1484 SECTION XII I Pediatric Critical Care Pharmacology and Toxicology isoenzymes of the mixed function oxidases among the antineo plastic agents For example, the vinca alkaloids, etoposide, cyclo pho[.]
1484 S E C T I O N X I I I Pediatric Critical Care: Pharmacology and Toxicology isoenzymes of the mixed-function oxidases among the antineoplastic agents For example, the vinca alkaloids, etoposide, cyclophosphamide, ifosfamide, and many of the tyrosine kinase inhibitors (TKIs) are substrates for CYP3A4 Known inhibitors and inducers of CYP3A4 increase and decrease plasma levels, respectively Toxicities are more likely when these agents are administered with classic CYP3A4 inhibitors, such as the azole antifungals, macrolide antibiotics, and non-DHP CCBs The azole antifungals modulate the metabolism of cyclophosphamide, increasing overall parent drug and metabolite exposure Fluconazole increases cyclophosphamide area under the concentrationtime curve (AUC) by inhibiting CYP2C9 metabolism that leads to formation of the toxic metabolite acrolein—in effect, reducing potential ADEs.219 However, the inhibition of the CYP3A4 metabolic pathway by itraconazole increases formation of the precursor to the acrolein metabolite, increasing toxicity risk.220 In order to minimize neurotoxicity, it is advisable to avoid concomitant administration of vincristine and azole antifungals—such as itraconazole, voriconazole and posaconazole—by temporarily withholding azole therapy.221,222 If clinically indicated, antifungal therapy can be substituted with another noninteracting alternative, such as an echinocandin antifungal (micafungin or caspofungin) or amphotericin B formulation On the other hand, prophylaxis with fluconazole (a less potent inhibitor) in pediatric patients with acute leukemia did not increase vincristine toxicity, and coadministration appeared to be safe in a retrospective study.223 Antiepileptic drugs—such as carbamazepine, phenytoin, and phenobarbital—are known inducers of the cytochrome P450 enzyme system and may contribute to therapeutic failure with chemotherapeutic agents In one study of pediatric patients with high-grade glioma, the presence of enzyme-inducing anticonvulsants increased irinotecan clearance.224 Colony-stimulating factors are often used to treat the ensuing neutropenia that accompanies cancer chemotherapy Patients with lymphomas undergoing their first cycle of vincristine and receiving treatment with filgrastim or sargramostim are at risk for developing severe atypical neuropathy This neuropathy has been described as a severe, sharp, burning pain in the feet and appears to occur more commonly in lymphoma patients receiving this combination than in patients receiving vincristine alone.225 The mechanism of action of this interaction is unclear Methotrexate elimination occurs in the kidneys via filtration and active secretion The process of tubular secretion requires a carrier, which is a saturable process Competition among other drugs for secretion may reduce the clearance of methotrexate, which may lead to toxicity Concurrent administration of methotrexate with any of the penicillins has demonstrated this interaction.226–228 NSAIDs, aspirin, and other salicylates all increase the likelihood of methotrexate toxicity by this same mechanism.229–231 Inhibition of renal prostaglandin synthesis and the resultant reduction in renal perfusion also contribute to renal toxicities seen with methotrexate because methotrexate can persist in renal tissue for weeks.229–231 Proton pump inhibitors also create interactions with methotrexate owing to effects on renal elimination By inhibiting the transmembrane H1/K1-ATPase pump, they may decrease active secretion of methotrexate.232 The antineoplastic activity of methotrexate stems from its inhibition of dihydrofolate reductase, the enzyme that catalyzes the reduction of folic acid to tetrahydrofolic acid In turn, tetrahydrofolic acid serves as a building block for purine and DNA synthesis TMP/SMX may increase methotrexate toxicity owing to additive inhibition of dihydrofolate reductase Sulfamethoxazole can also TABLE Cytochrome P450 Profile of Tyrosine Kinase 124.7 Inhibitors Drug CYP metabolism Inhibits Induces Crizotinib CYP3A4 CYP3A4 CYP2B6, CYP2C8, CYP2C9, UGT Dasatinib CYP3A4 CYP3A4 — Erlotinib CYP3A4 CYP3A4, CYP2C8, CYP1A1 — Imatinib CYP3A4 CYP3A4, CYP2D6, CYP2C9 — Nilotinib CYP3A4 CYP2C9 CYP3A4 CYP2B6, CYP2C8, Sorafenib CYP3A4 CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A4 — increase methotrexate plasma concentration by displacing methotrexate from plasma protein-binding sites and reducing renal tubular elimination of methotrexate.233 The most common DDIs associated with TKIs relate to absorption and metabolism by P450 isozymes The oral absorption of some TKIs is pH dependent (e.g., dasatinib, crizotinib, and erlotinib) and significantly reduced when concurrently administered with an acid-reducing agent (H2-blocker, proton pump inhibitor, or antacids).210,231,234 However, if acid suppression is clinically necessary, there should be an administration time gap between TKIs and H2-blockers/antacids according to the instructions of the drug package insert.207 TKIs are substrates of CYP3A4 and therefore are subjected to metabolism alteration by an inducer or inhibitor In addition, some TKIs are also inhibitors and/ or inducers of certain P450 isozymes (Table 124.7).207 As a result, DDI assessment is strongly encouraged with TKI therapy and is crucial to the safety of patients receiving these agents with other therapies Key References Anderson JR, Nawarskas JJ Cardiovascular drug-drug interactions Cardiol Clin 2001;19(2):215-234 Bjornsson E Hepatotoxicity by drugs: the most common implicated agents Int J Mol Sci 2016;17;224 Cuker A, Arepally GM, Chong BH, et al American Society of Hematology 2018 guidelines for management of venous thromboembolism: heparin– induced thrombocytopenia Blood Adv 2018;2(22):3360-3392 Curtis BR Non-chemotherapy drug-induced neutropenia: key points to manage the challenges Hematology 2017;2017(1):187-193 Haidar CH, Jeha S Drug interactions in childhood cancer Lancet Oncol 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