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At least 19 recordsLinked to original sources

Transfusion reaction. An immunologic hazard of blood transfusion.

Twenty-three cases of delayed hemolytic transfusion reaction (DHTR) occurring at the Mayo Clinic from 1964 through 1973 are reviewed. Nineteen patients had clinical manifestations of hemolysis, of which fever was the most frequent presenting symptom. The degree of hemolysis served as an index of morbidity. In four cases, there was oliguria, two of these patients experiencing renal shutdown. In one case, hemolysis led to a disseminated intravascular coagulation syndrome. Death occurred subsequent of DHTR in three patients. The direct antiglobulin test was positive in all but one case; this finding coincided with elevated unconjugated bilirubin in 14 cases and decreased haptoglobin levels in 15 cases. Anti-Jka antibody accounted for somewhat more than one-third of reactions and, along with anti-E, c, D, Fya, and K antibodies accounted for 91 per cent of cases.

Adult

Immediate haemolytic transfusion reaction due to anti-Inb.

An immediate haemolytic transfusion reaction was investigated in a patient with intestinal cancer. The causative antibody was directed against a high-frequency antigen Inb that was presumably produced as a result of pregnancies. This is the first case of a severe transfusion reaction due to this alloantibody.

Adult

Delayed overt hemolytic transfusion reaction due to anti-U antibody.

A patient is described who developed a delayed hemolytic transfusion reaction, 11 days posttransfusion, caused by anti-U. This case illustrates the difficulty that can occur in distinguishing a delayed transfusion reaction from autoimmune hemolytic disease when the antibody involved is directed against a high incidence blood group antigen.

Adult

Delayed hemolytic transfusion reactions. An often-missed entity.

Delayed hemolytic transfusion reactions in eight persons were manifested solely or primarily by an apparently unexplained posttransfusion decrease in the hematocrit value. Alloantibodies were eventually found in all eight patients, but were sometimes undetectable for as long as 72 hours after the reaction. This did not preclude the occurrence of a new, acute hemolytic reaction. There were three instances of reversible renal failure complicating the reaction. In two patients, some or all of the antibodies became undetectable after four and nine months. In a third, the indirect antiglobulin reactions became considerably weaker after 12 months. Patients previously sensitized to RBC antigens should have available records inspected and a warning device (wristband or wallet card) provided to help prevent reactions caused by an anamnestic antibody rise.

Adolescent

Frequency of delayed hemolytic transfusion reactions following antibody screening and immediate-spin crossmatching.

In view of the continuing controversy regarding the use of immediate-spin crossmatch procedures in preparing blood for transfusion to patients in whom unexpected clinically significant antibodies have not been found by antibody screening by the indirect antiglobulin test (IAT), a review of 8 years' experience with such a policy was conducted. In that period, 54,725 units of packed red cells or whole blood were transfused to 10,146 patients. Four clinically overt delayed hemolytic transfusion reactions and 18 clinically silent delayed serologic transfusion reactions were found. In 3 of the 22 patients, the offending antibody(ies) were detectable in the pretransfusion serum by an enzyme IAT, but none was detectable by routine saline IAT against either a three-cell screening panel or the transfused cells. Thus, the incorporation of saline indirect antiglobulin crossmatch would not have prevented the delayed reactions. It can be concluded that the use of a saline indirect antiglobulin crossmatch offers no significant advantage over the current policy of using only immediate-spin crossmatch for those patients whose pretransfusion serum gives negative results in a three-cell screen using a saline IAT.

Aged

Weak anti-IgA antibodies with limited specificity and nonhemolytic transfusion reactions.

Anti-IgA antibodies were studied in sera from patients with nonhemolytic transfusion reactions for which no serological reason had been found. Of the 158 sera that were studied by passive hemagglutination assay using twelve IgA myeloma proteins, 4 samples had class-specific antibodies and 10 samples antibodies with limited specificity. Titers were 1:8 or less. 100 multitransfused hemophilia patients were studied with two IgA myeloma proteins. Four of the sera had anti-IgA antibodies. Normal blood donor sera reacted with IgA only when antigens were first either digested with pepsin or stored for several months as dilute solutions in refrigerator. The results emphasize the need for fresh IgA proteins of good quality when human anti-IgA antibodies are investigated.

Antibodies, Anti-Idiotypic

Hemolytic transfusion reactions caused by failure of commercial antiglobulin reagents to detect complement.

Two definite acute hemolytic transfusion reactions occurred in a patient with chronic myelogenous leukemia in blastic crisis. Both suspect units were entirely compatible by routine crossmatch using commercial antiblobulin sera. However, both units were clearly incompatible using our own specific anti-C3 antiserum in the antiglobulin reaction phase of the crossmatch. Subsequently it was possible to predict in vivo compatibility using our anti-C3 antiserum in vitro. This case adds new evidence for the inadequacy of anticomplement activity in commercial antisera.

Adult

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

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

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

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