تداخلات فلوفاستاتين
فلوفاستاتين (Lescol؛ من فئة الستاتينات): 111 تداخلًا موثّقًا في نشرات FDA وصحائف الوقائع التي نفهرسها، وتوزيعها: شديدة 19، متوسطة 51، طفيفة 40، وحالات تفيد فيها نشرة بعدم وجود تداخل مهم 1. كل مُدخل أدناه يقتبس الجملة التي يستند إليها. صفحة الدواء هذه نقطة انطلاق، وليست حكمًا على حالتك.
تداخلات من النشرة
تداخلات شديدة (19)
Do not use erythromycin concomitantly with HMG CoA reductase inhibitors (statins) that are extensively metabolized by CYP 3A4 (lovastatin or simvastatin), due to the increased risk of myopathy, including rhabdomyolysis (see PRECAUTIONS - Drug Interactions ). (نشرة إريثرومايسين، موانع الاستعمال)
Lipid-modifying Agents: HMG-CoA Reductase Inhibitors: lovastatin simvastatin ↑ lovastatin ↑ simvastatin Coadministration with lovastatin or simvastatin is contraindicated due to potential for serious reactions such as myopathy including rhabdomyolysis. atorvastatin ↑ atorvastatin Initiate atorvastatin with the lowest starting dose of atorvastatin and titrate… (نشرة إلفيتيغرافير وكوبيسيستات وإمتريسيتابين وتينوفوفير، التداخلات الدوائية)
- إيزيتيميبشديد
When used in combination with a statin, fenofibrate, or other LDL-C lowering therapy, ZETIA is contraindicated in patients for whom a statin, fenofibrate, or other LDL-C lowering therapy are contraindicated. (نشرة إيزيتيميب، موانع الاستعمال)
HMG-CoA Reductase Inhibitors Primarily Metabolized through CYP3A4 ( 4.4 , 7.2 ) (نشرة بوساكونازول، موانع الاستعمال)
Co-administration of such combinations of a CYP2C9 inhibitor plus a strong or moderate CYP3A inhibitor with TRACLEER is not recommended. (نشرة بوسنتان، التداخلات الدوائية)
Steps to Prevent or Reduce the Risk of Myopathy and Rhabdomyolysis Avoid concomitant use of fluvastatin sodium extended-release tablets with gemfibrozil, cyclosporin, and fluconazole. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
• Statins: Avoid simvastatin doses greater than 10 mg daily. (نشرة درونيدارون، التداخلات الدوائية)
…2: Oral drugs that can be administered concomitantly with Ferric Citrate Tablets Amlodipine Aspirin Atorvastatin Calcitriol Clopidogrel Digoxin Diltiazem Doxercalciferol Enalapril Fluvastatin Glimepiride Levofloxacin Losartan Metoprolol Pravastatin Propranolol Sitagliptin Warfarin Oral drugs that have to be separated from Ferric Citrate Tablets and meals Dosing… (نشرة سترات الحديديك، التداخلات الدوائية)
…pitavastatin Coadministration with VOSEVI may increase the concentration of pitavastatin and is not recommended, due to an increased risk of myopathy, including rhabdomyolysis. atorvastatin fluvastatin lovastatin simvastatin ↑ atorvastatin ↑ fluvastatin ↑ lovastatin ↑ simvastatin Coadministration with VOSEVI may increase the concentrations of atorvastatin, fluvastatin,… (نشرة سوفوسبوفير وفيلباتاسفير، التداخلات الدوائية)
• Cyclosporine and Fluconazole : Avoid use with fluvastatin sodium extended-release tablets. (نشرة فلوفاستاتين، التداخلات الدوائية)
Steps to Prevent or Reduce the Risk of Myopathy and Rhabdomyolysis Avoid concomitant use of fluvastatin sodium extended-release tablets with gemfibrozil, cyclosporin, and fluconazole. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
Concomitant administration of clarithromycin tablets with HMG-CoA reductase inhibitors (statins) that are extensively metabolized by CYP3A4 (lovastatin or simvastatin) is contraindicated, due to the increased risk of myopathy, including rhabdomyolysis [see Warnings and Precautions ( 5.4 ) and Drug Interactions ( 7 )]. (نشرة كلاريثرومايسين، موانع الاستعمال)
Myopathy Coadministration of CYP3A4 metabolized HMG-CoA reductase inhibitors such as simvastatin, and lovastatin is contraindicated with ketoconazole tablets (see PRECAUTIONS: Drug Interactions ). (نشرة كيتوكونازول، موانع الاستعمال)
- ماسيتنتانشديد
Moderate dual CYP3A4 and CYP2C9 inhibitors (fluconazole, amiodarone) or use of combined CYP3A4 and CYP2C9 inhibitors may increase exposure to macitentan: avoid co-administration with OPSUMIT ( 7.3 , 12.3 ). (نشرة ماسيتنتان، التداخلات الدوائية)
تداخلات متوسطة (51)
HIV Protease inhibitor — Ritonavir (600 mg twice daily), a strong CYP3A4 inhibitor, which also inhibits CYP2C9, increased avanafil 50 mg single-dose C max and AUC equal to approximately 2-fold and 13-fold, and prolonged the half-life of avanafil to approximately 9 hours in healthy volunteers. (نشرة أفانافيل، التداخلات الدوائية)
Transporters Use caution when concomitantly administering ALVAIZ and drugs that are substrates of OATP1B1 (e.g., atorvastatin, bosentan, ezetimibe, fluvastatin, glyburide, olmesartan, pitavastatin, pravastatin, rosuvastatin, repaglinide, rifampin, simvastatin acid, SN-38 [active metabolite of irinotecan], valsartan) or breast cancer resistance protein (BCRP)… (نشرة إلترومبوباغ، التداخلات الدوائية)
Patients who consume substantial quantities of alcohol and/or have a history of liver disease may be at increased risk for hepatic injury. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
Effect of TRIKAFTA on Other Drugs CYP2C9 Substrates Ivacaftor may inhibit CYP2C9; therefore, monitoring of the international normalized ratio (INR) during concomitant use of TRIKAFTA with warfarin is recommended. (نشرة إليكساكافتور وتيزاكافتور وإيفاكافتور، التداخلات الدوائية)
HMG-CoA Reductase Inhibitors simvastatin, lovastatin, atorvastatin Increased plasma concentration of HMG-CoA reductase inhibitor. (نشرة أميودارون، التداخلات الدوائية)
Elevations in LDL cholesterol decreased to pre-treatment levels in response to statin therapy. (نشرة أوباداسيتينيب، التحذيرات والاحتياطات)
Dose adjustments for these HMG-CoA reductase inhibitors may be necessary. (نشرة إيترافيرين، التداخلات الدوائية)
The risk is also greater in patients taking VYTORIN 80 mg daily compared with patients taking lower VYTORIN dosages and compared with patients using other statins with similar or greater LDL-C-lowering efficacy [see Adverse Reactions (6.1) ] . (نشرة إيزيتيميب وسيمفاستاتين، التحذيرات والاحتياطات)
HMG-CoA reductase inhibitors: Atorvastatin PravastatinSimvastatin ↓ atorvastatin * ↓ pravastatin * ↓ simvastatin * Plasma concentrations of atorvastatin, pravastatin and simvastatin decreased. (نشرة إيفافيرينز، التداخلات الدوائية)
HMG-CoA reductase inhibitors: Atorvastatin Pravastatin Simvastatin ↓ atorvastatin ↓ pravastatin ↓ simvastatin Plasma concentrations of atorvastatin, pravastatin, and simvastatin decreased. (نشرة إيفافيرينز ولاميفودين وتينوفوفير، التداخلات الدوائية)
In a double-blind, placebo-controlled trial of 8,179 statin-treated subjects with established cardiovascular disease (CVD) or diabetes plus an additional risk factor for CVD, adjudicated atrial fibrillation or atrial flutter requiring hospitalization for 24 or more hours occurred in 127 (3%) patients treated with VASCEPA compared to 84 (2%) patients receiving… (نشرة إيكوسابنت إيثيل، التحذيرات والاحتياطات)
Interactions With Drugs Metabolized by CYP3A4 Gleevec will increase plasma concentration of CYP3A4 metabolized drugs (e.g., triazolo-benzodiazepines, dihydropyridine calcium channel blockers, certain HMG-CoA reductase inhibitors, etc.). Use caution when administering Gleevec with CYP3A4 substrates that have a narrow therapeutic window. (نشرة إيماتينيب، التداخلات الدوائية)
- بازوبانيبمتوسط
Insufficient data are available to assess the risk of concomitant administration of alternative statins and VOTRIENT. (نشرة بازوبانيب، التحذيرات والاحتياطات)
- بروبينيسيد وكولشيسينمتوسط
When used concomitantly with fluvastatin sodium extended-release tablets, lipid modifying doses (≥ 1 g/day) of niacin, fibrates, and colchicine may also increase the risk of myopathy and rhabdomyolysis [see Drug Interactions ( 7.1 )] . (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
HMG-CoA Reductase Inhibitors: lovastatin simvastatin ↑ lovastatin ↑ simvastatin Initiate lovastatin and simvastatin with the lowest starting dose and titrate carefully while monitoring for safety (e.g., myopathy). (نشرة بيكتيغرافير وإمتريسيتابين وتينوفوفير ألافيناميد، التداخلات الدوائية)
CYP2C9: Concomitant use with CYP2C9 inhibitors can decrease torsemide clearance. (نشرة توراسيميد، التداخلات الدوائية)
• Patients receiving more than 40 mg per day of simvastatin or lovastatin may be at increased risk of statin-related adverse effects. (نشرة تيكاغريلور، التداخلات الدوائية)
When used concomitantly with fluvastatin sodium extended-release tablets, lipid modifying doses (≥ 1 g/day) of niacin, fibrates, and colchicine may also increase the risk of myopathy and rhabdomyolysis [see Drug Interactions ( 7.1 )] . (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
In patients who receive Daptomycin for Injection, CPK levels should be monitored weekly, and more frequently in patients who received recent prior or concomitant therapy with an HMG-CoA reductase inhibitor or in whom elevations in CPK occur during treatment with Daptomycin for Injection. (نشرة دابتومايسين، التحذيرات والاحتياطات)
The risk of myopathy and rhabdomyolysis is increased by concomitant administration of danazol with statins such as simvastatin, atorvastatin and lovastatin. (نشرة دانازول، التداخلات الدوائية)
Monitor for increased dronabinol-related adverse reactions when dronabinol oral solution is co-administered with inhibitors of CYP2C9 (e.g., amiodarone, fluconazole) and inhibitors of CYP3A4 enzymes (e.g., ketoconazole, itraconazole, clarithromycin, ritonavir, erythromycin, grapefruit juice). (نشرة درونابينول، التداخلات الدوائية)
Co-administration of diclofenac with CYP2C9 inhibitors (e.g. voriconazole) may enhance the exposure and toxicity of diclofenac whereas co- administration with CYP2C9 inducers (e.g. rifampin) may lead to compromised efficacy of diclofenac. (نشرة ديكلوفيناك، التداخلات الدوائية)
Co-administration of diclofenac with CYP2C9 inhibitors (e.g., voriconazole) may enhance the exposure and toxicity of diclofenac [see Clinical Pharmacology (12.3) ] whereas co-administration with CYP2C9 inducers (e.g., rifampin) may lead to compromised efficacy of diclofenac. (نشرة ديكلوفيناك وميزوبروستول، التداخلات الدوائية)
Fluconazole (strong CYP2C9 inhibitor): Increases systemic exposure of ramelteon; administer with caution. (نشرة راميلتيون، التداخلات الدوائية)
Rosuvastatin plasma levels can be significantly increased with concomitant administration of inhibitors of CYP2C9 and transporters. (نشرة روسوفاستاتين، التداخلات الدوائية)
Decrease exposure Selective 5-HT 3 Receptor Antagonists Ondansetron Decrease exposure Statins Metabolized by CYP3A4 Simvastatin Decrease exposure Thiazolidinediones Rosiglitazone Decrease AUC by 66% Tricyclic Antidepressants Nortriptyline A tuberculosis treatment regimen including rifampin (600 mg/day), isoniazid (300 mg/day), pyrazinamide (500 mg 3× per day),… (نشرة ريفامبيسين، التداخلات الدوائية)
Zafirlukast exposure is likely to be increased by other moderate and strong CYP2C9 inhibitors. (نشرة زافيرلوكاست، الاحتياطات)
During sirolimus therapy with or without cyclosporine, patients should be monitored for elevated lipids, and patients administered an HMG-CoA reductase inhibitor and/or fibrate should be monitored for the possible development of rhabdomyolysis and other adverse effects, as described in the respective labeling for these agents. (نشرة سيروليموس، التحذيرات والاحتياطات)
Co-administration of celecoxib with drugs that are known to inhibit CYP2C9 (e.g., fluconazole) may enhance the exposure and toxicity of celecoxib whereas co-administration with CYP2C9 inducers (e.g., rifampin) may lead to compromised efficacy of celecoxib. (نشرة سيليكوكسيب، التداخلات الدوائية)
The risk is also greater in patients taking an 80 mg daily dosage of ZOCOR compared with patients taking lower ZOCOR dosages and compared with patients using other statins with similar or greater LDL-C-lowering efficacy [see Adverse Reactions (6.1) ] . (نشرة سيمفاستاتين، التحذيرات والاحتياطات)
• Glyburide : Monitor blood glucose levels when fluvastatin sodium extended-release tablets are initiated. (نشرة فلوفاستاتين، التداخلات الدوائية)
• Glyburide : Monitor blood glucose levels when fluvastatin sodium extended-release tablets are initiated. (نشرة فلوفاستاتين، التداخلات الدوائية)
Other benzodiazepines including triazolam and alprazolam (CYP3A4 Inhibition) In Vitro Studies Demonstrated Potential for Voriconazole to Inhibit Metabolism (Increased Plasma Exposure) HMG-CoA Reductase Inhibitors (Statins) (CYP3A4 Inhibition) In Vitro Studies Demonstrated Potential for Voriconazole to Inhibit Metabolism (Increased Plasma Exposure) Frequent monitoring… (نشرة فوريكونازول، التداخلات الدوائية)
…Sulfonamides Sulfamethizole, sulfaphenazole, sulfadiazine, sulfamethoxazole-trimethoprim Other Acute alcohol intake, amiodarone, chloramphenicol, chlordiazepoxide, disulfiram, estrogen, fluvastatin, isoniazid, methylphenidate, phenothiazines, salicylates, ticlopidine, tolbutamide, trazodone, warfarin Drugs that may decrease phenytoin serum levels Antineoplastic agents… (نشرة فوسفينيتوين، التداخلات الدوائية)
When used concomitantly with fluvastatin sodium extended-release tablets, lipid modifying doses (≥ 1 g/day) of niacin, fibrates, and colchicine may also increase the risk of myopathy and rhabdomyolysis [see Drug Interactions ( 7.1 )] . (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
• Phenytoin : Monitor plasma phenytoin levels when fluvastatin sodium extended-release tablets treatment is initiated. (نشرة فلوفاستاتين، التداخلات الدوائية)
Amiodarone Amiodarone and its metabolite desethyl amiodarone, inhibitors of CYP2C9, and P- glycoprotein increased concentrations of the S(-)-enantiomer of carvedilol by at least 2 fold [see Clinical Pharmacology (12.5) ]. (نشرة كارفيديلول، التداخلات الدوائية)
- كولشيسينمتوسط
When used concomitantly with fluvastatin sodium extended-release tablets, lipid modifying doses (≥ 1 g/day) of niacin, fibrates, and colchicine may also increase the risk of myopathy and rhabdomyolysis [see Drug Interactions ( 7.1 )] . (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
Thus, clinicians considering combined therapy of quinine sulfate with atorvastatin or other HMG-CoA reductase inhibitors ("statins") that are CYP3A4 substrates (e.g., simvastatin, lovastatin) should carefully weigh the potential benefits and risks of each medication. (نشرة كينين، التداخلات الدوائية)
Strong CYP3A4 or CYP2C9 Inhibitors Patients with renal or hepatic impairment who are taking strong inhibitors of CYP3A4 and CYP2C9 may have a significant increase in exposure to VIMPAT. (نشرة لاكوساميد، التداخلات الدوائية)
Examples of relevant classes of compounds where antacids have been demonstrated to reduce bioavailability include antibiotics (such as quinolones, ampicillin, and tetracyclines), thyroid hormones, ACE inhibitors, statin lipid regulators, and anti-malarials. (نشرة لانثانوم، التداخلات الدوائية)
However, another HMG-CoA reductase inhibitor has been found to produce a less than two-second increase in prothrombin time in healthy volunteers receiving low doses of warfarin. (نشرة لوفاستاتين، التداخلات الدوائية)
HMG-CoA Reductase Inhibitors: rosuvastatin ↑ rosuvastatin Coadministration of ledipasvir and sofosbuvir with rosuvastatin may significantly increase the concentration of rosuvastatin, which is associated with increased risk of myopathy, including rhabdomyolysis. (نشرة ليديباسفير وسوفوسبوفير، التداخلات الدوائية)
HMG-CoA Reductase Inhibitors: lovastatin simvastatin ↑ lovastatin ↑ simvastatin Initiate lovastatin and simvastatin with the lowest starting dose and titrate carefully while monitoring for safety (e.g., myopathy). (نشرة ليناكابافير، التداخلات الدوائية)
Mifepristone significantly increased exposure of fluvastatin, a typical CYP2C8/2C9 substrate, in healthy subjects. (نشرة ميفيبريستون، التداخلات الدوائية)
Thus concomitant usage of CYP2C9 inhibitors (such as amiodarone, fluconazole, and sulphaphenazole) may lead to abnormally high plasma levels of meloxicam due to reduced metabolic clearance [ see Use in Specific Populations ( 8.8 ); and Clinical Pharmacology ( 12.3 , 12.5 ) ]. (نشرة ميلوكسيكام، التداخلات الدوائية)
…salicylates, monoamine oxidase inhibitors, non-selective beta-adrenergic-blocking agents, anabolic hormones (e.g., methandrostenolone), guanethidine, gymnema sylvestre, glucomannan, thioctic acid, and inhibitors of CYP2C9 (e.g., amiodarone, fluconazole, voriconazole, sulfinpyrazone) or in patients known to be poor metabolizers of CYP2C9 substrates, alcohol. (نشرة ناتيغلينيد، التداخلات الدوائية)
- نياسينمتوسط
When used concomitantly with fluvastatin sodium extended-release tablets, lipid modifying doses (≥ 1 g/day) of niacin, fibrates, and colchicine may also increase the risk of myopathy and rhabdomyolysis [see Drug Interactions ( 7.1 )] . (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
HMG-CoA Reductase Inhibitors – When single 40 mg doses of simvastatin or atorvastatin, both substrates of CYP3A4, were given to healthy adult volunteers who had received nefazodone hydrochloride, 200 mg BID for 6 days, approximately 20 fold increases in plasma concentrations of simvastatin and simvastatin acid and 3 to 4 fold increases in plasma concentrations… (نشرة نيفازودون، التداخلات الدوائية)
Fluvastatin Sodium Extended-Release Tablets’ Effects on Other Drugs Warfarin Clinical impact There are postmarketing reports of clinically evident bleeding and/or increased INR in patients taking concomitant statins and warfarin. (نشرة فلوفاستاتين، التداخلات الدوائية)
إشارات طفيفة (40)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
Effient can be administered with aspirin (75 mg to 325 mg per day), heparin, GPIIb/IIIa inhibitors, statins, digoxin, and drugs that elevate gastric pH, including proton pump inhibitors and H 2 blockers [see Clinical Pharmacology (12.3) ] . (نشرة براسوغريل، التداخلات الدوائية)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
Toremifene is a weak inhibitor of CYP2C9. (نشرة توريميفين، التداخلات الدوائية)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
In vitro studies with human liver microsomes showed that terbinafine does not inhibit the metabolism of tolbutamide, ethinylestradiol, ethoxycoumarin, cyclosporine, cisapride and fluvastatin. (نشرة تيربينافين، التداخلات الدوائية)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
The interaction is a consequence of blocking hepatic metabolism of vardenafil by ritonavir, a HIV protease inhibitor and a highly strong CYP3A4 inhibitor, which also inhibits CYP2C9. (نشرة فاردينافيل، التداخلات الدوائية)
HMG-CoA Reductase Inhibitors The use of HMG-CoA reductase inhibitors that are CYP3A4 substrates in combination with verapamil has been associated with reports of myopathy/rhabdomyolysis. (نشرة فيراباميل، التداخلات الدوائية)
…acid, α-blockers, angiotensin-converting enzyme (ACE) inhibitors, analgesics, anti-convulsants, beta-adrenergic blocking agents, diuretics, calcium channel blockers, cardiac nitrates, HMG-CoA reductase inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), benzodiazepines, H 2 antagonists and quinolone anti-infectives without evidence of clinically significant… (نشرة فيناستيريد، التداخلات الدوائية)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
CYP2C9 Venlafaxine did not inhibit CYP2C9 in vitro . (نشرة فينلافاكسين، التداخلات الدوائية)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
However, at high concentrations in vitro , clopidogrel inhibits CYP2C9. (نشرة كلوبيدوغريل، التداخلات الدوائية)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
IMNM is characterized by proximal muscle weakness and elevated serum CK, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy, and improvement with immunosuppressive agents. (نشرة فلوفاستاتين، التحذيرات والاحتياطات)
Should treatment with any HMG-CoA reductase inhibitor (a lipid lowering agent) be needed to treat lipid elevations, evaluate the potential for a drug-drug interaction before initiating therapy as certain HMG-CoA reductase inhibitors are metabolized by the CYP3A4 pathway [see Drug Interactions ( 7.1 )] . (نشرة نيلوتينيب، التحذيرات والاحتياطات)
لم يُبلَّغ عن تداخل مهم (1)
Based on these data, ISENTRESS is not expected to affect the pharmacokinetics of drugs that are substrates of these enzymes or P-glycoprotein (e.g., protease inhibitors, NNRTIs, opioid analgesics, statins, azole antifungals, proton pump inhibitors and anti-erectile dysfunction agents). (نشرة رالتيغرافير، التداخلات الدوائية)
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