scholarly journals Gastric mucosal prolapse: A case of proton-pump inhibitor nonresponsive dyspepsia

2018 ◽  
Vol 6 (7) ◽  
pp. 1377-1378
Author(s):  
Tagore Sunkara ◽  
Emmanuel Ofori ◽  
Krishna Sowjanya Yarlagadda ◽  
Vinaya Gaduputi
Keyword(s):  
Proton Pump Inhibitor ◽  
Proton Pump ◽  
Mucosal Prolapse ◽  
Gastric Mucosal Prolapse

Duodenal Ulcer Induced by Hem-o-Lok clip after Reduced Port Laparoscopic Cholecystectomy

2016 ◽  
Vol 25 (1) ◽  
pp. 95-98 ◽  
Author(s):  
Koichi Soga ◽  
Kyoichi Kassai ◽  
Kenji Itani
Keyword(s):  
Laparoscopic Cholecystectomy ◽  
Proton Pump Inhibitor ◽  
Proton Pump ◽  
Cystic Duct ◽  
Duodenal Bulb ◽  
Mucosal Injury ◽  
Normal Mucosa ◽  
Surrounding Tissue ◽  
Inferior Wall ◽  
Endoscopic Clip

The patient was a 66-year-old woman who had undergone laparoscopic cholecystectomy (Lap-C) secondary to chronic cholecystitis status post endoscopic choledocholithotomy 13 months previously. During surgery, Hem-o-Lok clips were used to control the cystic duct and the cystic artery. Due to the presence of extensive adhesions of the cystic duct and surrounding tissue, the surgeons had difficulty in debriding the area. Thirteen months after Lap-C, the patient underwent a screening esophagogastroduodenoscopy (EGD), which demonstrated clip appearance at the inferior wall of the first part of the duodenum. In the EGD, duodenal erosions and edema were observed around the clip. We appreciated that endoscopic clip removal would be difficult because of the presence of severe adhesions and inflammation of the duodenal bulb. On clinical examination of the patient, no major abnormalities or physical findings were noted. Therefore, we decided not to attempt to remove the clip. The patient was treated with an oral proton pump inhibitor to prevent extensive duodenal mucosal injury. Two months later, we repeated the EGD, which revealed that the clip was no longer present, and the duodenum was covered with normal mucosa surrounding the scar. Abbreviations: EGD: esophagogastroduodenoscopy; Lap-C: laparoscopic cholecystectomy; PPI: proton pump inhibitor.

Potential reasons for proton pump inhibitor failure in the treatment of gastroesophageal reflux disease

2008 ◽  
Vol 149 (40) ◽  
pp. 1881-1888 ◽  
Author(s):  
Márk Juhász ◽  
Zsolt Tulassay
Keyword(s):  
Gastroesophageal Reflux Disease ◽  
Proton Pump Inhibitor ◽  
Gastroesophageal Reflux ◽  
Proton Pump ◽  
Reflux Disease

A protonpumpagátlók (protonpumpa-inhibitorok, PPI) bevezetése új fejezetet nyitott a gastrooesophagealis refluxbetegség (gastroesophageal reflux disease, GERD) kezelésében. A betegek kisebb, de nem jelentéktelen hányadában azonban a PPI sem hatékony. Ilyen esetekben az első kérdés mindig az, hogy a tünetek valóban GERD-nek tulajdoníthatók-e, vagy egyéb betegség után kell kutatnunk. Ha a GERD a legvalószínűbb lehetőség, akkor a további vizsgálatok és a több támadáspontú kezelés előtt fel kell térképeznünk a beteg együttműködését (compliance). Ha az eredménytelen PPI-kezelés hátterében nem helytelenül kezelt GERD áll, akkor számos egyéb kórkép lehetőségét is fel kell vetnünk. Összefoglaló közleményünkben az elkülönítő diagnosztikai kérdésekről adunk áttekintést.

Possibilities for treating aspirin-i lesions of the stomach and duodenum in patients with chronic coronary heart disease

2020 ◽  
Vol 98 (3) ◽  
pp. 231-235
Author(s):  
N. Yu. Borovkova ◽  
M. V. Buyanova ◽  
T. E. Bakka ◽  
M. P. Nistratova ◽  
T. V. Vlasova ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Proton Pump Inhibitor ◽  
Blood Serum ◽  
Proton Pump ◽  
The Body ◽  
Control Group ◽  
Pge2 Level ◽  
Endogenous Prostaglandins ◽  
Chronic Coronary Heart Disease

To evaluate possibilities of aspirin-induced gastroduodenopathy treatment in the patients with chronic ischemic heart disease by means of applying the internal endogenous prostaglandins stimulant.  Material and methods. 340 patients suffering from chronic coronary heart disease and receiving a long-term acetylsalicylic acid (ASA) therapy were examined on the base of the cardiovascular care unit of The Nizhny Novgorod Regional Clinical Hospital named after N.A. Semaschko. There were evaluated frequency, nature and severity of the aspirin-induced gastroduodenopathy. The patients with coronary heart disease and aspirin-induced gastroduodenopathy were divided in two groups. In the first group of patients there was applied rebamipide therapy (in a single daily dose 300 mg) in combination with the proton pump inhibitor (PPI) — pantoprazole. In the second group there was applied only pantoprazole therapy. For the purpose of specification of AIG pathogenetic mechanisms development, all the examined chronic coronary heart disease cases were tested on the prostaglandin E2 (PGE2) level in blood serum before the therapy beginning and after the treatment. The control group was formed of chronic coronary heart disease patients showing no AIG evidence. Statistical processing of the received data was fulfilled with the program «Statistika 10.0». Results. AIG was registered in 15% out of 340 chronic coronary heart disease patients. According to the endoscopic examination erosive disease of the body and antrum prevailed among the patients. The PGE2 level in the blood serum was significantly lower (р = 0,00087) in these patients in comparison with the control group. In association with PPI and rebamipide mixed therapy, esophagogastroduodenoscopy results showed no pathological findings in gastrointestinal mucosa and statistically significant (р = 0,00067) blood serum PGE2 level growing in all the treated patients. As a result of exclusive PPI therapy there was marked positive dynamics in endoscopic view in 19 out of 25 patients and a tendency to normalization of PGE2 level in the blood serum. However, PGE2 level growing was insignificant. Conclusion. The presented research demonstrates the possibility of AIG treatment with the use of internal endogenous prostaglandins stimulant — rebamipide in complex with proton pump inhibitor PPI therapy.

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