256 at 23 degrees C; it caused hemolysis of RBCs at 37 degrees C under conditions known to enhance hemolysis. An indirect monocyte monolayer assay gave results of 11.2 and 22 percent in testing of P1 + RBCs incubated with the patient's serum alone and with patient's serum plus fresh normal serum (as a source of complement), respectively (normal < or = 3%). CONCLUSION: An acute HTR was caused by a hemolytic anti-P1 that reacted at 37 degrees C. This antibody was not detected by the hospital in a prewarmed crossmatch that omitted 1) the addition of LISS, 2) the reading for agglutination after the 37 degrees C incubation, and 3) the use of antiglobulin sera containing anti-complement.

Acute Disease↗
PubMed1991

Delayed haemolytic transfusion reactions in patients with sickle cell disease.

We describe two cases which illustrate the difficult diagnostic and therapeutic problems posed by delayed haemolytic transfusion reactions in patients with sickle-cell disease. The cases emphasize the need for meticulous phenotypic and serological assessment of sickle-cell patients prior to transfusion therapy.

Adolescent↗
PubMed1976

Transfusion reaction with pulmonary infiltration associated with HL-A-specific leukocyte antibodies.

A case of a non-hemolytic transfusion reaction with pulmonary infiltration secondary to leukocyte antibodies is described, and previously reported cases are reviewed. This type of reaction can be diagnosed at the bedside when a patient develops fever, hypotension and dyspnea within a few hours following transfusion of whole blood or a plasma product. The roentgenogram of the chest shows pulmonary infiltrates with a normal cardiac silhouette constituting non-cardiac pulmonary edema. To provide laboratory confirmation of this reaction, it is essential to search for leukocyte antibodies by both leukoagglutinin and cytotoxic technics, as well as to determine HL-A phenotypes of both donor and recipient. As the plasma products involved usually come from multiparous women, donor parity should be a routine question in the donor interview in transfusion services. To prevent this reaction, which may prove fatal, blood donated by women who have two or more children should be used for packed cells only.

Adult↗
PubMed1991

Post-transfusion purpura as the main manifestation of a trilineal transfusion reaction, responsive to steroids: flow-cytometric investigation of granulocyte and platelet antibodies.

We report a typical case of post-transfusion purpura (PTP) due to anti-PlA1 in a 65-year-old woman. Serological studies were carried out using flow cytometry (FCM). The patient also developed red cell alloantibodies that produced a delayed hemolytic transfusion reaction (DHTR) and broad HLA antibodies. Treatment with high-dose intravenous IgG (HDIgG; a first-generation preparation) was ineffective, but a course of steroids resulted in a rapid increase in the the platelet count.

Aged↗
PubMed1995

The differentiation of delayed hemolytic and delayed serologic transfusion reactions: incidence and predictors of hemolysis.

BACKGROUND: After differentiation of the entities of clinically detectable delayed hemolytic (DHTR) and delayed serologic transfusion reactions (DSTR), previous investigators calculated a DHTR:DSTR incidence ratio of 18:72 from a retrospective review of patients with serologic evidence of DHTR or DSTR. There are no published data on factors that may influence the occurrence of DHTR versus DSTR in a given patient. STUDY DESIGN AND METHODS: Retrospective review was conducted of 292 patients at the Mayo Clinic who, between 1980 and 1992, received a clinical diagnosis of DHTR or DSTR concurrently with a serologic diagnosis. Red cell alloantibody specificity, the activity of the patient's reticuloendothelial system, and concurrent immunosuppression were evaluated as potential predictors of the occurrence of DHTR versus DSTR in different patients. RESULTS: The incidence of DHTR or DSTR was 1 in 1899 allogeneic red cell units transfused, with a DHTR:DSTR ratio of 36:64. Alloantibody specificity was the only variable that affected the occurrence of DHTR versus DSTR at the clinical level, with the anti-Jka and anti-Fya specificities, as well as multiple coexisting specificities, significantly associated with detectable hemolysis (p < 0.05). CONCLUSION: Clinically detectable DHTRs are found to occur more commonly than previously believed when the clinical and serologic diagnoses are made concurrently and appropriate work-ups for hemolysis are ordered. The association of certain alloantibody specificities with detectable DHTRs may have implications for clinical transfusion practice.

Adult↗
PubMed2005

Delayed and acute hemolytic transfusion reactions resulting from red cell antibodies and red cell-reactive HLA antibodies.

BACKGROUND: It has been controversial whether HLA antibodies cause hemolytic transfusion reactions (HTR) or shortened red blood cell (RBC) survival. A patient is reported who had two episodes of HTR, the latter of which was likely due to RBC-reactive HLA antibodies. CASE REPORT: A 77-year-old woman, admitted for gastric varix rupture, had no RBC-irregular antibodies detected before transfusion. On Hospital Day 12, after transfusion of 2 units of RBCs and 2 units of fresh-frozen plasma, the first delayed hemolytic episode occurred and anti-E, anti-c, anti-Jk(a), and unidentified RBC-reactive antibodies were detected in a serum sample from Day 14. Two additional units of matched RBCs were transfused with a leukoreduction filter on Days 19 and 22. After 4 hours of starting a transfusion on Day 22, the patient had fever, and a second hemolytic episode was recorded. Multireactive HLA antibodies (reactive against 20 of 20 donor panel lymphocytes) were detected in serum samples from Day 15 to Day 21. These HLA antibodies reacted strongly with HLA-A2 and HLA-B7 antigens, corresponding to Bg(c) and Bg(a) antigens on RBCs, respectively. RBCs transfused on Day 22 were found to be HLA-A2 by genotyping. CONCLUSION: Strong HLA alloantibodies in this recipient appear to have caused a HTR. It is suggested that HLA antibodies be considered in patients with unexplained HTRs.

Acute Disease↗