An endocrine tumour in kidney affecting small bowel structure, motility, and function.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R H Dowling.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
To determine the optimum dose for the medical treatment of gallstones with ursodeoxycholic acid (U.D.C.A.), 11 non-obese patients with radiolucent gallstones were given 5 mg, 10 mg, and 15 mg U.D.C.A. kg body-weight-1 day-1 for 6 weeks each. Apart from 3 patients who required surgery for gallstone complications, treatment was well tolerated, and both dyspeptic symptoms and frequency of biliary colic were reduced. Neither diarrhoea nor hypertransaminasaemia occurred during therapy. Of 3 patients completing 6 months' treatment with an average of 8 mg U.D.C.A. kg-1 day-1, 1 showed complete and 2 partial dissolution of gallstones. There were significant correlations between the biliary cholesterol-saturation index and (i) daily dose of U.D.C.A. in mg kg-1, (ii) percentage U.D.C.A., and (iii) percentage U.D.C.A. + chenodeoxycholic acid (C.D.C.A.) in biliary bile acids. Mean gamma-glutamyl transpeptidase fell significantly during treatment, whereas other liver-function tests and hepatic histology remained normal. Mean serum-cholesterol levels did not change, and although there was a 13-35% fall in fasting serum-triglycerides, this difference was not statistically significant. U.D.C.A., like C.D.C.A., seems to act by inhibiting hepatic cholesterogenesis. In 5 patients treated with 5 mg U.D.C.A. kg-1 day-1 for 1-6 months, mean hepatic hydroxymethylglutaryl-coenzyme-A-reductase activity was 28% lower than in untreated gallstone patients. These preliminary results suggest that U.D.C.A. is as effective as C.D.C.A. in 1/2--2/3 the dose and that 10 mg U.D.C.A. kg-1 day-1 should be effective in most gallstone patients.
Increasing evidence implicates prolonged intestinal transit (slow transit constipation) in the pathogenesis of conventional gallbladder stones (GBS), and that of gallstones induced by long term octreotide (OT) treatment. Both groups of GBS patients have multiple abnormalities in the lipid composition and physical chemistry of their gallbladder bile-associated with, and possibly due to, an increased proportion of deoxycholic acid (DCA) (percentage of total bile acids). In turn, this increase in the percentage of DCA seems to be a consequence of prolonged colonic transit. Thus, in acromegalic patients OT treatment significantly prolongs large bowel transit time (LBTT) and leads to an associated increase of the percentage of DCA in fasting serum (and, by implication, in gallbladder bile). LBTT is linearly related to the percentage of DCA in fasting serum and correlates significantly with DCA input (into the enterohepatic circulation) and DCA pool size. However, these adverse effects of OT can be overcome by the concomitant use of the prokinetic drug cisapride, which normalizes LBTT and prevents the rise in the percentage of serum DCA. Therefore, in OT-treated patients and other groups at high risk of developing stones, it may be possible to prevent GBS formation with the use of intestinal prokinetic drugs.
BACKGROUND: Although the prevalence of symptomatic gallbladder stone disease in Ghana increased almost four-fold between 1966 and 1991, little is known about the composition of and aetiopathogenesis of these stones, nor about their suitability for non-surgical (dissolution) treatments. METHODS: To study this, gallstones from 67 out of 90 patients coming to cholecystectomy were retrieved and, based on their external appearance, classified provisionally as cholesterol(chol) (n = 8), black pigment (n = 28) and brown pigment (n = 31) stones. The gallstones were then homogenised, their cholesterol(chol) content measured chemically and the stones re-classified as cholesterol-poor (< 10% chol by weight), intermediate (10-75% chol) and cholesterol-rich (> 75% chol). The relationship between the initial and the definitive classifications was then examined and the biliary bacteriology (carried out on fresh samples of gallbladder(GB) bile obtained by fine needle aspiration) on gallstone composition, analysed. RESULTS: The external appearance correctly predicted stone composition in the 28 thought, initially, to have black pigment stones (all of whom had stones containing < 10% chol by weight, on chemical analysis) and the eight believed, originally to have "cholesterol" stones (all of whom had stones with > 75% chol) but it proved unreliable in the 31 considered, at the time of surgery, to have brown pigment stones (mean chol content 58+ SEM 35%; range 0-98%. By chemical analysis, more than half the patients 35 of 67 or 52% had cholesterol-poor stones, nine (13% of the total) had intermediate stones, while 23 (34%) had cholesterol-rich stones. Cholesterol-rich gallstones were also more frequent in women than in men (p < 0.03). Only nine of 43 patients (21%) whose GB bile was aspirated, had positive bacterial cultures. There was no obvious difference in stone composition between those with positive, and those with negative, cultures. CONCLUSION: Since the majority of Ghanaian patients with cholecystolithiasis have gallbladder stones with < 75% chol by weight, when active treatment is indicated surgery is more appropriate than dissolution therapy. However contrary to common belief, cholesterol-rich gallstones do occur in West Africa: 34% of the present series had stones with > 70% chol by weight.