Tobacco Consumption Concerns With the Use of CYP1A2 Metabolized Antidepressants
A 47-year-old Caucasian woman was referred to our psychiatric department for a current, untreated severe major depressive episode without psychotic symptoms (score on the 17-item Hamilton Depressive Rating Scale (HAM-D), 28) in a context of major depressive disorder. She had severe tobacco dependence (30 cigarettes/day for 30 years). No other disorder was detected clinically. Results of blood serum screening (including thyroid hormones, glycemia, and calcemia) and cerebral contrast MRI were normal.She was treated with 125 mg/day of imipramine (in addition to oxazepam and zopiclone). Concomitantly, she reduced her smoking spontaneously while in the hospital, a smoke-free facility, to five cigarettes/day. At discharge, she had a full response and remission with 125 mg/day of imipramine (HAM-D score, 6). Imipramine and desipramine (its predominant metabolite) trough plasma concentrations (104 ng/mL and 238 ng/mL, respectively) were within the therapeutic range (180–350 ng/mL for imipramine and desipramine together).Four weeks later, despite good compliance, she relapsed (HAM-D score, 22), requiring an increase in her imipramine dosage to 175 mg/day. But with this dosage, her trough plasma concentrations were lower than expected (imipramine, 50 ng/mL; desipramine, 96 ng/mL).No decrease in compliance and no recent co-medication could explain such low levels except a tremendous increase in the patient’s smoking, which returned to 30 cigarettes/day after discharge.Because tobacco smoking is a CYP1A2 inducer and imipramine is mainly metabolized by CYP1A2, pharmacogenetic tests were performed (CYP1A2*1F, CYP2D6*3,*4,*5,*6,x2N, CYP2C19*17) showing that the patient was a carrier of a genotype heterozygous for the CYP1A2*1F allele (AC) that is associated with increased CYP1A2 activity in smokers.
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