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Does weight change following recovery from depression? Evidence from a randomized, placebo-controlled trial with fluoxetine
Pl Affective disorders and antidepressants
OB control groups. The higher dose of flesinoxan significantly reduced this deficit. Eltoprazine again, was unable to alter this hyperactive response. In addition both doses of flesinoxan significantly attenuated the I-OH-DPAT-induced hypothermic response whereas eltoprazine had little effect. From these studies it can be concluded that flesinoxan has potential antidepressant properties whereas eltoprazine appears to have little potential at the dose utilised. This further emphasises the role of the S-HT~Areceptor in the pathogenesis of depression. Eltoprazine has been proposed to have anti-agressive properties (Olivier et al. 1994) and these studies suggest that different S-HT receptor subtypes might underlie the antidepressive and antiaggressive action of psychotropic drugs. The authors wish to thank Solvay-Duphar (Weesp, Netherlands) for the gift of flesinoxan and eltoprazine and for financial assistance given for this study. References
[I] Olivxer, B., Mos, .I.,Raghoebar, M., de Koning, P. and Mak, M. (1994) Serenics. Proe. Drue Res. 42. 167-308. [2] SchTpper,y., IhIp, ti.T.M., Berkelmans, B., Mos, J., van der Heijden, J.A.M., Olivier, B. (1991) Preclinical pharmacology of flesinoxan: a potential aoxiolytic and antidepressant drug. Human Psychopharmacol., 1991, (supl. 6), 53-61
[p.1.103)
Chronic pindolol treatment disorders
and major affective
J. Tiihonen, F?R&sanen, H. Hakko. Department of Forensic Psychiatry. University of Kuopio, Niuoanniemi Hospital, Psychiatry, University of Oulu, Oulu, Finland
Kuopio; Department
of
Backgroud: It has been suggested that blockade of 5-HT autoreceptor
with pindolol during concomitant treatment with selective serotonin re-uptake inhibitors (SSRIs) would result in a rapid and augmented antidepressant effect, but it has also been argued that the possible augmenting effect of pindolol is due to the P-blocking properties of this drug. Results from the first human studies have also been controversial. Methods: National computer-based central register was used to study the cumulative incidence of the use of P-blockers and antidepressant drugs, as well as the point prevalence of disability pensions due to major affective disorders (296, DSM-III-R; F30-F34, ICD-10) in the end of a three-year follow-up period. Results: Our results from a very large database (total N = 30485) indicate that the use of pindolol is associated with a marked reduction (from 29% to 52%) in the prevalence of disability pensions due to major affective disorders when compared with the use of other p-blockers although the effect of age was controlled. The use of pindolol was associated with slightly lower rate of antidepressant use when compared with other @-blockers. Conclusions: The results suggest that long-term therapy with pindo101treatment augments the pharmacological effect of antidepressant drugs (especially SSRIs) among patients with major affective disorders. The finding that patients receiving pindolol have lower prevalence of disability pensions due to major affective disorders indicates that the prevalence of severe treatment resistant major affective disorders could be decreased markedly by using pindolol as the first choice P-blocker in the treatment of cardiovascular diseases whenever possible among those patients who have experienced at least one depressive episode and are receiving antidepressant treatment.
[m]
Does weight change following recovery from depression? kvkknce from a randomized, placebo-controlled trial with fluoxetine
J. Amsterdam’, I>. Michelson* *, Y. Kim’, K. Sundell*. ‘University of Pennsylvania Medical Center, Philadelphia, PA: “Eli Lilly and Company, Indianapolis. IN. USA Introduction: Fluoxetine is an effective, well-tolerated antidepressant medication associated with fewer adverse events than older agents such
s171
as tricyclic antidepressants. Although acute fluoxetine therapy is not associated with clinically significant weight gain, weight change over longer treatment periods has not been well-characterized. Methods: We examined weight change during continuation therapy with fluoxetine or placebo by analyzing data from a multi-site depression relapse prevention study. Patients whose depressive symptoms remitted after 12 weeks of treatment with open-label fluoxetine 20 mgiday were randomized to either continued fluoxetine 20 mg/day or placebo for 6 or 9 months. Patients were included in the analysis if they completed at least 26 weeks of therapy following randomization. Change in weight was calculated from study entry to the time of randomization, and from the time of randomization to 26 weeks following randomization. The number of patients with a 27% increase in weight from randomization to 26 weeks later was determined for the fluoxetine and placebo groups. Results: One-hundred patients completed at least 26 weeks of treatment following randomization (82 fluoxetine, 18 placebo) and bad weight data available. The treatment groups were similar for gender, mean Hamilton depression rating scale scores prior to and following acute treatment, and mean self-reported weight loss prior to treatment. Although the fluoxetine treatment group had higher baseline mean Body Mass Index (BMI) and weight than the placebo treatment group, both groups showed minimal change in weight during the 12 weeks of acute fluoxetine treatment and there was no correlation between baseline BMI and change in weight. After 26 weeks of continuation treatment, both groups showed modest weight gain (numerically but not statistically significantly greater in the placebo group); the percentage change in weight and number of patients gaining more than 7% of initial body weight were similar in both groups. Reanalysis of the data considering only patients who received at least 9 months of continuation therapy (fluoxetine N = 65, placebo N = 15) yielded similar results. Discussion: Patients randomized to fluoxetine 20 mg/day or placebo following 12 weeks of successful acute fluoxetine therapy experienced similar changes in weight over a 26-week period. Although patients appear predisposed to modest weight gain during the 6 to 9 months following successful acute treatment of depression, this analysis suggests that the weight gain is not related to long-term fluoxetine treatment. Also, this study does not provide evidence that fluoxetine treatment increases the risk for extreme weight gain, as the number of patients with a 27% increase in weight was similar in both placebo and fluoxetine treatment groups.
Ip.1.1051
A comparison of symptoms following treatment interruption: Evidence from a randomized, double-blind trial with fluoxetlne, sertrallne, and paroxetine
M. Fava’, J.F. Rosenbaum’S.L. , Hoo$,
W. Krebs*, J.A. Dillon*.
The Fluoxetine Collaboratioe Study Group; I Massachusetts General Hospital, Boston, Massachusetts; ‘Eli Lil[v and Company, Indianapolis, Indiana. USA Introduction: Evidence suggests that shorter-acting SSRls compared with fluoxetine are often associated with increased adverse events and dysphoria during brief treatment interruptions. Previous studies are limited by lack of prospective patient randomization; only one was conducted under controlled conditions. We report a prospective, randomized, double-blind study assessing the effects of brief SSRI treatment interruption following successful initial treatment of major depression. Methods: Drug-free outpatients (N = 284) with major depression were randomized under double-blind conditions to receive fluoxetine (initial dose: 20 mg/day; maximum dose: 60 mgiday), sertraline (initial dose: 50 mg/day; maximum dose: 200 mg/day), or paroxetine (initial dose: 20 mg/day; maximum dose: 60 mg/day). Patients who responded following 4-10 weeks of acute treatment (N = 213: fluoxetine, n = 67; sertraline, n = 75; paroxetine, n = 71) entered into a 5-month continuation phase. During this phase, treatment was interrupted for 4- to 6&y periods under double-blind conditions. Efficacy measures included the HAMD28 (primary), HAMD-17, CGI-Severity, CGI- and PGI-Improvement, Symptom Questionnaire, and the HAMD-28 subscales. Adverse event
OB control groups. The higher dose of flesinoxan significantly reduced this deficit. Eltoprazine again, was unable to alter this hyperactive response. In addition both doses of flesinoxan significantly attenuated the I-OH-DPAT-induced hypothermic response whereas eltoprazine had little effect. From these studies it can be concluded that flesinoxan has potential antidepressant properties whereas eltoprazine appears to have little potential at the dose utilised. This further emphasises the role of the S-HT~Areceptor in the pathogenesis of depression. Eltoprazine has been proposed to have anti-agressive properties (Olivier et al. 1994) and these studies suggest that different S-HT receptor subtypes might underlie the antidepressive and antiaggressive action of psychotropic drugs. The authors wish to thank Solvay-Duphar (Weesp, Netherlands) for the gift of flesinoxan and eltoprazine and for financial assistance given for this study. References
[I] Olivxer, B., Mos, .I.,Raghoebar, M., de Koning, P. and Mak, M. (1994) Serenics. Proe. Drue Res. 42. 167-308. [2] SchTpper,y., IhIp, ti.T.M., Berkelmans, B., Mos, J., van der Heijden, J.A.M., Olivier, B. (1991) Preclinical pharmacology of flesinoxan: a potential aoxiolytic and antidepressant drug. Human Psychopharmacol., 1991, (supl. 6), 53-61
[p.1.103)
Chronic pindolol treatment disorders
and major affective
J. Tiihonen, F?R&sanen, H. Hakko. Department of Forensic Psychiatry. University of Kuopio, Niuoanniemi Hospital, Psychiatry, University of Oulu, Oulu, Finland
Kuopio; Department
of
Backgroud: It has been suggested that blockade of 5-HT autoreceptor
with pindolol during concomitant treatment with selective serotonin re-uptake inhibitors (SSRIs) would result in a rapid and augmented antidepressant effect, but it has also been argued that the possible augmenting effect of pindolol is due to the P-blocking properties of this drug. Results from the first human studies have also been controversial. Methods: National computer-based central register was used to study the cumulative incidence of the use of P-blockers and antidepressant drugs, as well as the point prevalence of disability pensions due to major affective disorders (296, DSM-III-R; F30-F34, ICD-10) in the end of a three-year follow-up period. Results: Our results from a very large database (total N = 30485) indicate that the use of pindolol is associated with a marked reduction (from 29% to 52%) in the prevalence of disability pensions due to major affective disorders when compared with the use of other p-blockers although the effect of age was controlled. The use of pindolol was associated with slightly lower rate of antidepressant use when compared with other @-blockers. Conclusions: The results suggest that long-term therapy with pindo101treatment augments the pharmacological effect of antidepressant drugs (especially SSRIs) among patients with major affective disorders. The finding that patients receiving pindolol have lower prevalence of disability pensions due to major affective disorders indicates that the prevalence of severe treatment resistant major affective disorders could be decreased markedly by using pindolol as the first choice P-blocker in the treatment of cardiovascular diseases whenever possible among those patients who have experienced at least one depressive episode and are receiving antidepressant treatment.
[m]
Does weight change following recovery from depression? kvkknce from a randomized, placebo-controlled trial with fluoxetine
J. Amsterdam’, I>. Michelson* *, Y. Kim’, K. Sundell*. ‘University of Pennsylvania Medical Center, Philadelphia, PA: “Eli Lilly and Company, Indianapolis. IN. USA Introduction: Fluoxetine is an effective, well-tolerated antidepressant medication associated with fewer adverse events than older agents such
s171
as tricyclic antidepressants. Although acute fluoxetine therapy is not associated with clinically significant weight gain, weight change over longer treatment periods has not been well-characterized. Methods: We examined weight change during continuation therapy with fluoxetine or placebo by analyzing data from a multi-site depression relapse prevention study. Patients whose depressive symptoms remitted after 12 weeks of treatment with open-label fluoxetine 20 mgiday were randomized to either continued fluoxetine 20 mg/day or placebo for 6 or 9 months. Patients were included in the analysis if they completed at least 26 weeks of therapy following randomization. Change in weight was calculated from study entry to the time of randomization, and from the time of randomization to 26 weeks following randomization. The number of patients with a 27% increase in weight from randomization to 26 weeks later was determined for the fluoxetine and placebo groups. Results: One-hundred patients completed at least 26 weeks of treatment following randomization (82 fluoxetine, 18 placebo) and bad weight data available. The treatment groups were similar for gender, mean Hamilton depression rating scale scores prior to and following acute treatment, and mean self-reported weight loss prior to treatment. Although the fluoxetine treatment group had higher baseline mean Body Mass Index (BMI) and weight than the placebo treatment group, both groups showed minimal change in weight during the 12 weeks of acute fluoxetine treatment and there was no correlation between baseline BMI and change in weight. After 26 weeks of continuation treatment, both groups showed modest weight gain (numerically but not statistically significantly greater in the placebo group); the percentage change in weight and number of patients gaining more than 7% of initial body weight were similar in both groups. Reanalysis of the data considering only patients who received at least 9 months of continuation therapy (fluoxetine N = 65, placebo N = 15) yielded similar results. Discussion: Patients randomized to fluoxetine 20 mg/day or placebo following 12 weeks of successful acute fluoxetine therapy experienced similar changes in weight over a 26-week period. Although patients appear predisposed to modest weight gain during the 6 to 9 months following successful acute treatment of depression, this analysis suggests that the weight gain is not related to long-term fluoxetine treatment. Also, this study does not provide evidence that fluoxetine treatment increases the risk for extreme weight gain, as the number of patients with a 27% increase in weight was similar in both placebo and fluoxetine treatment groups.
Ip.1.1051
A comparison of symptoms following treatment interruption: Evidence from a randomized, double-blind trial with fluoxetlne, sertrallne, and paroxetine
M. Fava’, J.F. Rosenbaum’S.L. , Hoo$,
W. Krebs*, J.A. Dillon*.
The Fluoxetine Collaboratioe Study Group; I Massachusetts General Hospital, Boston, Massachusetts; ‘Eli Lil[v and Company, Indianapolis, Indiana. USA Introduction: Evidence suggests that shorter-acting SSRls compared with fluoxetine are often associated with increased adverse events and dysphoria during brief treatment interruptions. Previous studies are limited by lack of prospective patient randomization; only one was conducted under controlled conditions. We report a prospective, randomized, double-blind study assessing the effects of brief SSRI treatment interruption following successful initial treatment of major depression. Methods: Drug-free outpatients (N = 284) with major depression were randomized under double-blind conditions to receive fluoxetine (initial dose: 20 mg/day; maximum dose: 60 mgiday), sertraline (initial dose: 50 mg/day; maximum dose: 200 mg/day), or paroxetine (initial dose: 20 mg/day; maximum dose: 60 mg/day). Patients who responded following 4-10 weeks of acute treatment (N = 213: fluoxetine, n = 67; sertraline, n = 75; paroxetine, n = 71) entered into a 5-month continuation phase. During this phase, treatment was interrupted for 4- to 6&y periods under double-blind conditions. Efficacy measures included the HAMD28 (primary), HAMD-17, CGI-Severity, CGI- and PGI-Improvement, Symptom Questionnaire, and the HAMD-28 subscales. Adverse event