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R. C. Spiller
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Articles
Journal:
Clinical Science
Clin Sci (Lond) (1987) 72 (2): 217–223.
Published: 01 February 1987
Abstract
1. Coeliac patients are known to have an expanded bile salt pool which recirculates slowly due, at least in part, to impaired gall bladder contractility. We have investigated the possibility that delayed small bowel transit of chyme and bile may also contribute to this sluggish recycling. 2. Plasma cholylglycine, total bile acids and cholecystokinin concentrations were measured after a lactulose-labelled test meal whose mouth-caecum transit time (M–C TT) was assessed by the breath hydrogen technique. 3. Overall there were no significant differences in plasma bile acid profiles between seven healthy controls and a group of 25 coeliac patients. However, when subjects were divided according to their M–C TT, the 10 with the slowest transit were found to have significant elevation of fasting levels when compared with the 10 with the fastest transit, fasting total bile acids being 3.4 ± 1.3 versus 0.7 ± 0.6 μmol/l ( P < 0.02) and fasting cholylglycine being 0.43 ± 0.17 versus 0.06 ± 0.04 μmol/l ( P < 0.05) respectively. 4. Peak bile acid levels did not differ significantly between subjects with fast or slow transit. However, subjects with slow transit were found to have a delay in the return of plasma bile acid levels to fasting levels so that the 4 h postprandial levels were significantly elevated when compared with those observed in the subjects with fast transit (total bile acids 3.6 ± 1.2 versus 0.19 ± 0.1 μmol/l and cholylglycine 0.70 ± 0.13 versus 0.24 ± 0.07 μmol/l respectively, both P < 0.01). 5. We conclude that M–C TT is an important variable determining the postprandial plasma bile acid response, which should be considered when comparing different disease groups in whom gut motility may differ.
Articles
Journal:
Clinical Science
Clin Sci (Lond) (1984) 67 (1): 117–120.
Published: 01 July 1984
Abstract
1. A steady-state perfusion technique has been used in vivo in normal subjects to show that at concentrations occurring during therapeutic use (500 mg/l, 1.1 mmol/l) the antibiotic clindamycin reversibly inhibits bicarbonate-stimulated water and electrolyte absorption from the human jejunum. 2. Lactose-stimulated water and electrolyte absorption was not affected by the addition of clindamycin at the same concentration. 3. Clindamycin-induced malabsorption of water and electrolytes may contribute significantly to the diarrhoea that occurs during clindamycin therapy in the absence of pseudomembranous colitis.