Drugs online research references
Psychiatr Serv. 1997 Jun;48(6):835-7.
Psychiatrists' responses to failure of maintenance therapy with antidepressants.
Byrne S, Rothschild AJ.
McLean Hospital, Belmont, MA, USA.
Some patients being treated for recurrent major depression experience a return of depressive symptoms despite a constant maintenance dose of an antidepressant, a phenomenon known as breakthrough depression. A total of 145 psychiatrists who were members of the Massachusetts Psychiatric Society responded to a survey about intervention in hypothetical cases of breakthrough depression if the patient was taking either 20 mg of fluoxetine, 100 mg of sertraline, 100 mg of nortriptyline, or 40 mg of fluoxetine. For all drugs and dosages, the most popular choice was increasing the dosage, followed by augmenting with lithium or another antidepressant or changing to a different drug.
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unmc.edu
This retrospective chart review examines the impact of selective serotonin reuptake inhibitors on 20 patients with both depression and psychosis complicating dementia of the Alzheimer type (DAT) and other dementias. Fifteen of the 20 patients had moderate to marked improvement in depressive and psychotic symptoms. Eleven of 12 patients with DAT had moderate to marked improvement compared to only four of eight patients with dementia from other causes. The drugs were effective in diminishing or eliminating psychotic symptoms in six patients who had previously not responded to a trial of a neuroleptic. The selective serotonin reuptake inhibitors may have an important role to play in patients with DAT who have coexisting depression and psychosis. These drugs are very well tolerated and may have a place as first-line agents in non-emergent settings where a clinician might otherwise think of instituting a neuroleptic or as a second-line agent when a neuroleptic has proven ineffective.
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Br J Clin Pharmacol. 1997 Jun;43(6):619-26.
Venlafaxine: in vitro inhibition of CYP2D6 dependent imipramine and desipramine metabolism; comparative studies with selected SSRIs, and effects on human hepatic CYP3A4, CYP2C9 and CYP1A2.
Ball SE, Ahern D, Scatina J, Kao J.
Drug Safety and Metabolism, Wyeth-Ayerst Research, Princeton, NJ 08543-8000, USA.
AIMS: In order to anticipate drug-interactions of potential clinical significance the ability of the novel antidepressant, venlafaxine, to inhibit CYP2D6 dependent imipramine and desipramine 2-hydroxylation was investigated in human liver microsomes. The data obtained were compared with the selective serotonin re-uptake inhibitors, fluoxetine, sertraline, fluvoxamine and paroxetine. Venlafaxine's potential to inhibit several other major P450 s was also studied (CYP3A4, CYP2D6, CYP1A2). METHODS: Ki values for venlafaxine, paroxetine, fluoxetine, fluvoxamine and sertraline as inhibitors of imipramine and desipramine 2-hydroxylation were determined from Dixon plots of control and inhibited rate data in human hepatic microsomal incubations. The inhibitory effect of imipramine and desipramine on liver microsomal CYP2D6 dependent venlafaxine O-demethylation was determined similarly. Venlafaxine's IC50 values for CYP3A4, CYP1A2 CYP2C9 were determined based on inhibition of probe substrate activities (testosterone 6 beta-hydroxylation, ethoxyresorufin O-dealkylase and tolbutamide 4-hydroxylation, respectively). RESULTS: Fluoxetine, paroxetine, and fluvoxamine were potent inhibitors of imipramine 2-hydroxylase activity (Ki values of 1.6 +/- 0.8, 3.2 +/- 0.8 and 8.0 +/- 4.3 microM, respectively; mean +/- s.d., n = 3), while sertraline was less inhibitory (Ki of 24.7 +/- 8.9 microM). Fluoxetine also markedly inhibited desipramine 2-hydroxylation with a Ki of 1.3 +/- 0.5 microM. Venlafaxine was less potent an inhibitor of imipramine 2-hydroxylation (Ki of 41.0 +/- 9.5 microM) than the SSRIs that were studied. Imipramine and desipramine gave marked inhibition of CYP2D6 dependent venlafaxine O-demethylase activity (Ki values of 3.9 +/- 1.7 and 1.7 +/- 0.9 microM, respectively). Venlafaxine did not inhibit ethoxyresorufin O-dealkylase (CYP1A2), tolbutamide 4-hydroxylase (CYP2C9) or testosterone 6 beta-hydroxylase (CYP3A4) activities at concentrations of up to 1 mM. CONCLUSIONS: It is concluded that venlafaxine has a low potential to inhibit the metabolism of substrates for CYP2D6 such as imipramine and desipramine compared with several of the most widely used SSRIs, as well as the metabolism of substrates for several of the other major human hepatic P450s.
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