Nonsteroidal Antiinflammatory Drugs Are Associated with Gastric Outlet Obstruction

Weaver, Gary A.; Harper, Rebecca L.; Storey, James A.; Jenkins, Paul; Merrell, Nancy

doi:10.1097/00004836-199504000-00006

Cited by 17 publications

(7 citation statements)

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“…These ulcers might thus lead to pyloric scarring and gastric outlet obstruction as they are recurrent and can be overlooked in asymptomatic patients. In a recent study by Weaver et al [14], prolonged NSAIDs use was associated with gastric outlet obstruction. Ulcers in RA patients receiving chronic NSAIDs are more frequent when concomitant corticosteroids are used [12].…”

Section: Discussionmentioning

confidence: 91%

“…Patients with rheumatoid arthritis (RA), who require longterm nonsteroidal antiinflammatory drugs (NSAIDs) and corticosteroids, have a tendency to develop relapsing gastric antral ulcers which infrequently result in pyloric channel stenosis [3,8,11,12,14]. In addition, secondary gastrointestinal amyloidosis (SGIA) is a well-known serious complication in RA patients [13].…”

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confidence: 99%

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Endoscopic hydrostatic balloon dilation of ulcer-induced pyloric stenosis in rheumatoid arthritis and secondary amyloidosis

et al. 1997

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We describe a 50-year-old Japanese woman with rheumatoid arthritis who presented with near-complete gastric outlet obstruction. The patient also suffered from secondary gastrointestinal and cardiac amyloidosis. Gastroscopy revealed multiple huge gastric antral ulcers in which amyloid deposits were identified on histologic examination. The ulcers became scars after treatment with omeprazole, which cause in severe pyloric stenosis. Endoscopic hydrostatic balloon dilation under fluoroscopic guidance was performed twice for 10 min. The pyloric outlet remained sufficiently patent 22 months later.

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Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 99%

Endoscopic hydrostatic balloon dilation of ulcer-induced pyloric stenosis in rheumatoid arthritis and secondary amyloidosis

et al. 1997

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“…NSAID ingestion is an uncommon cause of GOO [3, 4]. Mechanism of GOO caused by NSAID abuse is not entirely clear.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Response to endoscopic dilatation depends upon the etiology, length, and site of stricture [4]. Patients with chronic pancreatitis-related duodenal stricture have been reported to have the worst outcome with endoscopic dilatation [4]. Need for more than two sessions of endoscopic dilatation to relieve symptom is also a predictor for failure of endoscopic therapy in patients with peptic ulcer disease [14].…”

Section: Discussionmentioning

confidence: 99%

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NSAIDs-Related Pyloroduodenal Obstruction and Its Endoscopic Management

Noor

Dixit

Kochhar

et al. 2011

Diagnostic and Therapeutic Endoscopy

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Endoscopic balloon dilatation (EBD) has important role in the management of benign gastric outlet obstruction. Although there are many reports on the role of EBD in the management of corrosive-induced and peptic benign GOO, there is scanty data on its role in the management of NSAID-induced GOO. We report 10 cases of NSAID-induced pyloroduodenal obstruction and their endoscopic management. The most common site of involvement was duodenum (5/10) followed by both pylorus and duodenum (4/10) and pylorus (1/10). Most of the strictures were short web-like, and the mean (SD) number of stricture was 2.0 (0.94). Endoscopic balloon dilatation was successful in 90% (9/10) cases requiring mean (SD) of 2.0 (1.6) sessions of dilatation to achieve target diameter of 15 mm and mean (SD) of 5.3 (2.7) sessions to maintain it over a treatment period of 4.5 months (IQR 2–15 months). There was no procedure-related complication or mortality.

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Gastric secretion of acid and pepsin in patients with esophageal stricture and appropriate controls

Hirschowitz

1996

Digest Dis Sci

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Most cases of esophageal stricture are associated with acid/peptic reflux esophagitis. While patients with strictures commonly have disordered lower esophageal sphincters and poor clearance and neutralization mechanisms, it is not known whether they also have abnormal gastric secretion. This study examined fasting, basal, and stimulated acid and pepsin secretion. With an endoscopic diagnosis of esophagitis, patients with stricture (< 12.5 mm) were matched for age, sex, concurrent gastrointestinal disease (duodenal ulcer, N = 9), Zollinger-Ellison syndrome (N = 6), and postgastric surgery state (N = 5), as well as the absence of ulcer disease (non-DU, N = 37). Fasting, basal, and pentagastrin-stimulated acid and pepsin secretion were measured. Overall, the 57 stricture patients had the same acid and pepsin secretion as their matched controls with esophagitis; the same was true for each of the subgroups (ZES, DU, non-DU, and postsurgical). Stricture patients weighed less and had a lower body mass index (P < 0.01). Patients with esophageal peptic stricture have the same acid and pepsin output as control patients matched for sex, age, background gastrointestinal disease, and the presence of esophagitis.

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Nonsteroidal Antiinflammatory Drugs Are Associated with Gastric Outlet Obstruction

Cited by 17 publications

References 0 publications

Endoscopic hydrostatic balloon dilation of ulcer-induced pyloric stenosis in rheumatoid arthritis and secondary amyloidosis

Endoscopic hydrostatic balloon dilation of ulcer-induced pyloric stenosis in rheumatoid arthritis and secondary amyloidosis

NSAIDs-Related Pyloroduodenal Obstruction and Its Endoscopic Management

Gastric secretion of acid and pepsin in patients with esophageal stricture and appropriate controls

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