Adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs, aspirin and coxibs) on upper gastrointestinal tract

Sostres, Carlos; Gargallo, Carla J.; Arroyo, María Teresa; Lanas, Fernando

doi:10.1016/j.bpg.2009.11.005

Cited by 566 publications

(382 citation statements)

References 73 publications

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“…The resulting hydrogen ions are responsible of cellular toxicity; oxidative phosphorylation is compromised with impaired mithocondrial energy production, reduced cellular integrity and increased permeability. All these changes, lead to retrodiffusion of H + and pepsin with consequent amplification of cellular toxicity (Sostres C., 2010).…”

Section: Injury Mechanismsmentioning

confidence: 99%

“…First of all, PGs reduce gastric acid secretion and stimulate the production of glycoprotein (mucin), bicarbonate and phospholipid by epithelial cells. Moreover, PGs guarantee mucosal blood flow and oxygen delivery through vasodilatation, promote epithelial cells migration towards the luminal surface during restitution and finally enhance cells proliferation (Brzozowski, 2008;Sostres, 2010).…”

Section: Injury Mechanismsmentioning

confidence: 99%

See 1 more Smart Citation

Chronic NSAIDs Therapy and Upper Gastrointestinal Tract – Mechanism of Injury, Mucosal Defense, Risk Factors for Complication Development and Clinical Management

Azzaroli¹,

Lisotti²,

Calvanese³

et al. 2012

New Advances in the Basic and Clinical Gastroenterology

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Section: Injury Mechanismsmentioning

confidence: 99%

Section: Injury Mechanismsmentioning

confidence: 99%

Chronic NSAIDs Therapy and Upper Gastrointestinal Tract – Mechanism of Injury, Mucosal Defense, Risk Factors for Complication Development and Clinical Management

Azzaroli¹,

Lisotti²,

Calvanese³

et al. 2012

New Advances in the Basic and Clinical Gastroenterology

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“…In addition, the inhibition blocks the platelet production of thromboxane (TXA), which causes increased bleeding during active gastric bleeding (2).…”

Section: Introductionmentioning

confidence: 99%

Histopathological Study of Hydroalcoholic Extract of Terminalia catappa Leaves in Treatment of Indomethacin-Induced Gastric Ulcer in Rats

Arzi

Karampour

Rezaei

et al. 2016

Jundishapur J Nat Pharm Prod

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Background: Traditional medicine discussed in the literature introduced Terminalia catappa (TC) L. as an antiulcer plant. Objectives: In this study, we investigated the activity of hydroalcoholic extract from TC leaves against indomethacin-induced gastric ulcers in rats. Methods: Animals were divided into 13 groups, each consisting of six rats. The rats fasted for 48 hours. Various doses of Terminalia catappa leaf extract (TCLE) (100, 200, 400, and 600 mg/kg), ranitidine (50 mg/kg), and normal saline (5 mL/kg) were administered orally to the assigned group of rats. Indomethacin (30 mg/kg) was administered to all six groups before treatment. Other groups received only TCLE (100, 200, 400, and 600 mg/kg), ranitidine (50 mg/kg), CMC (1% solution), or indomethacin. Five hours after the drugs were administered, the animals' stomachs were opened through the large curvature and lesions were observed. One-way ANOVA and LSD tests were used for data analysis, and the minimum significance level was P < 0.05. Results:The results showed that all doses of TCLE and ranitidine had a significant effect (P > 0.05) against the gastric damage caused by indomethacin. There was no significant difference (P > 0.05) between TCLE (400 mg/kg) and ranitidine. Conclusions: The flavonoids, saponins, tannins, alkaloids, and antioxidant properties of TCLE can decrease some of the effects of an indomethacin-induced gastric ulcer.

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“…Though the efficacy of NSAIDs for the management of several painful conditions has been widely demonstrated, drugs in this class also carry potential concerns related to gastrointestinal (GI), hematologic, renal, and cardiovascular safety [16][17][18][19][20]. Owing to these concerns, NSAID-containing products include warnings outlining the GI, renal, and bleeding risks associated with NSAID use [21,22].…”

Section: Introductionmentioning

confidence: 99%

Clinical and Laboratory Hematologic Findings in Patients Receiving Repeated-Dose Injectable HPBCD-Diclofenac for Acute Postoperative Pain: Pooled Analysis of Two Randomized Controlled Phase III Clinical Trials

Gan¹,

Singla²,

Daniels³

et al. 2015

J Anesth Clin Res

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Objective: While the non-steroidal anti-inflammatory drugs (NSAIDs) represent an important option for the management of acute postoperative pain, their use can be limited due to potential safety concerns, including bleeding risks. This study examined the bleeding-related safety of injectable diclofenac formulated with hydroxypropyl-β-cyclodextrin (HPβCD-diclofenac) when used for postoperative pain management. Methods:Data from two randomized, double-blind, placebo-and active comparator-controlled phase III trials were pooled. Patients in both studies received HPβCD-diclofenac, placebo, or the active comparator ketorolac via intravenous injection every 6 hours for ≤ 5 days following abdominal/pelvic or orthopedic surgery. Bleeding adverse events (AEs) were evaluated through the treatment period and follow-up (≤ 37 days), and relative bleeding AE risks (RR) were estimated. Changes in hematology laboratory values were also assessed.Results: Overall, 608 surgical patients received ≥ 1 dose of study medication. Bleeding AEs occurred in n=9/318 (2.8%) patients receiving HPβCD-diclofenac, n=8/142 (5.6%) patients receiving ketorolac, and n=4/148 (2.7%) patients receiving placebo. Over the period examined, HPβCD-diclofenac was not associated with increased bleeding AE RR versus placebo (1.05 [0.33, 3.35]; p=0.93), nor was ketorolac (2.08 [0.64, 6.77]; p=0.22). Bleeding AEs were predominantly mild or moderate in severity. No treatment-related bleeding AEs occurred in the HPβCD-diclofenac group (1 in both the placebo and ketorolac groups). Among the subset of patients receiving concomitant anticoagulants, bleeding AEs occurred in n=3/60 (5.0%) patients receiving HPβCD-diclofenac, n=2/29 (6.9%) patients receiving ketorolac, and n=0/35 patients receiving placebo. In the HPβCD-diclofenac group, postsurgical shifts to low hematocrit and hemoglobin occurred in 35.7% and 28.3% of patients, respectively (versus 31.4% and 21.5%, respectively, with placebo). Postsurgical shifts in platelet count were uncommon (<3.0% across treatment groups). Conclusions:While follow-up studies in larger populations are warranted, this analysis suggests that HPβCD-diclofenac may not present a significant incremental bleeding AE risk versus placebo when used for acute postoperative pain management.

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Adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs, aspirin and coxibs) on upper gastrointestinal tract

Cited by 566 publications

References 73 publications

Chronic NSAIDs Therapy and Upper Gastrointestinal Tract – Mechanism of Injury, Mucosal Defense, Risk Factors for Complication Development and Clinical Management

Chronic NSAIDs Therapy and Upper Gastrointestinal Tract – Mechanism of Injury, Mucosal Defense, Risk Factors for Complication Development and Clinical Management

Histopathological Study of Hydroalcoholic Extract of Terminalia catappa Leaves in Treatment of Indomethacin-Induced Gastric Ulcer in Rats

Clinical and Laboratory Hematologic Findings in Patients Receiving Repeated-Dose Injectable HPBCD-Diclofenac for Acute Postoperative Pain: Pooled Analysis of Two Randomized Controlled Phase III Clinical Trials

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