View clinical trials related to GI Bleeding.
Filter by:The GI-FLX Registry is intended to create a registry of patients with a history of Atrial Fibrillation (AF) and Gastrointestinal (GI) bleed who will receive Left Atrial Appendage Closure (LAAC) with WATCHMAN FLX device and compare to patients with AF and GI bleed who do not have LAAC. The GI-FLX Registry will be a multi-center, non-randomized registry. Approximately 250 prospective patients will be enrolled at all 4 sites. Historical cohort of 250 patients after propensity score matching with WATCHMAN-FLX arm will be included in the final analysis.
This study is designed as a multicenter prospective data recording study to document the performance of the DAT clip as part of standard medical care of patients. No experimental interventions will be performed.
Peptic ulcer bleeding is the most common etiology in upper gastrointestinal bleeding all over the world. After endoscopic treatment, proton pump inhibitor (PPI) is recommended to prevent re-bleeding. Intravenous PPI is recommended as a standard treatment.In the past, there were many trials showing the efficacy of high-dose oral PPI after endoscopic hemostasis but most were industrial sponsor which assessing an expensive PPI. Moreover, the number of patients in those studies were insufficient to confirm a non-inferiority outcome in term of rebleeding by using oral PPI. This study will evaluate a high-dose, local-made PPI (omeprazole) in peptic ulcer treatment after successful endoscopic hemostasis compared to standard IV PPI continuous drip.
Primary objective: Evaluation of capsule endoscopy in the emergency setting of severe GI-Bleeding.
Current guidelines recommend the addition of proton pump inhibitors (PPI) to patients taking double anti-platelet therapy (Aspirin and Clopidogrel) to prevent upper GI bleeding1. Many post percutaneous coronary intervention (PCI) patients are treated with dual anti-platelet medications as well as PPI to prevent upper GI bleeding. Recently, it was shown that PPI interact with the P450 system in the liver and reduce the platelet inhibitory effect of Clopidogrel2,3. Clopidogrel is activated by CYP2C19, which also metabolizes PPI4. Furthermore, a recent article showed increased mortality in patients taking PPI and clopidogrel compared with patients taking clopidogrel without PPI protection5. The degree of reduction in the platelet inhibitory properties of clopidogrel might vary among the different PPI4. The use of PPI for GI protection in patients treated with dual anti-platelet therapy is not based on randomized trials, but rather on expert opinion. Since H2 blockers are also effective in preventing acid secretion and are not known to interact with the P450 system that affects clopidogrel, the investigators hypothesized that these group of drugs will not interfere with the positive antiplatelet effects of clopidogrel and therefore will offer a good alternative treatment option.