Search

Iodine/silver(I) oxide (I(2)/Ag(2)O) reacts highly stereoselectively in the single, double, and triple anti epoxidation of the spherical 1,4,7-triene, 10-methyl-2,3:5,6:8,9-tris(cyclohexano)triquinacene 1. All of the three epoxides 3, 4, and 5 obtained with this reagent contain the epoxy groups at the convex side of the triquinacene framework. The stereochemical course of the epoxidation with I(2)/Ag(2)O is clearly distinct from that observed with m-chloroperbenzoic acid (MCPBA), which gives the same monoepoxide (3) but exclusively anti,syn di- and triepoxides (6-8) bearing at least one epoxy group at the concave side of the triquinacene framework. Epoxidation of the related three-fold 1,4-cyclohexadiene, tris(cyclohexeno)triquinacene 2, with MCPBA occurs similarly to the conversion of 1, whereas I(2)/Ag(2)O reacts with high regioselectivity at the less electron-rich peripheral double bonds of 2 giving triepoxides 12 and 13. The molecular structure of triepoxide 8 has been elucidated in detail by X-ray crystal structure analysis.

Anti-Yta is an antibody to a high-frequency (99.8%) antigen and has been reported to have variable clinical significance. A retrospective review of monocyte monolayer assay (MMA) results on sera from 79 patients with anti-Yta was conducted to determine the reliability of this assay to predict the clinical significance of anti-Yta. Results of the MMA, other serological tests, and patient transfusion histories were analyzed. The MMA was found to be a reliable predictor of the clinical significance of anti-Yta when samples for analysis were collected at least six weeks after initial detection of the antibody. Only 18.2 percent of those examples of anti-Yta tested appeared to be clinically significant.

Positive direct antiglobulin tests (DATs) associated with cephalosporin therapy have been reported, but rarely were associated with immune hemolytic anemia (IHA). In 1989, we described the first case of IHA associated with cefotetan (Cefotantrade mark) causing hemolysis by the drug-adsorption mechanism. We now report the full details of ow investigation. The patient was a 23-year-old female with a 2 1/2 year history of chronic ulcerative colitis. After 4 days of therapy with cefotetan (2 g/day), her hematocrit (Hct) decreased from 34.351 to 23.3%. The reticulocyte count was 6.9%. The DAT was 2+ (IgG only), and the serum and an eluate were nonreactive with a panel of standard reagent red blood cells (RBCs). Cefotetan therapy continued and the patient was transfused with two units of RBCs. On day 6 of therapy, the patient experienced an anaphylactoid reaction attributed to sensitivity to cefotetan. Cefotetan therapy was discontinued, the patient was treated with corticosteroids and epinephrine, and she was transfused with an additional unit of RBCs. Her Hct rose to 34.1% prior to her discharge on day 11. Further investigation revealed that the patient's serum and an eluate contained an antibody that reacted with cefotetan- and cephalothin-coated RBCs by the indirect antiglobulin test. In a monocyte monolayer assay, monocytes readily phagocytized cefotetan- and cephalothin-coated reagent RBCs but not uncoated reagent RBCs. The patient's serum did not react by the so-called immune-complex mechanism when cefotetan or cephalothin was added to the patient's serum + complement + RBCs.

Four methods were compared as to their suitability for excluding IgA deficiency in the investigation of suspected anti-IgA transfusion reactions. The methods were radial immunodiffusion, passive hemagglutination inhibition, sandwich enzyme-linked immunosorbent assay, and membrane enzyme immunoassay. Parallel testing was performed on sera from 40 patients or blood donors previously found to have anti-IgA and low or undetectable levels of IgA. All test methods identified the 40 sera as having abnormally low IgA levels. The membrane enzyme immunoassay required 10 minutes or less for testing, as compared to 3 hours for passive hemagglutination inhibition, 4 hours for sandwich enzyme-linked immunosorbent assay, and 48 hours for radial immunodiffusion. The membrane enzyme immunoassay offers the potential for a rapid, instrument-free screen of IgA levels and therefore may be useful in identifying those patients with suspected anti-IgA anaphylactic transfusion reactions who are not IgA deficient and do not require IgA-deficient blood components for additional transfusions.

During a serologic study on red cell samples from individuals representing three generations of a Chinese family, an unusual pattern of reactivity was noted in a sample from a daughter of an A1B2 individual. The results of direct ABO grouping, titration, and adsorption studies demonstrated that the red blood cells (RBCs) from the proposita and two of the proposita's uncles (1) expressed more B antigen than group B2 RBCs but less than group B1 RBCs; (2) expressed the B1 antigen but at a lower level than group B1 RBCs; and (3) expressed more H antigen than B1 RBCs but slightly less than B2 RBCs. The saliva from the proposita contained soluble B and H antigens, and her serum contained a weak B-gene-specified transferase. Serologic reactivity of her RBCs was intermediate between that of B1 and B2, RBCs. That is similar to reactivity of Aint RBCs, which is intermediate between A, and A2 RBCs. The proposita may represent a Bint phenotype.

An alloantibody to a high-incidence antigen, associated with multiple other alloantibodies, made it impossible to supply antigen-negative red blood cells (RBCs) for a chronically transfused sickle cell anemia patient. Anti-Cra,-E,K,-S, -Fya, -Fyb, as well as anti-M reactive at 37 degrees C and in the antiglobulin phase of testing, were identified in the patient's serum. An extensive search of rare donor files at the American Red Cross and at the American ASsociation of Blood Banks (AABB) failed to identify Cr(a-),M-,E-,K-,S-, Fy(a-b-) donors. Various studies were performed to predict the clinical significance of the anti-Cra and anti-M. Results of 51chromium survival studies showed 91.8 percent survival at 10 minutes and 87.2 percent survival at 60 minutes with Cr(a +),M-, K-,S-,Fy(a-b-) donors. Various studies were performed to predict the clinical significance of the anti-Cra and anti-M. Results of 51chromium survival studies showed 91.8 percent survival at 10 minutes and 87.2 percent survival at 60 minutes with Cr(a +),M-,E -,K-,S-,Fy(a-b-) red cells, suggesting that immediate destruction of transfused CrCa+) red cells would he unlikely. However, further analysis revealed diminished long-term survival of the donor's red cells with only 60.1 percent recovery at six days (T 1/2 = 12 days) and 10.8 percent at 14 days (T 1/2 = 4.5 days). A monocyte- monolayer assay (MMA) indicated that both the anti-Cra (5.9%) and anti-M (18%) would probably be clinically significant (normal value 0-3%). Mass screening continues at several blood centers for Cr(a-),M-, E-,K-,S-,Fy(a-b-) donors. However, if no suitable donors are found, the results of the 51chromium survival studies and the MMA support the decision to transfuse this patient with Cr(a+),M-,F(a- b-),S-,K- ,E- red cells, if necessary.