Articles: ketoprofen-adverse-effects.
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The mechanism of immunosuppression induced by severe sepsis is not fully understood. The production of prostaglandin E2 (PGE2) during sepsis is well known, but its role in long-term consequences of sepsis has not been explored. The current study evaluates the role of PGE2 in the development of immunosuppression secondary to sepsis and its potential as therapeutic target. ⋯ Furthermore, sepsis also altered key enzymes in PGE2 synthesis and degradation. Our results indicate the involvement of PGE2 in severe sepsis-induced immunosuppression. Inhibition of PGE2 production represents an attractive target to improve innate immune response against secondary infection in the immunocompromised host.
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J Am Assoc Lab Anim · Nov 2012
Randomized Controlled TrialA therapeutic dose of ketoprofen causes acute gastrointestinal bleeding, erosions, and ulcers in rats.
Perioperative treatment of several rats in our facility with ketoprofen (5 mg/kg SC) resulted in blood loss, peritonitis, and death within a day to a little more than a week after surgery that was not related to the gastrointestinal tract. Published reports have established the 5-mg/kg dose as safe and effective for rats. Because ketoprofen is a nonselective nonsteroidal antiinflammatory drug that can damage the gastrointestinal tract, the putative diagnosis for these morbidities and mortalities was gastrointestinal toxicity caused by ketoprofen (5 mg/kg). ⋯ Our results showed marked gastrointestinal bleeding, erosions, and small intestinal ulcers in the ketoprofen-treated rats and minimal damages in the saline-treated group. The combination of ketoprofen and anesthesia resulted in worse clinical signs than did ketoprofen alone. We conclude that a single 5-mg/kg dose of ketoprofen causes acute mucosal damage to the rat small intestine.
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Non-steroidal anti-inflammatory drugs (NSAIDs) are known to have adverse effects on kidney function. Situations with a stimulated renin-angiotensin system such as volume depletion or pre-existing chronic renal failure predispose to acute renal failure (ARF) via inhibition of prostaglandin synthesis by NSAIDs. To date, NSAIDs are frequently used as antipyretic drugs even in situations predisposing to ARF. Within 20 months, seven children presenting with diarrhoea and/or vomiting and fever were treated with therapeutic doses (11.5-32 mg/kg per day) of ibuprofen for 1 to 3 days before developing ARF. Maximum plasma creatinine levels were 180-650 micromol/l. One patient required emergency dialysis for hyperkalaemia, uraemia, and hyperphosphataemia. After cessation of NSAID treatment and rehydration, all patients recovered completely with a normalised creatinine level after 3 to 9 days. Once the acute phase is controlled, long-term outcome is excellent. Interstitial nephritis, another possible adverse effect of NSAIDs, might require steroid treatment and is the major differential diagnosis. Only histological examination can confirm the exact pathomechanism of ARF after NSAID exposure. If immunological events are responsible for the ARF, the recovery period is usually longer. ⋯ non-steroidal anti-inflammatory drugs are potentially dangerous in situations with even moderate volume depletion.
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The American surgeon · Jan 2002
Case ReportsStercoral perforation of the sigmoid colon: report of a rare case and its possible association with nonsteroidal anti-inflammatory drugs.
Stercoral perforation of the colon is a rare phenomenon with fewer than 90 cases reported in the literature to date. The pathogenesis of stercoral ulceration is thought to result from ischemic pressure necrosis of the bowel wall caused by a stercoraceous mass. Stercoral perforation in more than 90 per cent of cases involves the sigmoid or rectosigmoid colon with associated fecal mass causing localized mucosal ulceration and bowel wall thinning due to localized pressure effect. ⋯ Stercoral perforation is often a consequence of chronic constipation; however, there are other predisposing factors as the condition is rare compared with the frequency of severe constipation. One of the hypotheses includes the association of nonsteroidal anti-inflammatory drugs (NSAIDs) with stercoral perforation of the colon. Our case report lends support to this association with NSAID use; thus there need to be greater awareness and caution when using NSAIDs in chronically constipated patients.