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Biomedical subjects

G Garratty

Publications and source records attributed to G Garratty.

At least 109 records · Page 6Linked to original sources
PubMed1985

Immune hemolytic anemia associated with probenecid.

Upon hospital admission a patient was found to have severe anemia and a strongly positive direct antiglobulin test (DAT). The patient was taking probenecid periodically for gout. An antibody was detected in the patient's serum that only reacted with red blood cells (RBCs) when probenecid was added. Eluates from the patient's RBCs, with and without the presence of drug, were nonreactive. Upon the discontinuation of probenecid, the patient's hemoglobin level improved steadily. We believe this to be the first reported case of immune hemolytic anemia associated with probenecid.

ABO Blood-Group System↗
PubMed1985

High frequency antigens of human erythrocyte membrane sialoglycoproteins. I. Ena receptors in the glycosylated domain of the MN sialoglycoprotein.

The specificity of various allo- and autoantibodies, which agglutinate normal erythrocytes, but do not react with En(a-) red cells and normal erythrocytes, treated with trypsin (anti-EnaTS) or ficin (anti-EnaFS), was investigated. Various fragments and modification products of the major (MN) red cell membranes sialoglycoprotein were used in hemagglutination inhibition assays. Six anti-EnaFS sera were found to be directed against the residues approx. 46-56 of the molecule. Five of these require the carbohydrate unit, attached to Thr50, for binding. One anti-EnaTS serum was found to be directed against the residues approx. 36-42. Another antibody with anti-EnaTS specificity was shown to react with the residues 31-39 in some of the MN sialoglycoprotein molecules, namely those not glycosylated at a certain position (probably Thr33). A third anti-EnaTS serum, directed against the sequence domain around Lys30, was also found to react only with a fraction of the molecules, apparently due to the variable attachment of oligosaccharides in that region. The heterogeneity of glycosylation, detected by these two sera, appears to account for the partial tryptic and chymotryptic cleavage in this domain of the MN sialoglycoprotein, which has been described previously. Heterogeneity of the glycosylation at various positions of the molecule could be established by the isolation and analysis of peptides.

Amino Acid Sequence↗
PubMed1984

The significance of complement in immunohematology.

In vitro detection of red cell-bound complement can be important in the differential diagnosis of autoimmune and drug-induced immune hemolytic anemias; it can also be a sensitive test for the detection of complement-binding alloantibodies, e.g., in compatibility testing. Red cell-bound complement can be detected by the antiglobulin test if suitable antiglobulin sera (AGS) are utilized. In 1971, the Federal Standards for AGS were criticized because so-called broad spectrum AGS used routinely in blood banks were shown to often be deficient in anticomplement reactivity. In the new few years commercial regents changed with regard to the quantity and specificity of their anticomplement components. A great deal of controversy developed as to the true importance of detecting red cell-bound complement, the particular fragments of complement that should be detected, and the causes of nonspecific reactions that seemed to be occurring, especially with the increasing usage of new techniques utilizing low ionic strength media. When monospecific anti-IgG and anti-C3 became available commercially, the controversy regarding diagnostic testing was resolved as direct antiglobulin testing could be performed with these reagents rather than the broad spectrum reagents. Two main questions remained: how rare are alloantibodies that are only detectable by the anticomplement component of AGS? How clinically significant are such antibodies? The results of our 3-year study indicated that such antibodies (usually anti-Kidd) occurred with a incidence of 1/8000 sera tested. Some of these antibodies seemed capable of shortening the life span of transfused red cells, as determined by 51Cr survival studies; some showed negligible cell destruction. Severe transfusion reactions due to such antibodies would seem unlikely. Individual laboratories will have to balance the risk of missing some complement-dependent antibodies of possible clinical significance with the increased nonspecificity encountered in their own laboratory with AGS containing anticomplement.

Anemia, Hemolytic↗
PubMed1984

Increased IgG molecules bound to the surface of red blood cells of patients with sickle cell anemia.

We have used the complement-fixing antibody consumption ( CFAC ) test to detect small concentrations of IgG on red blood cells from patients with hemolytic anemias that are not thought to be caused by an immune mechanism. Although patients with hereditary spherocytosis, pyruvate kinase deficiency, and mechanical hemolytic anemias generally had normal concentrations of IgG bound to their red cells (less than 25 molecules IgG per red cell), we found that 39/62 (63%) patients with sickle cell anemia had elevated values. These 39 patients had a mean of 195 and a maximum of 890 molecules of IgG per red cell. None of the patients had been transfused within the previous 90 days, and some had never been transfused. Direct antiglobulin tests were positive in only two instances and autoantibodies were not found in the serum of any patient. However, eluates from the red cells of 6 of 23 patients demonstrated antibody activity against all of a panel of normal red cells by the indirect antiglobulin test. There was no correlation between the number of IgG molecules on patients' red cells and the severity of their anemia, the incidence of painful sickle cell crises, the reticulocyte count, or with blood transfusion history. We conclude that further study of immunohematologic abnormalities in patients with sickle cell anemia is warranted, especially in view of previous reports in this population of patients with red cell autoantibodies, autoimmune hemolytic anemia, hemolytic transfusion reactions without detectable alloantibodies, and an association of some episodes of pain crises with immunologically mediated red cell destruction.

Adolescent↗
PubMed1983

Mechanisms of immune red cell destruction, and red cell compatibility testing.

The immune destruction of red cells can occur as a complement-mediated intravascular process, or extravascularly, where the red cells are destroyed by macrophages following interaction with cell-bound IgG1, IgG3, and/or C3b. Many of the factors that affect this in vivo destruction are not taken into account during in vitro pretransfusion compatibility testing. At present, even by use of more elaborate tests, it is difficult to accurately predict the fate of a transfused unit of blood. By using some simple information, such as antibody specificity and thermal range, it is sometimes possible to predict the outcome of transfusing a unit of blood that is incompatible in vitro. At other times it may be necessary to utilize 51Cr-labeled red cells to determine the risk of transfusing such units. Because of the paucity of reported clinical correlations, macrophage/monocyte monolayer assays are of little practical value at present.

Anemia, Hemolytic, Autoimmune↗
PubMed1981

Acute immune intravascular hemolysis due to hydrochlorothiazide.

Acute near-fatal intravascular hemolysis and renal failure developed in a patient after he had ingested 15 to 20 tablets of both methyldopa (Aldomet) nd hydrochlorothiazide (HydroDiuril). Serologic test results were inconsistent with those associated with methyldopa-induced hemolytic anemia and suggested that hemolysis was caused by hydrochlorothiazide antibodies reacting by an immune complex mechanism.

Acute Kidney Injury↗
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↗