Search PubMed⌕ Search

Biomedical subjects

G Garratty

Publications and source records attributed to G Garratty.

At least 55 records · Page 3Linked to original sources
PubMed1998

False-positive eluate reactivity due to the low-ionic wash solution used with commercial acid-elution kits.

BACKGROUND: During the use of commercial red cell (RBC) acid-elution kits for adsorption and elution (adsorption/elution) studies with anti-D, unexpected reactive eluates (anti-D) were obtained from D- RBCs. Such results were not obtained with a parallel xylene method or, historically, with heat and ether methods. STUDY DESIGN AND METHODS: Single-donor and commercial polyclonal anti-D samples were incubated with D+ and D- RBCs. Acid eluates were prepared by the manufacturers' directions. Variations in the wash step of the eluate preparation included the use of commercial kit wash solution versus phosphate-buffered saline versus solutions of various ionic strengths. RESULTS: Anti-D was eluted from 20 of 22 samples of D- RBCs after incubation with commercial polyclonal anti-D (titer 512) and from 2 of 3 samples of D- RBCs incubated with single-donor anti-D (titer 256). With a low-titer (16) single-donor anti-D, 0 of 4 eluates from D- RBCs reacted. When phosphate-buffered saline was substituted for the commercial wash solution, 0 of 11 D- RBC eluates reacted, as compared with 9 of 11 D- RBCs that yielded positive 1+(-)2+ eluates with the commercial wash solution. If the recommended initial phosphate-buffered saline wash was omitted before the use of the commercial wash solution, the eluate reactivity was stronger (2+(-)3+). When low-ionic-strength (< 0.03 M) saline was substituted, anti-D was eluted from D- RBCs. All last washes were nonreactive. Antiglobulin tests on all adsorbing D- were negative. CONCLUSION: Commercial wash solutions used for acid elution are at low ionic strength and commonly yield superior eluates, but in the presence of high-titer antibodies, false-positive eluates can result. It is our belief that the low-ionic-strength wash solution caused aggregation of IgG and nonspecific attachment of IgG on RBCs. Aggregates will contain IgG serum antibodies in proportion to the titer of the antibody. It is this nonspecifically bound antibody that is eluted from antigen-negative RBCs.

Acids↗
PubMed1998

Evaluation of the Amicus Separator in the collection of apheresis platelets.

BACKGROUND: A new apheresis instrument, the Amicus Separator with software versions 2.13 and 2.34, was evaluated for component yields, collection efficiency, and incidence of donor and transfusion recipient reactions. The Amicus was also compared to the Spectra Leukocyte Reduction System (LRS) with version 5 software. STUDY DESIGN AND METHODS: Single and double apheresis platelets (APs) were collected at two locations. The targeted platelet yields were 4.0 x 10(11) for single APs and 6.8 x 10(11) for double APs. One location used a double-needle procedure, and the other used a single-needle procedure. Along with 28 of the Amicus procedures (14 at each of two locations), the same donors underwent single or double AP collections on the Spectra LRS. APs were tested for platelet yields and residual white cells. APs were transfused in three hospitals. Donor and transfusion recipient reactions and technical problems were documented. RESULTS: The Amicus Separator efficiently collected single APs (n = 59) and double APs (n = 62) with mean platelet yields of 4.2 x 10(11) and 6.5 x 10(11), respectively. When inlet line alarms occurred in single-needle procedures, platelet yields were lower and collection times were longer. All APs were white cell-reduced below 5.0 x 10(6), and all but one AP were white cell-reduced below 1.0 x 10(6) without filtration. Component yields from the paired Amicus and Spectra LRS procedures were comparable. Collection times (excluding reinfusion/rinseback) were 20 to 23 minutes faster on the Amicus Separator. No serious donor or transfusion recipient reactions occurred. CONCLUSION: The Amicus Separator provided satisfactory platelet yields and collection efficiency, with shorter collection times than did the Spectra LRS, and it white cell-reduced components without filtration.

Blood Donors↗
PubMed1998

Warm autoimmune hemolytic anemia associated with an IgM autoanti-Ge.

A 28-year-old male with a prior history of Hodgkin's disease and a recent upper respiratory tract infection presented with autoimmune hemolytic anemia (AIHA). The patient's red blood cells (RBCs) were spontaneously agglutinated after room temperature and 37 degrees C washes. Dithiothreitol-treated RBCs reacted strongly with anti-C3 and were nonreactive with anti-IgG, -IgM, and -IgA; they reacted with anti-IgM (kappa light chains only) by flow cytometry. The patient's serum was nonreactive. An acid eluate was only weakly reactive, but a 56 degrees C heat eluate strongly agglutinated untreated RBCs (3+). Ficin-treated RBCs were nonreactive. En(a-) RBCs were strongly reactive, but Ge- RBCs were nonreactive. The anti-Ge in the eluate was IgM. The patient's untreated RBCs were shown, by flow cytometry, to be weakly Ge+. This is the first report of IgM-mediated warm AIHA associated with autoanti-Ge.

Journal Article↗
PubMed1997

Severe autoimmune hemolytic anemia associated with IgM warm autoantibodies directed against determinants on or associated with glycophorin A.

BACKGROUND AND OBJECTIVES: Autoimmune hemolytic anemiA (AIHA) is rarely caused by IgM warm autoantibodies, and is sometimes difficult to diagnose. We describe three patients with severe AIHA caused by IgM warm autoantibodies; in two of the three, the hemolysis was fatal. MATERIALS AND METHODS: Conventional hematologic and serologic procedures were used. RESULTS: The IgM autoantibodies in all three cases were directed against determinants on or associated with glycophorin A (Ena, Wrb, and Pr). The IgM autoantibodies and unusual serological characteristics, in that the agglutinins were detected or greatly enhanced only by the presence of albumin or a low pH, and/or the agglutinins reacted optimally at 20-30 degrees C. CONCLUSIONS: IgM warm autoantibodies directed at determinants on or associated with glycophorin A appear to cause severe (often fatal) hemolytic anemia.

Aged↗
PubMed1997

Clinical significance of an anti-Dib assessed by flow cytometry.

Although antibodies to the Dib antigen are generally considered to be of potential clinical significance, we know of no reports assessing the clinical significance of anti-Dib (in vivo or in vitro). We report on an 88-year-old Japanese male gastrectomy patient who had alloanti-Dib. After transfusion of two Di(b-) units, three Di(b+) units had to be transfused, and there were no clinical signs of acute hemolysis. Di(b+) RBC survival was followed retrospectively by flow cytometry. On days 1, 7, and 10, the percent of circulating Di(b+) RBCs was determined to be 39, 30, and 11 percent, respectively, compared to an expected 49, 43, and 41 percent based on calculations. The Di(b+) RBCs appear to have been tolerated for about 6 days, then were removed from the circulation. Direct anti-IgG tests were 1-2+ mixed field with all posttransfusion samples. Monocyte monolayer assays (MMAs), which have been reported to predict the clinical significance of alloantibodies, gave borderline positive results. MMA results using sera from days 0, 3, and 9 were 2.7 and 5.5, 0.8 and 4.8, and 3.0 and 3.7 percent, respectively, without and with added fresh normal serum as a source of complement (clinical significance = > 3% reactivity). The subclass of the anti-Dib was IgG1. This is the first documentation of the clinical significance of an anti-Dib.

Journal Article↗
PubMed1996

Fatal hemolytic transfusion reaction resulting from ABO mistyping of a patient with acquired B antigen detectable only by some monoclonal anti-B reagents.

BACKGROUND: Some monoclonal anti-B reagents are prepared exclusively from an anti-B clone, ES4, that is known to detect acquired B antigens that are not detectable by other anti-B clones or polyclonal anti-B reagents. CASE REPORT: A 92-year-old group A, Rh-negative man with diverticulitis was mistyped as group AB with the use of a monoclonal anti-B. The hospital did not detect anti-B in the patient's serum. After a negative antibody screen, blood was issued through an abbreviated crossmatch (i.e., immediate-spin crossmatch). The patient was given 3 units of group AB blood and 1 unit of group A blood, and no problems were reported. After the transfusion of a ¿fourth unit of AB blood the patient had a severe hemolytic transfusion reaction which resulted in kidney failure and death 10 days later. After the transfusion reaction, the patient's pretransfusion red cells were found to be group A with an acquired B antigen. The monoclonal anti-B used the hospital was formulated from the ES4 clone. A sample of the patient's serum taken before the transfusion was later found to contain a weak anti-B, detectable most obviously by the antiglobulin test, which was not performed at the crossmatch stage. The manufacturers of monoclonal anti-B reagents prepared from ES4 have since modified their reagents (i.e., lowered the pH) so that they now detect only the strongest examples of acquired B antigen. CONCLUSION: A fatal hemolytic transfusion reaction resulted because a monoclonal anti-B that detected acquired B antigen was used to type red cells from an elderly man whose serum had weak anti-B that was not detected by abbreviated compatibility testing.

ABO Blood-Group System↗
PubMed1996

A new form of polyagglutination related to Cad.

Four phenotypes of Cad (Cad 1-4) have been characterized by a continuum of polyagglutinability and reactivity with lectins, with the strongest Cad+ red blood cells (RBCs) being polyagglutinable because of the presence of anti-Cad (anti-Sda) in most normal sera. Over a period of 7 years, a French male blood donor's RBCs demonstrated polyagglutinability with 50 percent to 70 percent of normal adult sera. The reactivity was characteristic of anti-Sda (refractile agglutination at 4 degrees C, 20 degrees C, 37 degrees C, and anti-human globulin test), and was inhibitable by two examples of Sd(a+) urine, but not by Sd(a-) urine or dialysate from Sd(a+) urine. The donor's RBCs reacted 1+ with Glycine max, but did not react with Dolichos biflorus, Leonurus cardiaca, Salvia horminum, or Arachis hypogaea. The first four of these lectins were reactive with five of five Cad+ RBCs, including one example of Cad 4 RBCs. Polybrene(R) aggregated the donor RBCs. Dilutions of nine samples of anti-Sda reacted more strongly with the donor RBCs than with normal RBCs. Even though lectin studies failed to classify this donor's RBCs as Cad, the persistent polyagglutinability and serologic characteristics are consistent with Cad and demonstrate the heterogeneity of this antigen.

Journal Article↗
PubMed1996

Association of blood groups and disease: do blood group antigens and antibodies have a biological role?

Although there are probably over a thousand publications on the associations of blood groups and disease, many are based totally on statistical analyses. Most of the earlier studies have been controversial, because they were small studies and/or had inadequate controls and/or had been analyzed incorrectly. Nevertheless, it is difficult to argue with the general pattern that emerges from the large body of statistical data on malignancy, coagulation and infection. Recent findings in membrane chemistry, rumor immunology and infectious disease (especially relating to bacterial receptors), add a scientific rationale for some of these findings, and there is an increasing rationale for some of the earlier statistical findings. Some of the more recent findings on parasitic/bacterial/viral receptors, the hematological abnormalities seen when high frequency blood group antigens are missing, and the association with immunologically important proteins are most convincing and suggest that blood group antigens do sometimes play a biological role; this role may relate directly, or often be completely unrelated, to the red cell.

Blood Coagulation Disorders↗
PubMed1995

Clinical significance of anti-At(a).

Ata is a high-frequency red blood cell (RBC) antigen. Anti-At(a) has been reported in rare At(a-) black subjects. We report two cases of anti-At(a). A clinically significant anti-At(a) was found in a 26-year-old black woman with systemic lupus erythematosus. The patient had a transfusion reaction with chills and nausea during a RBC survival study, and 95% of the radiolabeled At(a+) RBCs were destroyed within 3 h. A concurrently performed monocyte monolayer assay was strongly reactive. Anti-At(a) thus can cause rapid hemolysis of transfused RBCs, but At(a-) donor units are extremely scarce in rare donor registries. A second patient at our hospital had anti-At(a) which did not affect her newborn. She also had autoimmune disease, insulin-dependent diabetes mellitus.

Adult↗