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Aspirin / pravastatin Disease Interactions

There are 15 disease interactions with aspirin / pravastatin:

Major

Aspirin (Includes Aspirin/pravastatin) ↔ Coagulation

Severe Potential Hazard, High plausibility

Applies to: Coagulation Defect, Bleeding, Thrombocytopathy, Thrombocytopenia, Vitamin K Deficiency

The use of aspirin is contraindicated in patients with significant active bleeding or hemorrhagic disorders such as hemophilia, von Willebrand's disease, or telangiectasia. Aspirin interferes with coagulation by irreversibly inhibiting platelet aggregation and prolonging bleeding time. The non-aceylated salicylates (i.e. salicylate salts such as sodium or magnesium salicylate) do not demonstrate these effects and may be appropriate substitutions in these patients. However, all salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially aspirin, should be administered with extreme caution in patients with hypoprothrombinemia, vitamin K deficiency, thrombocytopenia, thrombotic thrombocytopenic purpura, severe hepatic impairment, or anticoagulant use.

References

  1. Buerke M, Pittroff W, Meyer J, Darius H "Aspirin therapy: optimized platelet inhibition with different loading and maintenance doses." Am Heart J 130 (1995): 465-72
  2. Ferraris VA, Ferraris SP "Preoperative aspirin ingestion increases operative blood loss after coronary artery bypass grafting - update." Ann Thorac Surg 59 (1995): 1036-7
  3. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  4. Patrono C "Aspirin as an antiplatelet drug." N Engl J Med 330 (1994): 1287-94
  5. Moroz LA "Increased blood fibrinolytic activity after aspirin ingestion." N Engl J Med 296 (1977): 525-9
  6. Garg SK, Sarker CR "Aspirin-induced thrombocytopenia on an immune basis." Am J Med Sci 267 (1974): 129-32
  7. "Product Information. Bayer aspirin (aspirin)." Bayer, West Haven, CT.
  8. Bochner F, Williams DB, Morris PM, Siebert DM, Lloyd JV "Pharmacokinetics of low-dose oral modified release, soluble and intravenous aspirin in man, and effects on platelet function." Eur J Clin Pharmacol 35 (1988): 287-94
  9. Sbarbaro JA, Bennett RM "Aspirin hepatotoxicity and disseminated intravascular coagulation." Ann Intern Med 86 (1977): 183-5
  10. Colwell JA "Aspirin and risk of hemorrhagic stroke." JAMA 282 (1999): 731-2
  11. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
  12. Petty GW, Brown RD, Whisnant JP, Sicks JD, O'Fallon WM, Wiebers DO "Frequency of major complications of aspirin, warfarin, and intravenous heparin for secondary stroke prevention: a population study." Ann Intern Med 130 (1999): 14-22
  13. Hirsh J, Dalen JE, Fuster V, Harker LB, Patrono C, Roth G "Aspirin and other platelet-active drugs: the relationship among dose, effectiveness, and side effects." Chest 108 Suppl (1995): s247-57
  14. He J, Whelton PK, Vu B, Klag MJ "Aspirin and risk of hemorrhagic stroke: a meta-analysis of randomized controlled trials." JAMA 280 (1998): 1930-35
View all 14 references
Major

Hmg-Coa Reductase Inhibitors (Includes Aspirin/pravastatin) ↔ Liver Disease

Severe Potential Hazard, High plausibility

Applies to: Liver Disease, Alcoholism

The use of HMG-CoA reductase inhibitors is contraindicated in patients with active liver disease or unexplained, persistent elevations of serum transaminases. HMG-CoA reductase inhibitors are extensively metabolized by the liver. Decreased drug metabolism may lead to accumulation and increased risk of toxicity, including biochemical abnormalities of liver function and, rarely, jaundice, hepatitis, cirrhosis, fatty change in the liver, and fulminant hepatic necrosis. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with a history of liver disease and/or heavy alcohol use. A lower initial dosage may be appropriate, and clinical monitoring of liver transaminase levels according to the individual product package labeling is recommended. Patients who develop elevated ALT or AST levels during therapy should be monitored until abnormalities resolve. If an increase above 3 times the upper limit of normal persists, consideration should be given to a reduction in dosage or withdrawal of therapy.

References

  1. Mauro VF "Clinical pharmacokinetics and practical applications of simvastatin." Clin Pharmacokinet 24 (1993): 195-202
  2. Smit JWA, Wijnne HJA, Schobben F, Sitsen A, Debruin TWA, Erkelens DW "Effects of alcohol consumption on pharmacokinetics, efficacy, and safety of fluvastatin." Am J Cardiol 76 (1995): a89-96
  3. Pan HY, Morrison RA, Singhvi SM, Frantz BM, Waclawski AP, Willard DA "Disposition of pravastatin sodium (SQ 31,000), a tissue-selective HMG-CoA reductase inhibitor, in healthy subjects." Clin Res 36 (1988): a368
  4. "Lovastatin 5-year safety and efficacy study. Lovastatin Study Groups I through IV." Arch Intern Med 153 (1993): 1079-87
  5. Pentikainen PJ, Saraheimo M, Schwartz JI, Amin RD, Schwartz MS, Brunner-Ferber F, Rogers JD "Comparative pharmacokinetics of lovastatin, simvastatin and pravastatin in humans." J Clin Pharmacol 32 (1992): 136-40
  6. "Product Information. Pravachol (pravastatin)." Bristol-Myers Squibb, Princeton, NJ.
  7. Quion JAV, Jones PH "Clinical pharmacokinetics of pravastatin." Clin Pharmacokinet 27 (1994): 94-103
  8. Grimbert S, Pessayre D, Degott C, Benhamou JP "Acute hepatitis induced by HMG-coa reductase inhibitor, lovastatin." Dig Dis Sci 39 (1994): 2032-3
  9. Duggan DE, Chen IW, Bayne WF, Halpin RA, Duncan CA, Schwartz MS, Stubbs RJ, Vickers S "The physiological disposition of lovastatin." Drug Metab Dispos 17 (1989): 166-73
  10. Walker JF "Simvastatin: the clinical profile." Am J Med 87 (1989): s44-6
  11. Smit JW, Wijnne HJ, Schobben F, Sitsen A, Debruin TW, Erkelens DW "Effects of alcohol and fluvastatin on lipid metabolism and hepatic function." Ann Intern Med 122 (1995): 678-80
  12. Cilla DD Jr, Gibson DM, Whitfield LR, Sedman AJ "Pharmacodynamic effects and pharmacokinetics of atorvastatin after administration to normocholesterolemic subjects in the morning an evening." J Clin Pharmacol 36 (1996): 604-9
  13. Lea AP, McTavish D "Atorvastatin. A review of its pharmacology and therapeutic potential in the management of hyperlipidaemias." Drugs 53 (1997): 828-47
  14. Halpin RA, Ulm EH, Till AE, Kari PH, Vyas KP, Hunninghake DB, Duggan DE "Biotransformation of lovastatin .5. species differences in invivo metabolite profiles of mouse, rat, dog, and human." Drug Metab Dispos 21 (1993): 1003-11
  15. Boberg M, Angerbauer R, Fey P, Kanhai WK, Karl W, Kern A, Ploschke J, Radtke M "Metabolism of cerivastatin by human liver microsomes in vitro. Characterization of primary metabolic pathways and of cytochrome P45 isozymes involved." Drug Metab Dispos 25 (1997): 321-31
  16. "Product Information. Lipitor (atorvastatin)." Parke-Davis, Morris Plains, NJ.
  17. "Product Information. Lescol (fluvastatin)." Novartis Pharmaceuticals, East Hanover, NJ.
  18. Davidson MH, on behalf of the FLUENT Investigators Group "Fluvastatin long-term extension trial (FLUENT): summary of efficacy and safety." Am J Med 96 Suppl (1994): 96 (suppl)
  19. Cilla DD Jr, Whitfield LR, Gibson DM, Sedman AJ, Posvar EL "Multiple-dose pharmacokinetics, pharmacodynamics, and safety of atorvastatin, an inhibitor of HMG-CoA reductase, in healthy subjects." Clin Pharmacol Ther 60 (1996): 687-95
  20. Arnon R, Eisenberg S "Lovastatin-induced hepatitis." Isr J Med Sci 28 (1992): 101-2
  21. McQueen MJ "Cholestatic jaundice associated with lovastatin (Mevacor) therapy." Can Med Assoc J 142 (1990): 841-2
  22. "Product Information. Zocor (simvastatin)." Merck & Co, Inc, West Point, PA.
  23. Pan HY, DeValut AR, Wang-Iverson D, et al "Comparative pharmacokinetics and pharmacodynamics of pravastatin and lovastatin." J Clin Pharmacol 30 (1990): 1128-35
  24. "Product Information. Mevacor (lovastatin)." Merck & Co, Inc, West Point, PA.
  25. Bakker-Arkema RG, Davidson MH, Goldstein RJ, Davignon J, Isaacsohn JL, Weiss SR, Keilson LM, Brown WV, Miller VT, Shurzinske LJ, Black DM "Efficacy and safety of a new HMG-CoA reductase inhibitor, atorvastatin, in patients with hypertriglyceridemia." JAMA 275 (1996): 128-33
  26. Nakad A, Bataille L, Hamoir V, Sempoux C, Horsmans Y "Atorvastatin-induced acute hepatitis with absence of cross-toxicity with simvastatin." Lancet 353 (1999): 1763-4
  27. "Product Information. Baycol (cerivastatin)." Bayer, West Haven, CT.
  28. Bilheimer DW "Long-term clinical tolerance of lovastatin and simvastatin." Cardiology 77 (1990): 58-65
  29. Jokubaitis LA "Updated clinical safety experience with fluvastatin." Am J Cardiol 73 (1994): d18-24
  30. Muck W, Unger S, Kawano K, Ahr G "Inter-ethnic comparisons of the pharmacokinetics of the HMG-CoA reductase inhibitor cerivastatin." Br J Clin Pharmacol 45 (1998): 583-90
  31. Dain JG, Fu E, Gorski J, Nicoletti J, Scallen TJ "Biotransformation of fluvastatin sodium in humans." Drug Metab Dispos 21 (1993): 567-72
  32. Simons LA "Simvastatin in severe primary hypercholesterolemia: efficacy, safety, and tolerability in 595 patients over 18 weeks. The Principal Investigators." Clin Cardiol 16 (1993): 317-22
  33. Mauro VF, MacDonald JL "Simvastatin: a review of its pharmacology and clinical use." DICP 25 (1991): 257-64
  34. Geddes JA "Cholestatic jaundice associated with lovastatin (mevacor) therapy." Can Med Assoc J 143 (1990): 13-4
  35. McGovern ME, Mellies MJ "Long-term experience with pravastatin in clinical research trials." Clin Ther 15 (1993): 57-64
  36. Tse FL, Jaffe JM, Troendle A "Pharmacokinetics of fluvastatin after single and multiple doses in normal volunteers." J Clin Pharmacol 32 (1992): 630-8
  37. Everett DW, Chando TJ, Didonato GC, Singhvi SM, Pan HY, Weinstein SH "Biotransformation of pravastatin sodium in humans." Drug Metab Dispos 19 (1991): 740-8
  38. Hartleb M, Rymarczyk G, Januszewski K "Acute cholestatic hepatitis associated with pravastatin." Am J Gastroenterol 94 (1999): 1388-90
  39. Levy RI, Troendle AJ, Fattu JM "A quarter century of drug treatment of dyslipoproteinemia, with a focus on the new HMG-CoA reductase inhibitor fluvastatin." Circulation 87 (1993): i45-53
  40. Posvar EL, Radulovic LL, Cilla DD Jr, Whitfield LR, Sedman AJ "Tolerance and pharmacokinetics of single-dose atorvastatin, a potent inhibitor of HMG-CoA reductase, in healthy subjects." J Clin Pharmacol 36 (1996): 728-31
  41. Lennernas H, Fager G "Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Similarities and differences." Clin Pharmacokinet 32 (1997): 403-25
View all 41 references
Major

Hmg-Coa Reductase Inhibitors (Includes Aspirin/pravastatin) ↔ Rhabdomyolysis

Severe Potential Hazard, Moderate plausibility

Applies to: Myopathy, Myoneural Disorder, Renal Dysfunction, Hypothyroidism

Severe myopathy, including rhabdomyolysis with acute renal failure secondary to myoglobinuria, has been reported rarely with the use of HMG-CoA reductase inhibitors. The myopathy may be dose-related and is characterized by muscle aches and/or weakness in conjunction with increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

References

  1. Norman DJ, Illingworth DR, Munson J, Hosenpud J "Myolysis and acute renal failure in a heart-transplant recipient receiving lovastatin." N Engl J Med 318 (1988): 46-7
  2. Vanpuijenbroek EP, Dubufvereijken PWG, Spooren PFMJ, Vandoormaal JJ "Possible increased risk of rhabdomyolysis during concomitant use of simvastatin and gemfibrozil." J Intern Med 240 (1996): 403-4
  3. "Product Information. Zocor (simvastatin)." Merck & Co, Inc, West Point, PA.
  4. Ahmand S "Lovastatin-induced myopathy in a hypothyroid patient." J Fam Pract 41 (1995): 227-8
  5. Walker JF "Simvastatin: the clinical profile." Am J Med 87 (1989): s44-6
  6. van Puijenbroek EP, Du Buf-Vereijken PW, Spooren PF, van Doormaal JJ "Possible increased risk of rhabdomyolysis during concomitant use of simvastatin and gemfibrozil." J Intern Med 240 (1996): 403-4
  7. Pierce LR, Wysowski DK, Gross TP "Myopathy and rhabdomyolysis associated with lovastatin-gemfibrozil combination therapy." JAMA 264 (1990): 71-5
  8. "Product Information. Pravachol (pravastatin)." Bristol-Myers Squibb, Princeton, NJ.
  9. "Product Information. Baycol (cerivastatin)." Bayer, West Haven, CT.
  10. Bakker-Arkema RG, Davidson MH, Goldstein RJ, Davignon J, Isaacsohn JL, Weiss SR, Keilson LM, Brown WV, Miller VT, Shurzinske LJ, Black DM "Efficacy and safety of a new HMG-CoA reductase inhibitor, atorvastatin, in patients with hypertriglyceridemia." JAMA 275 (1996): 128-33
  11. Pogson GW, Kindred LH, Carper BG "Rhabdomyolysis and renal failure associated with cerivastatin-gemfibrozil combination therapy." Am J Cardiol 83 (1999): 1146
  12. "Lovastatin 5-year safety and efficacy study. Lovastatin Study Groups I through IV." Arch Intern Med 153 (1993): 1079-87
  13. Reaven P, Witztum JL "Lovastatin, nicotinic acid, and rhabdomyolysis." Ann Intern Med 109 (1988): 597-8
  14. Wallace CS, Mueller BA "Lovastatin-induced rhabdomyolysis in the absence of concomitant drugs." Ann Pharmacother 26 (1992): 190-2
  15. Chariot P, Abadia R, Agnus D, Danan C, Charpentier C, Gherardi RK "Simvastatin-induced rhabdomyolysis followed by a MELAS syndrome." Am J Med 94 (1993): 109-10
  16. Corpier CL, Jones PH, Suki WN, et al. "Rhabdomyolysis and renal injury with lovastatin use. Report of two cases in cardiac transplant recipients." JAMA 260 (1988): 239-41
  17. Lees RS, Lees AM "Rhabdomyolysis from the coadministration of lovastatin and the antifungal agent itraconazole." N Engl J Med 333 (1995): 664-5
  18. Fernandezzatarain G, Navarro V, Garcia H, Villatoro J, Calvo C "Rhabdomyolysis and acute renal failure associated with lovastatin." Nephron 66 (1994): 483-4
  19. Grunden JW, Fisher KA "Lovastatin-induced rhabdomyolysis possibly associated with clarithromycin and azithromycin." Ann Pharmacother 31 (1997): 859-63
  20. Bilheimer DW "Long-term clinical tolerance of lovastatin and simvastatin." Cardiology 77 (1990): 58-65
  21. Jokubaitis LA "Updated clinical safety experience with fluvastatin." Am J Cardiol 73 (1994): d18-24
  22. Simons LA "Simvastatin in severe primary hypercholesterolemia: efficacy, safety, and tolerability in 595 patients over 18 weeks. The Principal Investigators." Clin Cardiol 16 (1993): 317-22
  23. "Product Information. Lipitor (atorvastatin)." Parke-Davis, Morris Plains, NJ.
  24. Schalke BB, Schmidt B, Toyka K, Hartung H-P "Pravastatin-associated inflammatory myopathy." N Engl J Med 327 (1992): 649-50
  25. Pedersen TR, Berg K, Cook TJ, Faergeman O, Haghfelt T, Kjekshus J, Miettinen T, Musliner TA, Olsson AG, Pyorala K, Thorgeirsso "Safety and tolerability of cholesterol lowering with simvastatin during 5 years in the scandinavian simvastatin survival study." Arch Intern Med 156 (1996): 2085-92
  26. "Product Information. Lescol (fluvastatin)." Novartis Pharmaceuticals, East Hanover, NJ.
  27. McDonagh J, Winocour P, Walker DJ "Musculoskeletal manifestations during simvastatin therapy." Br J Rheumatol 32 (1993): 647-8
  28. Iliadis EA, Rosenson RS "Long-term safety of pravastatin-gemfibrozil therapy in mixed hyperlipidemia." Clin Cardiol 22 (1999): 25-8
  29. Alvarez JM, Rawdanowiz TJ, Goldstein J "Rhadbdomyolysis after coronary artery bypass grafting in a patient receiving simvastatin." J Thorac Cardiovasc Surg 116 (1998): 654-5
  30. Levy RI, Troendle AJ, Fattu JM "A quarter century of drug treatment of dyslipoproteinemia, with a focus on the new HMG-CoA reductase inhibitor fluvastatin." Circulation 87 (1993): i45-53
  31. McGovern ME, Mellies MJ "Long-term experience with pravastatin in clinical research trials." Clin Ther 15 (1993): 57-64
  32. East C, Alivizatos PA, Grundy SM, Jones PH, Farmer JA "Rhabdomyolysis in patients receiving lovastatin after cardiac transplantation." N Engl J Med 318 (1988): 47-8
  33. "Product Information. Mevacor (lovastatin)." Merck & Co, Inc, West Point, PA.
View all 33 references
Major

Nsaids (Includes Aspirin/pravastatin) ↔ Asthma

Severe Potential Hazard, High plausibility

Applies to: Asthma

Approximately 10% of patients with asthma may have aspirin-sensitive asthma, characterized by nasal polyposis, pansinusitis, eosinophilia, and precipitation of asthma and rhinitis attacks after ingestion of aspirin. The use of aspirin in these patients has been associated with severe bronchospasm and fatal anaphylactoid reactions. Since cross-sensitivity has been noted between aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), therapy with any NSAID should be avoided in asthmatic patients with a history of aspirin or other NSAID sensitivity, and administered cautiously in all patients with preexisting asthma. Prior to initiating therapy with NSAIDs, patients should be questioned about previous allergic-type reactions to these agents. Salicylate salts, salsalate, salicylamide, and acetaminophen may be appropriate alternatives in patients with a history of NSAID-induced bronchospasm, since cross-sensitivity to these agents appears to be low. However, cross-sensitivity has been demonstrated occasionally with high dosages of these agents (e.g., acetaminophen >= 1000 mg), thus it may be appropriate to initiate therapy with low dosages and increase gradually. There is some evidence suggesting that COX-2 inhibitors may be safely used in patients with aspirin-sensitive asthma, although the labeling for these products contraindicate such use. If necessary, aspirin desensitization may also be attempted in some patients under medical surveillance.

References

  1. "Product Information. Naprosyn (naproxen)." Syntex Laboratories Inc, Palo Alto, CA.
  2. Stevenson DD, Hougham AJ, Schrank PJ, Goldlust MB, Wilson RR "Salsalate cross-sensitivity in aspirin-sensitive patients with asthma." J Allergy Clin Immunol 86 (1990): 749-58
  3. Stevenson DD, Simon RA "Lack of cross-reactivity between rofecoxib and aspirin in aspirin-sensitive patients with asthma." J Allerg Clin Immunol 108 (2001): 47-51
  4. "Product Information. Motrin (ibuprofen)." Pharmacia and Upjohn, Kalamazoo, MI.
  5. Lewis RV "Severe asthma after naproxen." Lancet 05/30/87 (1987): 1270
  6. "Product Information. Voltaren (diclofenac)." Novartis Pharmaceuticals, East Hanover, NJ.
  7. "Product Information. Feldene (piroxicam)." Pfizer US Pharmaceuticals, New York, NY.
  8. Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser SL, Longo DL, eds. "Harrison's Principles of Internal Medicine. 14th ed." New York, NY: McGraw-Hill Health Professionals Division (1998):
  9. "Product Information. Clinoril (sulindac)." Merck & Co, Inc, West Point, PA.
  10. "Product Information. Ansaid (flurbiprofen)." Pharmacia and Upjohn, Kalamazoo, MI.
  11. Settipane RA, Stevenson DD "Cross sensitivity with acetaminophen in aspirin-sensitive subjects with asthma." J Allergy Clin Immunol 84 (1989): 26-33
  12. "Product Information. Vioxx (rofecoxib)." Merck & Co, Inc, West Point, PA.
  13. Carmona MJ, Blanca M, Garcia A, Fernandez S, Burgos F, Miranda A, Vega JM, Garcia J "Intolerance to piroxicam in patients with adverse reactions to nonsteroidal antiinflammatory drugs." J Allergy Clin Immunol 90 (1992): 873-9
  14. Szczeklik A, Stevenson DD "Aspirin-induced asthma: Advances in pathogenesis and management." J Allerg Clin Immunol 104 (1999): 5-13
  15. "Product Information. Mobic (meloxicam)" Boehringer-Ingelheim, Ridgefield, CT.
  16. Israel E, Fischer AR, Rosenberg MA, Lilly CM, Callery JC, Shapiro J, Cohn J, Rubin P, Drazen JM "The pivotal role of 5-lipoxygenase products in the reaction of aspirin-sensitive asthmatics to aspirin." Am Rev Respir Dis 148 (1993): 1447-51
  17. Haddow GR, Riley E, Isaacs R, McSharry R "Ketorolac, nasal polyposis, and bronchial asthma: a cause for concern." Anesth Analg 76 (1993): 420-2
  18. Nasser SMS, Lee TH "Aspirin-induced early and late asthmatic responses." Clin Exp Allergy 25 (1995): 1-3
  19. Cohen RD, Bateman ED, Potgieter PD "Near-fatal bronchospasm in an asthmatic patient following ingestion of flurbiprofen. A case report." S Afr Med J 61 (1982): 803
  20. Chan TY "Severe asthma attacks precipitated by NSAIDs." Ann Pharmacother 29 (1995): 199
  21. "Product Information. Bextra (valdecoxib)." Pharmacia Corporation, Peapack, NJ.
  22. Schreuder G "Ketoprofen: possible idiosyncratic acute bronchospasm." Med J Aust 152 (1990): 332-3
  23. Lee TH "Mechanism of bronchospasm in aspirin-sensitive asthma." Am Rev Respir Dis 148 (1993): 1442-3
  24. Ayres JG, Fleming DM, Whittington RM "Asthma death due to ibuprofen." Lancet 05/09/87 (1987): 1082
  25. Shapiro N "Acute angioedema after ketorolac ingestion - report of case." J Oral Maxillofac Surg 52 (1994): 626-7
  26. "Product Information. Daypro (oxaprozin)." Searle, Skokie, IL.
  27. Dahlen B, Szczeklik A, Murray HH "Celecoxib in patients with asthma and aspirin intolerance." N Engl J Med 344 (2000): 142
  28. "Product Information. Indocin (indomethacin)." Merck & Co, Inc, West Point, PA.
  29. Lee TH "Mechanism of aspirin sensitivity." Am Rev Respir Dis 145 (1992): s34-6
  30. "Product Information. Celebrex (celecoxib)." Searle, Chicago, IL.
  31. Salberg DJ, Simon MR "Severe asthma induced by naproxen: a case report and review of the literature." Ann Allergy 45 (1980): 372-5
  32. "Product Information. Tolectin (tolmetin)." McNeil Pharmaceutical, Raritan, NJ.
  33. "Product Information. Relafen (nabumetone)." SmithKline Beecham, Philadelphia, PA.
  34. Zikowski D, Hord AH, Haddox JD, Glascock J "Ketorolac-induced bronchospasm." Anesth Analg 76 (1993): 417-9
  35. "Product Information. Nalfon (fenoprofen)." Xspire Pharma, Ridgeland, MS.
  36. "Product Information. Orudis (ketoprofen)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  37. Woessner KM, Simon RA, Stevenson DD "The safety of celecoxib in patients with aspirin-sensitive asthma." Arthritis Rheum 46 (2002): 2201-6
  38. "Product Information. Lodine (etodolac)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
View all 38 references
Major

Pravastatin (Includes Aspirin/pravastatin) ↔ Renal Dysfunction

Severe Potential Hazard, Moderate plausibility

Applies to: Renal Dysfunction

Pravastatin is partially eliminated by the kidney. Drug and/or metabolite accumulation may occur in patients with significant renal impairment, which may increase the risk of adverse effects, including hepatic and musculoskeletal toxicities. Therapy with pravastatin should be administered cautiously in patients with severely impaired renal function. A lower initial dosage may be appropriate, accompanied by close clinical monitoring.

References

  1. Sigurbjornsson S, Kjartansdottir T, Johannsson M, Kristinsson J, Sigurdsson G "A pharmacokinetic evaluation of pravastatin in middle-aged and elderly volunteers." Eur J Drug Metab Pharmacokinet 23 (1998): 13-8
  2. Pan HY, Morrison RA, Singhvi SM, Frantz BM, Waclawski AP, Willard DA "Disposition of pravastatin sodium (SQ 31,000), a tissue-selective HMG-CoA reductase inhibitor, in healthy subjects." Clin Res 36 (1988): a368
  3. Halstenson CE, Triscari J, DeVault A, Shapiro B, Keane W, Pan H "Single-dose pharmacokinetics of pravastatin and metabolites in patients with renal impairment." J Clin Pharmacol 32 (1992): 124-32
  4. Quion JAV, Jones PH "Clinical pharmacokinetics of pravastatin." Clin Pharmacokinet 27 (1994): 94-103
  5. "Product Information. Pravachol (pravastatin)." Bristol-Myers Squibb, Princeton, NJ.
  6. Lennernas H, Fager G "Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Similarities and differences." Clin Pharmacokinet 32 (1997): 403-25
  7. Pan HY, DeValut AR, Wang-Iverson D, et al "Comparative pharmacokinetics and pharmacodynamics of pravastatin and lovastatin." J Clin Pharmacol 30 (1990): 1128-35
View all 7 references
Major

Salicylates (Includes Aspirin/pravastatin) ↔ Gi Toxicity

Severe Potential Hazard, High plausibility

Applies to: Peptic Ulcer, Duodenitis/Gastritis, Gastrointestinal Hemorrhage, Gastrointestinal Perforation, History - Peptic Ulcer, Alcoholism, Colitis/Enteritis (Noninfectious), Colonic Ulceration

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

References

  1. Lanas A, Serrano P, Bajador E, Esteva F, Benito R, Sainz R "Evidence of aspirin use in both upper and lower gastrointestinal perforation." Gastroenterology 112 (1997): 683-9
  2. Savon JJ, Allen ML, Dimarino AJ, Hermann GA, Krum RP "Gastrointestinal blood loss with low dose (325 mg) plain and enteric-coated aspirin administration." Am J Gastroenterol 90 (1995): 581-5
  3. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  4. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
  5. Stalnikowiczdarvasi R "Gastrointestinal bleeding during low-dose aspirin administration for prevention of arterial occlusive events: a critical analysis." J Clin Gastroenterol 21 (1995): 13-6
  6. Marks RD "Aspirin use and fecal occult blood testing." Am J Med 100 (1996): 596-7
  7. Mehta S, Dasarathy S, Tandon RK, Mathur M, Malaviya AN "A prospective randomized study of the injurious effects of aspirin and naproxen on the gastroduodenal mucosa in patients with rheumatoid arthritis." Am J Gastroenterol 87 (1992): 996-1000
  8. Naschitz JE, Yeshurun D, Odeh M, Bassan H, Rosner I, Stermer E, Levy N "Overt gastrointestinal bleeding in the course of chronic low-dose aspirin administration for secondary prevention of arterial occlusive disease." Am J Gastroenterol 85 (1990): 408-11
  9. Bergmann JF, Chassany O, Geneve J, Abiteboul M, Caulin C, Segrestaa JM "Endoscopic evaluation of the effect of ketoprofen, ibuprofen and aspirin on the gastroduodenal mucosa." Eur J Clin Pharmacol 42 (1992): 685-8
  10. Weil J, Colinjones D, Langman M, Lawson D, Logan R, Murphy M, Rawlins M, Vessey M, Wainwright P "Prophylactic aspirin and risk of peptic ulcer bleeding." BMJ 310 (1995): 827-30
  11. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  12. Graham DY, Smith JL "Aspirin and the stomach." Ann Intern Med 104 (1986): 390-8
  13. Roderick PJ, Wilkes HC, Meade TW "The gastrointestinal toxicity of aspirin: an overview of randomised controlled trials." Br J Clin Pharmacol 35 (1993): 219-26
  14. Wilcox CM, Shalek KA, Cotsonis G "Striking prevalence of over-the-counter nonsteroidal anti- inflammatory drug use in patients with upper gastrointestinal hemorrhage." Arch Intern Med 154 (1994): 42-6
  15. Prichard PJ, Kitchingman GK, Walt RP, Daneshmend TK, Hawkey CJ "Human gastric mucosal bleeding induced by low dose aspirin, but not warfarin." BMJ 298 (1989): 493-6
  16. Silagy CA, McNeil JJ, Donnan GA, Tonkin AM, Worsam B, Campion K "Adverse effects of low-dose aspirin in a healthy elderly population." Clin Pharmacol Ther 54 (1993): 84-9
  17. Sabesin SM, Boyce HW Jr, King CE, Mann JA, Ruoff G, Wall E "Comparative evaluation of gastrointestinal intolerance produced by plain and tri-buffered aspirin tablets." Am J Gastroenterol 83 (1988): 1220-5
  18. Greenberg PD, Cello JP, Rockey DC "Asymptomatic chronic gastrointestinal blood loss in patients taking aspirin or warfarin for cardiovascular disease." Am J Med 100 (1996): 598-604
  19. Levy M, Miller DR, Kaufman DW, Siskind V, Schwingl P, Rosenberg L, Strom B, Shapiro S "Major upper gastrointestinal tract bleeding. Relation to the use of aspirin and other nonnarcotic analgesics." Arch Intern Med 148 (1988): 281-5
View all 19 references
Major

Salicylates (Includes Aspirin/pravastatin) ↔ Renal Dysfunction

Severe Potential Hazard, High plausibility

Applies to: Renal Dysfunction

Salicylate and its metabolites are eliminated almost entirely by the kidney. Therapy with salicylate drugs should be administered cautiously in patients with renal impairment, especially if it is severe. Reduced dosages may be necessary to avoid drug accumulation. Clinical monitoring of renal function is recommended during prolonged therapy, since the use of salicylate drugs has rarely been associated with renal toxicities, including elevations in serum creatinine, renal papillary necrosis, and acute tubular necrosis with renal failure. Most of the data have been derived from experience with aspirin but may apply to other salicylates as well. In patients with impaired renal function, aspirin has caused reversible and sometimes marked decreases in renal blood flow and glomerular filtration rate. Adverse renal effects have usually reversed rapidly following withdrawal of aspirin therapy.

References

  1. "Product Information. Rexolate (sodium thiosalicylate)" Hyrex Pharmaceuticals, Memphis, TN.
  2. Carmichael J, Shankel SW "Effects of nonsteroidal anti-inflammatory drugs on prostaglandins and renal function." Am J Med 78 (1985): 992-1000
  3. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  4. Riegger GA, Kahles HW, Elsner D, Kromer EP, Kochsiek K "Effects of acetylsalicylic acid on renal function in patients with chronic heart failure." Am J Med 90 (1991): 571-5
  5. Kimberly RP, Plotz PH "Aspirin-induced depression of renal function." N Engl J Med 296 (1977): 418-24
  6. Maher JF "Analgesic nephropathy. Observations, interpretations, and perspective on the low incidence in America." Am J Med 76 (1984): 345-8
  7. Wen SF, Parthasarathy R, Iliopoulos O, Oberley TD "Acute renal failure following binge drinking and nonsteroidal antiinflammatory drugs." Am J Kidney Dis 20 (1992): 281-5
  8. Muther RS, Potter DM, Bennett WM "Aspirin-induced depression of glomerular filtration rate in normal humans: role of sodium balance." Ann Intern Med 94 (1981): 317-21
  9. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  10. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
  11. Whelton A "Renal effects of over-the-counter analgesics." J Clin Pharmacol 35 (1995): 454-63
View all 11 references
Major

Salicylates (Includes Aspirin/pravastatin) ↔ Reye's Syndrome

Severe Potential Hazard, High plausibility

Applies to: Influenza, Varicella-Zoster

The use of salicylates, primarily aspirin, in children with varicella infections or influenza-like illnesses has been associated with an increased risk of Reye's syndrome. Although a causal relationship has not been established, the majority of evidence to date seems to support the association. Most authorities, including the American Academy of Pediatrics Committee on Infectious Diseases, recommend avoiding the use of salicylates in children and teenagers with known or suspected varicella or influenza and during presumed outbreaks of influenza. If antipyretic or analgesic therapy is indicated under these circumstances, acetaminophen may be an appropriate alternative. The same precautions should also be observed with related agents such as salicylamide or diflunisal because of their structural and pharmacological similarities to salicylate.

References

  1. Belay ED, Bresee JS, Holman RC, Khan AS, Shahriari A, Schonberger LB "Reye's syndrome in the United States from 1981 through 1997." N Engl J Med 340 (1999): 1377-82
  2. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  3. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  4. "Product Information. Rexolate (sodium thiosalicylate)" Hyrex Pharmaceuticals, Memphis, TN.
  5. American Academy of Pediatrics. Committee on Infectious Diseases; Peter G, ed. "Red BooK: Report of the Committee on Infectious Diseases. 24th" Grove Village, IL: American Academy of Pediatrics (1997):
  6. Hasking GJ, Duggan JM "Encephalopathy from bismuth subsalicylate." Med J Aust 2 (1982): 167
  7. Epidemiology Office, Divisiion of Viral and Rickettsial Diseasses, Center for Infectious Diseases, Centers for Disease Control. "Leads from the MMWR. Reye syndrome surveillance--United States, 1987 and 1988." JAMA 261 (1989): 3520,
  8. Behrman R, Kliegman R, Arvin A, Nelson W, eds. "Nelson Textbook of Pediatrics. 15th ed." Philadelphia, PA: W.B. Saunders Company (1996):
  9. "Product Information. Pepto-Bismol (bismuth subsalicylate)." Procter and Gamble Pharmaceuticals, Cincinnati, OH.
View all 9 references
Moderate

Hmg-Coa Reductase Inhibitors (Includes Aspirin/pravastatin) ↔ Cognitive Impairment

Moderate Potential Hazard, Moderate plausibility

Applies to: CNS Disorder

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) have been observed in patients receiving statins. The reports are usually not serious, and reversible upon statin discontinuation. Caution is recommended when using these agents in patients with cognitive impairment.

Moderate

Hmg-Coa Reductase Inhibitors (Includes Aspirin/pravastatin) ↔ Diabetes

Moderate Potential Hazard, Moderate plausibility

Applies to: Diabetes Mellitus

Increases in HbA1c and fasting serum glucose levels have been reported with the use of certain HMG-CoA reductase inhibitors. Caution should be exercised when using these agents in diabetic patients and close monitoring is recommended.

Moderate

Hmg-Coa Reductase Inhibitors (Includes Aspirin/pravastatin) ↔ Renal Disease

Moderate Potential Hazard, Moderate plausibility

Applies to: Renal Dysfunction

Some HMG-CoA reductase inhibitors such as fluvastatin, have not been studied in patients with severe renal impairment or end-stage renal disease. Some others such as pitavastatin and simvastatin, require a dose reduction when used in this group of patients. Caution and close monitoring is advised when using these drugs in patients with renal impairment.

Moderate

Salicylates (Includes Aspirin/pravastatin) ↔ Anemia

Moderate Potential Hazard, Moderate plausibility

Applies to: Anemia

Occult, often asymptomatic GI blood loss occurs quite frequently with the use of normal dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. Other salicylates reportedly cause little or no GI blood loss at usual dosages, but may do so at high dosages. Prolonged therapy with salicylates, particularly aspirin, should be administered cautiously in patients with or predisposed to anemia. Periodic monitoring of hematocrit is recommended. The same precautions should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

References

  1. Naschitz JE, Yeshurun D, Odeh M, Bassan H, Rosner I, Stermer E, Levy N "Overt gastrointestinal bleeding in the course of chronic low-dose aspirin administration for secondary prevention of arterial occlusive disease." Am J Gastroenterol 85 (1990): 408-11
  2. Savon JJ, Allen ML, Dimarino AJ, Hermann GA, Krum RP "Gastrointestinal blood loss with low dose (325 mg) plain and enteric-coated aspirin administration." Am J Gastroenterol 90 (1995): 581-5
  3. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  4. Stalnikowiczdarvasi R "Gastrointestinal bleeding during low-dose aspirin administration for prevention of arterial occlusive events: a critical analysis." J Clin Gastroenterol 21 (1995): 13-6
  5. Marks RD "Aspirin use and fecal occult blood testing." Am J Med 100 (1996): 596-7
  6. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  7. Prichard PJ, Kitchingman GK, Walt RP, Daneshmend TK, Hawkey CJ "Human gastric mucosal bleeding induced by low dose aspirin, but not warfarin." BMJ 298 (1989): 493-6
  8. Greenberg PD, Cello JP, Rockey DC "Asymptomatic chronic gastrointestinal blood loss in patients taking aspirin or warfarin for cardiovascular disease." Am J Med 100 (1996): 598-604
View all 8 references
Moderate

Salicylates (Includes Aspirin/pravastatin) ↔ Dialysis

Moderate Potential Hazard, High plausibility

Applies to: hemodialysis

Salicylate and its metabolites are readily removed by hemodialysis and, to a lesser extent, by peritoneal dialysis. Doses should either be scheduled for administration after dialysis or supplemental doses be given after dialysis.

References

  1. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  2. "Product Information. Rexolate (sodium thiosalicylate)" Hyrex Pharmaceuticals, Memphis, TN.
  3. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
Moderate

Salicylates (Includes Aspirin/pravastatin) ↔ G-6-Pd Deficiency

Moderate Potential Hazard, Moderate plausibility

Applies to: G-6-PD Deficiency

Salicylates, particularly aspirin, may cause or aggravate hemolysis in patients with pyruvate kinase or glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. However, this effect has not been clearly established. Until more data are available, therapy with salicylates should be administered cautiously in patients with G-6-PD deficiency. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

References

  1. "Product Information. Ecotrin (aspirin)." SmithKline Beecham, Philadelphia, PA.
  2. "Product Information. Rexolate (sodium thiosalicylate)" Hyrex Pharmaceuticals, Memphis, TN.
  3. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
Moderate

Salicylates (Includes Aspirin/pravastatin) ↔ Hepatotoxicity

Moderate Potential Hazard, Moderate plausibility

Applies to: Liver Disease

The use of salicylates has occasionally been associated with acute, reversible hepatotoxicity, primarily manifested as elevations of serum transaminases, alkaline phosphatase and/or, rarely, bilirubin. Hepatic injury consistent with chronic active hepatitis has also been reported in a few patients, which resulted rarely in encephalopathy or death. Salicylate-induced hepatotoxicity appears to be dependent on serum salicylate concentration (> 25 mg/dL) and has occurred most frequently in patients with juvenile arthritis, active systemic lupus erythematosus, rheumatic fever, or preexisting hepatic impairment. Therapy with salicylates, particularly when given in high dosages, should be administered cautiously in these patients, and periodic monitoring of liver function is recommended. The same precautions should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate. A dosage reduction may be necessary if liver function abnormalities develop and serum salicylate concentration exceeds 25 mg/dL, although serum transaminase elevations may sometimes be transient and return to pretreatment values despite continued therapy without dosage adjustment.

References

  1. Wolfe JD, Metzger AL, Goldstein RC "Aspirin hepatitis." Ann Intern Med 80 (1974): 74-6
  2. "Product Information. Rexolate (sodium thiosalicylate)" Hyrex Pharmaceuticals, Memphis, TN.
  3. "Product Information. Salflex (salsalate)." Carnrick Laboratories Inc, Cedar Knolls, NJ.
  4. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
  5. Patel DK, Hesse A, Ogunbona A, Notarianni LJ, Bennett PN "Metabolism of aspirin after therapeutic and toxic doses." Hum Exp Toxicol 9 (1990): 131-6
  6. Jorup-Ronstrom C, Beermann B, Wahlin-Boll E, Melander A, Britton S "Reduction of paracetamol and aspirin metabolism during viral hepatitis." Clin Pharmacokinet 11 (1986): 250-6
  7. Seaman WE, Ishak KG, Plotz PH "Aspirin-induced hepatotoxicity in patients with systemic lupus erythematosus." Ann Intern Med 80 (1974): 1-8
  8. Sbarbaro JA, Bennett RM "Aspirin hepatotoxicity and disseminated intravascular coagulation." Ann Intern Med 86 (1977): 183-5
View all 8 references

aspirin / pravastatin drug Interactions

There are 660 drug interactions with aspirin / pravastatin

aspirin / pravastatin alcohol/food Interactions

There are 2 alcohol/food interactions with aspirin / pravastatin

Drug Interaction Classification

The classifications below are a general guideline only. It is difficult to determine the relevance of a particular drug interaction to any individual given the large number of variables.
Major Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
Moderate Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.
Minor Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.
Unknown No information available.

Do not stop taking any medications without consulting your healthcare provider.

Further information

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

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