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A fatal pancytopenia occurred in a patient with an history of depression with hypomanic rebounds, admitted for a manic episode and treated with levomepromazine, diazepam and lithium carbonate.
Levomepromazine (previously known as methotrimeprazine), despite virtually no high quality scientific data to support its use, has become a very popular antiemetic for use in patients with advanced cancer. This article considers the reasons for this.
The neuroleptic drug levomepromazine (1, previously known as methotrimeprazine) is photolabile under UV-A and UV-B light in aerobic conditions. Irradiation of a methanol solution of this drug produces one photoproduct, resulting from the oxidation of 1 to its sulfoxide parent. It is demonstrated that photodegradation occurs via type II mechanism involving irreversible trapping of self-photogenerated singlet molecular oxygen. 1 shows a photohemolytic effect on human erythrocytes and photoinducers lipid peroxidation.
OBJECTIVE: We compared the effect of levomepromazine (LMP) with chlorpromazine (CPZ) in treatment-resistant schizophrenia (TRS). METHODS: We carried out a double-blind, parallel group study (n = 19/arm) with balanced randomization in blocks of 4 and stratification by sex. Subjects entered a 30-week trial, of which phases I-III were open: phase I (wk 0-6) baseline; phase II (wk 7-9) stepwise transition to haloperidol (HAL), 30 mg/d, plus benztropine (BT), 4 mg/d; phase III (wk 10-15) HAL, 40-60 mg/d, plus BT, 4-6 mg/d; phase IV (wk 16-20) stepwise transition to LMP or CPZ (500 mg/d) following randomization; phase V (wk 21-28) stepwise increase of LMP or CPZ (600-1000 mg/d, dose reduction permitted) to establish optimum dose; and phase VI (wk 29-30) optimized dose maintained. Criteria for TRS were based on those established by Kane et al in 1988. The criterion for a response to treatment was a reduction of 25% or more in total Brief Psychiatric Rating Scale score. RESULTS: Both LMP (p = 0.007) and CPZ (p = 0.030) improved TRS relative to baseline. Although there was no significant difference between the 2 groups in treatment response at study end point, hierarchical linear modelling of longitudinal outcome revealed a significant (p = 0.006) advantage of LMP over CPZ for the BPRS total score. Ten of 19 participants on LMP and 8 of 19 on CPZ met the criterion for treatment response, and 9 of the 18 responders did so on 200-700 mg/d phenothiazine. The mean dose of responders was 710 (standard deviation [SD] 265) mg/d (LMP) and 722 (SD 272) mg/d (CPZ). Akathisia was associated with a nonresponse to phenothiazines (p = 0.010). BPRS scores increased significantly on HAL (p = 0.006). Two of 19 participants on LMP and 5 of 19 on CPZ withdrew early from the study. CONCLUSION: LMP and CPZ may be useful in the management of TRS. A modest advantage of LMP compared with CPZ was seen in longitudinal analysis. High doses of neuroleptics may contribute to TRS; reduction of neuroleptics to modest or moderate doses should be considered before categorizing a patient as treatment resistant.
In contrast to imipramine, chlorprothixene (CPX) and levomepromazine (LMZ) given chronically did not affect clonidine-induced hypothermia and depression of noradrenaline synthesis rate, while similarly to imipramine and citalopram depressed the density of cortical 3H-clonidine binding sites and increased their affinity. Two week treatment with the antidepressants did not affect the parameters of 3H-dihydroalprenolol binding sites, while spiroperidol administration increased their density, without changing KD values. The data suggest that changes in alpha 2 adrenoceptor population parameters may be a general characteristics of antidepressant treatment, but not necessarily followed by changes in clonidine effects.
Nonenzymatic FeCl2-catalyzed oxidation of methotrimeprazine (levomepromazine) yielded three ring-hydroxylated derivatives that had different GC retention times but almost identical mass spectra. Two of these, together with O-desmethylmethotrimeprazine, were identified by combined GC/MS in enzymatically hydrolyzed urine from four psychiatric patients, who had been treated with oral doses of methotrimeprazine. The mass chromatograms indicated that the three metabolites were formed in similar amounts. Small amounts of three other metabolites were also found in the urine after enzymatic hydrolysis. These were identified as O-desmethyl-N-monodesmethylmethotrimeprazine and two monohydroxy-N-monodesmethyl derivatives that had different GC retention times. None of those metabolites were found in unconjugated form in the urine.
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