Patients with primary biliary cirrhosis have marked disturbances of humoral and cellular immunity, but an increased susceptibility to infection has not been described previously. We have observed, however, that patients with primary biliary cirrhosis have a high incidence of bacteriuria. This increased susceptibility to urinary infection has been studied and our findings are repoated. Methods PATIENTSPatients with primary biliary cirrhosis were diagnosed by the usual criteria,1 and classified into prefibrotic (stage 1 and 2) and fibrotic disease (stage 3 and 4). Women with other forms of chronic liver disease (non-primary biliary cirrhosis) confirmed by liver biopsy, and women with rheumatoid arthritis,

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Membrane glycolipids contain the lactose sequence (galactose linked to glucose), and the oligosaccharide is variously extended such that there is a cell-type-specific repertoire. In this study, binding of Pseudomonas aeruginosa M35 to lipid-linked lactose (Galj1-4Glc [structure 1]), lacto-N-neotetraose (Gal11-4GlcNAc01-3Gall-4Glc [structure 2]), lacto-N-tetraose (Gal,B1-3GlcNAc,B1-3Gal,B1-4Glc [structure 31), and asialo GM, (Ga431-3GalNAc1-4Ga4l1-4Glc [structure 4]) was evaluated and compared with binding of Escherichia coli C600 to these compounds. Oligosaccharides were linked to the lipid phosphatidylethanolamine dipalmitoate, and the resulting neoglycolipids were resolved on thin-layer chromatograms or coated onto plastic microtiter wells. Lipid-linked structures 1 to 4 were bound by P. aeruginosa and E. coli in the chromatogram assay, but only structure 4 was bound in the microtiter well assay. As shown previously for E. coli binding to lipid-linked structures 1 to 3, binding to lipid-linked structure 4 was not inhibited with oligosaccharide, indicating a requirement for lipid and oligosaccharide. With few exceptions, sialylation and fucosylation of structures 1 to 4 resulted in impaired or abolished binding. Comparisons of binding intensities in the chromatogram assay indicated that recognition by P. aeruginosa and recognition by E. coli are not identical. Presence of the additional disaccharide unit, as in structure 2, resulted in enhanced binding of P. aeruginosa but diminished

SUMMARY 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.We have recently shown that women with primary biliary cirrhosis have a high prevalence (19%) and incidence (35%) of significant bacteriuria compared with women with other types of chronic liver disease (7%) or rheumatoid arthritis (8%).' The prevalence and incidence are also significantly higher than those in age matched normal healthy women.2 Factors which predispose patients with primary biliary cirrhosis (who are predominantly female) to recurrent bacteriuria are as yet unknown.A relation between ABO blood group or secretor status and susceptibility to certain infectious diseases has been previously documented.

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