Desipramine

Serum or plasma

1 mL

0.3 mL

Red-top tube, lavender-top (EDTA) tube, or green-top (heparin) tube. Do not use a gel-barrier tube. The use of gel-barrier tubes is not recommended due to slow absorption of the drug by the gel. Depending on the specimen volume and storage time, the decrease in drug level due to absorption may be clinically significant.

Desipramine, a metabolite of imipramine, has actions and uses similar to those of the parent compound and is as effective as imipramine in the treatment of mood disorders. Untoward effects are similar to those produced by imipramine, but anticholinergic and sedative actions are less pronounced. Thus, desipramine may be especially useful in patients who are particularly sensitive to these effects (eg, the elderly).

This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.

Liquid chromatography/tandem mass spectrometry (LC/MS-MS)

When administered alone: therapeutic: 150−250 ng/mL

All the tricyclic antidepressants have significant drug interactions. Being potent inducers of hepatic drug-metabolizing enzymes, particularly CYP3A4, CYP1A2, and CYP2C9, the antiepileptic drugs, carbamazepine, phenytoin, phenobarbital, and primidone, stimulate the oxidative transformation of concurrently prescribed antidepressants.¹ This results in decreased drug levels of the antidepressant. With desipramine, it has been noted that up to a 36-fold difference in plasma levels can be observed in patients receiving the same dose.² One study compared desipramine monotherapy with carbamazepine co-administered.³ The monotherapy group exhibited a 4.6-fold increase in plasma levels and a 62% longer half-life as compared to the co-medicated group. To a lesser extent, co-administration of oxcarbazepine, topiramate, and felbamate can also result in decreased antidepressant levels. Other tricyclic antidepressant drug interactions: hydrocortisone, methylphenidate, and phenothiazines increase tricyclic levels; tricyclics impair the antihypertensive effectiveness of clonidine and guanethidine; tricyclics and alcohol produce additive sedative effects, tricyclics and antiparkinsonism agents have potent anticholinergic side effects, and tricyclics and MAO inhibitors should not be co-administered because of the potential for antihypertensive and CNS crises.

Tricyclics should be avoided in pregnant and lactating women because these drugs have not been established as safe. Geriatric patients are especially prone to postural hypotension, urinary retention, and sedation.⁴ In general, it has been reported that, “Therapeutic drug monitoring of antidepressants allows us to take into account the influence of factors such as co-medications, diet, smoking habit, impaired organ function, and compliance. Therapeutic drug monitoring and genotyping are thus complementary, and their combined use contributes to improve pharmacotherapy with antidepressants and other drugs.”⁵