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RESEARCH ON THE DRUG-DRUG INTERACTIONS WITH METABOLISM AND BRAND NAMES

ABSTRACT

Drug interactions are the harmful or beneficial effects of co administered medicinal products, these interaction may be synergistic or antogon istic pharmco kinetics or pharmaco dynamics, drug interactions exists between drugs anddrugs, drug and foods, drugs and herbs, benefits effects include convenience . Reduced toxicity and reduction. ANTIHISTIMINE, ANTIHISTIMINE, ASTHMA, ANALAGESIC, TYPHOID, HYPERTENSION, TUBERCULOSIS ANTIBIOTICS, FILARIA, RHEUMATOID ARTHRITIS, ANTIPYRITIC, ANTICANCER IMMUNOLOGICAL DISEASES, ECTOPIC PREGNANCY, FEVER, O


STEOARTHRITIS AND ANTIPYRITIC, ANALAGESIC, HIV AIDS, CHICKEN POX, SALICYLATE, PHENYTOIN, ESTROGENS, HMG COA REDUCTASE INHIBITORS, BARBITURATES, CHLORAMPHENICAL, ANTACIDS, ANTICOAGULANT. When two or more drugs are administered concurrently or within a reasonable time or after each other (both prescription drugs and non prescription drugs are involved) , the result may be in difference, synergisim, potentation, antagonisim this is called AS .DRUG-DRUG INTRACTION. Drug metabolism interactions results in the increase of biological half life or reduction of clearance there requiring lower doses, imipramine reduces the clearance of epinephrine, some examples of the drugs that inhibit metabolism like Erythromycin, ketocanazole, fluxetin, cimitidine, Allopurinol , carbamazepine, phenobarbital, Rifampacin , and phenytoin. Risk of Therapeutic failure, stoppage of induced may lead to toxic concentration of substrate and induction may lead to formation of toxic metabolites.

1.INTRODUCTION Drug interactions are the harmful or beneficial effects of co administered medicinal products, these interaction may be synergistic or antogon istic pharmco kinetics or pharmaco dynamics, drug interactions exists between drugs anddrugs, drug and foods, drugs and herbs, benefits effects include convenience Reduced toxicity and reduction.

2.DEFINATION When two or more drugs are administered concurrently or within a reasonable time or after each other (both prescription drugs and non prescription drugs are involved) , the result may be in difference, synergisim, potentation, antagonisim this is called AS .DRUG-DRUG INTRACTION

3.DRUG DRUG INTERACTIONS

1.ASTHMA Salbutamol +(diuretic) furosmide-hypokalemiea(muscle weakness, paralysis) Salbutamol( sympathomimitic) +(beta blocker) propranolol-narrowing the air way vessels difficult in breathing severe inaccute attacks . Salbutamol brand names-aerotaz, salbrel

2.ANALAGESIC Aspirin (ANALAGESIC) +(beta blocker) atenalol – effectiveness decreases and metabolism of atenolal increases Brand name of atenolal – tenerific, atezon

3.ANTIHISTIMINE Citrizen HCl (ANTIHISTIMINE) +theophylline (asthma) – decreases the clearance activity Brand name of citrizen – allorox syrup, allatral tablet, antrin tablet.

4.TYPHOID Norflaxacin +warfarin(anticoagulant) – enhances the effect of anticoagulant Norflaxacin +NSAIDS (analagesic) – increase the risk of cns stimulant Brand name of Norflaxacin – alflox, biflox norflox

5.ANTIHYPERTENSION Nifedipine +beta blocker – increase the chf, severe heart failure Nifedipine +cimitidine – decreases the Nifideipine action through enzyme inhibition Brand name of Nifedipine-adolat, procardia xl, nifidipine xl

6.ANTITUBERCULOSIS Rifampacin +cyclosporin – reduced the cyclosporin risk of organ rejection Rifampacin +isoniazid – risk of liver damage Rifampacin +pyrazinmide – risk of liver damage Rifampacin +quinine – decreases the blood levels Rifampacin brand name – acox, coxid, fampacin, rificillin,

7.ANTIBIOTICS Ampicillin+tetracycline-decreases the effect Ampicillin +atenolal – decreases the effect of ampicillin Ampicillin +typhoid vaccine – decreases the immunological resp of typhoid vaccine

8.FILARIA Alabinidazole +clozapine – decreases the blood count Brand name of Alabinidazole – albenzole, eskazole zentel, andizole

9.RHEUMATOID ARTHRITIS ANTICANCER, AUTOIMMUNODISORDERS, ECTOPIC PREGNANCY Methotrexate sodium +penicillin – increase the risk of toxicity Methotrexate +aminoglycosides – inhibit the Gi absorption, decreases the Gi absorption of Methotrexate sodium

10.FEVER , OSTEOARTHRITIS, ANALAGESIC, ANTIPYRITIC Nimesulide+furosimide – rate of binding action is decreased. Nimesulide +tolubutimide, fibirates, salcyclates – displacement of protein binding capacity Nimesulide +sulphonylureeas-increaese the action of hypoglycemic agent Brand name of nimesulide – nimulid, nisc, insulide gel

11.HIV AIDS, CHICKEN POX Aciclair +ketocanazole – synergistic effect Aciclair +probencid-half life time increases renal clearance Aciclair +zidovidine – neurotoxic effects

4.OTHER INTRACTION AND ASSOCIATED WITH DISEASES

1.Salicylates Interference with renal excretion of drugs that undergo active tubular secretion, salicylates renal excretion dependent on urinary pH when large doses used. Clinically documented INTRACTION Carbonic anhydrase inhibitors – increased acetazolamide serum concentration, increase salicylate toxicity due to decrease the pH Coticosteriods-increased the salicylate elimination toxic effect on gastric mucosa

2.Phenytoin Induces the hepatic microsmal ldrug metabolism Coticosteriods – decreases the serum corticosteroids levels Doxycycline – decreases the serum Doxycycline levels Quinidine – decreases the serum Quinidine levels Chloramphenical – increased the serum phenytoin

3.ESTROGENS Metabolism inducible, enter hepatic circulation of estrogen may be intruppted by alteration in bowel flora. Ampicillin – interruption of enter hepatic circulation of estrogen. Phenytoin – increased the estrogen metabolism Rifampin – increased the estrogen metabolism

4.HMG COA REDUCTASE INHIBITORS Lovostatin, simastatin and to lesser extent, increase the risk of myopathy Atazanavir – decreases the statin metabolism Clofibrate-increased the risk of myopathy Cyclosporin – decreased statin metabolism Rifampin – increased the statin metabolism Ritinovir – decreases the statin metabolism

5.CHLORAMPHENICAL Inhibit hepatic drug metabolizing enzyme Phenytoin – decreases phenytoin metabolism Sulfonylureas – decreases the Sulfonylureas metabolism Calcium channel blockers Cyclosporin – decreased cyclosporin metabolism Rifampin – increased the metabolism of calcium channel blocker

6.BARBITURATES Tacrolimus – increased the Tacrolimus metabolism Theophylline – increased the theophylline metabolism reduced theophylline effect ANTIFUNGAL azole derivative Barbiturate – increased metabolism of itraconazole

7.Anticoagulant NSAIDS – inhibit the platelet function Simvastatin – decreases the warfarin metabolism Barbiturate – enzyme induction

8. ANTACIDS

antacids may absorb drugs in gastrointestinal tract, reducing absorption, antacid tend to speed gastric emptying Atazanavir – decreases the absorption of Atazanavir Itraconazole – reduced gastrointestinal absorption of itraconazole due to increase pH Tetracycline – decreases gastrointestinal absorption of Tetracycline Allopurinol – inhibit the hepatic drug metabolism enzyme +anticoagulant – increased the hypo pro thrombinemia effect

5. MONITORING AND MANAGING DRUG INTERACTIONS IT is important to under stand the patient current medication, including drugs prescribed by other physician, herbal products and nutrition suppliments, diologue with patients about diet and alcohol consumption is required, the goals of the medication therapy should be fewest drugs in the lowest doses for the short test possible period, the Pharmacology effect expected, wanted and unwanted, of all drugs taken should be determined because these effects usually include the spectrum of drug interaction as far as possible, drugs with wide margin should be preferable so that unexpected interaction do not lead to toxicity effects,

6. monitoring patients Monitoring of patients after a change of treatments is important as some interaction may take about week of more time to observe, if dosage adjustments does not work, the drug may be replaced with another one which has lesser interaction, they are many sources available as reference tools for verification of the drug interaction, some of the sources are metck manual, drugs. Com, rxlist. Com,, drug has specific tool I. E INTRACTION checker for verfying drug interactions, with this tool persons can verify the interaction of many drug, informed decisions saves lives,

7.DISCUSSION Drug interactions are the harmful or beneficial effects of co administered medicinal products, these interaction may be synergistic or antogon istic pharmco kinetics or pharmaco dynamics, drug interactions exists between drugs anddrugs, drug and foods, drugs and herbs, benefits effects include convenience Reduced toxicity and reduction., Synergistic interaction are those that give added benefits Examples of synergistic drug interaction increase the analgesic effect of paracetamol with codiiene, reduction of bacterial resistance with co administration of clavonic acid with Amoxicillin cytotoxic drugs combination in treatment of cancer requires lower doses, of each drug to obtain better Therapeutic effects with less side effects, saquinaver is poorly absorbed, treatment is three times dosing when combined with Ritinovir there is multiple features increasing the blood concentration , antagonisim interaction are those may interact and conteract the action of one another example is oxybutin in for treating in contience in a patients taking donapezil for alzheimers diseases and also alcohol and caffeine , phenobarbital and cimitidine, acetylcholine and ATROPINE,. 8.Results of drug drug interactions Pharmacodynamic interaction are the actions that you are produced by the drug on the body, one drug alter the sensitive, or responsiveness of the body to other drug by producing antagonisim, effect, pharmacokinetics interactions are the action that are produced by the body on drugs, these interaction affect the intensity and duration of the drug action and not the effect, they usually alter drug absorption, distribution, metabolism, and excretion on of another drug nisim this is called AS .DRUG-DRUG INTRACTION. Drug metabolism interactions results in the increase of biological half life or reduction of clearance there requiring lower doses, imipramine reduces the clearance of epinephrine, some examples of the drugs that inhibit metabolism like Erythromycin, ketocanazole, fluxetin, cimitidine, Allopurinol , carbamazepine, phenobarbital, Rifampacin , and phenytoin. Risk of Therapeutic failure, stoppage of induced may lead to toxic concentration of substrate and induction may lead to formation of toxic metabolites.

9.CONCLUSION TETRACYCLINE AND QUINOLINES form insoluble complexes with metals and there by their absorption is reduced that I’d reason for advising to avoid antacids preparations, milk products with certain products, some drugs reduced, absorbed and causes effects, absorption of Methotrexate or digixin by cholestyramine, antacids also alters pH decreases the absorption of week acids and increasing the absorption of the week bases, prestalic movements regulates the passage of drugs, laxatives causes the drug to move rapidly through the intestine resulting poor drug absorption

REFERENCES

1. MERCK.MANNUAL 2.DRUGS.COM 3.RXLIST. COM 4.DRUGS DESCRIPTION. COM 5TRIPATI PHARMACOLOGY 6ROGER WALKER THERPEUTICS 7.antibiotics and infection. Com 8medicinalchemistery.com 9community pharmacy. Com 10hospital pharmacy. Com

References 1. Ancrenaz V, Daali Y, Fontana P et al. Impact of polymorphisms and drugdrug interacons on clopidogrel and prasugrel response variability . Curr Drug Metabo. 2010; 11:667-77. 2. Nguyen TA, Dioda JG, Pharand C. R esistance to clopidogrel: a review of the evidence. J Am Coll Cardiol. 2005; 45(8):1157-64. 3. Wang Y, Wang Y, Zhao X et al. Clopidogrel with aspirin in acute minor stroke or transient ischemic a ack. N Engl J Med. 2013; 369:11-19. 4. Steinhubl SR, Berger PB, Mann JT et al. Early and sustained dual oral an- plat elet therapy following percutaneous coronary intervenon: a random – ized controlled trial. J Am Med Assoc. 2002; 288(19):2411-20. 5. Yusuf S, Zhao F, Mehta SR et al. E ects of clopidogrel in addion t o aspirin in paen ts with acute coronary syndromes without ST-segment elevaon. N Engl J Med. 2001; 345(7):494-502. 6. Leon MB, Baim DS, Popma JJ et al. A clinical trial comparing three an – thrombic-drug regimens a er coronary-artery stenng. N E ngl J Med. 1998; 339(23):1665-71. 7. Bha DL , Scheiman J, Abraham NS et al. ACCF/ACG/AHA Expert consensus document on reducing the gastrointesnal risk s of anplat elet therapy and NSAID use. J Am Coll Cardiol. 2008; 52(18):1502-17. 8. Gilard M, Arnaud B, Cornily JC et al. Inuenc e of omeprazole on the an – platelet acon of clopidogrel associat ed with aspirin. J Am Coll Cardiol. 2008; 51(3):256-60. 9. Juurlink DN, Gomes T, Ko DT et al. A populaon-based s tudy of the drug interacon be tween proton pump inhibitors and clopidogrel. Can Med Assoc J. 2009; 180(7):713-8. 10. Ho PM, Maddox TM, Wang L et al. Risk of adverse outcomes associated with concomitant use of clopidogrel and proton pump inhibitors following acute coronary syndrome. J Am Med Assoc. 2009; 301(9):937-44. 11. Sibbing D, Morath T, Stegherr J et al. Impact of proton pump inhibitor on the anplat elet e ects of clopidogrel. Throm Haemost. 2009; 101(4):714-9. 12. Siller-Matula JM, Spiel AO, Lang IM et al. E ects of pantoprazole and esomeprazole on platelet inhibion b y clopidogrel. Am Heart J. 2009; 157(1):148e1-e5. 13. Dunn SP, Steinhubl SR, Bauer D et al. Impact of proton pump inhibitor therapy on the ec acy of clopidogrel in the CAPRIE and CREDO trials. J Am Heart Assoc. 2013; 2(1):e004564 14. Kowk CS, Loke YK. Meta-analysis: the e ects of proton pump inhibitors on cardiovascular events and mortality in paen ts receiving clopidogrel. Aliment Pharmacol Ther. 2000; 14:1191-98 15. Naonal Choles terol Educaon Program (NCEP) Expert P anel on Detec- on, E valuaon, and T reatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third Report of the Naonal Choles terol Educaon Program (NCEP) Expert Panel on Detecon, E valuaon, and T reatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) nal report. Circulaon. 2002;106(25):3143-421. Food-Drug Interactions 16. Kamanna VS, Ganji SH, Kashyap ML. Recent advances in niacin and lipid metabolism. Curr Opin Lipidol. 2013;24(3):239-45. 17. Digby JE, Ruparelia N, Choudhury RP. Niacin in cardiovascular disease: recent preclinical and clinical developments. Arterioscler Thromb Vasc Biol. 2012;32(3):582-8. 18. Villines TC, Kim AS, Gore RS et al. Niacin: the evidence, clinical use, and future direcons. Curr A theroscler Rep. 2012;14(1):49-59. 19. HPS2-THRIVE Collaborave Group. HPS2-THRIVE random – ized placebo-controlled trial in 25 673 high-risk paen ts of ER niacin/laropiprant: trial design, pre-specied muscle and liver outcomes, and reasons for stopping study treatment. Eur Heart J. 2013;34(17):1279-91. 20. Stone NJ, Robinson J, Lichtenstein AH et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Athero- scleroc Cardio vascular Risk in Adults: A Report of the American College of Cardiology/American Heart Associaon T ask Force on Pracc e Guidelines. Circulaon. 2013[epub ahead of prin t]. 21. Pieper JA. Overview of niacin formulaons: di erences in pharmacokinecs, e c acy, and safety. Am J Health Syst Pharm. 2003;60(13 Suppl 2):S9-14;quiz S25. 22. Bhardwaj SS, Chalasani N. Lipid-lowering agents that cause drug-induced hepatotoxicity. Clin Liver Dis. 2007;11(3):597-613, vii. 23. McKenney J. Niacin for dyslipidemia: consideraons in product selecon. Am J Health S yst Pharm. 2003;60(10):995-1005. 24. Kelley VE, Fere A , Izui S et al. A sh oil die t rich in eicosapen- taenoic acid reduces cyclooxygenase metabolites, and suppresses lupus in mrl-lpr mice. J Immunol. 1985; 134(3):1914-19. 25. Kar S, Webel R. Fish oil supplementaon and c oronary artery disease: does it help? Mo Med. 2012; 109(2):141-5. 26. Weitz D, Weintraub H, Fisher E et al. Fish oil for the treatment of cardiovascular disease. Cardiol Rev. 2010; 18(5):258-69. 27. Shahar E, Folsom AR, Dennis BH et al. Associaon of sh in take and dietary n-3 polyunsaturated fay acids with a h ypocoagula- ble prole. The atherosclerosis risk in c ommunies (ARIC) s tudy. Arterioscler Thromb Vasc Biol. 1993; 13: 1205-12. 28. Kim DN, Eastman A, Baker JE et al. Fish oils, atherogenesis, and thrombogenesis. Ann N Y Acad Sci. 1995; 748:474-80. 29. Kaminski WE, Jendraschak E, Kie R e t al. Dietary omega-3 fay acids lo wer levels of platelet-derived growth factor mRNA in human mononuclear cells. Blood. 1993; 81:1871-9. 30. Mayer K, Merfels M, Muhly-Reinholz M et al. Omega-3 fay acids suppress monocyte adhesion to human endothelial cells: role of endothelial PAF generaon. Am J Ph ysio Heart Circ Physiol. 2002; 283:H811-8. 31. Buckley MS, Go AD , Knapp WE. Fish oil interacon with war – farin. Ann Pharmacother. 2004; 38:50-3. 32. Eritsland J, Arnesen H, Seljeot I e t al. Long-term e ects of n-3 polyunsaturated fay acids on haemos tac variables and bleeding episodes in paen ts with coronary artery disease. Blood Coagul Fibrinolysis. 1995; 6:17-22 33. Bender NK, Kraynak MA, Chique e E et al. E ects of marine sh oils on the an c oagulaon s tatus of paen ts receiving chronic warfarin therapy. J Thromb Thrombolysis. 1998; 5:257-61. 34. Bays HE. Safety consideraons with omega-3 f ay acid thera – py. Am J Cardiol. 2007; 99:35C-43C. 35. Fung WT, Subramaniam G, Lee J et al. Assessment of extracts from red yeast rice for herb-drug interacon b y in-vitro and in-vivo assays. Sci Rep. 2012;2:298. 36. Gordon RY, Becker DJ. The role of red yeast rice for the physi- cian. Curr Atheroscler Rep. 2011;13(1):73-80. 37. Childress L, Gay A, Zargar A et al. Review of red yeast rice content and current Food and Drug Administraon o versight. J Clin Lipidol. 2013;7(2):117-22 38. Klimek M, Wang S, Ogunkanmi A. Safety and ec acy of redyeast rice (Monascus purpureus) as an alternave therap y for hyperlip- idemia. P T. 2009;34(6):313-27. 39. Chen CH, Uang YS et al. Interacon be tween Red Yeast Rice and CYP450 Enzymes/P-Glycoprotein and Its Implicaon f or the clinical pharmacokinecs of lo vastan. E vid Based Complement Alternat Med.2012;2012:127043. 40. European Associaon f or Cardiovascular Prevenon & R ehabili- taon, R einer Z,Catapano AL, De Backer G et al. ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the man- agement of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). Eur Heart J. 2011;32(14):1769-818. 41. Heber D, Lembertas A, Lu QY et al. An analysis of nine proprietary Chinese red yeast rice dietary supplements: implicaons of vari – ability in chemical prole and c ontents. J Altern Complement Med. 2001;7(2):133-9. 42. Gordon RY, Cooperman T, Obermeyer W et al. Marked variability of monacolin levels in commercial red yeast rice products: buyer beware! Arch Intern Med. 2010;170(19):1722-7. 43. Ernst E. The risk-benet prole of c ommonly used herbal therapies: Ginkgo, St. John’s Wort, Ginseng, Echinacea, Saw Palme o, and Kava. Ann Intern Med. 2002;136(1):42-53. Review. 44. Linde K, Berner MM, Kriston L. St John’s wort for major depression. Cochrane Database Syst Rev. 2008; (4):CD000448.Review. 45. Shelton RC, Keller MB, Gelenberg A et al. E ecveness of St John’ s wort in major depression: a randomized controlled trial. JAMA. 2001;285(15):1978-86. 46. Hypericum Depression Trial Study Group. E ect of Hypericum perforatum (St John’s wort) in major depressive disorder: a randomized controlled trial. JAMA.2002;287(14):1807-14. 47. American Psychiatric Associaon. Pracc e Guideline for the Treatment of Paen ts With Major Depressive Disorder, Third Edi- on. h p://p sychiatryonline.org/content.aspx?bookid=28&secon – id=1667485#654006. (accessed 2014 Jan 20). 48. Benne D A Jr, Phun L, Polk JF et al. Neuropharmacology of St. John’s Wort (Hypericum). Ann Pharmacother. 1998;32(11):1201-8. Review. 49. Müller WE, Singer A, Wonnemann M, et al. Hyperforin represents the neurotransmi er reuptake inhibing c onstuen t of hypericum extract. Pharmacopsychiatry. 1998;31 Suppl 1:16-21. 50. Markowitz JS, Donovan JL, DeVane CL et al.E ect of St John’s wort on drug metabolism by inducon of cy tochrome P450 3A4 enzyme. JAMA. 2003;290(11):1500-4. 51. IMS Instut e for Healthcare Informacs. The Use of Medicines in the United States: Review of 2010.hp://w ww.imshealth.com/im- shealth/Global/Content/IMS%20Instut e/Documents/IHII_UseOfMed_ report%20.pdf. (accessed 2013 Jan 20). 52. Dürr D, Seger B , Kullak-Ublick GA et al. St John’s wort induces intesnal P -glycoprotein/MDR1 and intesnal and hepac CYP3A4. Clin Pharmacol Ther.2000; 68:598-604. 53. Andrén L, Andreasson A, Eggertsen R. Interacon be tween a commercially available St. John’s wort product (Movina) and ator- vastan in paen ts with hypercholesterolemia. Eur J Clin Pharmacol. 2007;63(10):913-6. 54. Kullak-Ublick GA, Becker MB. Regulaon of drug and bile salt transporters in liver and intesne. Drug Me tab Rev. 2003;35(4):305-17. Review. 55. Moore LB, Goodwin B, Jones SA et al. St. John’s wort induces hepat- ic drug metabolism through acvaon of the pregnane X rec eptor. Proc Natl Acad Sci U S A. 2000;97:7500-7502. 56. Dahan A, Altman H. Food-drug interacon: grape fruit juice aug- ments drug bioavailability–mechanism, extent and relevance. Eur J Clin Nutr. 2004;58(1):1-9. Review. 57. Zhou S, Chan E, Pan SQ et al. Pharmacokinec in teracons of drugs with St John’s wort. J Psychopharmacol. 2004;18(2):262-76. Review. CONTINUING EDUCATION Food-Drug Interactions 58. Sugimoto K, Ohmori M, Tsuruoka S et al. Di erent e ects of St John’s wort and the pharmacokinecs of sim vastan and pravas tan. Clin Pharmacol Ther. 2001;70(6):518- 24. 59. Eggertsen R, Andreasson A, Andrén L. E ects of treatment with a commercially available St John’s Wort product (Movina) on cholesterol levels in paen ts with hypercholesterolemia treated with simvastan. Scand J Prim Health Care. 2007;25(3):154-9. 60. Iuliano L, Mauriello A, Sbarigia E et al. Radiolabeled nave lo w-den- sity lipoprotein injected into paen ts with carod s tenosis accumulates in macrophages of atheroscleroc plaque : e ect of vitamin E supple- mentaon. Circulaon. 2000;101(11):1249-54. 61. Tsimikas S, Brilakis ES, Miller ER et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronaryartery disease. N Engl J Med. 2005;353(1):4657. 62. Centers for Disease Control and Prevenon. Health, Unit ed States, 2012. Selected prescripon drug classes used in the pas t 30 days, by sex and age: United States, selected years 1988–1994 through 2007–2010. hp://w ww.cdc.gov/nchs/data/hus/hus12.pdf#092. (accessed 2013 January 20th). 63. Lilja JJ, Neuvonen M, Neuvonen PJ. E ects of regular consumpon of grapefruit juice on the pharmacokinecs of sim vastan. Br J Clin Pharmacol. 2004;58(1):56-60. 64. Fuhr U. Drug interacons with grape fruit juice. Extent, probable mechanism and clinical relevance. Drug Saf. 1998;18(4):251-72. Review. 65. Kantola T, Kivistö KT, Neuvonen PJ. Grapefruit juice greatly increases serum concentraons of lo vastan and lo vastan acid. Clin Pharmac ol Ther. 1998;63(4):397-402. 66. Lilja JJ, Kivistö KT, Neuvonen PJ. Grapefruit juice-simvastan interacon: e ect on serum concentraons of sim vastan, sim vas- tan acid, and HMG-CoA reduct ase inhibitors. Clin Pharmacol Ther. 1998;64(5):477-83. 67. Lilja JJ, Kivistö KT, Neuvonen PJ. Grapefruit juice increases serum concentraons of at orvastan and has no e ect on pravastan. Clin Pharmacol Ther. 1999;66(2):118-27. 68. Lilja JJ, Neuvonen M, Neuvonen PJ. E ects of regular consumpon of grapefruit juice on the pharmacokinecs of sim vastan. Br J Clin Pharmacol. 2004;58(1):56-60. 69. Fukazawa I, Uchida N, Uchida E et al. E ects of grapefruit juice on pharmacokinecs of at orvastan and pravas tan in Japanese. Br J Clin Pharmacol. 2004;57(4):448-55. 70. Ando H, Tsuruoka S, Yanagihara H et al. E ects of grapefruit juice on the pharmacokinecs of pit avastan and at orvastan. Br J Clin Pharmacol. 2005;60(5):494-7. 71. Go o AM Jr. Safety and stan therap y: reconsidering the risks and benets. Arch In tern Med. 2003;163(6):657-9. 72. Phillips PS, Haas RH, Bannykh S et al. Stan-associat ed myopathy with normal creane kinase le vels. Ann Intern Med. 2002;137(7):581-5. 73. Corsini A, Bellosta S, Bae a R et al. New insights into the pharma- codynamic and pharmacokinec properes of s tans. Pharmac ol Ther. 1999;84(3):413-28. Review. 74. Kajinami K, Takekoshi N, Brousseau ME et al. Pharmacogenecs of HMG-CoA reductase inhibitors: exploring the potenal f or geno- type-based individualizaon of c oronary heart disease management. Atherosclerosis. 2004;177(2):219-34. Review. 75. Omar MA, Wilson JP. FDA adverse event reports on stan-associat – ed rhabdomyolysis. Ann Pharmacother. 2002;36(2):288-95. Review. 76. Mazokopakis EE. Unusual causes of rhabdomyolysis. Intern Med J.

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