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Results
The sample included 7 women and 1 man (mean age 32.6 years, SD10.3).
Seven patients identified themselves as white, and one as black.
The patients did not present any comorbid DSM-IV Axis I disorders.
Six patients attended all 6 visits. Four patients displayed a total
remission of the binge eating episodes, and 2 had a marked reduction
in binge frequency. Two patients discontinued the trial: 1 due to
diurnal somnolence at visit 2 and 1 because of lack of efficacy
at visit 3. Most of the adverse events reported were transient in
nature; the most common were paresthesias (4 patients), fatigue
(2 patients), somnolence (2 patients), psychomotor slowing (1 patient),
impaired concentration (1 patient), and nausea (1 patient).
All patients who completed the trial showed reduced binge eating
at the end of treatment. The mean DBE fell significantly from 4.3
(SD 1.7) at baseline to 1.1 (SD 2.4) at the end of the study (t
= 4.4, df 7, P = 0.03), as did the BES scores, which fell
from 31.8 (SD 7.5) to 15.3 (SD 9.2) (t = 4.2, df =
7, P = 0.04). There was a statistically significant weight
loss (mean 4.1 kg) (t = 2.4, df = 7, P = 0.04).
The depressive symptoms also had a significant change, as shown
by the decrease of BDI scores from 25.3 (SD 7.5) to 15.8 (SD 5.7)
(t = 3.0, df = 7, P = 0.02).
Discussion
In this open-label study of topiramate use in obese patients with
BED and no psychiatric comorbidities, 6 out of 8 patients improved.
The treatment with topiramate was well tolerated, and all adverse
events reported were benign and transient in nature. Thus, topiramate
appears to be an effective agent for the treatment of patients in
this category.
Although topiramate’s mechanism of action in BED remains unknown,
there are some putative explanations for our results. For example,
Shapira and others (8) were uncertain whether topiramate could act
on BED in the absence of mood disorder. Even though all patients
did not present a DSM-IV Axis I comorbid diagnosis, as a group they
displayed mean BDI scores above 17, which suggests clinically significant
depressive symptoms (12). Thus, one could argue that the observed
binge eating reduction could be related to a topiramate antidepressant
property (13). However, depressive symptoms appear to be secondary
to the disturbed eating and a state-dependent feature that in many
cases resolves with the remission of binge eating (14). In our view,
this observation weakens the hypothesis that an antidepressant effect
reduces binge eating in this sample. One possibility is that the
response to topiramate may be due to a direct effect on the eating-disturbed
psychopathology, rather than an indirect effect on other psychiatric
symptoms, such as depression.
A comorbid impulsive personality was also suggested as having an
important role in triggering binge eating episodes (15). As such,
another possible mechanism of action is one wherein topiramate acts
like other mood stabilizers to control impulsiveness and thereby
reduces the urges to eat.
Finally, the patients showed a significant weight reduction during
the study. Thus, an alternative mechanism underlying the observed
binge eating remission could be the action of topiramate influencing
weight control.
This study has several limitations. First, this is an open-label
trial with very few patients. Additionally, we cannot reject the
hypothesis that the favourable response to topiramate was due to
a placebo effect: it is well known that patients with BED have a
high placebo response. Stunkard and others have described a 44%
placebo response rate in a run-in period of a d-fenfluramine trial
(16). Thus, only limited conclusions can be drawn from this study,
and our clinical observations need to be confirmed in randomized
double-blind placebo-controlled trials.
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Manuscript received July 2001, revised, and
accepted February 2002.
Previously presented as a poster at the American Psychiatric Association
2001 Annual Meeting; 2001; New Orleans (LA).
1 Research Coordinator, Obesity and Eating Disorders Group of the
Institute of Psychiatry of the Federal University of Rio de Janeiro
(IPUB/UFRJ) and State Institute of Diabetes and Endocrinology of
Rio de Janeiro (IEDE), Rio de Janeiro, Brazil.
2 Staff Psychiatrist, Obesity and Eating Disorders Group of the
Institute of Psychiatry of the Federal University of Rio de Janeiro
(IPUB/UFRJ) and State Institute of Diabetes and Endocrinology of
Rio de Janeiro (IEDE), Rio de Janeiro, Brazil.
3 Resident in Psychiatry, Institute of Psychiatry of the Federal
University of Rio de Janeiro (IPUB/UFRJ), Rio de Janeiro, Brazil.
4 Professor of Psychiatry, Institute of Psychiatry of the Federal
University of Rio de Janeiro (IPUB/UFRJ), Rio de Janeiro, Brazil.
5 Professor of Endocrinology, Pontifical Catholic University of
Rio de Janeiro, Rio de Janeiro, Brazil.
Address for correspondence: Dr JC Appolinario, Rua Visconde de
Pirajá, 550/2002 Ipanema, Rio de Janeiro, Brazil 22410-001
e-mail: appolinario@biohard.com.br
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