to inhibition of renal prostaglandin synthesis

Patients with Chronic hepatic failure, cirrhosis, diuretic-induced volume depletion or renal insufficiency require local synthesis of vasodilating prostaglandins to maintain renal perfusion and therefore these patients are at greater risk of developing renal dysfunction due to NSAID-induced inhibition of renal prostaglandin synthesis.
In view of the product's inherent potential to cause oedema, heart failure may be precipitated in some compromised patients

KNOWN SYMPTOMS OF OVERDOSAGE AND PARTICULARS OF ITS TREATMENT
See side effects and special precautions.
Treatment of overdosage should be symptomatic and supportive.

IDENTIFICATION
Round, biconvex with a score notch, uniform white to light yellow tablet 9 mm x 4 mm.

PRESENTATION
PIXICAM 20 is available in packs of 30 and 100 tablets.

STORAGE INSTRUCTIONS
Store below 25°C.

Numerous studies suggest that inhibition of renal prostaglandin synthesis by ..
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Patients with congestive heart failure, cirrhosis, diuretic-induced volume depletion, or renal insufficiency are at greater risk of developing renal dysfunction due to NSAID-induced inhibition of renal prostaglandin synthesis.


Nonsteroidal anti-inflammatory drug - Wikipedia

13/11/2014 · The adverse renal effects of prostaglandin-synthesis inhibition in ..
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Figure 3. Pathogenesis of gastric damage by NSAIDs. Current evidence indicates that the majority of harmful effects mediated by NSAIDs result from inhibition of the synthesis of mucosal-protective prostaglandins produced by constitutive COX-1 activity. Direct drug-mediated irritant effects on epithelial cells appear to play only a minor role in GI toxicity. The presence of infections by the bacterium H pylori represents a separate risk factor that increases the likelihood of developing duodenal ulcers (Feldman, 2014).


NSAIDs (Ibuprofen, Naproxen, Aspirin) and …

Concurrent administration of two or more NSAIDs may alter the pharmacokinetic profile of at least one of the medication; which may alter the therapeutic effect and/or increase the risk of adverse effects, specifically aspirin decreases the bioavailability of ibuprofen by 50%.
Bone marrow depressants:
Leukopenic and/or thrombocytopenic effects of these medications may be increased with concurrent or recent therapy; dosage adjustment of the bone marrow depressant, if necessary, should be based on blood counts.
Digoxin:
Ibuprofen has been reported to increase digoxin plasma concentration.
Cefamandole or cefoperazone or cefatetan or plicamycin or valproic acid:
These medications may cause hypoprothrombinemia; in addition, plicamycin or valproic acid may inhibit platelet aggregation; concurrent use with ibuprofen may increase the risk of bleeding because of additive interferences with platelet function and/or the potential occurrence of ibuprofen-induced gastro-intestinal ulceration or hemorrhage.
Cyclosporine or Gold Compounds and other nephrotoxic compounds:
Inhibition of renal prostaglandin activity by ibuprofen may increase the plasma concentration of cyclosporine and/or the risk of cyclosporine induced nephrotoxicity; patients should be carefully monitored during concurrent use.
Lithium
Ibuprofen has been reported to increase the steady state concentration of lithium possibly by decreasing its renal clearance.
Methotrexate
NSAIDs may decrease protein binding and/or renal elimination of methotrexate, resulting in increased and prolonged methotrexate plasma concentrations and increased risk of toxicity, especially during high dose methotrexate infusion therapy.
Laboratory Value Alterations
Bleeding time may be prolonged with the use of ibuprofen.

Celebrex 100mg capsule - - (eMC) - Medicines

The very low neonatal GFR (absolute inulin clearance: approximately 2 to 3 mL/min; corrected for mean adult body surface area: less than 20 mL/min/1.73m2) is maintained by a delicate interplay between strong vasoconstrictory (mainly angiotensin II) and prominent vasodilatory renal forces (almost exclusively PGs), even when stressed (). The interested reader is referred to a recent review by Toth-Heyn, Drukker and Guignard () that discusses the various hemodynamic forces that regulate GFR in the newborn. When in the neonatal situation PG-synthesis is inhibited by the administration of NSAIDs, the already basically very high vasoconstrictor state of the newborn kidney is not sufficiently opposed anymore. This will lead to a reduction in renal blood flow (RBF), GFR and urine volume, or, in other words, to oliguric ARF. Fortunately the impairment of neonatal renal function due to NSAIDs is generally reversible but it, nevertheless, is a significant complication of the administration of NSAIDs in newborns (). This is particularly true when there are additional factors that independently can cause ARF in the neonate, such as hypoxemia and septicemia.