PPI treatment compared with placebo or H2RA reduces mortality following PU bleeding among patients with high-risk endoscopic findings, and reduces re-bleeding rates and surgical intervention. PPI treatment initiated prior to endoscopy in UGI bleeding significantly reduces the proportion of patients with SRH at index endoscopy but does not reduce mortality, re-bleeding or the need for surgery. The strategy of giving oral PPI before and after endoscopy, with EHT for those with major SRH, is likely to be the most cost-effective. Treatment of H. pylori infection was found to be more effective than antisecretory therapy in preventing recurrent bleeding from PU. H. pylori eradication alone or eradication followed by misoprostol (with switch to PPI, if misoprostol is not tolerated) are the two most cost-effective strategies for preventing bleeding ulcers among H. pylori-infected NSAID users, although the data cannot exclude PPIs also being cost-effective. Further large randomised controlled trials are needed to address areas such as PPI administration prior to endoscopic diagnosis, different doses and administration of PPIs, as well as the primary and secondary prevention of UGI bleeding.
We have found increased small intestinal permeability to 51Cr-ethylenediaminetetra acetate in patients with ankylosing spondylitis compared with controls. There is no significant difference between patients with ankylosing spondylitis and patients with rheumatoid arthritis taking non-steroidal anti-inflammatory drugs (NSAID). The increased intestinal permeability in ankylosing spondylitis is independent ofdisease activity. These findings suggest that the increased permeability is caused by NSAID treatment and is probably not a primary lesion of small bowel mucosa. PATIENTSSeventeen patients with ankylosing spondylitis taking NSAIDs who were attending our rheumatology outpatient clinic were studied. They were compared with two control groups, the first comprising 16 healthy volunteers and the second 19 patients with rheumatoid arthritis being treated with NSAIDs. In our clinical practice we had insufficient patients with ankylosing spondylitis who were not taking NSAIDs to form a separate control group. In these groups, coeliac disease, inflammatory bowel disease, alcohol abuse, and, in the volunteers, NSAID therapy were excluded on the basis ofhistory and clinical examination. The ankylosing spondylitis patients were all men aged 29-63 years, healthy volunteers (eight men and eight women) were aged 24-63 years, and the rheumatoid group (10 men and nine women) were aged 37-82 years. All tests were performed on an outpatient basis and informed consent was obtained before each procedure. METHODSAfter an overnight fast, patients and controls received 150 ml of solution containing 2 g mannitol, 5 g lactulose, 1 g L-rhamnose, 20 g sucrose, 20 g lactose, and 4 MBq of 51Cr-EDTA. The patients' urine was collected for 24 hours after taking the test solution. The collection period was divided into 0-6 hours and 6-24 hours. One ml of thiomersol (10% w/v) was added to the containers as preservative. The addition ofsugars (sucrose and lactose) to the test solution rendered the final solution hyperosmolar at 1200 mOsmol/l.Estimation of urinary recovery of 51Cr-EDTA used the methods described by Bjarnason.56 Urinary L-rhamnose, mannitol, and lactulose were estimated by modification of two gas liquid chromatography methods.910Statistical tests were performed using the Wilcoxon rank sum test, Mann-Whitney U test, and Pearson's correlation test. ResultsWe found that intestinal permeability to 5 Cr-EDTA in the 0-6 hours collection was median 0.35% (range 0.09-0 70) in controls, 0-61% (range 0. 15-1-29) in ankylosing spondylitis and 0 54% (range 0. 12-1.27) in rheumatoid arthritis. In the 6-24 hours collection values were: median 1.23% (range 0@43-21) control; 1.31% (0 3-2.28) ankylosing spondylitis, and 2.12 (0-12-11-40) rheumatoid arthritis. The sugar permeability results were: lactulose 0.25% (0.05-1 1), rhamnose 8-6% (4 9-24 9), and lactulose/ rhamnose (L/R) ratio 0.02 (0.01-0.05) in controls; lactulose 0-26% (0.04-0 59), rhamnose 8-8% (1-2-11-6), and L/R ratio 0.03 (0-01-0-27) in ankylosing spondylitis; and lactulose 0...
Omeprazole, a substituted benzimidazole, is a potent inhibitor of gastric acid secretion which is currently being evaluated in patients with peptic ulcer and Zollinger-Ellison syndrome. Drugs which possess an imidazole nucleus have previously been shown to inhibit cortisol release from the adrenal cortex, secondary to inhibition of mitochondrial cytochrome P-450 dependent hydroxylation reactions. In a double-blind placebo-controlled crossover study in healthy male volunteers, omeprazole (60 mg daily for 7 days) did not alter basal cortisol levels. The peak cortisol response to ACTH stimulation was significantly reduced. Cortisol levels 60 min after ACTH were 824 +/- 27 nmol/l on omeprazole (mean +/- SEM), and 929 +/- 35 on placebo (P less than 0.005). In vitro, omeprazole caused a concentration-dependent inhibition of ACTH-stimulated cortisol release from isolated bovine adrenal cells (ED50 = 20 micrograms/ml). This was associated with a decrease in deoxycortisol synthesis. Therefore, unlike some other imidazole-containing drugs, the inhibitory effects of omeprazole are not entirely due to steroid 11 beta-hydroxylase inhibition. Substantial inhibition occurred at omeprazole concentrations which are higher than plasma levels normally achieved in clinical use. However, impairment of adrenocortical function may occur in patients on long-term high dose omeprazole treatment for Zollinger-Ellison syndrome.
1. Perindopril, a new ACE inhibitor, is a prodrug requiring conversion into its active form perindoprilat by hydrolysis in the liver. 2. The pharmacodynamics and pharmacokinetics of perindopril (8 mg oral) and perindoprilat (2 mg intravenously) were studied in a double‐blind randomised crossover study in a group of patients with compensated biopsy‐proven hepatic cirrhosis. 3. Blood pressure and heart rate responses were similar after the two routes of administration as were plasma renin activity and aldosterone levels following dosing. 4. The AUC of perindoprilat after oral administration of perindopril represented 46 +/‐ 4% of the total AUC of perindopril and its metabolite when expressed in molar terms. Comparison with the AUC of perindoprilat after its intravenous administration suggested that 30 +/‐ 6% of the oral dose of perindopril was converted to its active metabolite. 5. The findings are comparable with those in healthy subjects. It appears that the presence of relatively mild hepatic cirrhosis does not significantly alter the pharmacokinetics of perindopril.
Letters to the Editors 779 al., 1974). The coefficient of variation of the assay was less than 3% at 10 and 30 mg 1-(n = 50).
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