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Biomedical subjects

G Garratty

Publications and source records attributed to G Garratty.

At least 19 recordsLinked to original sources
PubMed1992

Selection of platelets for refractory patients by HLA matching and prospective crossmatching.

A multi-site clinical study compared platelets chosen for refractory patients by prospective platelet crossmatching using stored donor platelets and HLA-based selection. Seventy-three patients who were refractory to random-donor platelets received two plateletpheresis components, one chosen by HLA-based criteria and the other by crossmatching. Patients were carefully evaluated to exclude nonimmune factors that could adversely affect transfusion results. Each of the five study sites used a crossmatch procedure with which it had experience. Results from this study indicate the following: 1) The overall rate of successful transfusion was similar when an HLA-based method of donor selection that includes all grades of matching and mismatching was compared to a crossmatch-based method of donor selection. 2) HLA-based selection that restricts recipients to grade A and BU matches was superior to a selection method based upon crossmatching alone. Donor selection based on HLA matching (grades A or BU) was also superior to selection based on any degree of HLA mismatching (grades BX, C, or D). 3) Selection of donors based on HLA-cross-reactive groups (defined by in vitro serologic crossreactivity) was no more successful than that based on grade C and D mismatches and was no more successful than selection by crossmatching alone. 4) Lymphocytotoxic and platelet antibodies were not detected in many of the enrolled patients, even though patients demonstrating nonimmune factors were eliminated from the study. It can be concluded that HLA-compatible (grades A and BU) platelets provide optimal support for refractory patients, but that crossmatch-selected platelets are acceptable as an alternative component.

Adult↗
PubMed1991

A fatal case of ceftriaxone (Rocephin)-induced hemolytic anemia associated with intravascular immune hemolysis.

Fatal hemolytic anemia developed in a 52-year-old woman who was treated with a cephalosporin, ceftriaxone. The patient's red cells (RBCs) were coated with C3, but no RBC-bound IgG, IgA, or IgM was detected. Her serum contained an antibody that did not react with cephalosporin-coated RBCs but reacted strongly with RBCs in vitro when her serum was added to drug and RBCs. This is the first case of immune hemolytic anemia associated with ceftriaxone, the first case of fatal cephalosporin-induced hemolytic anemia, and the second case in which a cephalosporin antibody showed in vitro and in vivo characteristics usually thought to be associated with the so-called immune complex mechanism.

Anemia, Hemolytic↗
PubMed1991

Effect of cell-bound proteins on the in vivo survival of circulating blood cells.

Normal circulating red blood cells (RBCs) and platelets have been shown to have small amounts of IgG on their membranes. The cell-bound IgG may be cytophilic (IgG nonspecifically adsorbed from the plasma) and/or IgG autoantibody. It has been suggested that most of the RBC-bound IgG is on older RBCs and is an autoantibody directed against senescent cell antigen (SCA). The accumulation of this RBC-bound IgG leads to Fc-dependent removal of senescent RBCs by macrophages in the reticuloendothelial system. RBCs also have complement components on their membrane; it is not clear how this accumulates on RBCs and whether it has a physiologic function. This small amount of nonpathogenic RBC-bound IgG is not detected by the antiglobulin test. It is still unclear whether the major difference between pathogenic and nonpathogenic IgG autoantibodies is qualitative, quantitative, or both. Seemingly healthy blood donors (1 in 1,000 donors) and patients without hemolytic anemia (up to 8% of patients) have increased amounts (greater than 200 molecules/RBC) of RBC-bound IgG and complement that is detected by the antiglobulin test. This RBC-bound IgG has been shown to be an IgG autoantibody directed against blood group antigens, and/or IgG anti-idiotype, and/or IgG nonspecifically adsorbed onto the RBC membrane when plasma IgG levels are high. Most patients with autoimmune hemolytic anemia (AIHA) have RBC-bound IgG and/or complement detectable by the antiglobulin test. Most of the RBC-bound IgG is of the IgG1 subclass, whether one examines the RBCs of healthy blood donors or hospitalized patients with and without AIHA. Although the quantity of RBC-bound IgG is generally higher in patients with AIHA, there is no clear correlation with the quantity of RBC-bound IgG and the rate of in vivo RBC destruction. There is some recent evidence that the SCA autoantibody may at times be pathogenic and cause autoimmune disease.

Anemia, Hemolytic↗
PubMed1979

Cell surface heterogeneity of human blood neutrophils and monocytes.

Until recently, human blood neutrophils (PMN) and monocytes have been considered to be homogeneous cell populations. However, much evidence has accumulated on their functional heterogeneity. This functional heterogeneity suggests the existence of different subsets of myeloid cells analogous to T and B subsets of lymphoid cells. The goal of this study was to investigate this question of myeloid subsets by examining myeloid cells for cell surface reactivity for IgG and complement (C). Normal PMN and monocytes were examined from 60 subjects for the presence of two types of IgG-Fc receptors and two activated C components, C3b and C3d. Most PMN and monocytes showed Fc receptor activity for rabbit IgG (Fc-R). In addition, the majority of monocytes but very few PMN reacted with human IgG (anti-Rh0) coated Rh-positive erythrocytes (Fc-H). Most PMN and monocytes showed C receptor reactivity for C3b, but only a minor subpopulation of both myeloid cells had C3d receptors. These data provide evidence that human blood myeloid cells may be composed of subsets with different membrane marker reactivities.

Complement C3↗
PubMed1979

Tn polyagglutination preceding acute leukemia.

Tn polyagglutination (persistent mixed-field polyagglutination) was detected in the blood of a 66-yr-old male laborer at the time of a splenectomy for life-threatening thrombocytopenia. Confirmation that the polyagglutination was caused by Tn activation was established by the use of lectins, by failure of the patient's red cells to react with sera from other patients with Tn polyagglutination, by weak aggregation with polybrene, by low red cell sialic acid levels, and by the persistence of polyagglutination over several years of testing. Two years after the discovery of the Tn polyagglutination, the patient developed acute myelomonocytic leukemia. Vigorous chemotherapy regimens resulted in clinical remission of the leukemia and the Tn polyagglutination. This report describes the first known case of Tn polyagglutination preceding the development of acute myelogenous leukemia.

Aged↗
PubMed1979

Immune hemolytic anemia associated with anti-Kell and a carrier state for chronic granulomatous disease.

A patient presented with immune hemolytic anemia associated with a strongly positive direct antiglobulin test (IgG and complement). Anti-K was eluted from the patient's red cells, which were shown to be K negative. A powerful complement-binding anti-K was present in the serum together with another antibody(ies) showing characteristics resembling anti-Bg. Leukocyte antibodies were also present in the patient's serum. The anti-K could be adsorbed and eluted from K negative red cells in vitro. It is suggested that either non-specific adsorption of the anti-K may have occurred due to the Matuhasi-Ogata phenomenon; or, the antibody was an auto "minicking anti-K" capable of reacting with a broader specificity within the Kell system. A serendipitous finding was that the patient was a carrier for chronic granulomatous disease. The associations of immune hemolytic anemia, chronic granulomatous disease, and the Kell system are discussed.

Absorption↗
PubMed1977

The correlation of cold agglutinin titrations in saline and albumin with haemolytic anaemia.

Cold agglutinin syndrome (CAS) is usually associated with IgM cold agglutinins with titres exceeding 1000 at 4 degrees C and a thermal amplitude of 30-32 degrees C. Occasionally patients are encountered who although having clinical and laboratory findings compatible with CAS do not have the characteristic serological findings. Thirty-two patients with a positive direct antiglobulin test due to complement sensitization were studied. Thirty-one of these patients had cold agglutinin titres greater than 64. Twenty-eight had haemolytic anaemia, including one patient with a cold agglutinin titre of only 8 against saline-suspended red cells. 53.6% of sera from patients with haemolytic anaemia reacted at 30 degrees C and 7.1% at 37 degrees C when albumin was not present, whereas in the presence of albumin all of the sera reacted at 30 degrees C and 67.9% reacted at 37 degrees C. None of the four patients without haemolytic anaemia reacted at 30 degrees C or 37 degrees C in the presence of albumin, even though one serum reacted to a titre of 1280 at 4 degrees C. Cold agglutinin titres and thermal amplitudes in the presence of bovine albumin were found to correlate better with haemolytic anaemia than reactions without albumin. If bovine albumin is utilized in compatibility testing, multiple cold autoabsorptions may be necessary before alloantibody activity at 37 degrees C can be excluded.

Agglutinins↗
PubMed1976

Immunologic reactions in penicillin factory workers.

One hundred sixty-nine employees of a synthetic penicillin plant participated in this study to correlate immunologic reactions, allergic symptomatology and dustiness of the work area. Statistically significant positive correlations existed among the following: (1)presence or absence of symptomatology and increasing dustiness of the work area; (2)presence or absence of symptoms and the presence or absence of benzyl-penicilloyl specific hemagglutinating antibody (BPO-specific antibody); (3)the absence, presence and level of titer of BPO-specific antibody with the dustiness of the work area. Because synthetic penicillin dust in the workroom air is able to evoke immunologic responses and produce symptoms among workers exposed to high levels, it is recommended that a reasonable air level for penicillin in factories be in the range of those demonstrated in the least symptomatic group in the study with measurements below 0.1 mg/m3.

Agglutination Tests↗
PubMed1976

Problems in pre-transfusion tests related to drugs and chemicals.

Ingestion of drugs can cause patients or blood donors to have a positive direct and sometimes indirect antiglobulin test. The most common cause of these positive reactions and immune hemolytic anemia due to drugs is the formation of red cell autoantibodies. These autoantibodies will react with the patient's own red cells and usually most other normal red cells in vitro without the drug being present. The prototype drug causing this type of reaction is alpha methyldopa (Aldomet). Other drugs cause positive antiglobulin tests by three different mechanisms, the drug antibodies reacting with red cells in vitro only in the presence of the drug. The first of these mechanisms causes positive reactions because the drug binds firmly to the red cell membrane, and antibody against the drug will combine with the drug on the membrane leading to IgG-sensitized red cells. The prototype drug for this mechanism is penicillin. The second mechanism involves chemical modification of the red cell membrane by the drug so that it takes up many proteins nonspecifically; the cephalosporins are the only group of drugs known to react in this fashion. The final mechanism involves the formation of an immune complex by the drug and its specific antibody. This immune complex will attach to cell membranes, usually activating complement in the process. Examples of drugs thought to operate by this mechanism are phenacetin, quinine, and quinidine. Some individuals have antibodies present in their serum that will react with chemical added to commercial blood bank reagents. Examples of these are antibodies to dyes added to ABO typing sera, antibodies to sodium caprylate in bovine albumin, and antibodies to chemicals added to red cell diluents, e.g., chloramphenicol, neomycin, and hydrocortisone. If these antibodies are present they can create problems in pretransfusion testing; in particular, they can present anomalies in ABO, Rh grouping, and antibody detection.

Agglutination↗
PubMed1975

Penicillin-induced immune hemolytic anemia. Occurrence of massive intravascular hemolysis.

A patient with penicillin-induced immune hemolytic anemia had massive intravascular hemolysis with hemoglobinemia and hemoglobinuria. Substantial amounts of complement components C3 and C4 were detected on the patient's red blood cells (RBCs), in addition to the usual IgG antibody to penicillin. The patient's serum demonstrated a high titer of antibody to penicillin (8,000), which did not cause hemolysis in vitro, but did cause complement fixation when incubated with normal serum. The presence of complement components on the patient's RBCs, and the finding that the serum fixed complement in vitro suggests that penicillin-antipenicillin immune complexes may have been present in the serum. We attribute the severity of the hemolysis to participation of the complement system in the hemolytic process and to the high titer of antibody to pencillin.

Acute Disease↗
PubMed1975

Drug-induced immune hemolytic anemia.

Drug administration causes from 16 to 18 per cent of cases of acquired immune hemolytic anemia. The pathogenesis of erythrocyte sensitization by drug-related antibody with or without fixation of complement is variable, and there is a relationship between the responsible drug, the mechanism of red cell sensitization, clinical manifestations and laboratory methods of diagnosis. Drugs such as phenacetin and quinidine form a complex with the antidrug antibody, and the immune complex attaches to red cells usually fixing complement and causing acute intravascular hemolysis. Other drugs (e.g., penicillins), when given in large doses, coat normal red cells in vivo and in some patients a high titer IgG anti-drug antibody develops which reacts with the coated cells. Hemolytic anemia may develop with red cell destruction being primarily extravascular. Cephalosporins cause positive direct antiglobulin tests in a small percentage of patients either by the same mechanism as penicillins or by modification of the red cell membrane leading to nonimmunologic absorption of serum proteins. Hemolytic anemia has been reported only rarely. A few drugs (notably alpha methyldopa) cause the development of autoimmune hemolytic anemia. Knowledge of clinical manifestations and laboratory aids to diagnosis is necessary to distinguish immunohematologic abnormalities caused by drugs from other causes.

Adsorption↗
PubMed1975

Another example of anti-IB.

Another example of anti-IB is reported. The antibody would only react with cells having both B and I antigens and was transient.

ABO Blood-Group System↗
PubMed1975

Drug-induced haemolytic anemia.

Drug administration causes 16 to 18 per cent of cases of acquired immune haemolytic anaemia. The pathogenesis of erythrocyte sensitisation by drug-related antibody with or without fixation of complement is variable and there is a relationship between the responsible drug, the mechanism of red cell sensitisation, clinical manifestations, and laboratory methods of diagnosis. Drugs such as phenacetin and quinidine form a complex with the antidrug antibody, and the immune complex attaches to red cells usually fixing complement and causing acute intravascular haemolysis. Other drugs (e.g. penicillins) when given in high doses coat normal red cells in vivo and some patients develop a high titre IgG antidrug antibody which reacts with the coated cells. Haemolytic anaemia may develop, with red cell destruction being primarily extravascular. Cephalosporins cause positive direct antiglobulin tests in a small percentage of patients either by the same mechanism as penicillins or by modification of the red cell membrane leading to non-immunological absorption of serum proteins. Haemolytic anaemia has been reported only rarely. A few drugs (notably alpha-methyldopa) cause the development of autoimmune haemolytic anaemia. A knowledge of clinical manifestations and laboratory aids to diagnosis are necessary to distinguish immunohaematological abnormalities caused by drugs fron other causes. Drugs may also cause haemolytic anaemia by nonimmunologic mechanisms as a result of oxidative denaturation of haemoglobin. Factors which make red cells particularly susceptible to the effects of oxidant drugs are intraerythrocytic metabolic abnormalities or the presence of unstable haemoglobins.

Anemia, Hemolytic↗