Drug Interactions between efavirenz / emtricitabine / tenofovir and Omnipaque 180 Redi-Unit

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.

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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.

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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.

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