PubMed · 7615218
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E W Moore, J D Ostrow. 1995. Some Ca2+ electrodes misrepresent Ca2+ binding by bile salts.. https://doi.org/10.1016/0016-5085(95)90364-x
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Clostridium scindens is a keystone bacterial species in the mammalian gut that, while low in abundance, has a significant impact on bile acid and steroid metabolism. Numerous studies indicate that the two most studied strains of C. scindens (i.e. ATCC 35704 and VPI 12708) are important for a myriad of physiological processes in the host. We focus on both historical and current microbiological and molecular biology work on the Hylemon-Björkhem pathway and the steroid-17,20-desmolase pathway that were first discovered in C. scindens. Our most recent analysis now calls into question whether strains currently defined as C. scindens represent two separate taxonomic groups. Future directions include developing genetic tools to further explore the physiological role of bile acid and steroid metabolism by strains of C. scindens and the causal role of these pathways in host physiology and disease.
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The management of patients with biliary colic without gallstones has remained controversial in part because a mechanism for "biliary dyskinesia" has not been elucidated. A prospective study was done on patients presenting with biliary colic symptoms but without demonstrable gallstones. Thirty-six patients were evaluated with ultrasound and hepatobiliary/cholecystokinin scintigraphic scanning. Patients with gallbladder ejection fractions of less than 35 per cent and/or symptoms reproducible with cholecystokinin were offered cholecystectomy. At cholecystectomy, bile was aspirated from the gallbladder for crystal analysis. A random sample of 36 patients with gallstones undergoing cholecystectomy were analyzed as a control group. Pathologic evaluation was done; the gallbladder wall was examined using polarized microscopy to determine the presence of crystals within the gallbladder wall. The mean gallbladder ejection fraction in patients without stones was 24.1 per cent and in patients with stones, 34.6 per cent (P = 0.14). 89.7 per cent of patients without stones had crystals in their gallbladder bile. 61.8 per cent of patients without stones and 81.3 per cent of patients with stones (P = 0.22) had crystals within their gallbladder walls. 94.1 per cent of patients without stones and 100 per cent of patients with stones (P = 0.49) had pathologic evidence of chronic cholecystitis. These data suggest that a spectrum of biliary disease exists in which bile saturation and gallbladder dysmotility lead to crystal growth and subsequent gallstone formation and chronic inflammation. Biliary pain may be generated at any point in this spectrum.