Depression Symptoms Treatment

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The most common drug interaction with antidepressants is their influence on the metabolism of other drugs. Antidepressants are metabolized through catabolic enzymes located in a variety of places, but primarily in the smooth endoplasmic reticulum of hepatocytes: the cytochrome P450 (CYP) enzymes. Many other drugs are also metabolized through similar pathways: it is estimated that about half of all drugs prescribed depend on CYP for their metabolism.

Of these enzymes, most drugs are metabolized by the enzymes CYP3A4 (50%) and CYP2D6 (20%). Other clinically important CYP enzymes include CYP2C9, and CYP2C19 and CYP1A2, the latter which is found in the brain and may affect CNS distribution of antidepressants. A list of the enzymes and some drugs commonly affected by them is found in Table: Cytochrome P-450 Isoenzymes and Common Medications Inhibiting or Inducing Them.

Table: Cytochrome P-450 Isoenzymes and Common Medications Inhibiting or Inducing Them

Tricyclic Antidepressants

As with any combination therapy, the side effects described previously can be additive with other similar drugs. Most problematical are the antichohnergic effects of the tricyclic antidepressants (TCAs). Such cholinergic blockade is a property shared by many other medications, including numerous over-the-counter preparations. The general sedative properties of these medications can also augment any soporific. The slowing of cardiac conduction can also potentiate other medications that produce similar effects, such as type IA antiarrhythmics and antichohnergic medications. Adrenergic receptor blockade can worsen the orthostatic hypotension caused by other medications, including vasodilators and low-potency antipsychotic medications.

Pharmacokinetic Effects

Absorption of tricyclic antidepressants (TCAs) can be inhibited by cholestyramine, which therefore must be given at different time intervals than the antidepressants. Specific substances reported to increase TCA levels include fluoxetine, antipsychotic medications, methylphenidate, and cimetidine. Methylphenidate has been combined with desipramine to treat attention deficits and depression in children. The combination therapy had a higher incidence of ECG changes (particularly higher ventricular rates), nausea, dry mouth, and tremor. Enzyme “inducers” that can lower tricyclic agent levels include phenobarbital and carbamazepine. The nicotine from cigarettes can also induce enzyme activity.

Guanethidine is contraindicated with TCAs, as it relies on neuronal reuptake for its antihypertensive effect. Clonidine, a presynaptic alpha-₂-receptor noradrenergic agonist, is also contraindicated, as it works in an antithetical fashion to tricyclic medications.

Monoamine Oxidase Inhibitors

As with the dietary proscriptions, any medication that increases tyramine can precipitate a hypertensive crisis; such medications include numerous over-the-counter preparations for coughs, colds, and allergies. The same rule applies to sympathomimetic drugs (such as epinephrine and amphetamines or cocaine) and dopaminergic drugs such as anti-parkinsonian medications.

The combination of monoamine oxidase inhibitors (MAOIs) and narcotics, particularly meperidine, may cause a fatal interaction. The reaction can vary from symptoms of agitation and hyperpyrexia to cardiovascular collapse, coma, and death. A similar reaction has also been reported when propoxyphene, diphenoxylate hydrochloride, and atropine are used with MAOIs. The combination of MAOIs with agents such as selective serotonin reuptake inhibitors (SSRIs) can cause the serotonin syndrome.

Serotonin Reuptake Inhibitors

Serotonin reuptake inhibitors are potent inhibitors of the CYP2D6 pathway and can slow the metabolism of any drug that is also metabolized by that pathway. Such drugs include tricyclic antidepressants (TCAs), carbamazepine, phenothiazines, butyrophenones, opiates, diazepam, alprazolam, verapamil, diltiazem, cimetidine, and bupropion. Paroxetine appears to be the most potent inhibitor of this metabolic pathway, with fluoxetine also showing high potency. Sertraline is a somewhat less potent inhibitor. These pharmacokinetic interactions are best managed with dosage adjustment. Fluoxetine, for example, can be safely used with tricyclic medications if TCA blood levels and, possibly, electrocardiograms are monitored. Although it binds more weakly to the CYP2D6, sertraline has also been reported to raise the level of TCAs significantly. In the case of bupropion, this relative increase in the blood level can increase the risk for seizures.

Particular caution should be used when a patient using multiple medications starts a serotonin reuptake inhibitor, as the interactions with other drugs can cause dangerous increases in levels. For example, in the cardiac patient, levels of warfarin should be monitored as fluoxetine has been reported to raise these levels. Several case reports exist of increased antiarrhythmic levels after introduction of fluoxetine, which resulted in potential serious bradyarrhythmias.

Fluoxetine has also been reported to raise lithium levels. The mechanism for this is not clear, as lithium is primarily excreted through the kidneys.

Other Second-Generation Antidepressants

Few reports exist of interactions with other drugs and trazodone, although trazodone may increase levels of digoxin, phenytoin, and possibly warfarin. Bupropion causes few drug-drug interactions. The main interactions reported have occurred when bupropion is combined with another dopaminergic agent. For example, when bupropion was used with l-dopa, the combination caused excitement, restlessness, nausea, vomiting, and tremor.

Third-Generation Antidepressants

Venlafaxine does not substantially inhibit the CYP enzyme, and is not highly protein-bound, thus it tends to have few clinically significant drug-drug interactions. Duloxetine is metabolized by 1A2 and 2D6 P450 isoenzymes, and may increase plasma levels of other antidepressants, antipsychotics, and Type 1C antiarrhythmics, such as flecainide (Tambocor). Nefazodone is highly protein-bound, and has several active metabolites. It is also a strong inhibitor of CYP3A4, and affects other drugs also metabolized by that pathway; however, it has little affinity for the CYP2D6 enzyme. Mirtazapine is highly protein-bound as well, but appears to only weakly affect the cytochrome enzymes.