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In the Poitou-Charentes area, a regional pilot program was implemented over a two year-period to improve transfusion safety in public and private hospitals. This program consisted in: (i) an evaluation of the transfusion chain in hospitals; (ii) a regional program to guide hospitals in improving the quality process. Five workgroups were set up. Three persons in each hospital should participate in the workgroup: one representing the administration, one the medical staff and one the nursing staff. After a six months follow-up several hospitals were prompted to implement corrective and preventive measures to improve transfusion safety; (iii) a letter was regularly published to contribute to set-up a regional haemovigilance network. Such a quality improvement program revealed to be a relevant method to steer the changing blood transfusion process in hospitals.

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We compared a new Elisa assay to detect malaria antibodies: Malaria IgG Celisa (BMD) with the IFAT technique Falciparum-spot IF (Biomérieux): sensitivity, specificity, predictive positive and negative values were 81%, 99%, 95%, 95%, respectively. Eight patients had positive thick blood smear out of 23 performed. For these eight confirmed acute malaria cases, the Elisa assay was negative in five instances. For two recent malaria attacks both Elisa and IFI were negative. With blood donors, two sera were IFAT positive and Elisa negative; 16 were IFAT doubtful and Elisa negative. Doubtful results rose up to 13.5% by IFAT against 1.5% by Elisa assay. We preferred kappa coefficient instead of chi 2 test for data analysis, which measures the concordance degree between the two techniques. Here concordance is moderate. Choosing an Elisa assay to detect the transmission of malaria for at-risk blood donors collides with the method sensitivity compared with IFAT as reference.

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BACKGROUND: The utility of a pretransfusion bedside blood compatibility protocol to decrease immunohemolytic accidents has been questioned for years. STUDY DESIGN AND METHODS: The reliability of a standard bedside ABO compatibility test was evaluated with a stratified random sample of 48 nurses who performed agglutination testing by using Bristol cards, interpreted compatibility, and decided whether to transfuse red cells for 12 randomly and blindly selected donor-and-recipient blood sample pairs. An expert judged technical performance and the interpretation of each card. RESULTS: Erroneous decisions occurred in 18.2 percent of 576 tests, including 12 decisions to transfuse incompatible blood. Errors involved both testing protocols and the interpretation of compatibility. Anti-A and anti-B were detected with 92.8-percent sensitivity and 95.9-percent specificity. The expert judged 17.7 percent of tests to be technically inadequate, most often because of the application of excess blood to the card and a lack of rotation of the card. Testing errors (16.1% of tests) were significantly linked to infrequent transfusion activity by the nursing service, inexperience, and insufficient training. Compatibility misinterpretation occurred in 14.6 percent of the tests and was significantly linked to the nurses' infrequent transfusion activity, inexperience, insufficient training, lack of practical experience, and confusion regarding the use of ABO-compatible but not identical blood. CONCLUSION: Bedside pretransfusion compatibility determination should not be considered a reliable supplemental safety procedure in the hands of inexperienced and insufficiently trained operators.

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The ultrastructural localization of peroxidase activity has been studied in the circulating neutrophils and in a neutrophilic series of bone marrow cells from a patient with preleukaemia. Light microscopic examination showed 36% of the polymorphonuclear leucocytes to be totally devoid of myeloperoxidase, while 50% were normally stained and 14% were slightly positive for this enzyme. Electron microscopic studies revealed considerable heterogeneity in the promyelocyte population, since the number of peroxidase-deficient azurophil granules was seen to vary from 0 to 100% in these cells. Thus, several types of promyelocytes were identified. One cell type, which resembled that seen in normal subjects, contained myeloperoxidase within its azurophil granules and also within the cisternae of the rough endoplasmic reticulum and Golgi complex. A second type of promyelocyte, which was at an early stage of development, lacked myeloperoxidase in its secretory apparatus. These cells contained two species of azurophil granules, the first of which was devoid of peroxidase activity whereas the other reacted positively. These observations suggest that the premature arrest of myeloperoxidase synthesis in the promyelocytes from a preleukaemic patient may give rise to several populations of circulating neutrophils which can exhibit varying contents of myeloperoxidase.

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A patient with a refractory anaemia preceding acute myeloblastic leukaemia had an increased susceptibility to infection due to Staphylococcus aureus. 36% of neutrophils lacked myeloperoxidase (MPO) activity and, in vitro, these polymorphonuclear neutrophils (PMN) had a defect of bactericidal activity against Staphylococcus aureus. Cytochemical studies of phagocytosis with the electron miscroscope have shown that the degranulation of primary granules (MPO+ or MPO-) was normal after phagocytosis of Escherichia coli which were normally lysed. A defective destruction of Staphylococcus aureus and Candida albicans was observed in some PMN with or without MPO activity, suggesting that MPO deficiency itself was not the only cause of this defect. In PMN which appeared normal, most MPO(+) granules were unable to fuse with the phagocytic vacuole containing intact germs even after 90 min of contact. There was, therefore, in addition to a partial MPO deficiency, a defect in cellular degranulation. This defect, the mechanism of which is unknown, may be in part responsible for the defective bacterial degradation.

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