GASTROINTESTINAL INVOLVEMENT IN PROGRESSI V-SYSTEMIC SCLEROSIS [PSS]

The complained gastrointestinal symptoms in PSS are probably caused by several complex disturbances like intestinal transit disturbances (IT D), bacterial overgrowth of the small intestine caused malabsorption o f bile acids and altered kinetics of intestinal hormones. 25 patients with PSS and eleven healthy controls were tested for the existence of ITD by use of the metal-detector test (MDT). Twelve patients were also tested for a malabsorption of primary bile acids by radioimmunologica l measurement of cholylglycine serumlevels before and after a meal. In addition serumconcentrations of gastrin (nine patients) and plasmacon centrations of cholecystokinin (CCK) (eight patients) and motilin (ele ven patients) were measured by radioimmunoassay pre- and postprandial. Interdigestive gastric emptying was accelerated in patients with PSS (53 +/- 3 min. vs. 73 +/- 7 min.; p < 0.01). Small intestinal transit times were similar in both groups (115 +/- 17 min. vs. 121 +/- 13 min. ). Colonic transit in patients with PSS was significantly prolonged (6 3 +/- 6 h vs. 39 +/- 5 h; p < 0.05). There were no significant differe nces between the two groups concerning the pre- and postprandial level s of cholylglycin. Basic and postprandial levels of gastrin, CCK and m otilin were higher in the PSS group. In contrast to scintigraphic stud ies using semisolid meals gastric emptying of the copper pellet in PSS was accelerated. A general malabsorption of primary bile acids was no t found. Prolonged colonic transit times correlate well with frequentl y complained obstipation. Gastric hypacidity could be the reason of el evated gastrin levels. The high motilin-levels in PSS could be due to a lack of the feed-back inhibition as a result of diminished phase-ill activity of the interdigestive migrating motor complex. The elevation of CCK-levels could reflect compensation of neurogenic or myogenic di sturbances of gallbladder contraction.