Recurrent bacteriuria and primary biliary cirrhosis: ABO blood group, P1 blood group, and secretor status.

Patients with primary biliary cirrhosis have an abnormally high incidence of urinary tract infection (35%). Susceptibility to urinary infection and other infectious diseases has been linked with certain blood group antigens and secretor status. We have therefore studied these characteristics in patients with primary biliary cirrhosis. We were unable to show any abnormal distribution in blood groups or secretor status in patients with primary biliary cirrhosis (compared with a normal population) which might reflect their predisposition to urinary infection. The distribution of blood groups and secretor status in patients with primary biliary cirrhosis with a history of urinary infections was not significantly different from patients without such a history. Escherichia coli strains isolated from patients with primary biliary cirrhosis did not bind in any greater numbers to the uroepithelial cells of primary biliary cirrhosis patients than to the cells of a normal healthy control. We therefore conclude that blood group distribution, abnormal secretor status, and epithelial cell type are not important factors in the predisposition of primary biliary cirrhosis patients to urinary infections.

A and B blood group antigen expression on mixed colony cells and erythroid precursors: relevance for human allogeneic bone marrow transplantation.

Using anti-A and anti-B blood group monoclonal antibodies and fluorescent activated cell sorting of human bone marrow, A (or B) blood group antigen was shown to be on 5.2 +/- 5.9 (mean +/- SD) % of CFU-GEMM and 12.5 +/- 19.6% of the erythroid burst forming cells (designated BFU-GEMM) as defined by the mixed colony assay, and 49.5 +/- 20% of the BFU-E and 83.5 +/- 9.9% of the CFU-E as defined by the erythroid colony assay. This antigen expression on the BFU-GEMM is consistent with the concept that erythroid bursts stimulated by leucocyte conditioned medium are less mature, and are closer in development to the pluripotent stem cell than the BFU-E. These results help to explain the delayed erythropoiesis, and perhaps impaired engraftment of all cell lineages, that may occur in some recipients of ABO incompatible bone marrow transplants with persistent and high anti-A titres.

Haemolysis after T-cell depleted bone marrow transplantation involving minor AB0 incompatibility.

9 recipients of T-cell depleted allogeneic bone marrows (8 group A, 1 group AB) from group 0 donors were monitored after transplantation. Free anti-A/B was demonstrable in 8 of the 9 recipients 10-19 d post-transplant, 5 patients developed a positive direct anti-globulin test and 7 showed a rise in bilirubin. The presence of antibody was generally unrelated to the infusion of incompatible plasma, although 2 patients who also received anti-CMV immunoglobulin subsequently shown to contain high titre IgG anti-A/B were more severely affected, sustaining a fall in Hb of up to 2 g/d. These observations suggest that, after T-cell depleted bone marrow transplantation, immunocompetent B lymphocytes of donor origin are transferred, secrete antibody in the recipient, and may be responsible for self-limiting haemolytic episodes.

ABO-incompatible bone-marrow transplantation: removal of red blood cells from donor marrow avoiding recipient antibody depletion.

Eight patients with acute leukaemia undergoing allogeneic bone-marrow transplantation from ABO-incompatible donors received red-cell-depleted donor marrow without any procedure to diminish their anti-ABO antibody titres. Successful marrow red-cell removal (mean 98.8%) was achieved by means of a large-volume separation technique on Ficoll-Metrizoate in the IBM 2991 blood-cell processor. Clinically significant ABO-haemolytic reaction was prevented in all patients, and there was neither failure of engraftment nor rejection. This approach used alone is satisfactory for most ABO-incompatible marrow-transplant recipients, although combining this with some method of recipient antibody depletion, such as plasma exchange, is recommended in the occasional patient with high anti-ABO titres.