Transfusion-related acute lung injury (TRALI) is a hazardous but little-known complication of blood transfusion, characterized by non-cardiogenic lung oedema after blood transfusion. Leucoagglutinating antibodies in the donor plasma are considered to play a central role in the pathogenesis of TRALI but no recommended procedure currently exists for their detection, and most of them have not yet been well characterized. Serum samples of two patients who have developed TRALI within 30 min of blood transfusion and the sera of the involved blood donors were investigated for leucocyte antibodies by granulocyte immunofluorescence, granulocyte agglutination and lymphocytotoxicity assays using typed test cells. Suspected specificities of the detected antibodies were confirmed by a luminoimmunoblot assay and the antigen capture assay MAIGA. One case was associated with granulocyte agglutinating anti-HLA-A2 antibodies in the recipient's (i.e. patient's) own blood and the other with donor-related non-agglutinating antibodies directed against the granulocyte-specific antigen NB1. Leucocyte incompatibility between donor and recipient was shown in both cases by crossmatching and typing of the incompatible cells for the appropriate antigen. The results show that TRALI is associated not only with donor- but also with recipient-related leucocyte antibodies. In addition to leucoagglutinating antibodies, non-agglutinating granulocyte-specific antibodies can be also involved. For immunodiagnosis, sera from both must be investigated by a combination of granulocyte and lymphocyte (HLA) antibody screening tests and leucocyte incompatibility verified by crossmatching.

SYNOPSIS A method for the measurement of serum folic acid activity is described, which is a modification of previous methods.The from normal subjects and patients with primary vitamin B12 deficiency. Normal subjects had serum folic acid levels from 5 9 to 210 m,ug./ml. (mean 9-9 m,ug./ml. ± 0-3 m.tg./ml. S.E.). In patients with megaloblastic anaemia requiring treatment with folic acid, other than megaloblastic anaemia of pregnancy, the levels were less than 4-0 mptg./ml. Patients with uncomplicated pernicious anaemia had levels from 6-0 to 27-0 m,tg./ml. (mean 16-6 m,ug./ml. ± 11 m,ug./ml. S.E.). The mean level in this group was higher than in normal subjects, and the highest levels of all were found in patients with subacute combined degeneration of the cord with minimal anaemia (range 14-4 to 36-8 mp,g./ml.; mean 24-8 mpg./ml. ± 2-4 mpig./ml. S.E.).The L. casei activity of the labile component is lost during autoclaving or storage at -20°C. This loss can be prevented during autoclaving by using adequate amounts of ascorbic acid in the phosphate buffer used to dilute the serum for assay and by adding ascorbic acid to serum that is to be stored. Moreover, the activity lost during the storage of serum not protected by ascorbic acid could be restored, for periods up to three months, by adding ascorbic acid to this serum before assay.The folic acid activity of blood and serum has been measured in the past by a number of workers using Streptococcus faecalis (Schweigert and Pearson, 1947; Wolff, Drouet, and Karlin, 1949;Toennies and Gallant, 1949;Girdwood, 1953;Nieweg, Faber, de Vries, and Kroese, 1954;Condit and Grob, 1958;and Cox, Meynell, Cooke, and Gaddie, 1960) and/or Lactobacillus casei (Schweigert, 1948;Simpson and Schweigert, 1949;Spray, 1952;and Spray and Witts, 1952) as test organisms. These workers were unable to demonstrate a consistent difference in the levels of folic acid activity of blood or serum in normal 'University of Queensland Travelling Scholar in Medicine.

In this prospective study, 26 consecutive patients being treated for haematological malignancies receiving standard (i.e. non-leucocyte-depleted) blood components were observed for the development of refractoriness to platelet transfusions. One hundred and sixteen of the 266 (44%) platelet transfusions failed to produce a satisfactory response. In 102/116 (88%), the poor response was in the presence of non-immune factors known to be associated with platelet refractoriness. Non-immune factors were present alone in 78/116 (67%), and in combination with immune factors in a further 24/116 (21%). Immune factors (HLA and platelet-specific antibodies) were present during 29/116 (25%) of unsuccessful platelet transfusions. Statistical analysis confirmed that platelet refractoriness was significantly associated with the presence of non-immune factors. The non-immune factors associated with refractoriness were often multiple, most frequently a combination of fever, infection and antibiotic therapy. This study provides evidence that immune mechanisms were not the predominant cause of platelet refractoriness in the patient population studied. It also suggests that measures for the prevention of HLA alloimmunisation, such as leucocyte depletion, may have a limited impact in reducing the incidence of refractoriness to platelet transfusions.