Antiretrovirals/escitalopram/ondansetron interaction
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Nausea, serotonergic toxicity and myoclonus: case report A 26-year-old man developed nausea following treatment with cobicistat/elvitegravir/emtricitabine/tenofovir alafenamide and elvitegravir/emtricitabine/tenofovir disoproxil fumarate/cobicistat for HIV infection. Additionally, he developed myoclonus secondary to serotonergic toxicity following the concomitant administration of ondansetron, escitalopram and elvitegravir/emtricitabine/tenofovir disoproxil fumarate/cobicistat for nausea, generalised anxiety disorder and HIV infection. The man, who had HIV infection, started receiving antiretroviral therapy with elvitegravir/emtricitabine/tenofovir disoproxil fumarate/cobicistat [Stribild] comprising of elvitegravir 150mg, emtricitabine 200mg, tenofovir disoproxil fumarate 300mg and cobicistat 150mg [route and frequency not stated]. Subsequently, he developed nausea secondary to the antiretroviral therapy. Therefore, the man started receiving oral ondansetron 40mg. He also started receiving escitalopram 5mg [route and frequency not stated] and alprazolam for generalised anxiety disorder. Within 4 months, escitalopram dose was gradually titrated to 15mg. He was receiving ondansetron upto five times a day. Subsequently, he started experiencing myoclonic jerks in his upper extremities 5–6 times a day. The frequency of jerks increased upto 12 times a day when he missed his alprazolam doses. He was diagnosed with serotonergic toxicity manifesting as myoclonus. Therefore, his ondansetron dose frequency was reduced to 3 times a day. Thereafter, the frequency of his myoclonic jerks improved to 1–2 episodes per day. Escitalopram dose was also decreased to 10mg. However, he continued to experience myoclonus once or twice a week. Due to nausea, elvitegravir/emtricitabine/tenofovir disoproxil fumarate/cobicistat was switched to cobicistat/elvitegravir/ emtricitabine/tenofovir alafenamide [Genvoya] comprising of cobicistat 150mg, elvitegravir 150mg, emtricitabine 200mg and tenofovir alafenamide 10mg [route and frequency not stated]. Thereafter, he continued to experience nausea; however at lesser extent. Subsequently, his myoclonus resolved. Three months later, escitalopram dose was increased again to 15mg. However, no recurrence of myoclonus was observed. A pharmacokinetic genetic testing showed that he was an intermediate metaboliser of cytochrome P450 2D6 (CYP2D6). The serotonergic toxicity was suspected to have developed secondary to escitalopram and ondansetron therapy. Additionally, it was considered that escitalopram, which is a weak CYP2D6 inhibitor, could have increased the plasma levels of ondansetron and further contributed in the development of serotonergic toxicity. Cobicistat could have also increased the level of ondansetron and escitalopram resulting in serotonergic toxicity [duration of treatments to reaction onsets not stated]. Author comment: "We hypothesize that the higher levels of escitalopram and ondansetron, and their serotonergic actions, increased the risk of serotonin toxicity in our patient." "
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