Effect of pepsin on ionic permeability of canine esophageal mucosa

Safaie-Shirazi, Siroos

doi:10.1016/0022-4804(77)90117-2

Cited by 18 publications

(5 citation statements)

References 5 publications

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“…Many of them have developed stricture and a few of them perforation or nonfatal hemorrhage 1 . Aspirin disrupts the normal cytoprotective barrier in the mucosa of the stomach and a similar process has been found to occur in the esophagus 39 . The nonsteroidal anti‐inflammatory drugs may exert their ulcerogenic effect by reducing the cytoprotective action of the prostaglandins on the gastric mucosa.…”

Section: Pathogenesismentioning

confidence: 89%

Drug-induced esophagitis

Zografos¹,

Georgiadou²,

Thomas

et al. 2009

Diseases of the Esophagus

124

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Drug-induced esophagitis is being recognized increasingly in the past few years. Since 1970 more than 650 cases have been reported worldwide caused by 30 or more medications. We have reviewed these cases with a view to classifying this disease based on underlying pathological mechanism. Drug-induced esophageal injury tends to occur at the anatomical site of narrowing, with the middle third behind the left atrium predominating (75.6%). The disease is broadly classified into two groups. The first group being transient and self-limiting as exemplified by the tetracycline group induced injury (65.8%). The second is the persistent esophagitis group, often with stricture, with two distinct entities: (i) patients on nonsteroidal anti-inflammatory agents whose injury is aggravated by gastroesophageal reflux (21.8%) (reflux aggravated); and (ii) patients with potasium chloride and quinidine sulphate induced injury (12.4%) (persistent drug injury). Severe esophageal injury has been reported in some women taking biphosphonates as treatment for postmenopausal osteoporosis. Endoscopic findings in such patients with esophageal injury generally suggested a chemical esophagitis, with erosions or ulcerations and exudative inflammation accompanied by thickening of the esophageal wall. Most cases of medication-induced esophageal injury heal without intervention within a few days. Thus, the most important aspect of therapy is to make the correct diagnosis and then to avoid reinjury with the drug. When possible, potentially caustic oral medications should be discontinued.

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Section: Pathogenesismentioning

confidence: 89%

Drug-induced esophagitis

Zografos¹,

Georgiadou²,

Thomas

et al. 2009

Diseases of the Esophagus

124

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“…The influence of gastric acidity on bile acid toxicity has not been investigated in humans. Animal model studies on the influence of acid on various components of duodenogastric reflux have shown a damaging potential between pepsin and taurine conjugated bile acids in acidic conditions,16 30 whereas trypsin and unconjugated bile acids have been found to be damaging in alkaline conditions 3132 Armstrong et al ,33 studying the relative toxicity of 12 bile acid fractions in a rat gastric mucosa model, showed that at neutral pH the most gastrotoxic bile acids were the unconjugated forms of the dihydroxy bile acids.…”

Section: Discussionmentioning

confidence: 99%

Toxic bile acids in gastro-oesophageal reflux disease: influence of gastric acidity

Nehra

Howell

Williams

et al. 1999

Gut

361

372

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Background-Bile acid toxicity has been shown in the gastric, colonic, and hepatic tissues; the eVect on oesophageal mucosa is less well known. Aims-To determine the spectrum of bile acids refluxing in patients with gastrooesophageal reflux disease and its relation to oesophageal pH using a new technique of combined oesophageal aspiration and pH monitoring. Methods-Ten asymptomatic subjects and 30 patients with symptoms of gastrooesophageal reflux disease (minimal mucosal injury, erosive oesophagitis (grade 2 or 3 Savary-Miller), Barrett's oesophagus/stricture; n=10 in each group) underwent 15 hour continuous oesophageal aspiration with simultaneous pH monitoring. Bile acid assay of the oesophageal samples was performed using modified high performance liquid chromatography. Results-The peak bile acid concentration and DeMeester acid scores were significantly higher in the patients with oesophagitis (median bile acid concentration 124 µmol/l; acid score 20.2) and Barrett's oesophagus/stricture (181 µmol/l; 43.3) than patients with minimal injury (14 µmol/l; 12.5) or controls (0 µmol/l; 11.1). The predominant bile acids detected were cholic, taurocholic, and glycocholic acids but there was a significantly greater proportion of secondary bile acids, deoxycholic and taurodeoxycholic acids, in patients with erosive oesophagitis and Barrett's oesophagus/stricture. Although bile acid reflux episodes occurred at variable pH, a temporal relation existed between reflux of taurine conjugates and oesophageal acid exposure (r=0.58, p=0.009). Conclusion-Toxic secondary bile acid fractions have been detected in patients with extensive mucosal damage. Mixed reflux is more harmful than acid reflux alone with possible toxic synergism existing between the taurine conjugates and acid. (Gut 1999;44:598-602)

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“…Pepsin is considered to be a very harmful agent since it causes injury typical of erosive esophagitis in a dose-dependent manner at acid pH. When in contact with the esophageal mucosa, it also increases permeability to H + (34). At an alkaline pH pepsin is not associated with significant morphologic injury or permeability changes (35).…”

Section: Pepsin Exposurementioning

confidence: 98%

How to Make a Barrett Esophagus: Pathophysiology of Columnar Metaplasia of the Esophagus

Guillem

2005

Dig Dis Sci

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Barrett esophagus is defined as a specialized intestinal replacing the squamous epithelium of the esophageal mucosa in response to gastroesophageal reflux. Barrett metaplasia is a healing process that develops to protect the esophagus from further damage. Although mechanisms by which Barrett metaplasia evolves toward dysplasia and adenocarcinoma have been extensively studied, the process by which squamous epithelium is replaced by specialized intestinal metaplasia is poorly understood. Barrett esophagus develops when defense mechanisms in the esophageal mucosa (luminal secretion of mucus, bicarbonate, growth factors, etc.) are overwhelmed by an ongoing cycle of mucosal injury and repair. Hydrogen ion, pepsin, trypsin, and bile acids are considered harmful agents that synergistically invade the esophageal mucosa. Areas of destroyed squamous epithelium are then progressively reepithelized by a columnar epithelium that may originate from multipotent stem cells located within the basal layer of the normal esophageal mucosa or in the ducts of submucosal glands.

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Effect of pepsin on ionic permeability of canine esophageal mucosa

Cited by 18 publications

References 5 publications

Drug-induced esophagitis

Drug-induced esophagitis

Toxic bile acids in gastro-oesophageal reflux disease: influence of gastric acidity

How to Make a Barrett Esophagus: Pathophysiology of Columnar Metaplasia of the Esophagus

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