Concurrent use with inhibitors or inducers of the cytochrome (CYP) P450 isoenzymes CYP1A2, CYP2D6, and/or CYP3A4 can result in altered concentrations of<unk> , as these are the main enzymes responsible for its metabolism. As examples, fluoxetine and paroxetine, inhibitors of these enzymes, are known to modestly increase<unk>  levels, while carbamazepine, an inducer, considerably decreases them. Liver impairment and moderate chronic kidney disease have been reported to decrease the oral clearance of<unk>  by about 30%; severe kidney disease decreases it by 50%.<unk>  in combination with an SSRI, , or TCA as an augmentation strategy is considered to be relatively safe and is often employed therapeutically, with a combination of venlafaxine and<unk> , sometimes referred to as "California rocket fuel". Several case reports document serotonin syndrome induced by the combination of<unk>  with other agents (olanzapine, quetiapine, tramadol and venlafaxine). According to information from the manufacturers,<unk>  should not be started within two weeks of any monoamine oxidase inhibitor (MAOI) usage; likewise, MAOIs should not be administered within two weeks of discontinuing<unk> . The addition of<unk>  to a monoamine oxidase inhibitor (MAOI), while potentially having typical or idiosyncratic (unique to the individual) reactions not herein described, does not appear to cause serotonin syndrome. This is in accordance with the fact that the 5-HT2A receptor is the predominant serotonin receptor thought to be involved in the pathophysiology of serotonin syndrome (with the 5-HT1A receptor seeming to be protective).<unk>  is a potent 5-HT2A receptor antagonist, and cyproheptadine, a medication that shares this property, mediates recovery from serotonin syndrome and is an antidote against it. There is a possible interaction that results in a hypertensive crisis when<unk>  is given to a patient that has already been on steady doses of clonidine. This involves a subtle consideration, when patients have been on chronic therapy with clonidine and suddenly stop the dosing, a rapid hypertensive rebound sometimes (20%) occurs from increased sympathetic outflow. Clonidine's blood pressure lowering effects are due to stimulation of presynaptic α2 autoreceptors in the CNS which suppress sympathetic outflow.<unk>  itself blocks these same α2 autoreceptors, so the effect of adding<unk>  to a patient stabilized on clonidine may precipitate withdrawal symptoms.
Mirtazapine
Sertraline
Citalopram
Fluparoxan
Quetiapine
Asenapine
Loxapine
Escitalopram