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.     

Secondary anti-D immunization by Del red blood cells

BACKGROUND: Recent molecular studies of the RHD gene have revealed that D(el) individuals retain a grossly intact RHD gene or have a portion of RHD in their genomes. No D(el) phenotype has yet been shown to induce a primary or secondary alloanti-D immunization, however. CASE REPORT: A 67-year-old D- Japanese woman with a history of allosensitization from transfusion of D+ red blood cells (RBCs) was negative for anti-D at admission. After she received RBCs from 19 apparently D- donors, she developed anti-D with an 8-fold titer. The titer of anti-D increased further to 128-fold after transfusions of cross-match-compatible D- negative RBCs from 40 donors over the next 2 years. Two of 59 donors were found to be RHD gene-positive and antigen D- with a D(el) phenotype, that is, RHD(K409K). CONCLUSION: This is the first case in which RBCs having the D(el) phenotype induced a secondary alloanti-D immunization. A D- donor with the RHD(K409K) allele was associated with the development of anti-D. Adverse episodes or evidence of hemolysis was not observed after the transfusion of RHD(K409K) RBCs. Further clinical evidence is needed to reveal whether the D(el) phenotype has a clinically relevant potential for anti-D immunization.     

Absence of D- alloimmunization in AIDS patients receiving D-mismatched RBCs

BACKGROUND: More than 80 percent of D- patients who receive D+ blood become alloimmunized to the D antigen. Anemia occurs in most AIDS patients at some point in the disease. D- patients with AIDS may require blood transfusion and, during times of blood shortage, may receive D+ RBCs. They would be expected to become alloimmunized to the d antigen. STUDY DESIGN AND METHODS: The records of the transfusion service between January 1996 and July 2000 were reviewed for D- patients who received D+ blood. IATs were performed before the initial transfusion and subsequently when the patient required further RBC transfusion. RESULTS: Eight D- AIDS patients who received multiple transfusions (three women and five men; age range, 31-44 years; mean, 44 years) who received between 2 and 11 units (mean, 6.25) of D+ RBCs were identified. Antibody screens were performed at 8 to 65 weeks after transfusion. It was found that none of the eight D- AIDS patients developed anti-D. ABO antibodies were found as expected. During the same period, it was found that six D- patients admitted with other diagnoses who received 1 to 9 units of D+ RBCs, all developed anti-D within 7 to 19 weeks of transfusion. CONCLUSION: Patients with AIDS may not form alloantibodies to the D antigen. This may be attributable to their immunodepressed state, particularly to the decrease in CD4+ T lymphocytes. Therefore, during blood shortages, transfusion of D+ blood to D- AIDS patients may be without any subsequent consequence.     

Taiwan experience suggests that RhD typing for blood transfusion is unnecessary in southeast Asian populations

BACKGROUND: The high frequency of RhD (D) antigen among Taiwanese persons (99.67%) often imposes unnecessary risks of under-transfusion on D- patients awaiting D- blood. Also because of the rare occurrence of anti-D among Taiwanese persons, routine pretransfusion D typing has been discontinued in the Mackay Memorial Hospital since 1988. This report is the retrospective evaluation of the outcome of abolishing RhD typing for Taiwanese. STUDY DESIGN AND METHODS: More than 10 years of alloantibody data at Mackay Memorial Hospital Blood Bank were reviewed. The cases with anti-D were further used to analyze the potency of D antigen and to observe whether there were differences in the incidence of anti-D before and after discontinuation of routine D typing among Taiwanese individuals. RESULTS: The incidence of anti-D before and after discontinuation of routine pretransfusion D typing has remained unchanged. The immunogenicity of D and "Mi(a)" in Taiwanese persons is found to be similar. In terms of opportunity for immunization, however, the "Mi(a)" antigen (phenotype frequency 7.3% in Taiwanese persons) has become the most important blood group antigen in Taiwan. CONCLUSION: The results strongly support the exclusion of D typing from routine compatibility testing for individuals of Taiwanese origin. Because the low incidence of D- and relatively high incidence of "Mi(a)"+ phenotypes are common findings throughout southeast Asia, and because a population genetic study revealed that the Taiwanese people are genetically related to southern Asian populations, it is suggested that RhD typing for blood transfusion is unnecessary among southeast Asian populations.     

Prospective evaluation of a transfusion policy of D+ red blood cells into D- patients.

BACKGROUND: Although D- patients should receive red blood cells (RBCs) from D- donors, the scarcity of D- blood components in certain situations makes the transfusion of D+ RBCs unavoidable. Therefore it is recommended that guidelines be developed in order to standardize transfusion policy in these scenarios. STUDY DESIGN AND METHODS: We have prospectively evaluated a policy for the use of D+ RBCs in 905 D- patients. The amount of D- RBCs saved as well as the incidence of hemolytic reactions and anti-D alloimmunization were assessed. RESULTS: 554 patients received D- RBCs while 351 received a total of 1032 D+ RBCs, all of them within our criteria for the acceptable use of D+ RBCs. This strategy allowed us to save 25.6 percent of D- RBCs (1032 out of 4024 RBCs requested). No hemolytic reactions were reported. The incidence of alloimmunization was 21.4 percent. Most patients who developed anti-D did so within the first 2 or 4 RBCs transfused (64% after the first 2 RBCs transfused and 88% after the first 4). In multivariate analysis the age of less than 77 years was the only predictor for alloimmuization (HR = 2.48 [95% CI = 1.21-3.81]; p = 0.014). CONCLUSION: The use of D+ RBCs in selected D- patients does not induce adverse reactions and allows the saving of a significant number of D- RBCs.     

Detection of anti-D in D- recipients transfused with D+ red blood cells

BACKGROUND: The D antigen is highly immunogenic, requiring only a small quantity of transfused red blood cells (RBCs) to cause alloimmunization in D- immunocompetent recipients. The relatively low sensitization rate in oncology patients transfused with D+ platelets is well documented. A study of the alloimmunization rate of primarily nononcology D- recipients transfused with D+ RBCs was undertaken. STUDY DESIGN AND METHODS: Transfusion service records were examined to identify D- recipients who were not alloimmunized to the D antigen and who had a follow-up antibody screen performed at least 10 days after the initial D+ RBC transfusion(s). The age and sex of the recipients, date and number of D+ RBC transfusion(s) and their leukoreduction status, all subsequent serologic investigations, and the hospital ward where the units were issued were recorded. RESULTS: There were 98 study-eligible recipients identified who received a total of 445 D+ RBC units. The mean follow-up length was 182 days. Most recipients (87%) had antibody screens performed more than 21 days after the initial D+ RBC transfusion. In total, 24 recipients made 44 new alloantibodies: 22 anti-D (22%), 11 anti-E, 5 anti-C, 2 anti-K, and 1 each of anti-Kp(a), anti-Jk(a), anti-Bg, and anti-Fy(b). The rate of anti-D alloimmunization among recipients of entirely leukoreduced D+ units was 13 percent (1/8). Reexposure to D+ RBCs after the initial bleeding episode did not increase the rate of alloimmunization. CONCLUSIONS: The 22 percent rate of anti-D alloimmunization in patients requiring urgent RBC transfusion was intermediate between the rates previously reported for D- oncology patients transfused with D+ RBCs and that in immunocompetent volunteer recipients.     

The RHCE allele ceSL: the second example for D antigen expression without D-specific amino acids

BACKGROUND: The example of ceRT proved that the expression of some D epitopes does not require D-specific amino acids. This allele denoted as RHce(R154T) caused the "false-positive" reactions that were observed in ccddee blood donors who typed positive for the D antigen with some monoclonal anti-D. No other example exposing a similar molecular mechanism was known. STUDY DESIGN AND METHODS: Eleven donor and 1 patient ccddee samples were collected in Switzerland that typed "false-positive" with some monoclonal anti-D in bromelain technique. Their RHCE alleles were determined by nucleotide sequencing from genomic DNA and by a polymerase chain reaction with sequence-specific priming. The D epitope profile was compared to ceRT. The population frequencies were estimated in Switzerland and Germany by serology or at the molecular level, respectively. RESULTS: The "false-positive" reactions were caused by the RHCE allele RHce(S122L) occurring in the cde haplotype. Its ceSL phenotype expressed few D epitopes that belonged to the D epitope 6 group. The frequency of ceSL among D- donors was about 1:675 in the region of Bern, Switzerland. No ceSL donors were found elsewhere in Switzerland or in southwestern Germany. CONCLUSION: ceSL represented the second molecular mechanism for D antigen expression without any D-specific amino acids. ceSL and ceRT were useful to delineate the molecular mechanisms of D expression by RhCE proteins carrying amino acids not representative for the RhD proteins. The ceSL population frequencies differed significantly among three Swiss and German populations.     

Massive fetomaternal hemorrhage: clearance of fetal red blood cells after intravenous anti-D prophylaxis monitored by flow cytometry

BACKGROUND: The clearance of D+ red blood cells (RBCs) from the circulation in D- individuals mediated by passively administered anti-D occurs by opsonization with the antibody and subsequent removal in the spleen. Few data exist on the kinetics of clearance of large volumes of D+ RBCs from the maternal circulation by anti-D in clinical cases of massive fetomaternal hemorrhage (FMH). CASE REPORT: A 33-year-old D- woman delivered a D+ female infant by emergency cesarean section for suspected fetal anemia. A massive FMH, initially estimated to be approximately 142 mL of RBCs, was found. In addition to the standard dose of intramuscular (IM) anti-D (300 microg) given immediately after delivery, 2700 microg of anti-D was administered intravenously (IV). The clearance of D+ fetal cells from the maternal circulation was monitored by flow cytometry in samples obtained on a daily basis using anti-D. The mother had no detectable anti-D 6 months after delivery. RESULTS: No clearance of fetal cells was apparent after the insufficient dose of IM anti-D. The IV administration of anti-D caused accelerated clearance of D+ fetal RBCs with a t1/2 of 24.5 hours. D+ reticulocytes comprised 4.2 percent of all D+ cells in the maternal circulation at delivery suggesting acute fetal blood loss. CONCLUSIONS: The approach used in this report allowed a detailed analysis of the kinetics related to the clearance of fetal D+ RBCs. Simultaneous measurements of fetal reticulocytes and fetal RBCs in maternal blood may establish the timing of an FMH.     

Analysis of factors affecting quantification of fetomaternal hemorrhage by flow cytometry

BACKGROUND: An analysis was carried out to determine the sources and extent of errors encountered in the quantitation of the volume of fetomaternal hemorrhage (FMH) by flow cytometry. Different assay conditions were compared, to define the simplest, most accurate protocol. STUDY DESIGN AND METHODS: D-, D+, and artificial FMH (mixtures of D+ and D- RBCs) were stained either by a direct method (using FITC-conjugated IgG3 D MoAb [BRAD-3]), with or without dual labeling with PE-conjugated anti-GPA, or by indirect methods (using polyclonal anti-D followed by FITC- or biotin-conjugated anti-IgG reagents). Cells were selected for flow cytometric analysis on the basis of either forward or side scatter (log FSC/log SSC) characteristics or of GPA+ labeling or were unselected. The numbers of events labeled with anti-D were determined from histograms. For some samples, 10 replicates of 500,000 events each were analyzed. RESULTS: Background fluorescent events in 10 directly labeled gated D- samples ranged from 0.007 to 0.023 percent, equivalent to 0.15- to 0.51-mL FMH. Both the use of a gate on log FSC/SSC or the selection of GPA+ events only resulted in a reduction in FMH of 0.3 mL or less. The intra-assay variation in FMH, or sampling error, was found to be approximately 10 percent at low artificial FMH (<10 mL) but greater (< or =50% with a CV of 15%) with D- samples. Direct staining was quicker and produced a lower background than indirect staining. CONCLUSION: The inherent sampling error that is due to the random distribution of rare events throughout the blood sample contributed greatly to the variation in the volume of FMH calculated by flow cytometry. The FMH should not be underestimated. For a routine assay, a simplified protocol and calculation will be sufficiently accurate to determine the dose of prophylactic anti-D that should be given to the patient.     

Anti-D alloimmunization after D-mismatched allogeneic hematopoietic stem cell transplantation in patients with hematologic diseases

BACKGROUND: The de novo development of anti-D after D-mismatched allogeneic hematopoietic stem cell transplantation (AHSCT) is a possibility that must be considered. The transfusion of D- blood components after AHSCT has been recommended but anti-D alloimmunization in this setting has been studied little. Thus, the aim of this study was to analyze anti-D formation after D-mismatched AHSCT. STUDY DESIGN AND METHODS: Thirty patients with a hematologic disease who underwent D-mismatched AHSCT were retrospectively studied. Support therapy included red blood cells (RBCs) and platelet (PLT) concentrates (PCs) from whole-blood donations and PLTs from apheresis. After AHSCT, patients received D+ PCs without administering Rh immunoglobulin (RhIG). An antibody screening to detect anti-D was performed by low-ionic-strength saline-indirect antiglobulin test with the tube test. RESULTS: Fifteen D+ patients received stem cells (SCs) of D- donors and 15 D- patients received SCs of D+ donors. After AHSCT, patients received a median of 11.5 (range, 0-32) D- RBC units. D+ patients received 682 (83%) of 825 PLT units from D+ donors, and D- patients received 573 (85%) of 678 PLT units from D+ donors. None of the 30 patients developed anti-D after a median follow-up of 32 weeks (range, 4-310 weeks). CONCLUSION: Anti-D alloimmunization after performing a D-mismatched AHSCT is infrequent in patients with hematologic diseases although patients receive D-mismatched PLT transfusions without RhIG administration.     

Postdelivery levels of anti-D IgG prophylaxis in D- mothers depend on maternal body weight

BACKGROUND: Current recommendations for anti-D prophylaxis for women who deliver a D+ offspring vary from country to country, and the introduction of new reagents require pharmacokinetic studies that show serum levels after the injection. Serum levels of anti-D may depend on the maternal body mass index (BMI). STUDY DESIGN AND METHODS: Serum concentrations of total anti-D IgG and IgG1-4 subclasses were determined by flow cytometry in 26 D- women, who had received prophylaxis after delivery of a D+ offspring. Blood samples were drawn on Days 1, 2, 3, and 14 after injection, and the BMI was recorded. RESULTS: Anti-D levels increased continuously in all women during the first 3 days. The increase was significantly affected by the BMI if higher than 27 kg per m2 (p<0.001). The higher the BMI, the less was the increase of serum anti-D. Mean peak levels 72 hours after injection was 89 ng per mL in lean women, but estimated levels were 28 to 60 percent lower in women with a BMI of 28 to 40 kg per m2. The effect of a BMI higher than 27 kg per m2 on anti-D was not gradual but progressive. Similarly, the BMI affected serum concentrations of anti-D subclasses IgG1-4 (p<0.001). CONCLUSION: The BMI needs consideration for the adjustment of the dosage of anti-D, provided its bioavailability to suppress alloimmunization is reflected by measurable amounts in the serum.     

An easy RHD genotyping strategy for D- East Asian persons applied to Korean blood donors

BACKGROUND: In East Asian populations RHD alleles are known to occur frequently among D- donors, requiring suitable genotyping strategies. The molecular basis of the "RHD(el)" allele previously reported in Taiwan to harbor a genomic 1013-bp deletion was questioned by several authors. STUDY DESIGN AND METHODS: The presence of the RHD gene was investigated in 126 random serologic D- blood donors from Gwangju, southwest Korea. Four donors who typed weakly positive for the D antigen were also analyzed. RH alleles were determined by polymerase chain reaction (PCR) with sequence-specific priming (PCR-SSP) or nucleotide sequencing. RESULTS: Seventy-five percent of the serologically D- samples lacked the RHD gene, 10 percent carried the hybrid RHD-CE(2-9)-D2 or RHD-CE(2-7)-D2 alleles, 13 percent represented the RHD(K409K), and 2 percent were weak D type 15 and type 17. Among the four donors typing weak D, two carried weak D type 15, one RHD(K409K), and one the novel weak D type 43. Critical molecular characteristics of RHD(K409K) and its population frequencies were indistinguishable to those reported for the RHDel allele. CONCLUSION: Korean RHD allele frequencies are comparable to Chinese and Japanese frequencies. It is concluded that the RHDel allele may actually not exist but is identical to RHD(K409K). A practical RHD genotyping strategy applicable to D- donors in all East Asian populations was devised. The strategy requires four PCR-SSP procedures only for RHD intron 4 and exon 7 as well as RHD(K409K) and non-RHD(K409K).     

Partial D, weak D types, and novel RHD alleles among 33,864 multiethnic patients: implications for anti-D alloimmunization and prevention

BACKGROUND: The D antigen includes category D, partial D, and weak D types, which are important because anti-D alloimmunization can occur in some but not all persons that express a variant RHD allele. At present, there is little prospective information on the prevalence of D variants among obstetric patients and potential transfusion recipients. STUDY DESIGN AND METHODS: The RHD alleles were prospectively examined in a large patient population identified on the basis of a difference in anti-D reactivity between two reagents. RESULTS: Fifty-five discrepancies (0.96% of D-) were noted among 33,864 ethnically diverse patients over 18 months, of which 54 represented mutated RHD alleles. Seven obstetric patients were assigned D- status based on serology; only 1 patient had a partial RHD allele. Ten of 25 (36%) obstetric patients and 4 of 6 (67%) female potential transfusion recipients of childbearing age or younger were assigned D+ status, and they expressed a D variant known to permit anti-D alloimmunization. In total 20 RHD alleles were identified including category, DVa or DVa-like alleles (n = 7), DAR (n = 8), and four novel RHD alleles including two new DAU alleles. CONCLUSION: Given the complexity of D antigen expression, it is concluded that some clinically important D variants identified by standard serologic analysis phenotype as D+ and are potentially at risk for the development of anti-D.     

The RHCE allele ceCF: the molecular basis of Crawford (RH43)

BACKGROUND: The Crawford antigen (RH43) was described in 1980. It occurred in African American people, as a low-prevalence Rhesus antigen, who were also VS+. STUDY DESIGN AND METHODS: Twelve blood samples were analyzed because of inquiries into discrepant reactions in routine anti-D typing. The RHCE alleles were determined by nucleotide sequencing from genomic DNA. The D epitope profile was determined with 60 monoclonal anti-D. The population frequency was estimated in four major US regional blood centers. RESULTS: The novel RHce(W16C, Q233E, L245V) allele, dubbed ceCF, was found to be occurring in the cde haplotype as cause of the reactivity with the immunoglobulin M anti-D GAMA401. The ceCF phenotype expressed few D epitopes resembling but not matching the reaction patterns observed with other RhCE variants, like R0 (Har), ceRT, and ceSL. The frequency of the ceCF phenotype was 0.056 percent among African American persons and 0.007 percent in the general US population. CONCLUSION: The novel RHce(W16C, Q233E, L245V) allele, which is a variant of the known ce(s) allele, RHce(W16C, L245V), occurs in a haplotype with the RHD deletion and represents the molecular basis of the Crawford antigen.     

The RoHar antigenic complex is associated with a limited number of D epitopes and alloanti-D production: a study of three unrelated persons and their families

BACKGROUND: the RoHar antigenic complex has been characterized serologically by difficulties in D typing, weak e expression, lack of G antigen, presence of Rh33, a low-frequency Rh antigen, and, more recently, a second low-frequency antigen, FPTT. Allocation to one of the partial D catagories was not considered because of the unuaual reactions of RoHar cells and because anti-D production was not observed in RoHar persons. STUDY DESIGN and METHODS: Three unrelated RoHar donors and their families were studied in detail with special emphasis on D epitope mapping, e and G typing, and screening for antibodies. RESULTS: Only D epitopes 5 and 6/7 were demonstrable, and D epitopes 1, 2, 3, 4, 8, and 9 seem to be absent in the RoHar complex. In one individual, the presence of alloanti-D with limited specificity, not reacting with RoHar red cells of other individuals, was found 6 months after a second D+ pregnancy. CONCLUSION: The finding of alloanti-D in an RoHar r person supports the concept that the D characteristic of this phenotype is a partial D antigen, which is consistent with the presence of the limited number of D epitopes found in epitope mapping. As has been suggested for other partial D antigens, RoHar individuals should be regarded as D- for the receipt of blood, and pregnant RoHar women who have had D+ pregnancies should receive anti-D prophylaxis.     

Six years' experience performing RHD genotyping to confirm D− red blood cell units in Germany for preventing anti-D immunizations

BACKGROUND: Red blood cell (RBC) units of D+ donors are falsely labeled D− if regular serologic typing fails to detect low D antigen expression or chimerism. The limitations of serology can be overcome by molecular typing.
STUDY DESIGN AND METHODS: In January 2002, we introduced a polymerase chain reaction (PCR)-based assay for RHD as a routine test for first-time donors who typed D− by serologic methods including the indirect antiglobulin test. Samples were tested in pools of 20 for the RHD -specific polymorphism in Intron 4. RHD alleles were identified by PCR and nucleotide sequencing.
RESULTS: Within 6 years, 46,133 serologically D− first-time donors were screened for the RHD gene. The prevalence of RHD gene carriers detected by this method was 0.21 percent. Twenty-three RHD alleles were found of which 15 were new. Approximately one-half of the RHD gene carriers harbored alleles expressing a DEL phenotype resulting in a prevalence of 0.1 percent.
CONCLUSION: The integration of RHD genotyping into the routine screening program was practical. We report 6 years' experience of this donor testing policy, which is not performed in most transfusion services worldwide. RBC units of donors with DEL phenotype have been reported to anti-D immunize D− recipients. We transferred those donors to the D+ donor pool with the rationale of preventing anti-D immunizations, especially dreaded in pregnancies. For each population, it will be necessary to adapt the RHD genotyping strategy to the spectrum of prevalent alleles.     

Anti-D immunization by DEL red blood cells

BACKGROUND: No data are available on the immunogenicity of extremely weak D variants called DEL. Evaluation of alloanti-D formation in a D- female patient after transfusion of apparently D- blood from an Austrian donor led to discovery of a so far unknown DEL type. STUDY DESIGN AND METHODS: Standard blood group serologic methods were applied. Molecular typing, RHD sequencing, and D epitope mapping was performed and the absolute D antigen density determined. RESULTS: After transfusion of RBCs typed D- by routine serology, the recipient developed alloanti-D. Further evaluation with an indirect antiglobulin test confirmed donor RBCs to be D-. Molecular typing, however, demonstrated the presence of the RHD gene in one donor, and RHD sequencing revealed a deletion of four nucleotides in RHD intron 5 (RHD IVS5-38del4) as the only difference compared to the normal RHD gene. Adsorption-elution techniques demonstrated a DEL phenotype without apparent loss of D epitopes. CONCLUSION: This study documents the clinical significance of the DEL phenotype in blood units that was capable of inducing anti-D in a recipient. Qualitative data are provided on D epitope expression in DEL RBCs.     

Platelet transfusion in an infant leading to formation of anti-D: implications for immunoprophylaxis

BACKGROUND: The immature infant immune system rarely makes RBC alloantibodies; however, most studies confirming the absence of alloantibodies in infants have involved transfusions that were matched for one of the most immunogenic antigens, rhesus D. The potential for D- infants to develop anti-D is unknown. Specifically, this issue has not been analyzed for infants receiving whole-blood-derived PLTs from D+ donors. The importance of understanding such risk is underscored by the fact that anti-D formation can be prevented by the administration of Rh immunoglobulin. CASE REPORT: A D- infant with congenital heart disease received two D-mismatched whole-blood-derived PLT units at 17 weeks of age. He did not receive Rh immunoglobulin prophylaxis. Upon a subsequent admission 13 months later, anti-D was identified in his plasma sample. CONCLUSION: The case presented here demonstrates that a young infant can respond to less than 0.6 mL of D+ RBCs and documents the youngest patient to have developed a RBC alloantibody from a PLT transfusion. To prevent anti-D formation, we recommend administering Rh immunoglobulin to all D- pediatric patients that receive PLT transfusions from D+ donors [correction].     

The Movement Assessment Battery for Children: a comparison of 4-year-old to 6-year-old children from Hong Kong and the United States.

OBJECTIVE: There is little information available on the appropriateness of tests developed in the West for children of different ethnicities. The aim of this study was to examine the suitability of the Movement Assessment Battery for Children (Movement ABC) for use with Hong Kong Chinese preschool children. METHOD: The performance of 255 Hong Kong Chinese children between the ages of 4 years and 6 years was compared with that of the 493 children of the same age from the United States who took part in the most recent standardization of the Movement ABC. RESULTS: The test content was found to be suitable for use with Hong Kong Chinese children. However, cross-cultural differences were found on a number of the test items. Chinese children performed significantly better on items contained in the manual dexterity and dynamic balance sections, whereas American children were better at the projection and reception of moving objects. CONCLUSION: These findings highlight the need to ensure that norms for all tests are appropriate for the specific cultural groups being assessed.     

Social sharing of bereavement experience by Chinese bereaved persons in Hong Kong

Contrary to the belief that the Chinese do not share emotionally intense experiences, findings from a cross-sectional study of 292 respondents who lost either a spouse or a parent in the previous 2 years in Hong Kong indicated that only 10% did not share their bereavement experiences with another person. The physical health and emotional state of non-sharers was found to be no different to those who shared. In addition, the Chinese are believed to limit their social sharing of personal experiences to family members only. In our study, we found that for those who shared, the persons they shared most with were their best friends, siblings, and professionals. Non-family members are clearly eligible "sharees" for Chinese people. Differences in the reactions of sharees in good and bad sharing experiences were identified. Based on these findings, implications for bereavement care for Chinese are delineated.