Drugs online research references
Am J Physiol Gastrointest Liver Physiol. 2002 Jan;282(1):G175-83.
Hypergastrinemia in response to gastric inflammation suppresses somatostatin.
Zavros Y, Rieder G, Ferguson A, Samuelson LC, Merchant JL.
Howard Hughes Medical Institute, Ann Arbor, Michigan 48109-0650, USA.
Hypergastrinemia and a reduction in tissue somatostatin occur in Helicobacter pylori-infected patients. We investigated whether the D cell may be a direct target of gastric inflammation and hypergastrinemia. D cells were quantified by morphometry and flow cytometry in 16-wk-old wild-type (G+/+) and gastrin-deficient (G-/-) mice. Hypochlorhydric G-/- mice were treated with either antibiotics for 20 days or infused with gastrin (G-17) for 14 days. G+/+ mice were made hypochlorhydric by treating them with omeprazole for 2 mo. G-/- mice showed significant inflammation compared with the G+/+ mice, which resolved after 20 days of antibiotic treatment. D cell numbers were not significantly different between G-/- and G+/+ mice. After G-17 was infused, fundic and antral D cell numbers decreased in the G-/- mice. G+/+ animals made hypergastrinemic with omeprazole exhibited decreased D cell numbers. When omeprazole-treated mice were treated with antibiotics alone, elevated plasma gastrin levels returned to baseline and D cell numbers returned to resting levels despite persistent hypochlorhydria. Hypergastrinemia, induced by inflammation, results in decreased D cell numbers. Thus the stomach responds to the presence of inflammation by reducing somatostatin levels, thereby releasing the inhibition on the G and parietal cells to maximize gastric acid output.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11751171&dopt=Abstract
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Gastrointest Endosc. 2002 Jan;55(1):23-6.
Effect of multipolar electrocoagulation on EUS findings in Barrett's esophagus.
Faigel DO, Lieberman DA, Weinstein WM, Fanning S, Fennerty MB, Sampliner RB.
Portland VA Medical Center, Oregon Health and Science University, Portland, Oregon, 97201, USA.
BACKGROUND: Restoration of squamous epithelium in patients with Barrett's epithelium may be achieved by treatment with a proton pump inhibitor plus selective electrocoagulation of the metaplastic epithelium. The effect of such treatment on esophageal wall thickness and morphology, as determined by EUS, is unknown. METHODS: Patients with Barrett's esophagus were treated with omeprazole (40 mg by mouth, twice daily) and underwent selective multipolar electrocoagulation of the metaplastic segment monthly until complete squamous re-epithelialization or a maximum of 6 treatments was achieved. EUS was performed before and 6 months after the end of treatment. Four-quadrant large-forceps biopsy specimens were taken every 2 cm at the 6-month follow-up. RESULTS: Twenty-five patients with Barrett's epithelium (mean length 3.1 cm, range 2-6 cm) were included. Complete endoscopic reversal was achieved in 24 patients. Residual intestinal metaplasia beneath squamous epithelium was observed in 1 patient. In 4 patients there was intestinalized mucosa at the neosquamocolunmar junction. The thickness of the treated distal esophageal wall decreased from 4.0 +/- 0.1 mm to 3.7 +/- 0.1 mm (mean +/- SEM; p < 0.05, 2-tailed paired t test). Untreated (control) esophageal wall thickness at the level of the aortic arch (2.1 +/- 0.1 mm vs. 2.2 +/- 0.1 mm) and the mid-body gastric wall thickness (2.9 +/- 0.1 mm vs. 3.1 +/- 0.1 mm) did not change. Among the 6 patients with residual intestinal metaplasia there was no change in mean wall thickness (3.7 +/- 0.2 mm vs. 3.8 +/- 0.2 mm); among the 19 without metaplasia, thickness decreased from 4.1 +/- 0.2 mm to 3.6 +/- 0.2 mm; p < 0.01. Of 11 patients with a decrease in wall thickness, only 1 had residual intestinal metaplasia. No changes in the 5-layer sonographic pattern of the esophageal wall were observed. CONCLUSIONS: Multipolar electrocoagulation of Barrett's esophagus results in a slight decrease in thickness of the treated esophageal wall. A decrease in wall thickness by EUS was associated with the absence of intestinal metaplasia in follow-up biopsy specimens.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11756909&dopt=Abstract
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Biol Pharm Bull. 2001 Dec;24(12):1395-9.
The influence of commonly prescribed synthetic drugs for peptic ulcer on the pharmacokinetic fate of glycyrrhizin from Shaoyao-Gancao-tang.
He JX, Akao T, Nishino T, Tani T.
Institute of Natural Medicine, Toyama Medical and Pharmaceutical University, Japan.
The influence of synthetic drugs prescribed for peptic ulcer on the pharmacokinetic fate of glycyrrhizin (GL) from Shaoyao-Gancao-tang (SGT, a traditional Chinese formulation, Shakuyaku-Kanzo-to in Japanese) was investigated in rats. Co-administration of histamine H2-receptor antagonist (cimetidine) and anticholinergic drug (scopolamine butyl bromide) with SGT didn't influence the area under the plasma concentration-time curves (AUC) of glycyrrhetic acid (GA), an active metabolite derived from GL in SGT. The AUC of GA from SGT were significantly reduced by co-administration of synthetic drugs commonly used for peptic ulcer in a triple therapy (OAM), a combination of a proton pump inhibitor (omeprazole) and two antibiotics (amoxicillin and metronidazole). We found that the reduction of AUC in OAM treatment was due to the antibacterial effect of amoxicillin and metronidazole on intestinal bacteria in rat which lead to the decrease of GL-hydrolysis activity. The present study suggests that it may not be a proper way to use triple therapy containing antibiotics simultaneously with SGT for healing of chronic ulcers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11767109&dopt=Abstract
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