Posted by Kimba on April 7, 2001, at 10:46:56
I think the people on this board should start a movement to force Smith Kline Beecham to take responsibility for the withdrawal symptoms and weight gain caused by this drug so other people might not have to go through this.
If we all go to our doctors armed with a written statement about our side effects, and ask he or she to submit an Adverse Event Report, SKB will soon have a huge file of evidence that might inspire them to run (and publicize) a study of their own, but at the least will provide subpeonable material if anyone ever tries to sue them.
Here are some suggestions: Try to mention in your statement things that will defeat SKB's standard excuses about these symptoms. For instance, on the weight gain issue they'll claim it's not metabolic - that you are just less depressed and therefore eating more, or that you're craving carbohydrates. So don't forget to mention in your statement if you've taken measures to control your food intake and activity level. On the withdrawal issue, their excuse is that you are just having a relapse. Make sure you mention it if you didn't have the electric shocks, sloshy brain and nausea when you were depressed before you went on the drug.
I'm also going to include my name, address, and phone number on my statement so that if anyone ever wants to contact me as a witness or study participant, they can.
I suggest that we ask our doctors to write a letter of their own, attach my statement, and send me a carbon copy of his letter. I'll question him if I never get that Carbon Copy.
After that, don't be ashamed to tell friends about your experience and if they've had the same problem, have them take this action also. I told my co-worker that I share an office with, and lo and behold, she had another friend that went through the same thing.
Also, if your doctor doesn't believe you yet, at the bottom of this post I'll put in a bunch of references from psychiatric journals that document these as real symptoms. You can bring these to him/her also.
Does anyone else think this might work? It can't hurt and can only help. I'll post again next week after I meet with my doctor and let people know how it goes. I think it will work.
Weight gain references
----------------------
< 1 >
Unique Identifier
20380041
Authors
Fava M.
Institution
Depression Clinical and Research Program, Massachusetts General Hospital,
Boston 02114, USA.
Title
Weight gain and antidepressants. [Review]
[44 refs]
Source
Journal of Clinical Psychiatry. 61 Suppl 11:37-41, 2000.
Abstract
Weight gain during antidepressant treatment
can be either a sign of improvement in patients who have
weight loss as a symptom of depression or a residual symptom
in patients who overeat when depressed. However, significant
weight gain during the acute phase of
treatment or weight gain that continues
despite achieving full remission of depressive symptoms is likely to be a
side effect of antidepressant treatment. Weight
gain is a relatively common problem during both acute and
long-term treatment with antidepressants, and it is an important contributing
factor to noncompliance. This article will review the literature with regard
to the relative risk for weight gain of
antidepressants. It appears that tricyclic antidepressants (TCAs) and perhaps
monoamine oxidase inhibitors (MAOIs) may be more likely to cause
weight gain than the selective serotonin
reuptake inhibitors (SSRIs) or the newer antidepressants, with the exception
of mirtazapine, which may be placed between the SSRIs and the TCAs in terms
of relative risk for weight gain.
Paroxetine may be more likely to cause
weight gain than the other SSRIs during
long-term treatment, and bupropion and nefazodone may be less likely to cause
weight gain than the SSRIs in the long
term, although more studies are necessary to confirm these impressions.
[References: 44]< 2 >
Unique Identifier
20329689
Authors
Hinze-Selch D. Schuld A. Kraus T. Kuhn M. Uhr M. Haack M. Pollmacher T.
Institution
Max Planck Institute of Psychiatry, Munich, Germany.
Title
Effects of antidepressants on weight and on the plasma
levels of leptin, TNF-alpha and soluble TNF receptors: A longitudinal study
in patients treated with amitriptyline or paroxetine.
Source
Neuropsychopharmacology. 23(1):13-9, 2000 Jul.
Local Messages
Abstract
Leptin, tumor necrosis factor-alpha (TNF-alpha), and soluble TNF receptors
are involved in weight regulation. Antipsychotic agents,
such as clozapine, induce weight gain and
increase circulating levels of these cytokines. To assess whether
obesity-inducing antidepressants have a similar effect, we measured plasma
cytokine levels in depressive inpatients during the first six weeks of
treatment with tricyclic agents (amitriptyline or nortriptyline, n = 12),
with paroxetine (n = 10), or without medication (n = 14).
There was an increase in the body mass index at week 6 of treatment with the
tricyclics, which was preceded by a significant increase in soluble TNF
receptor p75 plasma levels. Circulating levels of leptin were not affected.
Paroxetine and drug-free treatment did not affect any of
these parameters. We conclude that weight
gain induced by psychotropic agents may occur without
increased circulating levels of leptin. However, activation of the TNF-alpha
system might be an early and sensitive marker of ensuing
weight gain.< 3 >
Unique Identifier
20260944
Authors
Harvey BH. Bouwer CD.
Institution
Department of Pharmacology, Potchefstroom University for Christian Higher
Education, South Africa.
Title
Neuropharmacology of paradoxic weight gain
with selective serotonin reuptake inhibitors. [Review] [87 refs]
Source
Clinical Neuropharmacology. 23(2):90-7, 2000 Mar-Apr.
Abstract
It has been suggested that weight gain
associated with tricyclic antidepressants (TCA) reflect actions on dopamine
(DA) and histamine receptors. However, a definitive cause is purely
assumptive given the nonselective pharmacology of these agents. The selective
serotonin reuptake inhibitors (SSRIs), as well as agents like dexfenfluramine
(DFF), have emphasized the pivotal role of serotonin (5HT) in reducing
carbohydrate (CHO) intake, and have provided a more selective tool with which
to study appetite regulation. It would be expected that all SSRIs should
exert a similar anorectic action. However, recent reports provide evidence to
the contrary. Despite their claimed selectivity, SSRIs still interact, either
directly or indirectly, with various critical neurotransmitter systems. In
addition, although the anorectic action of fluoxetine (FLX) is well
recognized, long-term follow-up studies in depressed patients and in obese
nondepressed patients reveal that its weight-reducing
effects are transient, even leading to a gain in body
weight. Similarly, paroxetine (PRX) and
citalopram (CTP) have also been associated with weight
gain. These latter observations are unexpected because PRX
and CTP are highly potent and selective SSRIs. A neuropharmacologic rationale
for the apparent paradoxic effects of SSRIs on appetite not a review of
neuronal regulation of appetite is presented in this article. As with the
regulation of feeding, paradoxic weight
gain observed with SSRIs appears to rest on the interaction
of 5HT with multiple mechanisms, with the extent of weight
gain observed being dependent on subtle, yet important
pharmacologic differences within the group. Finally, the neurobiology of
depressive illness itself, and of recovery from it, is a major contributing
factor to individual response to these drugs. [References: 87]< 4 >
Unique Identifier
99397846
Authors
Masand PS. Gupta S.
Institution
Psychiatric Consultation Service, Regional Psychopharmacology Consultation
and Training Program, SUNY Health Science Center at Syracuse, NY 13210, USA.
Title
Selective serotonin-reuptake inhibitors: an update. [Review] [185 refs]
Source
Harvard Review of Psychiatry. 7(2):69-84, 1999 Jul-Aug.
Abstract
Selective serotonin-reuptake inhibitors (SSRIs), including fluoxetine,
sertraline, paroxetine, fluvoxamine, and citalopram,
represent an important advance in the pharmacotherapy of mood and other
disorders. They are chemically unrelated to tricyclic, heterocyclic, and
other first-generation antidepressants. SSRIs are the treatment of choice for
many indications, including major depression, dysthymia, panic disorder,
obsessive-compulsive disorder, eating disorders, and premenstrual dysphoric
disorder, because of their efficacy, good side-effect profile, tolerability,
and safety in overdose, as well as patient compliance. A review of the
literature was conducted using Medline and the terms "SSRIs," "fluoxetine,"
"sertraline," "paroxetine," "fluvoxamine," and "citalopram."
Articles were limited to those published in English within the last 15 years.
The search revealed that indications for antidepressants include unipolar
depression, dysthymia, bipolar depression, treatment-resistant depression,
depression in the medically ill, panic disorder, obsessive-compulsive
disorder, eating disorders, social phobia, and premenstrual dysphoric
disorder. One SSRI, fluoxetine, has demonstrated safety in pregnancy. Side
effects of SSRIs include gastrointestinal disturbances, headache, sedation,
insomnia, activation, weight gain, impaired
memory, excessive perspiration, paresthesia, and sexual dysfunction.
[References: 185]< 5 >
Unique Identifier
98140246
Authors
Amsterdam JD. Garcia-Espana F. Goodman D. Hooper M. Hornig-Rohan M.
Institution
Department of Psychiatry, University of Pennsylvania Medical Center,
Philadelphia 19104, USA.
Title
Breast enlargement during chronic antidepressant therapy.
Source
Journal of Affective Disorders. 46(2):151-6, 1997 Nov.
Abstract
Recent reports of mammoplasia during selective serotonin re-uptake inhibitor
(SSRI) therapy suggested that this side effect may be more common than
previously reported. We examined 59 women receiving > or = 2 months treatment
with an SSRI or venlafaxine for changes in breast size in relation to
menopausal status, weight gain and duration
of drug therapy. Serum prolactin, estradiol and beta-hCG were also measured
before and during treatment in a subgroup of patients. Twenty-three out of 59
patients (39%) reported some degree of mammoplasia. Significantly more SSRI
vs. venlafaxine patients reported mammoplasia (p < 0.01). Eighty-four percent
with mammoplasia had weight gain vs. 30%
without mammoplasia (p < 0.001). The rate of mammoplasia was unrelated to
age, menopausal status or duration of treatment. Serum prolactin increased
during treatment in the paroxetine subgroup (p < 0.03). In
conclusion, antidepressant-induced mammoplasia may be more common than
previously expected.< 6 >
Unique Identifier
98105197
Authors
Masand PS. Gupta S.
Institution
Department of Psychiatry, SUNY Health Science Center at Syracuse 13210, USA.
Title
Dexfenfluramine for weight gain secondary
to psychotropics.
Source
Depression & Anxiety. 6(3):119-23, 1997.
Abstract
We describe the use of dexfenfluramine (Redux) in six patients with mood
disorders (bipolar disorder = 3; major depression = 3) who developed
significant weight gain as a result of
their psychotropics. All patients were females with an age range of 27-58
years. The duration of the trial varied from 3 to 20 weeks, with the
dexfenfluramine dosage being 15 mg twice daily. Weight loss
ranged from 2 to 23 pounds. None of the patients had any evidence of primary
pulmonary hypertension or serotonin syndrome, despite being on serotonergic
agents such as fluoxetine, paroxetine, and sertraline.< 7 >
Unique Identifier
97253220
Authors
Davis R. Whittington R. Bryson HM.
Institution
Adis International Limited, Auckland, New Zealand.
Title
Nefazodone. A review of its pharmacology and clinical efficacy in the
management of major depression [see comments]. [Review] [110 refs]
Comments
Comment in: Drugs 1997 Jul;54(1);186-7
Source
Drugs. 53(4):608-36, 1997 Apr.
Abstract
Nefazodone hydrochloride is a phenylpiperazine antidepressant with a
mechanism of action that is distinct from those of other currently available
drugs. It potently and selectively blocks postsynaptic serotonin
(5-hydroxytryptamine; 5-HT) 5-HT2A receptors and moderately inhibits
serotonin and noradrenaline (norepinephrine) reuptake. In short term clinical
trials of 6 or 8 weeks' duration, nefazodone produced clinical improvements
that were significantly greater than those with placebo and similar to those
achieved with imipramine, and the selective serotonin reuptake inhibitors
(SSRIs) fluoxetine, paroxetine and sertraline. The optimum
therapeutic dosage of nefazodone appears to be between 300 and 600 mg/day.
Limited long term data suggest that nefazodone is effective in preventing
relapse of depression in patients treated for up to 1 year. Analyses of
pooled clinical trial results indicate that nefazodone and imipramine
produces similar and significant improvements on anxiety- and
agitation-related rating scales compared with placebo in patients with major
depression. Short term tolerability data indicate that nefazodone has a lower
incidence of adverse anticholinergic, antihistaminergic and adrenergic
effects than imipramine. Compared with SSRIs, nefazodone causes fewer
activating symptoms, adverse gastrointestinal effects (nausea, diarrhoea,
anorexia) and adverse effects on sexual function, but is associated with more
dizziness, dry mouth, constipation, visual disturbances and confusion.
Available data also suggest that nefazodone is not associated with abnormal
weight gain, seizures, priapism or
significant sleep disruption, and appears to be relatively safe in
overdosage. Nefazodone inhibits the cytochrome P450 3A4 isoenzyme and thus
has the potential to interact with a number of drugs. Further long term and
comparative studies will provide a more accurate assessment of the relative
place of nefazodone in the management of major depression. Nonetheless,
available data suggest that nefazodone is a worthwhile treatment alternative
to tricyclic antidepressants and SSRIs in patients with major depression.
[References: 110]Withdrawal references
---------------------
1 >
Unique Identifier
20313455
Authors
Belloeuf L. Le Jeunne C. Hugues FC.
Institution
Service de Medecine Interne et de Therapeutique, Hopital Laennec, Paris.
Title
[Paroxetine withdrawal syndrome]. [French]
Source
Annales de Medecine Interne. 151 Suppl A:A52-3, 2000 Apr.
Abstract
Withdrawal syndrome after discontinuing serotonin re-uptake
inhibitors, especially paroxetine, is largely unknown to
most physicians. Variable incidence has been reported. Our aim was to stress
the main clinical features of this syndrome. Serotonin re-uptake inhibitor
withdrawal syndrome generally begins within 24 to 48 hours
after discontinuing the drug. Signs reach their maximum on day 5 and usually
resolve within 2 to 3 weeks. Withdrawal syndrome is more
common with short half-life drugs (paroxetine, fluvoxamine).
The intensity of the clinical signs depends on the daily dose and how long
the drug has been given. The main signs are dizziness, vertigo, headache,
nausea, and flu-like symptoms as well as anxiety, confusion, irritability,
excessive dreaming and insomnia. Risk factors usually stressed are poor
treatment compliance, previous withdrawal syndrome with
another drug, concomitant medication and alcohol consumption. The syndrome
can be prevented by tapering off the dose and patient education. When a
withdrawal syndrome is present, it is advisable to
reintroduce the drug then withdraw gradually.< 2 >
Unique Identifier
20234123
Authors
Nuss S. Kincaid CR.
Institution
Dept. of Medicine, Robert C. Byrd Health Sciences Center of West Virginia
University, Morgantown, USA.
Title
Serotonin discontinuation syndrome: does it really exist?.
Source
West Virginia Medical Journal. 96(2):405-7, 2000 Mar-Apr.
Abstract
Treatment guidelines for depression have typically focused on diagnosis, how
to initiate antidepressants, and duration of therapy, while very little is
discussed about discontinuing treatment. With the advent of the
serotonin-specific reuptake inhibitors (SSRIs), there is now growing evidence
to support a "discontinuation syndrome" associated with
withdrawal of therapy. This article describes two cases and
presents a review of the literature.< 3 >
Unique Identifier
99351458
Authors
Peeters FP. Zandbergen J.
Institution
Universiteit Maastricht, vakgroep Psychiatrie en Neuropsychologie.
Title
[Severe withdrawal symptoms with fever during
paroxetine tapering off (see comments)]. [Dutch]
Comments
Comment in: Ned Tijdschr Geneeskd 1999 Aug 28;143(35):1794-5; discussion
1795-6
Source
Nederlands Tijdschrift voor Geneeskunde. 143(27):1429-31, 1999 Jul 3.
Abstract
A 30-year-old man with depression who was treated with
paroxetine (Seroxat) developed severe
withdrawal symptoms when the medication was gradually
diminished and stopped: agitation, irritability, vertigo, lightheadedness and
fever up to 40 degrees C. The symptoms disappeared after the medication was
reintroduced but recurred after rediscontinuation. When the dosage was
diminished very gradually the symptoms were mild. The depression did not
recur. Such withdrawal symptoms are most prevalent after
discontinuation of paroxetine but can occur after use of all
selective serotonin reuptake inhibitors. The withdrawal
syndrome includes both physical and psychiatric symptoms and needs to be
distinguished from a relapse of the psychiatric disorder. Good information
and gradual discontinuation of the antidepressant after long-term use are
adequate measures to prevent severe withdrawal symptoms.< 4 >
Unique Identifier
98207452
Authors
Bryois C. Rubin C. Zbinden JD. Baumann P.
Institution
Clinique psychiatrique universitaire, Departement Universitaire de
Psychiatrie Adulte (DUPA), Prilly-Lausanne.
Title
[Withdrawal syndrome caused by selective serotonin reuptake
inhibitors: apropos of a case]. [Review] [33 refs] [French]
Source
Schweizerische Rundschau fur Medizin Praxis. 87(10):345-8, 1998 Mar 4.
Abstract
During the past 4 years, several case reports have been published on the
withdrawal syndrome which may be observed after acute
interruption of a treatment with selective serotonin reuptake inhibiting
antidepressants (SSRI). Paroxetine is the most frequently
cited antidepressant in the literature, whereas fluoxetine is the less
frequently cited of this type of drugs. The withdrawal
symptoms appear a few days after stopping treatment or after a decrease of
the dose. The typical symptoms are of the gastro-intestinal type, such as
loss of appetite, nausea, vomiting, diarrhea and abdominal cramps. Other
symptoms are sensation of instability, vertigo, dizziness, headache, malaise,
muscular pains, asthenia, as well as a syndrome of pseudo-influenza. Brief
electric shocks throughout the body, which last one or two seconds, have also
been reported. A case is reported in detail by the authors, who observed some
of these symptoms in a patient after stopping his treatment with
paroxetine. This withdrawal syndrome may be
due to a rebound phenomenon of the serotonergic systems after interruption of
the treatment with SSRIs. It is, therefore, recommended that treatment with
SSRIs is progressively stopped over a period of several weeks. [References:
33]< 5 >
Unique Identifier
98136503
Authors
Stahl MM. Lindquist M. Pettersson M. Edwards IR. Sanderson JH. Taylor
NF. Fletcher AP. Schou JS.
Institution
Pharmacoepidemiology Unit, Medical Products Agency (MPA), Uppsala, Sweden.
Title
Withdrawal reactions with selective serotonin re-uptake
inhibitors as reported to the WHO system.
Source
European Journal of Clinical Pharmacology. 53(3-4):163-9, 1997.
Abstract
OBJECTIVE: The present study was performed both to investigate whether there
might be a difference between the selective serotonin re-uptake inhibitors,
(SSRIs) with regard to the incidence of withdrawal
reactions, and to describe the associated symptoms. From the WHO database,
therefore, all case reports from the year of introduction for each of the
SSRIs, fluoxetine, paroxetine and sertraline, were
retrieved. Sales figures were obtained from Intercontinental Medical
Statistics International. The reporting rates were calculated as the number
of reports per million defined daily doses (DDDs) sold per year. RESULTS: The
reporting rate of withdrawal reactions for
paroxetine was found to be higher than that for sertraline
and fluoxetine in each of the countries selected for detailed analyses (US,
UK and Australia), as well as for all 16 countries combined. Moreover, using
the WHO system of organ classification, the ratio of central nervous system
to psychiatric withdrawal symptoms was 1.9 and 2.1 for
paroxetine and sertraline, respectively, whereas that for
fluoxetine was 0.48, indicating a possible qualitative difference between the
SSRIs with respect to the nature of the withdrawal syndrome.< 6 >
Unique Identifier
97414556
Authors
Zajecka J. Tracy KA. Mitchell S.
Institution
Women's Board Depression Treatment and Research Center, Rush Preshyterian St.
Luke's Medical Center, Chicago, III., USA.
Title
Discontinuation symptoms after treatment with serotonin reuptake inhibitors:
a literature review. [Review] [36 refs]
Source
Journal of Clinical Psychiatry. 58(7):291-7, 1997 Jul.
Abstract
BACKGROUND: The discontinuation of many pharmacologic agents is associated
with characteristic withdrawal symptoms. Antidepressants,
particularly the tricyclic antidepressants (TCAs), are known to be associated
with a group of common symptoms upon discontinuation. Serotonin reuptake
inhibitors (SRIs) are also taking their respective place in the literature
with reports of discontinuation symptoms. This review summarizes case reports
and reports that allow systematic assessment of discontinuation symptoms
following SRI discontinuation. METHOD: A computerized literature search was
conducted using a MEDLINE search to identify reports of
withdrawal effects following discontinuation of SRIs.
Additional reports were found in the bibliographies of various published
reports. RESULTS: SRI discontinuation symptoms in adults are summarized in 24
case reports and 9 reports from controlled clinical trials. Additionally, 3
case reports addressing SRI discontinuation in the neonate are described. The
reports describe clusters of symptoms commonly associated with the
discontinuation of an SRI. CONCLUSION: We propose to define an antidepressant
discontinuation syndrome as the onset of a cluster of somatic and psychic
symptoms following the discontinuation of an SRI and not attributable to
other causes (e.g., concomitant medication, illness). These symptoms include
dizziness, light-headedness, insomnia, fatigue, anxiety/agitation, nausea,
headache, and sensory disturbance. The syndrome may last up to 3 weeks and
may be improved by restarting the antidepressant or starting an
antidepressant with a similar pharmacologic profile. [References: 36]< 7 >
Unique Identifier
97363163
Authors
Lejoyeux M. Ades J.
Institution
Department of Psychiatry, Bichat-Claude Bernard Hospital, Paris, France.
Title
Antidepressant discontinuation: a review of the literature. [Review] [39
refs]
Source
Journal of Clinical Psychiatry. 58 Suppl 7:11-5; discussion 16, 1997.
Abstract
Sudden or tapered withdrawal from treatment with
antidepressants, including monoamine oxidase inhibitors (MAOIs), tricyclic
antidepressants (TCAs), and serotonin selective reuptake inhibitors (SSRIs),
can produce phenomena consisting of somatic and psychological symptoms. The
literature about these discontinuation phenomena consists mainly of case
reports and a limited number of controlled prospective studies. The symptoms
are generally mild and transient for the TCAs and the SSRIs but may be
serious for the MAOIs. They are much more common with a shorter acting SSRI,
such as paroxetine, than with the longer acting agent
fluoxetine. Because the symptoms of antidepressant discontinuation include
changes in mood, affect, appetite, and sleep, they are sometimes mistaken for
signs of a relapse into depression. Thus, it is important to directly
question patients about new symptoms that occur during antidepressant
discontinuation to optimally manage treatment discontinuation. [References:
39]
poster:Kimba
thread:59019
URL: http://www.dr-bob.org/babble/20010403/msgs/59019.html