Autologous Anti‐I and Anti‐M Following Liver Transplant

A patient who received a liver transplant subsequently developed autologous anti‐I and anti‐M. The antibodies were demonstrated in the serum and in eluates from the patient's red blood cells, and could be separated by cross‐absorption with appropriate red blood cells. The patient received horse antilymphocyte globulin and the possibility could not be excluded that the anti‐M was transferred passively.     

Three New Antibodies to High‐incidence Antigenic Determinants (Anti‐El, Anti‐Dp, and Anti‐So)

Three new antibodies have been investigated relative to genetic control of the absent antigenic determinant. In each instance a family member has lacked the same antigenic determinant as the propositus. None of the three antibodies is identical with any previously reported one. Because a second case was found identical with one of these antibodies, it was felt that other cases may be resolved as a result of this report. The number of random donors tested with each of the individual antibodies varied from several hundred to several thousand. None was compatible with the specific antibodies.     

Three Examples of Rh‐Positive, Good Responders to Blood Group Antigens

Three patients are described who produced a variety of blood group antibodies following exposure to foreign red cells. These findings are considered in relation to the theory that a small group of individuals possess an ability, possibly genetically determined, to readily form antibodies and the theory that the first antibody formed may augment the production of other antibodies.     

Hemolytic Anemia Due to Anti‐A in Concentrated Antihemophilic Factor Preparations

Progressive anemia developed in a type A₁ hemophiliac after he had received a large amount of commercial Factor VIII concentrate. Anti‐A was found in the patient's serum as well as in eluates from his erythrocytes. Moreover, the product contained potent anti‐A. A positive direct antiglobulin test and increased osmotic fragility with microspherocytosis were additional laboratory findings which suggested passive transfer of anti‐A as the cause of the anemia. The possibility of anemia due to transfused anti‐A or anti‐B should be considered in patients, other than those of type O, who manifest progressive anemia following treatment with large volumes of a pooled plasma product.     

The Second Example of Anti‐Bea Causing Hemolytic Disease of the Newborn

The second example of anti‐Be^a which caused hemolytic disease of the newborn is reported. Confirmation was made by using the cells and serum of the original Berrens family. The antibody was stimulated by pregnancy only. Three of four children are Be(a+) and two had hemolytic disease of the newborn. No genetic relationship of Be^a with any other blood group system has been revealed.     

An Anti‐Diegob (Dib) Antibody Occurring during Pregnancy

A case is reported in which fetal erythrocytes were sensitized by IgG maternal anti‐Di^b, which indicates that Di^b incompatibility must be considered in cases of erythroblastosis fetalis caused by a high‐frequency erythrocyte antigen, especially in persons of Mongoloid or American Indian extraction.     

Demonstrating effectiveness—the concept of numbers‐needed‐to‐treat

When assessing a health-care intervention the main question is—does it work? Often, a more difficult question needs to be answered—how well does it work? Systematic reviews and meta-analyses help to provide answers to both questions. Too often though, the results are expressed in a way that leaves the reader asking, ‘what is the result?’ Numbers-needed-to-treat is a simple method for conveying the answers. It can be applied to any chosen clinical outcome with dichotomous data, and the results can be understood by doctor, patient and the public. This paper discusses the concept of numbers-needed-to-treat and gives worked examples using trials in H. pylori eradication and lowering of serumcholesterol.     

Primary anti-D immunization by weak D type 2 RBCs

BACKGROUND: D is the most immunogenic blood group antigen. In about 0.4 percent of whites, D is expressed on RBCs in a weak form. Recently, it was found that the weak D phenotypes are caused by a large number of distinct RHD alleles generally encoding altered D proteins. No particular molecular weak D type has yet been shown to induce anti-D. The threshold of D antigen density required for anti-D immunization is not known. CASE REPORT: A 72-year-old D- white man received apparently D- RBCs. Nineteen days later, he developed a positive DAT, and anti-D was found in his serum and an eluate from his RBCs. One donor was found to be D+ with a weak D type. The weak D type was determined by RHD exon 9-specific nucleotide sequencing from genomic DNA. The transfusion recipient showed alloanti-D. Ten months later, anti-D but no other antibody was detectable; the DAT was negative and the eluate was nonreactive. The donor of the incriminated unit was D+ (ccDEe) with weak D due to the weak D type 2 allele, expressing about 450 D antigens per RBC. CONCLUSION: This case provides formal proof that RBCs of weak D type 2 phenotype may cause alloanti-D immunization. Among the more prevalent weak D types in whites, weak D type 2 has the lowest D antigen density. Thus, units of blood from donors of the weak D type 2 phenotype should be labeled D+; the weak D type 2 phenotype may be useful for quality assurance.     

Circulation of Concentrated One‐day‐old Platelets in Vivo

Platelet concentrates of rat and human origin were stored at 22 C or at 4 C for up to 24 hours without additives. Transfusion of these concentrates into thrombocytopenic recipients demonstrated that: (1) storage of rat or human platelets at 4 C for up to 24 hours did not affect their recovery in vivo ; (2) storage at 22 C resulted in a marked reduction in the viability of rat platelets but only a slight reduction in the viability of human platelets as adjudged by these criteria; (3) at 24 hours posttransfusion, the residual increment of platelets stored at 22 C was significantly higher than that of platelets stored at 4 C. The pH of the concentrates (rat and human) stored at 4 C remained slightly alkaline while the pH of those stored at 22 C., especially rat platelets, was significantly reduced. The deleterious effects of storage of platelets at 4 C are well known. These effects, however, do not preclude their usefulness when a limited objective of arresting or preventing hemorrhage for short periods is pursued. When daily platelet transfusions are feasible, platelets stored for 24 hours at 4 C in the absence of fresh material are adequate for clinical use.     

Evaluation of Methods for the Preparation of HL‐A Antigen‐Poor Blood

More than 85 per cent of the leukocytes are removed from blood by dextran or Plasmagel sedimentation and by both high and low glycerol freeze‐thaw technics. Larger numbers of white cells and platelets remain in bloods processed by inverted centrifugation, saline washing, and agglomeration without freezing. Cytoglomeration is the least efficient method of removing HL‐A antigens from frozen blood. Units prepared by this and other freezing methods contain nonviable leukocytes which may or may not be antigenic.     

Di‐2‐ethylhexyl Phthalate, a Plasticizer Contaminant of Platelet Concentrates

Di‐2‐ethylhexyl phthalate (DEHP), a plasticizer used in polyvinyl chloride plastic blood bags, is extracted by human blood during storage at 4 C. The rate of extraction (0.25 mg/100 ml/day) suggested that after only two days of storage, a concentration of 0.5 mg/100 ml might be found in human blood. In contrast to this, five platelet concentrates that were stored at 22 C for two days had a calculated DEHP concentration of approximately 19 mg/100 ml. The concentration of DEHP in platelet‐poor plasma was 16.7 mg/100 ml while the platelets were found to contain 37.7 mg/100 ml packed platelet volume. This result might suggest that platelets can preferentially accumulate DEHP. It is not known if such concentrations of DEHP are injurious to humans who receive platelet transfusions.     

Exchange Transfusion with ACD‐Adenine Blood. A Follow‐up Study

Twenty‐seven children had received neonatal exchange transfusions (one to seven times) with ACD‐adenine red cell concentrate containing 7 mg adenine per 100 ml of blood. They were evaluated in a follow‐up study at about five years of age. The examination comprised a history and physical examination, routine blood and urine examination, urine culture, serum creatinine and pitressin test. In no case could any renal damage be demonstrated. No correlation was found between the number of transfusions with ACD‐adenine blood and the values of serum creatinine and pitressin test.     

Therapeutic drug monitoring of gentamicin: a 6‐year follow‐up audit

Background and objective : In 1984 a therapeutic drug monitoring (TDM) service was established in Hospital Universiti Sains Malaysia (HUSM) and gentamicin concentrations were measured and used to design optimal regimens for the antibiotic. In this study we report on a 6‐year follow‐up audit since our first assessment of the service. Method : Records of 733 requests for gentamicin monitoring were reviewed. Results : Of the 592 patients involved, 39% were neonates and 42% were adults. Peak gentamicin concentrations were within the therapeutic range in 65% of the patients at first monitoring and 79% of the corresponding trough concentrations were within the non‐toxic range. After dosage adjustment, 81% of the peak concentrations were within the therapeutic range and trough concentrations rose to levels regarded as toxic in 7% of patients. In patients with therapeutic peak concentrations at the first monitoring point, the average duration of gentamicin therapy was statistically shorter than in those patients who failed to achieve a therapeutic peak concentration. The distribution of gentamicin peak and trough concentrations in terms of therapeutic ranges were also better than those found in 1990. Conclusion : TDM for gentamicin is well accepted in HUSM and its application has contributed to improved gentamicin administration. Furthermore, our physicians are now able to choose more appropriate dosage regimens for their patients because the majority of gentamicin concentrations attained even at the first monitoring were within the therapeutic range.     

Near‐patient stability studies

Approaches to performing stability tests on formulations developed in hospitals, defined as the near‐patient situation, are reviewed. Emphasis is placed on the selection and validation of storage conditions and the statistical methodology necessary to ensure confidence in the results obtained.     

Spectrum of Albumin Auto‐Agglutinins

The properties of four albumin‐agglutinating sera demonstrating a spectrum of reactivities are reported. All cause pan‐ and auto‐agglutination in albumin. Direct and indirect reacting caprylate‐dependent agglutinins are described, as are two sera with undefined specificity not related to the presence of caprylate stabilizer in the albumin. Immunoelectrophoretic evidence was obtained to support the concept of albumin‐immunoglobulin complex formation in the genesis of albumin agglutination. Most albumin agglutinins react only with albumin stabilized by short‐chain fatty acids; however, other specificities may be represented. Albumin agglutinins should be clearly identified in the blood bank to prevent confusion with blood group antibodies.     

RhIg for the prevention Rh immunization and IVIg for the treatment of affected neonates

Rhesus D (RhD) negative pregnant women carrying an RhD positive fetus are at risk of developing anti-D during or after pregnancy. Anti-d-immunoglobulin (RhIg), which is mainly produced from special plasma donated in a few countries for the whole world, is able to prevent an anti-D alloimmunization. Through the introduction of ante- and postnatal anti-d-prophylaxis into clinical routine, the frequency of hemolytic disease of fetus and newborn decreased considerably. Postnatal prophylaxis from the beginning in the 1960s has been applied only to women who delivered an RhD positive newborn. Because the fetal RhD status can be determined with high sensitivity and accuracy from the mother’s peripheral blood, targeted antenatal anti-d-prophylaxis is becoming a new standard procedure in more and more countries. Phototherapy and exchange transfusion are still the main pillars for the treatment of RhD hemolytic disease of the newborn. The efficacy of IVIg in the management of these neonates is not conclusive and cannot be recommended until a larger randomized, double-blind, placebo-controlled study is performed.