Drug Interaction Report
9 potential interactions and/or warnings found for the following 2 drugs:
- betamethasone / iodixanol / lidocaine
- efavirenz / lamivudine / tenofovir disoproxil
Interactions between your drugs
iodixanol tenofovir
Applies to: betamethasone / iodixanol / lidocaine, efavirenz / lamivudine / tenofovir disoproxil
GENERALLY AVOID: Concomitant use of intravascular radiocontrast media with other nephrotoxic agents may potentiate the risk of contrast-induced nephropathy and renal impairment. Contrast-induced nephropathy is most commonly defined as an increase in serum creatinine >=0.5 mg/dL or 25% from baseline within 24 to 72 hours of intravascular contrast administration in the absence of alternative etiologies, although nephropathy may occur up to a week after contrast exposure. Pathogenesis has not been fully elucidated, but may involve renal hypoperfusion and ischemia, direct cytotoxicity on tubular epithelial cells, and generation of reactive oxygen species. While the condition is usually transient and asymptomatic, it can be associated with increased risk of renal failure, dialysis, prolonged hospitalization, significant long-term morbidity, and mortality. Patients at increased risk of developing contrast-induced nephropathy include those with diabetes (especially diabetic nephropathy), preexisting renal insufficiency (serum creatinine >1.5 mg/dL or GFR <60 mL/min/1.73 m2), volume depletion (e.g., diuretic use), advanced age (>70 years), congestive heart failure, multiple myeloma, hypoalbuminemia, and concomitant use of nephrotoxic agents (e.g., aminoglycosides; polypeptide, glycopeptide, and polymyxin antibiotics; amphotericin B; aminosalicylates; antiviral/antiretroviral agents such as acyclovir, adefovir, cidofovir, foscarnet, and tenofovir; antineoplastics such as aldesleukin, cisplatin, clofarabine, ifosfamide, streptozocin, and high intravenous dosages of methotrexate; chelating agents such as deferasirox, deferoxamine, edetate disodium, and edetate calcium disodium; immunosuppressants such as cyclosporine, everolimus, sirolimus, and tacrolimus; intravenous bisphosphonates; intravenous pentamidine; high dosages and/or chronic use of nonsteroidal anti-inflammatory agents; gallium nitrate; lithium; penicillamine). The incidence has been reported to be approximately 10% to 30% in patients with risk factors, and as high as 90% in diabetics with chronic kidney disease. Intraarterial administration of contrast media is also associated with increased risk of nephropathy relative to intravenous administration.
MANAGEMENT: Alternative imaging techniques that do not require contrast should be considered in patients who are at increased risk for contrast-induced nephropathy. Otherwise, experts recommend discontinuing other nephrotoxic drugs 1 to 2 days before administration of contrast media, depending on the clinical feasibility of doing so. The smallest effective dose (100 mL or less) of a nonionic, low-osmolar (e.g., iohexol, iomeprol, iopamidol, iopental, iopromide, ioversol) or iso-osmolar (e.g., iodixanol, iotrolan) contrast medium should be used whenever possible, since the risk of nephrotoxicity may be increased with increasing contrast dose, osmolarity, and ionicity. Some studies suggest a lower risk for iso-osmolar contrasts compared to low-osmolar contrasts, although data are limited. Serum creatinine levels should be measured before contrast administration (if procedure is not urgent) and continued for 24 to 48 hours after. In addition, patients should be adequately hydrated with either intravenous normal saline or sodium bicarbonate starting 3 (outpatient) to 6 (inpatient) hours before and continued for 6 to 24 hours after procedure. Oral fluids are also beneficial, but not as effective as intravenous hydration. N-acetylcysteine the day before and day of contrast administration, or theophylline up to 30 minutes before contrast administration, have also been used in high-risk or critically ill patients. Preferably, a nephrologist should be consulted to optimize prophylactic measures for preventing contrast-induced nephropathy in high-risk patients and to guide treatment if the condition occurs. Any repeat procedures with contrast media, if necessary, should not occur until at least 48 to 72 hours after the previous contrast exposure and renal function has fully recovered.
References (7)
- Bennett WM, Porter GA (1990) "Nephrotoxicity of common drugs used by urologists." Urol Clin North Am, 17, p. 145-56
- Bentley ML, Corwin HL, Dasta J (2010) "Drug-induced acute kidney injury in the critically ill adult: recognition and prevention strategies." Crit Care Med, 38(6 Suppl), S169-74
- Marcos LA, Camins BC, Ritchie DJ, Casabar E, Warren DK (2012) "Acute renal insufficiency during telavancin therapy in clinical practice." J Antimicrob Chemother, 67, p. 723-6
- Dubrovskaya Y, Prasad N, Lee Y, Esaian D, Figueroa DA, Tam VH (2015) "Risk factors for nephrotoxicity onset associated with polymyxin B therapy." J Antimicrob Chemother, 70, p. 1903-7
- Bansal R, Aflieco F, Kaplan AA (2016) Contrast-Induced Nephropathy. http://emedicine.medscape.com/article/246751-overview
- van den Berk G, Tonino S, de Fijter C, Smit W, Schultz MJ (2005) "Bench-to-bedside review: Preventative measures for contrast-induced nephropathy in critically ill patients." Crit Care, 9, p. 361-70
- Kellum JA, Leblanc M, Venkataraman R (2008) "Acute renal failure." BMJ Clin Evid, 9, p. 2001
betamethasone efavirenz
Applies to: betamethasone / iodixanol / lidocaine, efavirenz / lamivudine / tenofovir disoproxil
MONITOR: Coadministration with efavirenz may decrease the plasma concentrations of drugs that are substrates of the CYP450 3A4 isoenzyme. The mechanism is accelerated clearance due to induction of CYP450 3A4 activity by efavirenz.
MONITOR: Administration of efavirenz can cause central nervous system (CNS) toxicity. In controlled studies, patients receiving efavirenz reported central nervous system and psychiatric symptoms. These CNS toxicity symptoms included, but were not limited to, dizziness, impaired concentration, somnolence, insomnia, abnormal dreams, and hallucinations. Combining efavirenz with other centrally-acting CNS agents may add to the neurotoxic effects of efavirenz.
MANAGEMENT: Caution is advised if efavirenz must be used concomitantly with medications that undergo metabolism by CYP450 3A4, particularly those with a narrow therapeutic range. Dosage adjustments as well as clinical and laboratory monitoring may be appropriate for some drugs whenever efavirenz is added to or withdrawn from therapy. Additionally, patients treated with any medication that can cause CNS toxicity symptoms should be advised to seek prompt medical attention if they experience symptoms. Patients should be advised to avoid driving, operating machinery, or engaging in potentially hazardous activities requiring mental alertness and motor coordination until they know how the medications affect them.
References (4)
- (2001) "Product Information. Sustiva (efavirenz)." DuPont Pharmaceuticals
- (2023) "Product Information. Sustiva (efavirenz)." Bristol-Myers Squibb, SUPPL-59/47
- (2024) "Product Information. Stocrin (efavirenz)." Merck Sharp & Dohme (Australia) Pty Ltd
- (2024) "Product Information. Efavirenz (efavirenz)." Viatris UK Healthcare Ltd
lamiVUDine efavirenz
Applies to: efavirenz / lamivudine / tenofovir disoproxil, efavirenz / lamivudine / tenofovir disoproxil
MONITOR: Coadministration of efavirenz with other agents known to induce hepatotoxicity may potentiate the risk of liver injury. Efavirenz has been associated with hepatotoxicity during postmarketing use. Among reported cases of hepatic failure, a few occurred in patients with no preexisting hepatic disease or other identifiable risk factors.
MANAGEMENT: The risk of hepatic injury should be considered when efavirenz is used in combination with other agents that are potentially hepatotoxic (e.g., acetaminophen; alcohol; androgens and anabolic steroids; antituberculous agents; azole antifungal agents; ACE inhibitors; cyclosporine (high dosages); disulfiram; endothelin receptor antagonists; interferons; ketolide and macrolide antibiotics; kinase inhibitors; minocycline; nonsteroidal anti-inflammatory agents; other HIV reverse transcriptase inhibitors; proteasome inhibitors; retinoids; sulfonamides; tamoxifen; thiazolidinediones; tolvaptan; vincristine; zileuton; anticonvulsants such as carbamazepine, hydantoins, felbamate, and valproic acid; lipid-lowering medications such as fenofibrate, lomitapide, mipomersen, niacin, and statins; herbals and nutritional supplements such as black cohosh, chaparral, comfrey, DHEA, kava, pennyroyal oil, and red yeast rice). Patients should be advised to seek medical attention if they experience potential signs and symptoms of hepatotoxicity such as fever, rash, itching, anorexia, nausea, vomiting, fatigue, malaise, right upper quadrant pain, dark urine, pale stools, and jaundice. Monitoring of liver function tests should occur before and during treatment, especially in patients with underlying hepatic disease (including hepatitis B or C coinfection) or marked transaminase elevations. The benefit of continued therapy with efavirenz should be considered against the unknown risks of significant liver toxicity in patients who develop persistent elevations of serum transaminases greater than five times the upper limit of normal.
References (2)
- (2001) "Product Information. Sustiva (efavirenz)." DuPont Pharmaceuticals
- Elsharkawy AM, Schwab U, McCarron B, et al. (2013) "Efavirenz induced acute liver failure requiring liver transplantation in a slow drug metaboliser." J Clin Virol, 58, p. 331-3
efavirenz tenofovir
Applies to: efavirenz / lamivudine / tenofovir disoproxil, efavirenz / lamivudine / tenofovir disoproxil
MONITOR: Coadministration of efavirenz with other agents known to induce hepatotoxicity may potentiate the risk of liver injury. Efavirenz has been associated with hepatotoxicity during postmarketing use. Among reported cases of hepatic failure, a few occurred in patients with no preexisting hepatic disease or other identifiable risk factors.
MANAGEMENT: The risk of hepatic injury should be considered when efavirenz is used in combination with other agents that are potentially hepatotoxic (e.g., acetaminophen; alcohol; androgens and anabolic steroids; antituberculous agents; azole antifungal agents; ACE inhibitors; cyclosporine (high dosages); disulfiram; endothelin receptor antagonists; interferons; ketolide and macrolide antibiotics; kinase inhibitors; minocycline; nonsteroidal anti-inflammatory agents; other HIV reverse transcriptase inhibitors; proteasome inhibitors; retinoids; sulfonamides; tamoxifen; thiazolidinediones; tolvaptan; vincristine; zileuton; anticonvulsants such as carbamazepine, hydantoins, felbamate, and valproic acid; lipid-lowering medications such as fenofibrate, lomitapide, mipomersen, niacin, and statins; herbals and nutritional supplements such as black cohosh, chaparral, comfrey, DHEA, kava, pennyroyal oil, and red yeast rice). Patients should be advised to seek medical attention if they experience potential signs and symptoms of hepatotoxicity such as fever, rash, itching, anorexia, nausea, vomiting, fatigue, malaise, right upper quadrant pain, dark urine, pale stools, and jaundice. Monitoring of liver function tests should occur before and during treatment, especially in patients with underlying hepatic disease (including hepatitis B or C coinfection) or marked transaminase elevations. The benefit of continued therapy with efavirenz should be considered against the unknown risks of significant liver toxicity in patients who develop persistent elevations of serum transaminases greater than five times the upper limit of normal.
References (2)
- (2001) "Product Information. Sustiva (efavirenz)." DuPont Pharmaceuticals
- Elsharkawy AM, Schwab U, McCarron B, et al. (2013) "Efavirenz induced acute liver failure requiring liver transplantation in a slow drug metaboliser." J Clin Virol, 58, p. 331-3
lidocaine efavirenz
Applies to: betamethasone / iodixanol / lidocaine, efavirenz / lamivudine / tenofovir disoproxil
Coadministration with inducers of CYP450 1A2 and/or 3A4 may decrease the plasma concentrations of lidocaine, which is primarily metabolized by these isoenzymes. In four healthy volunteers (2 smokers and 2 nonsmokers), administration of a single 400 mg oral dose of lidocaine following pretreatment with the CYP450 inducer phenobarbital (15 mg/day for 4 weeks, followed by 30 mg/day for 4 weeks) decreased lidocaine systemic exposure (AUC) by 37% and increased its oral clearance by 56% compared to administration of lidocaine alone. In another study, the mean bioavailability of a single 750 mg oral dose of lidocaine in six patients receiving chronic antiepileptic drug therapy (consisting of one or more of the following enzyme-inducing anticonvulsants: phenobarbital, primidone, phenytoin, carbamazepine) was approximately 2.5-fold lower than that reported for six healthy control subjects, while intrinsic clearance was nearly threefold higher. By contrast, the interaction was modest for lidocaine administered intravenously, suggesting induction of primarily hepatic first-pass rather than systemic metabolism of lidocaine. When a single 100 mg dose of lidocaine was given intravenously, mean lidocaine AUC was reduced by less than 10% and serum clearance increased by just 17% in the epileptic patients compared to controls. These changes were not statistically significant. Likewise, mean lidocaine AUC decreased by approximately 11% and plasma clearance increased by 15% when a single 50 mg intravenous dose of lidocaine was administered following pretreatment with the potent CYP450 inducer rifampin (600 mg/day for six days) in ten healthy, nonsmoking male volunteers. Another pharmacokinetic study found that cigarette smoke, an inducer of CYP450 1A2, reduced the bioavailability of lidocaine when administered orally, but had only minor effects on lidocaine administered intravenously. When 4 smokers and 5 non-smokers received 2 doses of lidocaine (100 mg IV followed by 100 mg orally after a 2-day washout period), the smoker's systemic exposure (AUC) of oral lidocaine was 68% lower than non-smokers. The AUC of IV lidocaine was only 9% lower in smokers compared with non-smokers. The clinical impact of smoking on lidocaine has not been studied, however, a loss of efficacy may occur.
References (4)
- Heinonen J, Takki S, Jarho L (1970) "Plasma lidocaine levels in patients treated with potential inducers of microsomal enzymes." Acta Anaesthesiol Scand, 14, p. 89-95
- Perucca E, Richens A (1979) "Reduction of oral bioavailability of lignocaine by induction of first pass metabolism in epileptic patients." Br J Clin Pharmacol, 8, p. 21-31
- Perucca E, Ruprah M, Richens A, Park BK, Betteridge DJ, Hedges AM (1981) "Effect of low-dose phenobarbitone on five indirect indices of hepatic microsomal enzyme induction and plasma lipoproteins in normal subjects." Br J Clin Pharmacol, 12, p. 592-6
- Reichel C, Skodra T, Nacke A, Spengler U, Sauerbruch T (1998) "The lignocaine metabolite (MEGX) liver function test and P-450 induction in humans." Br J Clin Pharmacol, 46, p. 535-9
Drug and food interactions
lidocaine food
Applies to: betamethasone / iodixanol / lidocaine
MONITOR: Grapefruit and grapefruit juice may increase the plasma concentrations of lidocaine, which is primarily metabolized by the CYP450 3A4 and 1A2 isoenzymes to active metabolites (monoethylglycinexylidide (MEGX) and glycinexylidide). The proposed mechanism is inhibition of CYP450 3A4-mediated first-pass metabolism in the gut wall by certain compounds present in grapefruit. Inhibition of hepatic CYP450 3A4 may also contribute. The interaction has not been studied with grapefruit juice but has been reported with oral and/or intravenous lidocaine and potent CYP450 3A4 inhibitor, itraconazole, as well as moderate CYP450 3A4 inhibitor, erythromycin. A pharmacokinetic study of 9 healthy volunteers showed that the administration of lidocaine oral (1 mg/kg single dose) with itraconazole (200 mg daily) increased lidocaine systemic exposure (AUC) and peak plasma concentration (Cmax) by 75% and 55%, respectively. However, no changes were observed in the pharmacokinetics of the active metabolite MEGX. In the same study, when the moderate CYP450 3A4 inhibitor erythromycin (500 mg three times a day) was administered, lidocaine AUC and Cmax increased by 60% and 40%, respectively. By contrast, when intravenous lidocaine (1.5 mg/kg infusion over 60 minutes) was administered on the fourth day of treatment with itraconazole (200 mg once a day) no changes in lidocaine AUC or Cmax were observed. However, when lidocaine (1.5 mg/kg infusion over 60 minutes) was coadministered with erythromycin (500 mg three times a day) in the same study, the AUC and Cmax of the active metabolite MEGX significantly increased by 45-60% and 40%, respectively. The observed differences between oral and intravenous lidocaine when coadministered with CYP450 3A4 inhibitors may be attributed to inhibition of CYP450 3A4 in both the gastrointestinal tract and liver affecting oral lidocaine to a greater extent than intravenous lidocaine. In general, the effects of grapefruit products are concentration-, dose- and preparation-dependent, and can vary widely among brands. Certain preparations of grapefruit (e.g., high dose, double strength) have sometimes demonstrated potent inhibition of CYP450 3A4, while other preparations (e.g., low dose, single strength) have typically demonstrated moderate inhibition. While the clinical significance of this interaction is unknown, increased exposure to lidocaine may lead to serious and/or life-threatening reactions including respiratory depression, convulsions, bradycardia, hypotension, arrhythmias, and cardiovascular collapse.
MONITOR: Certain foods and behaviors that induce CYP450 1A2 may reduce the plasma concentrations of lidocaine. The proposed mechanism is induction of hepatic CYP450 1A2, one of the isoenzymes responsible for the metabolic clearance of lidocaine. Cigarette smoking is known to be a CYP450 1A2 inducer. In one pharmacokinetic study of 4 smokers and 5 non-smokers who received 2 doses of lidocaine (100 mg IV followed by 100 mg orally after a 2-day washout period), the smokers' systemic exposure (AUC) of oral lidocaine was 68% lower than non-smokers. The AUC of IV lidocaine was only 9% lower in smokers compared with non-smokers. Other CYP450 1A2 inducers include cruciferous vegetables (e.g., broccoli, brussels sprouts) and char-grilled meat. Therefore, eating large or variable amounts of these foods could also reduce lidocaine exposure. The clinical impact of smoking and/or the ingestion of foods that induce CYP450 1A2 on lidocaine have not been studied, however, a loss of efficacy may occur.
MANAGEMENT: Caution is recommended if lidocaine is to be used in combination with grapefruit and grapefruit juice. Monitoring for lidocaine toxicity and plasma lidocaine levels may also be advised, and the lidocaine dosage adjusted as necessary. Patients who smoke and/or consume cruciferous vegetables may be monitored for reduced lidocaine efficacy.
References (7)
- Huet PM, LeLorier J (1980) "Effects of smoking and chronic hepatitis B on lidocaine and indocyanine green kinetics" Clin Pharmacol Ther, 28, p. 208-15
- (2024) "Product Information. Lidocaine Hydrochloride (lidocaine)." Hospira Inc.
- (2015) "Product Information. Lidocaine Hydrochloride (lidocaine)." Hospira Healthcare Corporation
- (2022) "Product Information. Lidocaine Hydrochloride (lidocaine)." Hameln Pharma Ltd
- (2022) "Product Information. Xylocaine HCl (lidocaine)." Aspen Pharmacare Australia Pty Ltd
- Isohanni MH, Neuvonen PJ, Olkkola KT (2024) Effect of erythromycin and itraconazole on the pharmacokinetics of oral lignocaine https://pubmed.ncbi.nlm.nih.gov/10193676/
- Isohanni MH, Neuvonen PJ, Olkkola KT (2024) Effect of erythromycin and itraconazole on the pharmacokinetics of intravenous lignocaine https://pubmed.ncbi.nlm.nih.gov/9832299/
efavirenz food
Applies to: efavirenz / lamivudine / tenofovir disoproxil
ADJUST DOSING INTERVAL: Administration with food increases the plasma concentrations of efavirenz and may increase the frequency of adverse reactions. According to the product labeling, administration of efavirenz capsules (600 mg single dose) with a high-fat/high-caloric meal (894 kcal, 54 g fat, 54% calories from fat) or a reduced-fat/normal-caloric meal (440 kcal, 2 g fat, 4% calories from fat) was associated with mean increases of 39% and 51% in efavirenz peak plasma concentration (Cmax) and 22% and 17% in systemic exposure (AUC), respectively, compared to administration under fasted conditions. For efavirenz tablets, administration of a single 600 mg dose with a high-fat/high-caloric meal (approximately 1000 kcal, 500-600 kcal from fat) resulted in a 79% increase in mean Cmax and a 28% increase in mean AUC of efavirenz relative to administration under fasted conditions.
GENERALLY AVOID: Alcohol may potentiate the central nervous system (CNS) depressant effects of efavirenz. Concomitant use may result in additive CNS depression and impairment of judgment, thinking, and psychomotor skills. In more severe cases, hypotension, respiratory depression, profound sedation, coma, or even death may occur.
MANAGEMENT: Efavirenz should be taken on an empty stomach, preferably at bedtime. Dosing at bedtime may improve the tolerability of nervous system symptoms such as dizziness, insomnia, impaired concentration, somnolence, abnormal dreams and hallucinations, although they often resolve on their own after the first 2 to 4 weeks of therapy . Patients should be advised of the potential for additive central nervous system effects when efavirenz is used concomitantly with alcohol or psychoactive drugs, and to avoid driving or operating hazardous machinery until they know how the medication affects them.
References (4)
- (2001) "Product Information. Sustiva (efavirenz)." DuPont Pharmaceuticals
- (2023) "Product Information. Sustiva (efavirenz)." Bristol-Myers Squibb, SUPPL-59/47
- (2024) "Product Information. Stocrin (efavirenz)." Merck Sharp & Dohme (Australia) Pty Ltd
- (2024) "Product Information. Efavirenz (efavirenz)." Viatris UK Healthcare Ltd
lidocaine food
Applies to: betamethasone / iodixanol / lidocaine
MONITOR: Smoking cessation may lead to elevated plasma concentrations and enhanced pharmacologic effects of drugs that are substrates of CYP450 1A2 (and possibly CYP450 1A1) and/or certain drugs with a narrow therapeutic index (e.g., flecainide, pentazocine). One proposed mechanism is related to the loss of CYP450 1A2 and 1A1 induction by polycyclic aromatic hydrocarbons in tobacco smoke; when smoking cessation agents are initiated and smoking stops, the metabolism of certain drugs may decrease leading to increased plasma concentrations. The mechanism by which smoking cessation affects narrow therapeutic index drugs that are not known substrates of CYP450 1A2 or 1A1 is unknown. The clinical significance of this interaction is unknown as clinical data are lacking.
MANAGEMENT: Until more information is available, caution is advisable if smoking cessation agents are used concomitantly with drugs that are substrates of CYP450 1A2 or 1A1 and/or those with a narrow therapeutic range. Patients receiving smoking cessation agents may require periodic dose adjustments and closer clinical and laboratory monitoring of medications that are substrates of CYP450 1A2 or 1A1.
References (4)
- (2024) "Product Information. Cytisine (cytisinicline)." Consilient Health Ltd
- jeong sh, Newcombe D, sheridan j, Tingle M (2015) "Pharmacokinetics of cytisine, an a4 b2 nicotinic receptor partial agonist, in healthy smokers following a single dose." Drug Test Anal, 7, p. 475-82
- Vaughan DP, Beckett AH, Robbie DS (1976) "The influence of smoking on the intersubject variation in pentazocine elimination." Br J Clin Pharmacol, 3, p. 279-83
- Zevin S, Benowitz NL (1999) "Drug interactions with tobacco smoking: an update" Clin Pharmacokinet, 36, p. 425-38
tenofovir food
Applies to: efavirenz / lamivudine / tenofovir disoproxil
Food enhances the oral absorption and bioavailability of tenofovir, the active entity of tenofovir disoproxil fumarate. According to the product labeling, administration of the drug following a high-fat meal increased the mean peak plasma concentration (Cmax) and area under the concentration-time curve (AUC) of tenofovir by approximately 14% and 40%, respectively, compared to administration in the fasting state. However, administration with a light meal did not significantly affect the pharmacokinetics of tenofovir compared to administration in the fasting state. Food delays the time to reach tenofovir Cmax by approximately 1 hour. Tenofovir disoproxil fumarate may be administered without regard to meals.
References (1)
- (2001) "Product Information. Viread (tenofovir)." Gilead Sciences
Therapeutic duplication warnings
No duplication warnings were found for your selected drugs.
Therapeutic duplication warnings are only returned when drugs within the same group exceed the recommended therapeutic duplication maximum.
Drug Interaction Classification
| Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit. | |
| Moderately clinically significant. Usually avoid combinations; use it only under special circumstances. | |
| 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. | |
| No interaction information available. |
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