Patients Received Platelet Transfusions Research Articles

The Expression of IgG Allotypes on Platelets and Immunization to IgG Allotypes in Multitransfused Thrombocytopenic Patients

We investigated whether the platelet-membrane surface carries IgG allotypic antigens and whether these determinants may be important in platelet transfusion therapy. Using a hemagglutination inhibition assay, we showed that the G1m IgG allotypes (a, x, f) and K1m and K3m light-chain allotypes are expressed on the surface of platelets, whereas G3m allotype antigenic determinants were not detectable. In 146 multitransfused thrombocytopenic patients, 35 (24%) patients were found to have antiallotypic antibodies. To study the effect of antiallotypic antibodies on platelet transfusion outcome, patients received platelet transfusions from donors, either positive or negative for the IgG allotype to which patients were immunized. Of the 19 antigen-positive and 19 antigen-negative platelet transfusions given, respectively, the mean platelet count increments at 1 hour were 8,402 +/- 6,402 +/- 6,721 (1 SD) and 9,799 +/- 5,559 (1 SD) P less than .2. Transfusion reactions were not more common when antigen-positive platelet transfusions were given. Despite the presence of IgG allotypic determinants on platelets, allotypic antibodies do not decrease platelet transfusion recovery. Furthermore, passive administration of plasma containing IgG allotypes to patients with antiallotypic antibodies does not lead to innocent bystander-mediated platelet destruction.

The expression of IgG allotypes on platelets and immunization to IgG allotypes in multitransfused thrombocytopenic patients

We investigated whether the platelet-membrane surface carries IgG allotypic antigens and whether these determinants may be important in platelet transfusion therapy. Using a hemagglutination inhibition assay, we showed that the G1m IgG allotypes (a, x, f) and K1m and K3m light-chain allotypes are expressed on the surface of platelets, whereas G3m allotype antigenic determinants were not detectable. In 146 multitransfused thrombocytopenic patients, 35 (24%) patients were found to have antiallotypic antibodies. To study the effect of antiallotypic antibodies on platelet transfusion outcome, patients received platelet transfusions from donors, either positive or negative for the IgG allotype to which patients were immunized. Of the 19 antigen-positive and 19 antigen-negative platelet transfusions given, respectively, the mean platelet count increments at 1 hour were 8,402 +/- 6,402 +/- 6,721 (1 SD) and 9,799 +/- 5,559 (1 SD) P less than .2. Transfusion reactions were not more common when antigen-positive platelet transfusions were given. Despite the presence of IgG allotypic determinants on platelets, allotypic antibodies do not decrease platelet transfusion recovery. Furthermore, passive administration of plasma containing IgG allotypes to patients with antiallotypic antibodies does not lead to innocent bystander-mediated platelet destruction.

Autologous peripheral hematopoietic stem cell transplantation restores hematopoietic function following marrow ablative therapy

From ten patients with advanced malignant disease involving the bone marrow, autologous hematopoietic stem cells were collected from the peripheral blood during eight four-hour pheresis procedures and cryopreserved. No manipulations to increase the number of stem cells circulating in the blood were used during the collections. Following marrow ablative chemotherapy or chemoradiotherapy, the autologous cells were thawed and infused intravenously (IV). WBCs reappeared in the circulation at a median of eight days (range seven to 11 days) after stem cell infusion. Two patients died early, whereas the other eight reached normal numbers of circulating granulocytes that have persisted for up to greater than 20 months. These eight patients became independent of RBC transfusions (hemoglobin concentration greater than 10 g/dL) at a median of 27 days (range 11 to 58 days) after transplantation. One patient received platelet transfusions for counts less than 50 x 109)/L, one patient developed a clinical picture of idiopathic thrombocytopenic purpura, and six patients maintained a platelet count greater than 20 x 10(9)/L at a median of 23 days (range 14 to 25 days) following stem cell infusion. This technique allows patients ineligible for autologous bone marrow transplantation due to unacceptable anesthetic risks, prior pelvic irradiation, or bone marrow metastases to receive marrow ablative therapy.

Transient platelet and HLA antibody formation in multitransfused patients with malignancy

Fifty-nine patients receiving platelet transfusions for bone marrow failure secondary to malignancy were screened at regular intervals for the presence of antibodies to human leucocyte (HLA) and platelet specific antigens. HLA antibodies occurred in 19 patients, 10 of whom also developed platelet specific antibodies. The HLA antibodies disappeared in 10 of 15 patients followed for periods of 2-14 months. In two patients this occurred whilst still receiving platelet transfusions. Antibody reappeared in only two of six patients subsequently transfused. Antibodies to platelet specific antigens were detected in 28 patients. They were transient, often appeared in association with infection, and in 50% of cases tested demonstrated autoantibody activity. There was no association with antibiotic drug therapy, or PFA/EDTA-dependent cryptantigens. Platelet recovery at 1 h or 20 h post transfusion was not significantly reduced in the presence of platelet specific antibodies. These findings have important implications for the selection of platelet donors for alloimmunized recipients.

Autologous Peripheral Hematopoietic Stem Cell Transplantation Restores Hematopoietic Function Following Marrow Ablative Therapy

From ten patients with advanced malignant disease involving the bone marrow, autologous hematopoietic stem cells were collected from the peripheral blood during eight four-hour pheresis procedures and cryopreserved. No manipulations to increase the number of stem cells circulating in the blood were used during the collections. Following marrow ablative chemotherapy or chemoradiotherapy, the autologous cells were thawed and infused intravenously (IV). WBCs reappeared in the circulation at a median of eight days (range seven to 11 days) after stem cell infusion. Two patients died early, whereas the other eight reached normal numbers of circulating granulocytes that have persisted for up to greater than 20 months. These eight patients became independent of RBC transfusions (hemoglobin concentration greater than 10 g/dL) at a median of 27 days (range 11 to 58 days) after transplantation. One patient received platelet transfusions for counts less than 50 x 109)/L, one patient developed a clinical picture of idiopathic thrombocytopenic purpura, and six patients maintained a platelet count greater than 20 x 10(9)/L at a median of 23 days (range 14 to 25 days) following stem cell infusion. This technique allows patients ineligible for autologous bone marrow transplantation due to unacceptable anesthetic risks, prior pelvic irradiation, or bone marrow metastases to receive marrow ablative therapy.

Detection of platelet antibodies using the platelet migration inhibition assay.

We evaluated the usefulness of the Platelet Migration Inhibition (PMI) assay in detecting antibody to platelets in patients receiving platelet transfusions. Forty-one PMI assays were performed on pretransfusion sera from 19 patients. After each transfusion, each patient was evaluated clinically and by transfusion response for alloimmunization. Prevalence of antiplatelet antibody, the predictive value of positive and negative results, and efficiency of the PMI assay were calculated. The 41 PMI assays yielded true-positive, true-negative, false-positive, and false-negative results of 18, 14, 5, and 4, respectively. The sensitivity and specificity of the PMI assay were calculated at 81.8% and 73.7%. The PMI assay was comparable in sensitivity and specificity to immunofluorescence and superior to platelet aggregation and lymphocytotoxicity for detecting platelet (inhibition) antibodies. This test is simple and less costly than immunofluorescence; however, it lacks speed and efficiency for crossmatching purposes. It is useful as a clinical test in screening potential platelet pheresis donors and patients receiving platelet transfusions every other day. It may prove useful in research as a functional test to understand alloimmunization and restricted alloimmunization.

Expect the Unexpected in Hepatitis

Even though it is known that the virus of hepatitis A may be transmitted by the parenteral route, 1 we hardly ever think of this possibility when hepatitis follows transfusion of blood or blood products. Almost invariably, we assume that the disease is hepatitis B. Meyers et al 2 remind us that this assumption can be misleading. They have investigated an outbreak of hepatitis in a bone marrow transplant unit. Overt disease developed within a period of three months in nine patients with a marrow transplant and in six donor-members of their families. Subclinical hepatitis, evidenced by increased serum glutamic oxalacetic transaminase concentrations, was detected in 21 additional cases among family members, staff members, and other donors, and 69% of patients receiving platelet transfusion during the period of risk. Unexpectedly, the short incubation period as well as the clinical and serological features of the illness were compatible with hepatitis A

Parenterally transmitted hepatitis A associated with platelet transfusions. Epidemiologic study of an outbreak in a marrow transplantation center.

During 3 months, nine patients with a marrow transplant hospitalized in a leukemia research center and six donor-members of their families developed acute hepatitis. Serum glutamic-oxalacetic transaminase (SGOT) screening showed 21 subclinical cases among other family members, staff members, and other donors at the center. Epidemiologic investigation implicated platelet and plasma donation and platelet transfusion as the source of exposure. Twenty-six of 29 (90%) platelet and plasma donors and 9 of 13 (69%) patients receiving platelet transfusions during the period of risk developed clinical or biochemical evidence of acute hepatitis. The clinical illness, incubation period of 27 days, and results of serologic tests were compatible with hepatitis A. Observation of the platelet donation procedure showed practices possibly responsible for the contamination of blood products. This outbreak illustrates the risk of hepatitis for platelet and plasma donors and recipients and suggests the need for reexamination of platelet and plasma donation procedures in other institutions.