Pantoprazole before Endoscopy in Patients with Gastroduodenal Ulcer Bleeding: Does the duration of Infusion and Ulcer Location Influence the Effects?

The aim of this study was to investigate the effect of preemptive pantoprazole infusion on early endoscopic findings in patients with acute ulcer bleeding. Records of 333 patients admitted with acute ulcer bleeding were analyzed. Ulcer bleeders were given either 80 mg bolus of pantoprazole followed by continuous infusion of 8 mg per hour or saline infusion until endoscopy. In 93 patients saline infusion whereas in 240 patients bolus plus infusion of pantoprazole was administrated with mean (±SD) durations of 5.45±12.9 hours and 6.9±13.2 hours, respectively (P=0.29). Actively bleeding ulcers were detected in 46/240 (19.2%) of cases in the pantoprazole group as compared with 23/93 (24.7%) in the saline infusion group (P=0.26). Different durations of pantoprazole infusion (0–4 hours, >4 hours, and >6 hours) had no significant effect on endoscopic and clinical outcome parameters in duodenal ulcer bleeders. Gastric ulcer bleeders on pantoprazole infusion longer than 4 and 6 hours before endoscopy had actively bleeding ulcers in 4.3% and 5% compared to the 19.5% active bleeding rate in the saline group (P=0.02 and P=0.04). Preemptive infusion of high-dose pantoprazole longer than 4 hours before endoscopy decreased the ratio of active bleeding only in gastric but not in duodenal ulcer patients

Pantoprazole before Endoscopy in Patients with Gastroduodenal Ulcer Bleeding: Does the duration of Infusion and Ulcer Location Influence the Effects?

The aim of this study was to investigate the effect of preemptive pantoprazole infusion on early endoscopic findings in patients with acute ulcer bleeding. Records of 333 patients admitted with acute ulcer bleeding were analyzed. Ulcer bleeders were given either 80 mg bolus of pantoprazole followed by continuous infusion of 8 mg per hour or saline infusion until endoscopy. In 93 patients saline infusion whereas in 240 patients bolus plus infusion of pantoprazole was administrated with mean (±SD) durations of 5.45± 12.9 hours and 6.9 ± 13.2 hours, respectively (P = 0.29). Actively bleeding ulcers were detected in 46/240 (19.2%) of cases in the pantoprazole group as compared with 23/93 (24.7%) in the saline infusion group (P = 0.26). Different durations of pantoprazole infusion (0-4 hours, >4 hours, and >6 hours) had no significant effect on endoscopic and clinical outcome parameters in duodenal ulcer bleeders. Gastric ulcer bleeders on pantoprazole infusion longer than 4 and 6 hours before endoscopy had actively bleeding ulcers in 4.3% and 5% compared to the 19.5% active bleeding rate in the saline group (P = 0.02 and P = 0.04). Preemptive infusion of high-dose pantoprazole longer than 4 hours before endoscopy decreased the ratio of active bleeding only in gastric but not in duodenal ulcer patients

A tervezett ellenőrző endoszkópia értéke az akut gastroduodenalis fekélyvérzés ellátásában = The value of routine second-look endoscopy in the management of the acute gastroduodenal ulcer bleeding

A tervezett ellenőrző endoszkópiák szerepe az akut gastroduodenalis fekélyvérző betegek ellátásában mindmáig ellentmondásos. Endoszkópos és klinikai adatokra alapozott rizikócsoport meghatározására van szükség ahhoz, hogy kiválaszthatóak legyenek azok a betegek, akiknél a tervezett ellenőrző endoszkópia stratégiája hasznosnak bizonyulhat. Célkitűzés: A tervezett ellenőrző endoszkópiák klinikai hasznát kívántuk felmérni akut gastroduodenalis fekélyvérző betegeink klinikai és endoszkópos adatainak retrospektív elemzésével. Módszer: Összesen 274 fekélyvérző beteg adatait elemeztük. A tervezett ellenőrző endoszkópiák hatékonyságának lemérésére az újbóli endoszkópos vérzéscsillapító beavatkozások szükségességét használtuk fel. A betegeket a sürgősségi endoszkópia során észlelt Forrest szerinti fekélystádium alapján csoportosítottuk. Eredmények: Az aktívan vérző fekélybetegek (Forrest Ia, Ib) csoportjában a tervezett endoszkópiák alkalmával 23,8%-ban végeztünk újbóli endoszkópos vérzéscsillapítást. Az ércsonkos fekélyesek (Forrest IIa) csoportjában 13,0%-ban, míg a thrombussal fedett fekélyesek (Forrest IIb) körében 13,3%-ban volt szükség újabb endoszkópos hemosztatikus kezelésre az ellenőrző endoszkópiák kapcsán. Bár a beavatkozások gyakorisága közötti különbségek statisztikailag nem szignifikánsak, mégis klinikailag számottevőnek tartható az, hogy az eredetileg aktívan vérző betegek negyedében hasznos volt a tervezett ellenőrző endoszkópia. Következtetés: Az eredmények arra engednek következtetni, hogy a tervezett ellenőrző endoszkópia stratégiája a kezdetben aktívan vérző és nagy újravérzési kockázatú betegek számára kedvezőbb kórlefolyást ígér. | The role of routine second-look endoscopy in the management of patients with acute peptic ulcer bleeding is controversial. A more precise identification of higher risk patient group, based on both clinical and endoscopic criteria, is needed to determine whether there are high-risk patients who may benefit from this management strategy. Aim: Or aim was to find out whether scheduled second-look endoscopy has any beneficial effect in the clinical outcome. Methods: Both endoscopic and clinical data were analyzed in 274 acute gastroduodenal ulcer bleeding patients. The need for repeated endoscopic haemostatic intervention was used as a measure to evaluate the potential beneficial effect of the second look endoscopy. Patients were categorized according to the Forrest classification detected during the emergency endoscopy. Results: In the subgroup of actively bleeding patients (Forrest Ia, Ib) a second endoscopic haemostasis was performed in 23.8% of cases. In the patient subgroup with visible vessel ulcers (Forrest IIa) and in those with adherent clot covered ulcers (Forrest IIb) the needs for a repeated haemostasis were 13.0% and 13.3% respectively. Despite the not statistically significant differences, remarkable clinical impact was noted favoring scheduled second look endoscopy in patients with initially active ulcer bleeding. Conclusion: In the light of the retrospective study results it may be concluded that the scheduled second look endoscopy strategy offers a beneficial clinical outcome for selected patients estimated to be a very high risk of re-bleeding following the initial endoscopic therapy for active bleeding

Lysophosphatidic acid induces vasodilation mediated by LPA1 receptors, phospholipase C, and endothelial nitric oxide synthase.

Lysophosphatidic acid (LPA) has been implicated as a mediator of several cardiovascular functions, but its potential involvement in the control of vascular tone is obscure. Here, we show that both LPA (18:1) and VPC31143 (a synthetic agonist of LPA1-3 receptors) relax intact mouse thoracic aorta with similar Emax values (53.9 and 51.9% of phenylephrine-induced precontraction), although the EC50 of LPA- and VPC31143-induced vasorelaxations were different (400 vs. 15 nM, respectively). Mechanical removal of the endothelium or genetic deletion of endothelial nitric oxide synthase (eNOS) not only diminished vasorelaxation by LPA or VPC31143 but converted it to vasoconstriction. Freshly isolated mouse aortic endothelial cells expressed LPA1, LPA2, LPA4 and LPA5 transcripts. The LPA1,3 antagonist Ki16425, the LPA1 antagonist AM095, and the genetic deletion of LPA1, but not that of LPA2, abolished LPA-induced vasorelaxation. Inhibition of the phosphoinositide 3 kinase-protein kinase B/Akt pathway by wortmannin or MK-2206 failed to influence the effect of LPA. However, pharmacological inhibition of phospholipase C (PLC) by U73122 or edelfosine, but not genetic deletion of PLCepsilon, abolished LPA-induced vasorelaxation and indicated that a PLC enzyme, other than PLCepsilon, mediates the response. In summary, the present study identifies LPA as an endothelium-dependent vasodilator substance acting via LPA1, PLC, and eNOS.-Ruisanchez, E., Dancs, P., Kerek, M., Nemeth, T., Farago, B., Balogh, A., Patil, R., Jennings, B. L., Liliom, K., Malik, K. U., Smrcka, A. V., Tigyi, G., Benyo, Z. Lysophosphatidic acid induces vasodilation mediated by LPA1 receptors, phospholipase C, and endothelial nitric oxide synthase