Drugs online research references
J Gastrointest Surg. 1998 Jul-Aug;2(4):333-41.
Bile reflux in benign and malignant Barrett's esophagus: effect of medical acid suppression and nissen fundoplication.
Stein HJ, Kauer WK, Feussner H, Siewert JR.
Chirurgische Klinik und Poliklinik, Klinikum rechts der Isar der TU Munchen, Munchen, Germany.
Bile reflux has been implicated in the pathogenesis and malignant degeneration of Barrett's esophagus, but clinical studies in patients with adenocarcinoma arising in Barrett's esophagus are lacking. Ambulatory esophageal measurement of acid and bile reflux was performed with the previously validated fiberoptic bilirubin monitoring system (Bilitec) combined with a pH probe in 20 asymptomatic volunteers, 19 patients with gastroesophageal reflux disease (GERD) but no mucosal injury, 45 patients with GERD and erosive esophagitis, 33 patients with GERD and Barrett's esophagus, and 14 patients with early adenocarcinoma arising in Barrett's esophagus. Repeat studies were done in 15 patients under medical acid suppression and 16 patients after laparoscopic Nissen fundoplication. The mean esophageal bile exposure time showed an exponential increase from GERD patients without esophagitis to those with erosive esophagitis and benign Barrett's esophagus and was highest in patients with early carcinoma in Barrett's esophagus (P <0.01). Pathologic esophageal bile exposure was documented in 18 (54.5%) of 33 patients with benign Barrett's esophagus and 11 (78.6%) of 14 patients with early adenocarcinoma in Barrett's esophagus. Nissen fundoplication but not medical acid suppression resulted in complete suppression of bile reflux. Bile reflux into the esophagus is particularly prevalent in patients with Barrett's esophagus and early cancer. Bile reflux into the esophagus can be completely suppressed by Nissen fundoplication but not medical acid suppression alone.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9841990&dopt=Abstract
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Jpn J Pharmacol. 1998 Nov;78(3):313-22.
Histamine H2-receptor antagonism of T-593, an anti-ulcer agent: studies on aminopyrine accumulation in isolated canine gastric mucosal cells.
Inoie M, Marubuchi S, Arai H.
Research Laboratories, Toyama Chemical Co., Ltd., Japan.
Histamine H2-receptor antagonistic properties of the anti-ulcer agent T-593, (+/-)-(E)-1-[2-hydroxy-2-(4-hydroxyphenyl)ethyl] -3-[2[[[5-(methylamino)methyl-2-furyl]methyl]thio] ethyl] -2-(methylsulfonyl)guanidine, were investigated on [14C]aminopyrine accumulation in isolated canine gastric mucosal cells and compared with those of ranitidine and famotidine. The potency of T-593-inhibition of [14C]aminopyrine accumulation stimulated by 10(-4) M histamine, with an IC50 value of 1.85 x 10(-6) M, was approximately 5 times greater than that of ranitidine, but half that of famotidine. T-593 did not affect [14C]aminopyrine accumulation stimulated by carbachol or dibutyryl-cAMP. T-593 depressed the maximal response of the histamine concentration-response curve with a dose-related displacement to the right, indicating that the nature of the H2-receptor antagonism of T-593 was insurmountable and included non-competitive inhibition. The inhibitory efficacy of T-593 was time-dependent and was retained after the cells were washed. The inhibitory potency of (-)-S-T-593, one of the enantiomers, on the [14C]aminopyrine accumulation stimulated by histamine was approximately twice that of racemic T-593 and it also behaved as an insurmountable H2-receptor antagonist. However, the potency of (+)-R-T-593 was markedly weak. These results suggest that T-593 has H2-receptor antagonism that is insurmountable and this agent slowly associates and dissociates with the receptor in isolated canine gastric mucosal cells and that the specific substance causing H2-receptor antagonism is (-)-S-T-593.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9869265&dopt=Abstract
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hsc.usc.edu
OBJECTIVES: To present a potentially life-threatening manifestation of gastroesophageal reflux disease (GERD), laryngospasm. This review covers the diagnosis and management of eight patients treated by the authors. STUDY DESIGN: A retrospective analysis of 8 consecutive patients who were referred for the evaluation of unexplained laryngospasm. The medical therapy and lifestyle modifications of treatment are discussed. METHODS: The patient records were reviewed and tabulated for age, onset of symptoms, and history of GERD; the presence of an associated upper respiratory infection with persistent cough; and the development of syncope in the presence of laryngospasm. RESULTS: All 8 patients had initial control of laryngospasm. Three had complete control without relapse, 3 had initial control with rare relapse of mild laryngospasm, and 2 patients had initial control with frequent relapses. Six of the 8 had syncopal episodes as a consequence of the laryngospasm. All patients were initially treated with a proton pump inhibitor. Five of the 8 required the addition of an esophageal prokinetic agent to control the reflux and subsequent laryngospasm. Two patients are off all medications at the time of this writing and 4 of the 8 have had rare relapses after initial control of symptoms. Once control of the laryngospasm had been achieved, there were no subsequent episodes of syncope. CONCLUSIONS: Based on the data collected in these 8 individuals, patients with reflux disease (known or unknown) can develop severe laryngospasm and possible syncope. The key factor seems to be the association of a recent or concurrent upper respiratory infection that results in a protracted cough that is more severe when supine and at times violent. The cough increases the amount of the refluxate, which is the noxious insult to the larynx.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11801981&dopt=Abstract
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