Gastric adaptation

Dy, Graham; Jl, Smith; Hj, Spjut; Torres, E. L.

doi:10.1016/0016-5085(88)90487-8

Cited by 163 publications

(14 citation statements)

References 20 publications

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“…received four prescriptions for a NSAID before falling to baseline in those who have received 10 prescriptions That 67% of the patients sampled were not informed of adverse effects is consistent with the work of [ 6]. Mucosal adaptation may partly explain this [7 ]. Early bleeds may also result from NSAID exacerbation…”

Section: Short Report 255supporting

confidence: 67%

Patient awareness of the adverse effects of non‐steroidal anti‐inflammatory drugs (NSAIDs)

Wynne

Long

1996

Brit J Clinical Pharma

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We set out to determine the extent to which two groups of patients reported having been informed about the adverse effects of NSAIDs. These consisted of 50 patients who had suffered an acute gastrointestinal bleed while taking a NSAID, and 100 age, sex and drug matched controls who had not. Eight (16%) of the index patients, and 41 (41%) of the control patients remembered having been informed of potential adverse effects, an odds ratio of 3.65 (95% CI 1.55–8.58, P<0.002). Two (4%) of the index patients recalled having been advised what to do should adverse symptoms develop, whereas 21 (21%) of the control patients did so, an odds ratio of 6.38 (95% CI 1.4–28.4, P<0.01). Eighteen (36%) of patients who bled had experienced gastrointestinal pain prior to the bleed, but of these only two (11%) admitted reduced compliance with NSAID therapy. In contrast, 10 (67%) of the 15 control patients who had suffered epigastric discomfort admitted reduced compliance, an odds ratio of 16.0 (95% CI 2.6–98.8, P<0.001). Our results suggest that patients who report not having been informed of adverse effects of NSAIDs are less likely to reduce intake in response to epigastric pain than patients who report having received such information. If the patients who bled had reduced their intake of NSAIDs to the same extent as apparently better informed control patients in response to epigastric pain, it is possible that some episodes of acute gastrointestinal bleeding would have been avoided.

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Section: Short Report 255supporting

confidence: 67%

Patient awareness of the adverse effects of non‐steroidal anti‐inflammatory drugs (NSAIDs)

Wynne

Long

1996

Brit J Clinical Pharma

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“…The suggestion that patients with rheumatoid arthritis are more prone to gastric ulceration has been much dis cussed but it is not supported by clinical evi dence. Some studies in rheumatoid arthritis patients have found an excess of GUs [23][24][25], others have not [28] and some have found a large excess of GUs in the control group of osteoarthritis patients taking NSAIDs [27] -suggesting that the drugs themselves rather than the disease are of pri mary importance.…”

Section: Identifying At-risk Groupsmentioning

confidence: 99%

“…Acute administra tion of an oral NSAID results in acute gastric damage in almost all cases (erosions, petechlae, superficial ulceration, submucosal haem orrhages), which become fewer during contin ued administration with most damage resolv ing over a 4-to 8-week period. Such adapta tion as has been described is documented for aspirin [28], indomethacin [29,30], nabumetone and fenbufen [31]. Challenging epidemi ological parallels are provided by two studies, first, risks of bleeding during transient isch aemic attack prophylaxis with aspirin appear greatest in the first 3 months of treatment [32].…”

Section: Acute Versus Chronic Dosingmentioning

confidence: 99%

Nonsteroidal Anti-Inflammatory Drug-Induced Gastric Damage: Epidemiology

Shorrock

Langman²

1995

Dig Dis

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Although figures vary considerably, the ingestion of aspirin or other non-aspirin non-steroidal anti-inflammatory drugs is associated with an increased risk of gastric ulceration, ulcer bleeding, ulcer complications and of death by a factor of around 3. Evidence for duodenal ulcer (DU) disease is less convincing, but the risk of complications of DU disease, bleeding and perforation, are increased to much the same extent as for gastric ulcer. Whether this increase in complications for DU represents exacerbation of an existing DU diathesis remains unresolved.

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“…Instead, the gastnc mucosa may develop resistance or 'tolerance' to the ulcerogenic agents. This occurs in both humans and antmals and h,ls been demonstrated for ASA as well as for ethanol (49)(50)(51)(52).…”

Section: Trophic Effects Of Prost Aglandinsmentioning

confidence: 89%

Prostaglandins and Mucosal Defensive Mechanisms

Morris¹,

Williamson²,

Hynna³

1990

Canadian Journal of Gastroenterology

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The first line of mucosa! defence includes the juxtamucosal unstirred layer/pl I gradient and the apical surface~ of the luminal epithelial cells.Many damag ing age nts, including n onsteroidnl anti-inflammatory drugs (NSAIDs), can overwhelm Lhese defences and destroy ex tensive regions of the luminal cpiLhe lium. This damage is readily L olerated in the normal mucosa. Furthermore, a combination of inc reased mucosa! bloodflow, epi thelial migration, mucus release, and efflu x of bicarbonate-rich fluid usua lly allows rapid recovery of mucosa I integrity. In th e presence of vasc ular damage and congestion, however, luminal acid can kill mucosa! cells and destroy the substrate necessary for repair (by epithelial migration ). Damage of this type results in the production of hemorrhag ic erosion s, which may then develop into chronic ulceroinflammatory disease if healing is prevented by exec&, lu minal ac id or by impaired mucosa! immune response. Endogenous and exogenous prostaglandins could affect all aspects of the mucosa! defensive response~, fro m the juxcam ucosal unstirred layer/pH gradient ( via effects on secretion of bicarbonate, acid and mucus, as well as stimulation of fluid efflux) to the function of the mucosa! immune system. Protection against the acute damage produced by topically administered NSAIDs or concentrated etha nol can result from e ither administration of prostaglandins or topical applicaLion of'mild irritants'. This is referred to as 'adaptive cytopr~tection'. Parenterally adm in istereJ NSAIDs can also produce mucosa! erosions. Proteclion aga inst this type of damage may depend on the effects of proscaglandins on neura l and contractile elements in the mucosa. Studies on animal models also suggest that by preventing ac ute hemorrhagic erosions, prostaglandins may prevent the development of chronic ulcer in susceptible individuals. Can J Gastroenterol 1990;4(3 ):95 -107

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Gastric adaptation

Cited by 163 publications

References 20 publications

Patient awareness of the adverse effects of non‐steroidal anti‐inflammatory drugs (NSAIDs)

Patient awareness of the adverse effects of non‐steroidal anti‐inflammatory drugs (NSAIDs)

Nonsteroidal Anti-Inflammatory Drug-Induced Gastric Damage: Epidemiology

Prostaglandins and Mucosal Defensive Mechanisms

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