scholarly journals Two Cases of Proton Pump Inhibitor (PPI)-resistant Gastric Ulcers Caused by Gastric Empting Disturbance

2005 ◽  
Vol 54 (2/3) ◽  
pp. 69-74
Author(s):  
Yuki NISHINO ◽  
Jun NISHIKAWA ◽  
Masaaki SATAKE ◽  
Toshihiko MATSUMOTO ◽  
Keiko AKASHI ◽  
...  
Keyword(s):  
Proton Pump Inhibitor ◽  
Proton Pump ◽  
Gastric Ulcers

Peptic ulcer disease

2020 ◽  
pp. 2849-2861
Author(s):  
Joseph Sung
Keyword(s):  
Peptic Ulcer ◽  
Proton Pump Inhibitor ◽  
Peptic Ulcer Disease ◽  
Proton Pump ◽  
Gastric Ulcers ◽  
High Dose ◽  
Recurrent Bleeding ◽  
Ulcer Disease ◽  
H Pylori ◽  
Line Of Therapy

Helicobacter pylori infection, use of nonsteroidal anti-inflammatory drugs (NSAIDs) including aspirin, and smoking are the most important causes of peptic ulcer disease. Peptic ulcer disease is characterized by a history of waxing and waning symptoms of localized, dull, aching pain in the upper abdomen. Bleeding is the most common complication; free perforation of the stomach or duodenum into the peritoneal cavity is uncommon but serious. The diagnosis of peptic ulcer disease is made by endoscopy, which offers an opportunity for biopsy of gastric ulcers (which may be malignant) and reveals important prognostic indicators in patients with bleeding ulcers. A single daily dose of a proton pump inhibitor gives quick relief of symptoms and effective healing of peptic ulcers in 4 to 6 weeks. The management of patients with upper gastrointestinal haemorrhage requires a multidisciplinary medical and surgical approach. Early risk stratification based on clinical and endoscopic criteria allows delivery of appropriate care, with endoscopic intervention now widely accepted as the first line of therapy. This should be followed by administration of a high dose of an intravenous proton pump inhibitor to further reduce recurrent bleeding. Treatment of H. pylori is a cure for peptic ulcer disease in most patients. This usually requires at least two antimicrobial agents, with the most popular triple therapy combining a proton pump inhibitor with any two of amoxicillin, metronidazole, and clarithromycin for 7 to 14 days. Eradication of H. pylori infection, avoidance of high-dose NSAIDs or aspirin, and the maintenance use of proton pump inhibitors in high-risk individuals are the best ways to prevent recurrence of ulcer and ulcer complications.

scholarly journals Usefulness of Indocyanine Green Angiography for Evaluation of Blood Supply in a Reconstructed Gastric Tube During Esophagectomy

2013 ◽  
Vol 97 (4) ◽  
pp. 340-344 ◽  
Author(s):  
Toru Ishiguro ◽  
Youichi Kumagai ◽  
Tomojiro Ono ◽  
Hideko Imaizumi ◽  
Hiroaki Honjo ◽  
...  
Keyword(s):  
Proton Pump Inhibitor ◽  
Indocyanine Green ◽  
Proton Pump ◽  
Gastric Tube ◽  
Indocyanine Green Angiography ◽  
Blood Perfusion ◽  
Gastric Ulcers ◽  
Subtotal Esophagectomy ◽  
Icg Angiography ◽  
Time Of Admission

Abstract We report a case of necrosis of a reconstructed gastric tube in a 77-year-old male patient who had undergone esophagectomy. At the time of admission, the patient had active gastric ulcers, but these were resolved by treatment with a proton pump inhibitor. Subtotal esophagectomy with gastric tube reconstruction was performed. Visually, the reconstructed gastric tube appeared to be well perfused with blood. Using indocyanine green (ICG) fluorescence imaging the gastroepiploic vessels were well enhanced and no enhancement was visable 3 to 4 cm from the tip of the gastric tube. Four days after esophagectomy, gastric tube necrosis was confirmed, necessitating a second operation. The necrosis of the gastric tube matched the area that had been shown to lack blood perfusion by ICG angiography imaging. It seems that ICG angiography is useful for the evaluation of perfusion in a reconstructed gastric tube.

scholarly journals Polymorphism of CYP2C19 and Gastric Emptying in Patients with Proton Pump Inhibitor-Resistant Gastric Ulcers

2002 ◽  
Vol 30 (4) ◽  
pp. 413-421 ◽  
Author(s):  
F Wada ◽  
K Murase ◽  
H Isomoto ◽  
H Soda ◽  
F Takeshima ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Proton Pump Inhibitor ◽  
Healthy Volunteers ◽  
Proton Pump ◽  
Fragment Length Polymorphism ◽  
Gastric Ulcers ◽  
Peak Time ◽  
Cyp2c19 Polymorphism ◽  
Patient Groups ◽  
Polymerase Chain

The aim of the present study was to investigate whether CYP2C19 polymorphism status and gastric emptying are related to healing in patients with gastric ulcers. We studied the CYP2C19 status in seven patients with proton pump inhibitor (PPI)-resistant ulcers, 21 with PPI-sensitive ulcers and 46 healthy volunteers using polymerase chain reaction restriction fragment length polymorphism to detect CYP2C19m1 mutation in exon 5 and CYP2C19m2 mutation in exon 4. Gastric emptying was evaluated using the 13C-acetate breath test. The frequency of phenotypes, indicated by genotypes, did not differ significantly between the three patient groups. The peak time of 13C excretion in patients with PPI-resistant ulcers was significantly longer than that of patients with PPI-sensitive ulcers and healthy volunteers. Our results suggest that rate of gastric emptying, but not CYP2C19 polymorphism, is likely to be an important factor in the delayed healing of patients with PPI-resistant gastric ulcer.

Twelve-month endoscopic and histological analysis following proton-pump inhibitor-based triple therapy inHelicobacter pylori-positive patients with gastric ulcers

2010 ◽  
Vol 45 (9) ◽  
pp. 1048-1058 ◽  
Author(s):  
Zsolt Tulassay ◽  
Manfred Stolte ◽  
Lars Engstrand ◽  
Eugeniusz Butruk ◽  
Peter Malfertheiner ◽  
...  
Keyword(s):  
Proton Pump Inhibitor ◽  
Triple Therapy ◽  
Proton Pump ◽  
Histological Analysis ◽  
Gastric Ulcers

scholarly journals Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid Suppression

1999 ◽  
Vol 13 (2) ◽  
pp. 135-142 ◽  
Author(s):  
R Lad ◽  
D Armstrong
Keyword(s):  
Proton Pump Inhibitor ◽  
Proton Pump ◽  
Nsaid Therapy ◽  
Peptic Ulceration ◽  
Acid Suppression ◽  
Gastric Ulcers ◽  
Prostaglandin E ◽  
Duodenal Lesions ◽  
Mucosal Lesions ◽  
Anti Inflammatory

One major cause of peptic ulceration is the use of nonsteroidal anti-inflammatory drugs (NSAIDs). The precise mechanisms through which NSAIDs cause peptic ulceration are unknown, but the discovery that they reduce the production of ‘cytoprotective’ prostaglandins led to the hypothesis that coadministration of exogenous prostaglandins heals and prevents NSAID-induced gastroduodenal ulcers and other mucosal lesions. Studies using high doses of misoprostol have shown that it does have a protective effect; however, gastrointestinal intolerance of this prostaglandin E2analogue is common. Early indications that acid suppression was effective in the management of NSAID-related peptic ulcers came from studies showing that gastric ulcers could be healed by omeprazole in patients who continued to take NSAIDs. Other studies suggested that acid suppression reduces the incidence of mucosal lesions but that standard dose ranitidine protects only against duodenal lesions. Subsequent studies reported that higher dose H2receptor antagonist therapy can protect against both gastric and duodenal ulcers during continued NSAID therapy. An ideal therapeutic strategy would heal NSAID-related ulcers and prevent the development of new NSAID-related lesions and complications in patients who are unable to discontinue NSAID therapy. A number of recent studies indicate that effective acid-suppressive treatment with the proton pump inhibitor omeprazole can achieve these aims. Overall, data from recent studies show that acid suppression with the proton pump inhibitor omeprazole at a dose of 20 mg daily is the most effective means of healing NSAID-associated gastroduodenal lesions and that it is the most effective prophylactic therapy. In the long run, the role of omeprazole will have to be evaluated with respect to its cost effectiveness compared with other strategies and with respect to the development of less damaging NSAIDs.

The biochemical and pharmacological properties of a newly synthesized H+-K+ ATPase inhibitor, 2-dimethylamino-4,5-dihydrothiazolo[4,5:3,4]pyridol-[1,2-a]benzimidazole

1998 ◽  
Vol 76 (9) ◽  
pp. 921-929 ◽  
Author(s):  
Young-Kuk Chung ◽  
Man-Sik Chang ◽  
Kyu-Bong Kim ◽  
Sang-Kwon Sohn ◽  
Tae-Wook Woo ◽  
...  
Keyword(s):  
Proton Pump Inhibitor ◽  
Atpase Activity ◽  
Acid Secretion ◽  
Proton Pump ◽  
Water Immersion ◽  
Repeated Administration ◽  
Gastric Ulcers ◽  
Dependent Manner ◽  
Atpase Inhibitor ◽  
Concentration Dependent Manner

This study was designed to determine the effect of a newly synthesized proton pump inhibitor, 2-dimethylamino-4,5-dihydrothiazolo[4,5:3,4]pyridol[1,2-a]benzimidazole (YJA20379-2), on gastric H+-K+ ATPase activity, acid secretion, and experimental gastroduodenal lesions or ulcers in rats. YJA20379-2 inhibited in a concentration-dependent manner the proton pump (H+-K+ ATPase) activity in isolated hog gastric mucosal microsomes, therefore, confirming its classification as a proton pump inhibitor. The inhibitory efficacy of YJA20379-2 on the proton pump was about eight times higher than that of omeprazole at pH 7.4. The activity of the inhibited enzyme was not restored by dilution and washout method, so this implied that the inhibition of YJA20379-2 is not reversible. YJA20379-2, given intraduodenally or orally, potently suppressed acid secretion in pylorus-ligated rats, with ED50 values of 3.6 and 7.7 mg·kg-1, respectively. Pretreatment with YJA20379-2 dose dependently protected the gastric mucosa from damage induced by absolute ethanol, water-immersion stress, indomethacin, and the duodenal mucosa from damage induced by mepirizole in rats, with ED50 values of 11.0, 21.0, 0.5, and 18.7 mg·kg-1, respectively. Repeated administration of YJA20379-2 also dose dependently accelerated spontaneous healing of acetic acid induced gastric ulcers. These results suggest that YJA20379-2 has potent antisecretory and antiulcer effects, which are exerted by suppression of H+-K+ ATPase activity in gastric parietal cells, such that YJA20379-2 may be useful for the clinical treatment of peptic ulcer diseases.Key words: antisecretion, cytoprotection, H+-K+ ATPase, YJA20379-2.

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