scholarly journals ISOFORM(S) OF CYTOCHROME P450 RESPONSIBLE FOR THE METABOLISM OF NONSTEROIDAL ANTIINFLAMMATORY DRUGS: OXIDATIVE METABOLISM OF MEFENAMIC ACID AND DICLOFENAC BY CYP2C SUBFAMILY

1994 ◽  
Vol 9 (supplement) ◽  
pp. 144-147
Author(s):  
Kan CHIBA ◽  
Atuko SAITOH ◽  
Tomie CHIBA ◽  
Takashi ISHIZAKI ◽  
Masanao TANI ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Oxidative Metabolism ◽  
Mefenamic Acid ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Antiinflammatory Drugs

Adverse Interactions Between Warfarin and Nonsteroidal Antiinflammatory Drugs: Mechanisms, Clinical Significance, and Avoidance

1995 ◽  
Vol 29 (12) ◽  
pp. 1274-1283 ◽  
Author(s):  
Thomas Yk Chan
Keyword(s):  
Clinical Significance ◽  
Mefenamic Acid ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Bleeding Complications ◽  
High Dose ◽  
Antiinflammatory Drugs ◽  
Risk Of Bleeding ◽  
Dose Aspirin ◽  
Combined Use ◽  
High Dose Aspirin

Objective: To review the mechanisms and clinical significance of adverse interactions between warfarin and nonsteroidal antiinflammatory drugs (NSAIDs) and discuss how these interactions can be avoided. Data Sources: Previous studies of interactions between warfarin and NSAIDs or reports of adverse interactions were identified from a MEDLINE search (1976 to present) and from the reference lists of pertinent articles. Study Selection And Data Extraction: All articles were considered for inclusion in the review. Pertinent information was selected for discussion. Data Synthesis: All NSAIDs can prolong bleeding time by inhibiting platelet function. High-dose aspirin has a direct hypoprothrombinemic effect. Phenylbutazone and its analogs enhance the hypoprothrombinemic effect of warfarin through a pharmacokinetic interaction by inhibiting the hepatic metabolism of warfarin. Mefenamic acid also enhances the anticoagulant effect of warfarin, but the mechanism is not known. The clinical relevance of protein binding displacement in the interaction between warfarin and NSAIDs has been overstated, although a significant one may be more likely in the presence of high concentrations of NSAIDs in patients with slow elimination of warfarin (e.g., those with severe heart failure or impaired liver function). NSAIDs can induce gastrointestinal bleeding, which is likely to be more severe if warfarin is also given. Conclusions: The combined use of warfarin and NSAIDs is generally discouraged because of the increased risk of bleeding in these patients. In patients receiving warfarin who also require NSAIDs, phenylbutazone and its analogs, high-dose aspirin, mefenamic acid, excessive use of topical methyl salicylate, and NSAIDs that are associated with a higher risk of bleeding peptic ulcers should be avoided. Patients should be closely monitored for anticoagulant control and bleeding complications during the combined use of warfarin and NSAIDs.

Induction of Hemolytic Anemia by Nonsteroidal Antiinflammatory Drugs

1986 ◽  
Vol 20 (12) ◽  
pp. 925-934 ◽  
Author(s):  
Marcia Sanford-Driscoll ◽  
Leroy C. Knodel
Keyword(s):  
Hemolytic Anemia ◽  
Mefenamic Acid ◽  
Treated Patient ◽  
Case Reports ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Antiinflammatory Drugs ◽  
Drug Induced ◽  
Predisposing Factor ◽  
Increased Risk ◽  
Immune Hemolytic Anemia

The incidence of immune hemolytic anemia (IHA) is increasing. The proliferation of pharmaceuticals is a contributing factor to this increase. IHA is an uncommon, though significant, adverse effect of a wide variety of drugs. Several recent case reports have implicated the nonsteroidal antiinflammatory drugs (NSAIDs). Because of the extensive use of this class of drugs, a review of case reports, clinical studies, and in vitro research was conducted on NSAID-induced IHA. Mefenamic acid, ibuprofen, sulindac, naproxen, tolmetin, feprazone, and aspirin are reported to cause IHA, with mefenamic acid most frequently implicated. Mefenamic acid appears to cause hemolytic anemia by an autoimmune mechanism similar to methyldopa and aspirin by an immune complex mechanism. However, there is insufficient information concerning ibuprofen, sulindac, naproxen, tolmetin, and feprazone to assign specific mechanisms of immune hemolysis. In individuals with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, aspirin at usual therapeutic doses is not a predisposing factor to hemolysis unless other risk factors are present. Although individuals with G-6-PD deficiency are at increased risk of developing hemolytic anemia when exposed to oxidizing stresses, the use of NSAIDs does not appear to increase this risk significantly. Because NSAID-induced IHA occurs infrequently and the sensitivity of currently used tests to detect drug-dependent antibodies is limited, routine serologic testing in patients receiving NSAIDs is not justified. If hemolytic anemia occurs in a NSAID-treated patient and the history is consistent with a drug-induced etiology, the NSAID should be discontinued. With discontinuation of the offending agent, the prognosis is good. There is a rapid hematologic recovery, with a slow resolution of abnormal serologic findings.

Ototoxicity of Salicylate, Nonsteroidal Antiinflammatory Drugs, and Quinine

1993 ◽  
Vol 26 (5) ◽  
pp. 791-810 ◽  
Author(s):  
Timothy T.K. Jung ◽  
Chung-Ku Rhee ◽  
Charles S. Lee ◽  
Yong-Soo Park ◽  
Duck-Choo Choi
Keyword(s):  
Nonsteroidal Antiinflammatory Drugs ◽  
Antiinflammatory Drugs
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