Colitis associated with oral clindamycin therapy. A clinical study of 16 patients.

The clinical, radiologic, and histologic features of 16 patients hospitalized with clindamycin-associated colitis are presented. The findings are tabulated and compared to 33 cases reported in the literature. The majority of patients were caucasian females over 40 years of age. The clinical presentation varied from mild persistent diarrhea to acute surgical abdomen. Proctoscopic examination revealed nonspecific colitis in 9 and pseudomembranous colitis in 7 cases. No specific radiologic or histologic fingings for postanitbiotic colitis were found. Therapy was nonspecific and varied according to the severity of the clinical course. Clinically, there appeared to be some benefit from systemic steroid therapy. 4 of the 16 patients died. None of the recovered patients have had spontaneous relapses off medication during follow-up evaluation. The pathogenic mechanism for postantibiotic colitis secondary to clindamycin remains unknown and does not appear dose related. Clindamycin therapy should be limited to disorders with specific indications.

Studies of the prevalence and significance of radiolabeled bile acid malabsorption in a group of patients with idiopathic chronic diarrhea.

We studied radiolabeled fecal bile acid excretion in 11 normal subjects and 17 patients with idiopathic chronic diarrhea for three major purposes: to establish normal values for this test in the presence of increased stool volumes (induced in normal subjects by ingestion of poorly absorbable solutions); to test for bile acid malabsorption in the patients and to correlate this with an independent test of ileal function, the Schilling test; and to compare the results of the bile acid excretion test with the subsequent effect of a bile acid binding agent (cholestyramine) on stool weight. In normal subjects fecal excretion of the radiolabel was increased with increasing stool volumes. As a group, patients with idiopathic chronic diarrhea excreted radiolabeled bile acid more rapidly than normal subjects with induced diarrhea (t1/2 56 +/- 8 vs. 236 +/- 60 h, respectively, p less than 0.005). There was a statistically significant positive correlation between t1/2 of radiolabeled bile acid and Schilling test results in these patients. Although 14 of 17 patients absorbed labeled taurocholic acid less well than any of the normal subjects with comparable volumes of induced diarrhea, cholestyramine had no statistically significant effect on stool weight in the patient group, and in none of the patients was stool weight reduced to within the normal range. In summary, most patients with idiopathic chronic diarrhea have bile acid malabsorption (as measured by fecal excretion of labeled bile acid), but they do not respond to cholestyramine therapy with a significant reduction in stool weight. Although the significance of these findings was not clearly established, the most likely interpretation is that bile acid malabsorption is a manifestation of an underlying intestinal motility or absorptive defect rather than the primary cause of diarrhea.