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Biomedical subjects

S G Sandler

Publications and source records attributed to S G Sandler.

At least 37 records · Page 2Linked to original sources
PubMed1999

Successful prevention of post-transfusion Rh alloimmunization by intravenous Rho (D) immune globulin (WinRho SD).

Alloimmunization to the D blood group antigen following the transfusion of D-positive red blood cells to a D-negative recipient may be prevented in most persons by a prompt and adequate dose of Rho (D) immune globulin (RhIG). Until recently, the only RhIG approved by the US Food and Drug Administration (FDA) for this indication required intramuscular injection, an inconvenient and painful route for the relatively large volume that may be required. We describe the successful prevention of Rh alloimmunization following the unintentional transfusion of D-positive red blood cells to a D-negative infant by the intravenous infusion of WinRho SD, a new RhIG that is FDA-approved for prevention of post-transfusion Rh alloimmunization by intravenous administration. We believe that this more convenient and less painful approach should be the treatment of choice for preventing Rh alloimmunization following the transfusion of D-positive red cells to a D-negative recipient.

Anemia, Sickle Cell↗
PubMed1999

Impact of innovations on transfusion medicine.

The final decade of the last century of the second millennium ad has seen dramatic changes in all aspects of science and health care. In transfusion medicine, the blood supply is the safest it has ever been. Newer refinements and innovations are continuously being researched and implemented to achieve and further enhance safety. Advances in blood conservation, pharmacologic manipulation, engineered blood derivatives, and recombinant growth factors can now provide safer and more effective alternatives to blood transfusions for many patients. This overview highlights selective innovations in transfusion medicine and emphasizes some significant advances that have occurred in blood donor screening, blood component collections and therapy, and laboratory testing. Newer technologies are anticipated that will further enhance the safety of blood and transfusions and potentially augment annually the blood supply on a worldwide basis.

Blood Component Transfusion↗
PubMed1999

Naturally-occurring anti-Jka in infant twins.

Anti-Jka was detected by solid-phase red cell adherence (SPRCA) antibody detection and identification tests in the plasma of a 9-month-old female infant during a routine presurgical evaluation. The patient and her nonidentical twin sister, who also had anti-Jka in her plasma, were products of an uncomplicated in vitro fertilization, full-term pregnancy, and vaginal delivery. Neither twin had been transfused, recently infected, or treated with medication. Their mother had no prior pregnancies or transfusions. Red blood cells (RBCs) from the patient and her sister typed as Jk(a-b+) by direct hemagglutination, and this phenotype was confirmed by negative adsorption and elution studies. Both infants' plasma samples were strongly reactive with 20 examples of Jk(a+) RBCs and nonreactive with 20 examples of Jk(a-) RBCs by SPRCA assays. Anti-Jka was not detected in either twins' plasma by indirect antiglobulin tests by tube method in low-ionic- strength saline solution or polyethylene glycol, or with ficin- or papain-treated RBCs. Monocyte monolayer assays using Jk(a+) RBCs sensitized by either twins' serum were nonreactive (0%). RBCs from both parents typed as Jk(a+b+). Both parents' antibody detection test results by SPRCA assay were negative. The absence of a history of exposure to allogeneic RBCs or possible passive transfer of maternal or other alloantibody classifies these antibodies as naturally-occurring anti-Jka.

Journal Article↗
PubMed1998

Immunoprophylaxis using intravenous Rh immune globulin should be standard practice when selected D-negative patients are transfused with D-positive random donor platelets.

A 67-year-old female developed excessive bleeding and thrombocytopenia following cardiovascular surgery. Her blood type was group A, D-. The only platelet products available in the transfusion service were random donor platelet concentrates from D+ donors. She was transfused with a pool of 6 D+ random donor platelet concentrates. Anti-D undetected in her pretransfusion serum by solid-phase antibody screen was present 11 days later. Retrospectively, the patient provided a history of having two pregnancies more than 40 years ago, prior to the availability of immunoprophylaxis by Rh immune globulin (RhIG). Although studies have shown that as many as 19 percent of D- people may develop anti-D following transfusion of platelets from D+ donors, there is no specific standard requiring immunoprophylaxis with RhIG to prevent Rh alloimmunization after transfusion of random donor platelet concentrates from D+ donors. In contrast, vigorous efforts are routine for preventing Rh alloimmunization in D- patients requiring red cell transfusions or D- females during pregnancy or after delivery of D+ newborns. The absence of a comparable practice standard for platelet transfusions is based, in part, on concern that intramuscular injections of conventional RhIG may cause local hemorrhage in thrombocytopenic persons. The recent availability of a Food and Drug Administration-approved preparation of intravenous RhIG makes Rh immunoprophylaxis in thrombocytopenic patients safe and practical. We recommend that intravenous RhIG be considered if it is necessary to transfuse random donor platelet concentrates from D+ donors to D- recipients. As a minimal standard, intravenous RhIG should be administered to all D- females of childbearing age who are recipients of pools of random donor platelet concentrates from D+ donors.

Journal Article↗
PubMed1998

Management of patients with hematologic malignancies and aplastic anemia who are refractory to platelet transfusions.

Patients with hematologic malignancies or aplastic anemia may have reduced responses to platelet transfusions after multiple transfusions of standard red blood cells or platelet components. This situation, conventionally described as 'refractoriness' to platelet transfusions, may result from immune or non-immune causes. Non-immune causes include fever, infections, hypersplenism, disseminated intravascular coagulation, antibiotics, or veno-occlusive disease. Immune causes include platelet-reactive alloantibodies, which are typically antibodies to human leukocyte antigens (HLA) or, less commonly, antibodies to human platelet antigens (HPA). Transfused HLA-matched platelets often have satisfactory posttransfusion survivals, but few transfusion services have the donor and logistical resources to sustain a prolonged course of platelet transfusions requiring four-antigen matches. The availability of commercially marketed kits for crossmatching samples of potential donors' platelets with a recipient's serum has facilitated donor-recipient matching. Also, platelet crossmatching may be used to select a suitable unit of from several candidates platelets that have been identified to be partial HLA matches. The high likelihood of decreased efficacy of platelet transfusions in HLA-alloimmunized recipients makes avoidance of exposure to HLA-bearing leukocytes a priority. This goal is facilitated by lowering transfusion 'triggers' for cellular blood components, particularly for prophylactic platelet transfusions, by reducing the leukocyte content of components by leukocyte-reduction filters and, possibly by ultraviolet-B irradiation of leukocyte-containing products.

Anemia, Aplastic↗
PubMed1997

Screening with monoclonal anti-Fy3 to provide blood for phenotype-matched transfusions for patients with sickle cell disease.

BACKGROUND: In the United States, there is a shortage of blood group phenotype-matched red cells (RBCs) for patients with sickle cell disease (SCD). A protocol designed to supply phenotype-matched RBCs for these patients by combining the recruitment of African American blood donors and automated testing of RBCs for these patients for the presumptive Fy(a-b-) phenotype using monoclonal anti-Fy3 was evaluated. STUDY DESIGN AND METHODS: African American donors were recruited, to increase the likelihood of phenotype matches in the donor population. Samples of RBCs were tested for the presumptive Fy(a-b-) phenotype by using monoclonal anti-Fy3 and an automated blood typing analyzer. RBCs confirmed to be Fy(a-b-) were retyped for selected Rh, MNS, Kell, Duffy, and Kidd blood system antigens. The extended phenotypes were matched with those of 41 SCD patients requiring transfusions. RESULTS: Of 8323 blood donations during the study, approximately 40 percent (3329) were made by African Americans. Approximately 22 percent (737) of African Americans were identified as Fy(a-b-) by this protocol and 12 percent (410) were phenotype matches for the 41 SCD patients. CONCLUSION: Combining the recruitment of African American blood donors and automated phenotyping using monoclonal anti-Fy3 offers a practical, relatively low-cost strategy for supplying phenotype-matched RBCs for SCD patients. This protocol increases the options for addressing the shortage of phenotype-matched RBCs for SCD patients.

Anemia, Sickle Cell↗
PubMed1997

Alloimmune refractoriness to platelet transfusions.

Patients who are transfused on multiple occasions with red cells or platelets may develop platelet-reactive alloantibodies and experience decreased clinical responsiveness to platelet transfusion. This situation, conventionally described as "refractoriness to platelet transfusions," is defined by an unsatisfactory low post-transfusion platelet count increment. If antibodies to HLAs are detected, improved clinical outcomes may result from transfusions of HLA-matched or donor-recipient cross-matched platelets. Because refractoriness is an expected, frequently occurring phenomenon, prevention of HLA alloimmunization is an important management strategy. Prevention strategies include efforts to decrease the number of transfusions, filtration of cellular components to reduce the number of HLA-bearing leukocytes, or pretransfusion ultraviolet B irradiation of cellular components to decrease their immunogenicity. Other investigational approaches include reducing the expression of HLAs on transfused platelets, inducing a transient reticuloendothelial system blockade by infusions of specialized immunoglobulin products, or transfusing semisynthetic platelet substitutes (thromboerythrocytes, thrombospheres) or modified platelets (infusible platelet membranes, lyophilized platelets).

Biological Products↗
PubMed1997

Case report: reporting anti-G as anti-C+D may have misleading clinical implications.

Four months after a D- male was transfused with four units of D- red blood cells (RBCs), the results of a standard pretransfusion antibody screen and alloantibody identification panel detected anti-C+D in his serum. This report was interpreted by his physician to be evidence of alloimmunization to the D antigen, which triggered concern that the patient had been transfused previously with D+ RBCs as the result of an error in blood typing or personal identification. After a review of hospital records failed to identify such an error, consultation with a reference laboratory technologist confirmed that the serologic reactions resembled those of anti-C+D but were also consistent with anti- C + anti-G. Additional testing confirmed that the reactions were due to anti-G, not anti-C+D. One of the four donors was identified to have the C+D- RBC phenotype, which is typically G+, thus identifying the stimulus for anti-G. Routine reporting of the detection of anti-C+D in the serum of D- people, without confirmatory testing or commentary about the possibility that anti-G may resemble anti-C+D, may mislead health care providers who are not familiar with the pertinent blood group serology.

Journal Article↗
PubMed1996

Coexistent IgG2 and IgA deficiencies in blood donors.

BACKGROUND: To meet the transfusion requirements of IgA-deficient patients with anti-IgA, blood services screen random donors to identify potential donors of IgA-deficient blood components. New information reveals that some IgA-deficient persons may also be deficient in IgG2 and may be at increased risk for bacterial infections. STUDY DESIGN AND METHODS: Serum samples from IgA-deficient blood donors and patients were tested for IgG2 concentration by radial immunodiffusion using monospecific anti-IgG2. RESULTS: Four (9.0%) of 44 IgA-deficient blood donors and 14 (31.5%) of 44 IgA-deficient patients had coexistent IgG2 and IgA deficiencies. Follow-up interviews with the 4 donors who had coexistent IgG2 and IgA deficiencies revealed that 3 had recurrent respiratory infections and had been hospitalized at least once for pneumonia. The fourth donor did not report a history suggestive of recurrent infections. CONCLUSION: Some blood donors, recruited specifically because they are IgA deficient, may also be deficient in IgG2. Persons identified by donor screening programs as being IgA deficient should be tested for IgG2. If deficient in IgG2, they should be evaluated for a history of recurrent bacterial infections and counseled accordingly.

Blood Donors↗
PubMed1995

IgA anaphylactic transfusion reactions.

IgA anaphylactic transfusion reactions are rare events, estimated to occur in 1 in 20,000 to 47,000 transfusions. The signs and symptoms of these reactions do not differentiate them from other causes of anaphylaxis. The diagnosis of an anaphylactic transfusion reaction is established by showing an IgA-antibody in the patient's serum. Most laboratories that test for IgA antibodies rely on the PHA method, which uses red blood cells that are coated with serologically defined IgA multiple myeloma proteins. We tested sera referred from Red Cross regional blood centers and hospitals from patients with suspected IgA anaphylactic reactions and found an IgA antibody in 76.3% of IgA-deficient patients. However, only 17.5% of all samples referred contained an IgA antibody, indicating that most persons with suspected IgA anaphylactic reactions had experienced acute generalized reactions that were from causes other than anti-IgA transfusion. Using PHIA to measure serum concentrations of IgA and PHA to detect IgA antibodies, we found the frequency of IgA deficiency (< 0.05 mg/dL) and class-specific anti-IgA in random blood donors to be approximately 1 in 1,200. Titers of anti-IgA did not distinguish these seemingly healthy blood donors from patients with a history of an anaphylactic transfusion reaction. Because the frequency of 1 in 1,200 greatly exceeds the observed frequency of anaphylactic reactions in transfused persons, we conclude that using PHA for anti-IgA does not reliably predict risk for an anaphylactic transfusion reaction. Additional research is needed to define a more specific marker to identify those persons who are truly at risk for these serious, but rare, complications of blood transfusion.

Anaphylaxis↗
PubMed1995

Pooling blood donor samples to reduce the cost of HIV-1 antibody testing.

Accurate, low cost testing of donated blood is a goal of the global effort to reduce the spread of the human immunodeficiency virus (HIV-1). We describe a modified enzyme immunoassay (EIA) method for detecting HIV-1 antibody (anti-HIV-1) in 15-sample pools. In this preliminary study, the modified EIA was as sensitive for detecting weakly seropositive samples, and as specific for testing HIV-1 Western blot-negative or Western blot-indeterminate results, as testing individual samples by the standard EIA. A simulation of field operations was conducted using pools of blood donor samples collected in the United States and in Shanghai, People's Republic of China. Implementation of the modified EIA method and testing 15-sample pools for anti-HIV-1 is a reliable strategy for reducing the cost of large scale testing of donated blood for anti-HIV-1 in areas of low seroprevalence.

Blood Donors↗
PubMed1995

Biological functions of blood groups in health and disease.

Biochemical studies reveal that erythrocyte blood group antigens are the immunological expression of polymorphic and, frequently, biologically-active membrane structures. Some of these structures have been identified to be specific transport proteins, enzymes, or receptors for infectious agents. Certain erythrocyte phenotypes, for example, Rh(null), lack all or most antigens in a specific blood group system. Changes in erythrocyte morphology and function associated with these phenotypes provide insights into the roles of the corresponding proteins in the maintenance of membrane integrity. Other phenotypes, for example Oh, and p, also lack multiple blood group antigens, but the absence of changes in morphology or function in these erythrocytes suggests that their corresponding carbohydrate determinants are not essential for maintaining membrane integrity. Additional information on the function of erythrocyte membrane structures that express blood group antigens is likely to advance our understanding of the role of blood groups in health and disease.

Blood Group Antigens↗
PubMed1995

Correlation of monocyte monolayer assays and posttransfusion survival of Yt(a+) red cells in patients with anti-Yta.

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.

Journal Article↗
PubMed1994

Hemagglutination assays for the diagnosis and prevention of IgA anaphylactic transfusion reactions.

Passive hemagglutination assays (PHA) may be used to detect IgA antibodies to confirm clinical diagnoses of suspected IgA anaphylactic transfusion reactions. Passive hemagglutination inhibition assays (PHIA) may be used to identify IgA-deficient blood donors whose plasma-containing components are transfused to prevent anaphylactic transfusion reactions in prospective recipients at risk because of the presence of IgA antibodies. Using a standard PHA, we detected class-specific anti-IgA in 76.3% of 80 IgA-deficient patients with a history of an anaphylactic transfusion reaction, and in 21.7% of 97 asymptomatic IgA-deficient blood donors or their IgA-deficient family members. Using PHIA, we confirmed IgA deficiency (< 0.05 mg/dL) for the donors of 525 plasma-containing blood components that were transfused without acute clinical reactions to 48 IgA-deficient recipients with anti-IgA and/or a history of an anaphylactic transfusion reaction. The frequency of IgA-deficiency with class-specific anti-IgA among 32,376 random blood donors was 0.08% (1/1,200). The combined use of PHA for detecting anti-IgA and PHIA for measuring IgA concentration provides an effective and safe strategy for the diagnosis and prevention of IgA anaphylactic transfusion reactions. However, PHA for anti-IgA lacks specificity for identifying persons who are truly at risk for significant anaphylactic transfusion reactions. The consequence is an overdiagnosis of IgA anaphylactic transfusion reactions and an overestimation of the number of persons at risk for IgA anaphylactic transfusion reactions because of the detection of an IgA antibody in their serum.

Anaphylaxis↗
PubMed1994

Human T-lymphotropic virus type II in Panamanian Guaymi Indians.

BACKGROUND: Currently, human T-lymphotropic virus type II (HTLV-II) is the most prevalent human retrovirus, detected in persons presenting to donate blood in the United States. Only scant information is available with which to counsel HTLV-II-seropositive deferred donors or other persons about the ways in which they may spread HTLV-II to others. STUDY DESIGN AND METHODS: To increase understanding of the modes of transmission of HTLV-II, a seroepidemiologic study was conducted among Panamanian Guaymi Indians, a recently identified focus of endemic HTLV-II infection. Subjects were tested for serologic evidence of infection by HTLV-II, HTLV type I, hepatitis B virus, and nine other infectious agents by enzyme immunoassays and specific confirmatory tests. RESULTS: Nine (8.3%) of 109 persons tested HTLV-II-seropositive. HTLV-II seropositivity was more likely in persons with serologic evidence of prior hepatitis B virus infection. Sexual contact with HTLV-II-seropositive partners, but neither parenteral exposure nor breast-feeding, was identified as a risk factor for HTLV-II. CONCLUSION: In Guaymi Indians, HTLV-II appears to be spread primarily through sexual transmission.

Adolescent↗