[Deletion of ABH antigens in urine sediment cells from patients with prostatic adenoma]. / Deleción antigénica ABH en células de sedimento urinario de pacientes con adenoma de próstata.

OBJECTIVE: This study was conducted to analyze ABH antigenic expression in urinary sediment of patients with benign prostatic hyperplasia (BPH) before and after deobstructive surgery. METHODS/RESULTS: The agglutination inhibition technique was utilized to determine the ABH antigenic expression in urinary sediments of 30 healthy subjects and 34 patients with BPH. The presence of neoplastic cells was also determined in urinary sediments of the patients by Papanicolaou's stain. These studies were performed before and 12 months after surgery. Membrane antigen expression was found in 100% of the healthy subjects and in only 50% of the patients with BPH before surgery. Only 25 patients returned for control evaluation after surgery. Of these, 17 were positive and of the remaining 8 patients who were negative preoperatively, only one continued to be negative. Urine cytology demonstrated progression to malignancy in this patient. CONCLUSIONS: Determination of ABH antigenic expression appears to be able to identify premalignant conditions and could be a useful complementary diagnostic method to cytology.

Blood group B glycosphingolipids in alpha-galactosidase deficiency (Fabry disease): influence of secretor status.

Defect in degradation of blood group B-immunoactive glycosphingolipids in Fabry disease (deficiency of lysosomal alpha-galactosidase EC 3.2.1.22) has been studied using highly sensitive and specific TLC-immunostaining analysis of urinary sediments and tonsillar tissues of blood group B patients and healthy controls, secretors and nonsecretors. The B glycolipid antigens with hexasaccharide chains were consistently found increased (25- to 100-fold) in the urinary sediments of three Fabry patients, blood group B or AB secretors. Conversely, they were absent in the urinary sediment of one blood group B nonsecretor patient. In normal secretors, B glycosphingolipids were present only in traces. Moreover, significant increase in B glycolipid antigens (8-fold) was found in the tonsillar tissue of a Fabry patient blood group B secretor. We conclude that the secretor status is responsible for increased concentration of blood group B glycosphingolipids in both urinary cells and tonsils in alpha-galactosidase deficiency. The quantity of stored B-immunoactive glycosphingolipids, however, is much lower than that of the mainly accumulated glycosphingolipid Gb(3)Cer. The results clearly indicate that active or silent Se gene, which controls synthesis of B-antigen precursors, is responsible for notable difference in B-glycosphingolipids expression in Fabry patients - secretors and nonsecretors. Whether this novel aspect may be of prognostic significance, remains to be established.