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  • 1
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Previous data have indicated low bone formation as a mechanism of osteoporosis in inflammatory bowel disease. Fluoride can stimulate bone formation.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To assess the effect of fluoride supplementation on lumbar spine bone mineral density in osteoporotic patients with inflammatory bowel disease treated in parallel with calcium and vitamin D.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:In this prospective, randomized, double-blind, parallel and placebo-controlled study, 94 patients with inflammatory bowel disease (lumbar spine T score below − 2 standard deviations, normal serum 25OH vitamin D), with a median age of 35 years, were included. Bone mineral density was measured by dual-energy X-ray absorptiometry. Patients were randomized to receive daily either sodium monofluorophosphate (150 mg, n=45) or placebo (n=49) for 1 year, and all received calcium (1 g) and vitamin D (800 IU). The relative change in bone mineral density from 0 to 12 months was tested in each group (fluoride or placebo) and compared between the groups.〈section xml:id="abs1-4"〉〈title type="main"〉Results:Lumbar spine bone mineral density increased significantly in both groups after 1 year: 4.8 ± 5.6% (n=29) and 3.2 ± 3.8% (n=31) in the calcium–vitamin D–fluoride and calcium–vitamin D–placebo groups, respectively (P 〈 0.001 for each group). There was no difference between the groups (P=0.403). Similar results were observed according to corticosteroid intake or disease activity.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions:Calcium and vitamin D seem to increase lumbar spine density in osteoporotic patients with inflammatory bowel disease; fluoride does not provide further benefit.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1238
    Keywords: Peptic ulcer ; Gastrointestinal haemorrhage ; Endoscopic treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Endoscopic adrenaline-hypertonic injection was attempted in 40 patients admitted for oesophagogastroduodenal ulcer haemorrhage unresponsive to conventional medical treatment and presenting with severe underlying disease or advanced age (〈80 years). The results were compared with our own historical controls (43 patients) treated by conventional therapy, meeting the same inclusion criteria. Permanent haemostasis was achieved in 32 patients in the injection group and 30 in the control group (NS) but emergency surgery was less frequent in the injection group (2 vs 25,p〈0.001). Blood transfusion requirements were less in the injection group (8.5±6.2 vs 10.2±5.4,p〈0.05) but length of hospital stay was not really different (15.7 days±9.3 vs 20.9±14.4). Unfortunately, mortality was not reduced in the injection group (14/40 vs 17/43). Two lethal complications attributable to injection treatment occurred. This treatment could represent an alternative to conventional haemostatic treatment in high surgical risk patients with severe clinical bleeding, avoiding emergency surgery. In spite of the fact that we selected high-risk patients, endoscopic treatment was not able to lower the mortality (about 37%). Due to severe unpredictable side effects and potential risks of long-term massive rebleeding, this treatment should be performed electively in patients with severe clinical bleeding, as first line treatment when surgical risk factors exist or immediately before surgery in low risk patients.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: intravenous fat ; intraduodenal fat ; jejunum motility ; plasma cholecystokinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of intravenous and intraduodenal fat on jejunal motility were studied in nine normal volunteers. Using a nitrogen hydraulic infusion system, recording was performed continuously during 4 hr of fasting and 5 hr of 100 ml/hr infusion of fat (Intralipid 10%) given either intraduodenally (group ID) or intravenously (group IV) and 9 hr after the end of fat administration successively. The two experiments were performed at seven-day intervals in random order. In six of the nine subjects, a third experiment, in which 20 g of cholestyramine was given by mouth during intraduodenal fat infusion (group ID + C), was carried out. Venous blood samples were drawn for measurement of serum triglyceride levels and radioimmunoassay of plasma cholecystokinin. Intraduodenal fat, alone or plus cholestyramine, induced a significant reduction in incidence of phase III of the migrating motor complex. Intravenous fat reduced the incidence of phase III. However, this reduction was significant only during the last 3 hr of fat infusion, corresponding to the highest serum triglyceride concentration. In the three groups, fat infusion induced a significant increase in duration of phase II, leading to a postprandial-like pattern. Plasma cholecystokinin increased significantly in the three groups during fat administration, with a significant positive correlation between serum triglyceride concentration and plasma cholecystokinin in the group IV. The data suggest that, in addition to its known inhibitory effects on activity fronts when acting luminally, fat given intravenously may inhibit phase III activity. The effects in both instances may be mediated in part by cholecystokinin.
    Type of Medium: Electronic Resource
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