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Antidepressants |
Depressive disorders have been with man since
the beginning of recorded history. In the Bible, King David, as well as
Job, suffered from this affliction. Hippocrates referred to depression as
melancholia, which literally means black bile. Black bile, along with blood,
phlegm, and yellow bile were the four humors (fluids) that accounted for
the basic medical physiology of that time. Depression has been portrayed
in literature and the arts for hundreds of years, but what do we mean today
when we refer to a depressive disorder? In the nineteenth century, depression
was seen as an inherited weakness of temperament. In the first half of the
twentieth century, Freud linked the development (pathogenesis) of depression
to guilt and conflict. John Cheever, the author and a modern sufferer of
depressive disorder, wrote of conflict and experiences with his parents
as influencing his development of depression.
In the 1950's and 60's, depression was divided into two types, endogenous
and neurotic. Endogenous means that the depression comes from within the
body, perhaps of genetic origin, or comes out of nowhere. Neurotic or reactive
depression has a clear environmental precipitating factor, such as the death
of a spouse, or other significant loss, such as the loss of a job. In the
1970's and 80's, the focus of attention shifted from the cause of depression
to its effects on the afflicted people. |
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PROZAC-Floxet
Substance: Fluoxetine
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Dosage |
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20 mg |
14 caps |
USD 0.00 |
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20 mg |
28 caps |
USD 34.00 |
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Dosage |
Packing |
Price |
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20 mg |
30 caps |
USD 0.00 |
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20 mg |
60 caps |
USD 0.00 |
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20 mg |
90 caps |
USD 0.00 |
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PAXIL (SEROXAT)
Substance: Paroxetine
Manufacturer: SKB Pharma
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Dosage |
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20 mg |
30 tab |
USD 59.00 |
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20 mg |
90 tab |
USD 175.00 |
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Dosage |
Packing |
Price |
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20 mg |
100 tab |
USD 109.00 |
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30 mg |
100 tab |
USD 139.00 |
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ZOLOFT
Substance: Sertraline
Manufacturee: Pfizer Inc.
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50 mg |
28 tab |
USD 57.00 |
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50 mg |
84 tab |
USD 146.00 |
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Dosage |
Packing |
Price |
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50 mg |
30 tab |
USD 37.00 |
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50 mg |
60 tab |
USD 69.00 |
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50 mg |
90 tab |
USD 97.00 |
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100 mg |
30 tab |
USD 45.00 |
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100 mg |
60 tab |
USD 87.00 |
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100 mg |
90 tab |
USD 127.00 |
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RHODIOLA ROSEA
(dry roots)
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Dosage |
Packing |
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28 g |
USD 15.00 |
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Preparation of tea:
cut fine 5g of Rhodiola rosea roots. 1 cup of boiling water pour in roots
and leave for (brew) at least 4 hours. Than filter. Daily dosage: 1/5 cup - 3-5
times per day. For better taste dilute Rhodiola rosea tea with juice, tonic or
other herbal tea.
Preparation of tincture for personal usage: Mill
30 g of Rhodiola Rose roots in a coffee-grinder no less than 5-10 mm, add 150
ml of light spirits (30-40%), agitate and steep 3-5 days at room temperature.
Separate and filter the extract. Dosage: ? tsp. x 3 times per day.
RHODIOLA ROSEA
(dry extract tablets, total rosavins 40%)
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Health information and news
Dosage |
Packing |
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50 mg |
60 tab |
USD 18.00 |
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Dosage: 2 tablets 3 times daily
Course: 30 days, 180 tablets
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Dosage |
Packing |
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37.5 mg |
100 tab |
USD 59.00 |
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75 mg |
100 tab |
USD 94.00 |
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What treatments
are available for depression? |
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Antidepressant Medications
Selective serotonin reuptake inhibitors (SSRIs) are medications
that increase the amount of the neurochemical serotonin in the brain.
(Remember that brain serotonin levels are low in depression.) As their
name implies, the SSRIs work by selectively inhibiting (blocking) serotonin
reuptake in the brain. This block occurs at the synapse, the place where
brain cells (neurons) are connected to each other. Serotonin is one of
the chemicals in the brain that carries messages across these connections
(synapses) from one neuron to another.
The SSRIs work by keeping the serotonin present in high concentrations
in the synapses. These drugs do this by preventing the reuptake of serotonin
back into the sending nerve cell. The reuptake of serotonin is responsible
for turning off the production of new serotonin. Therefore, the serotonin
message keeps on coming through. This, in turn, helps arouse (activate)
cells that have been deactivated by depression, and relieves the depressed
person's symptoms.
In the United States, SSRIs have been used successfully for a decade to
treat depression. They have fewer side effects than the tricyclic antidepressants
(TCAs) and monoamine oxidase inhibitors (MAOIs), which are discussed below.
SSRIs do not interact with the chemical tyramine in foods, as do the MAOIs.
Also, SSRIs do not cause orthostatic hypotension and heart rhythm disturbances,
like the TCAs do. Therefore, SSRIs are often the first-line treatment
for depression. Examples of SSRIs include fluoxetine (Prozac), paroxetine
(Paxil), sertraline (Zoloft), citalopram (Celexa), and fluvoxamine (Luvox).
SSRIs are generally well tolerated and side effects are usually mild.
The most common side effects are nausea, diarrhea, agitation, insomnia,
and headache. However, these side effects generally go away within the
first month of SSRI use. Some patients experience sexual side effects,
such as decreased sexual desire (decreased libido), delayed orgasm, or
an inability to have an orgasm. Some patients experience tremors with
SSRIs. The so-called serotonergic (meaning caused by serotonin) syndrome
is a serious neurologic condition associated with the use of SSRIs. It
is characterized by high fevers, seizures, and heart rhythm disturbances.
This condition is very rare and has been reported only in very ill psychiatric
patients taking multiple psychiatric medications.
All patients are unique biochemically. Therefore, the occurrence of side
effects or the lack of a satisfactory result with one SSRI does not mean
that another medication in this group will not be beneficial. However,
if someone in the patient's family has had a positive response to a particular
drug, that drug would be the preferable one to try first.
Dual Action Antidepressants: The biochemical reality is that all classes
of medications that treat depression (MAOIs, SSRIs, TCAs, and atypical
antidepressants) have some effect on both norepinephrine and serotonin,
as well as on other neurotransmitters. However, the various medications
affect the different neurotransmitters in varying degrees.
Some of the newer antidepressant drugs, however, appear to have particularly
robust effects on both the norepinephrine and serotonin systems. These
drugs seem to be very promising, especially for the more severe and chronic
cases of depression. (Psychiatrists, rather than family practitioners,
see such cases most frequently.) Venlafaxine (Effexor) is one of these
dual action compounds. It is a serotonin reuptake inhibitor that, at lower
doses, shares many of the safety and low side effect characteristics of
the SSRIs. At higher doses, this drug appears to block the reuptake of
norepinephrine. Thus, venlafaxine can be considered an SNRI, a serotonin
and norepinephrine reuptake inhibitor.
Another newer antidepressant, mirtazapine (Remeron), is a tetracyclic
compound (four-ring chemical structure). It works at somewhat different
biochemical sites and in different ways than the other drugs. It affects
serotonin, but at a post-synaptic site (after the connection between nerve
cells.) It also increases histamine levels, which can cause drowsiness.
For this reason, mirtazapine is given at bedtime and is often prescribed
for people who have trouble falling asleep. Like venlafaxine, it also
works by increasing levels in the norepinephrine system. Other than causing
sedation, this medication has side effects that are similar to those of
the SSRIs, but to a lesser degree in many cases.
Atypical antidepressants are so named because they work in a variety of
ways. Thus, atypical antidepressants are not TCAs or SSRIs, but they act
like them. More specifically, they increase the level of certain neurochemicals
in the brain synapses (where nerves communicate with each other). Examples
of atypical antidepressants include nefazodone (Serzone), trazodone (Desyrel),
venlafaxine (Effexor), and bupropion (Wellbutrin). The United States Food
and Drug Administration (FDA) has also approved bupropion for use in weaning
from addiction to cigarettes. This drug is also being studied for treating
attention deficit disorder (ADD) or attention deficit hyperactivity disorder
(ADHD). These problems affect many children and adults and restrict their
ability to focus or concentrate on one thing at a time.
Lithium (Eskalith, Lithobid), valproate (Depakene, Depakote) carbamazepine
(Epitol, Tegretol), neurontin (Gabapentin), and lamictal (Lamotrigine)
are mood stabilizers and anticonvulsants. They have been used to treat
bipolar depression. Certain antipsychotic medications, such as ziprasidone
(Geodon), risperidone (Risperdal), and quetiapine (Seroquel), have sometimes
also been used to treat bipolar depression, usually in combination with
other antidepressants and/or the mood stabilizers.
Monoamine oxidase inhibitors (MAOIs) are the earliest developed antidepressants.
Examples of MAOIs include phenelzine (Nardil) and tranylcypromine (Parnate).
MAOIs elevate the levels of neurochemicals in the brain synapses by inhibiting
monoamine oxidase. Monoamine oxidase is the main enzyme that breaks down
neurochemicals, such as norepinephrine. When monoamine oxidase is inhibited,
the norepinephrine is not broken down and, therefore, the amount of norepinephrine
in the brain is increased.
MAOIs also impair the ability to break down tyramine, a substance found
in aged cheese, wines, most nuts, chocolate, and some other foods. Tyramine,
like norepinephrine, can elevate blood pressure. Therefore, the consumption
of tyramine-containing foods by a patient taking an MAOI drug can cause
elevated blood levels of tyramine and dangerously high blood pressure.
In addition, MAOIs can interact with over-the-counter cold and cough medications
to cause dangerously high blood pressures. The reason for this is that
these cold and cough medications often contain drugs that likewise can
increase blood pressure. Because of these potentially serious drug and
food interactions, MAOIs are usually only prescribed after other treatment
options have failed.
Tricyclic antidepressants (TCAs) were developed in the 1950's and 60's
to treat depression. They are called tricyclic antidepressants because
their chemical structures consist of three chemical rings. TCAs work mainly
by increasing the level of norepinephrine in the brain synapses, although
they also may affect serotonin levels. Doctors often use TCAs to treat
moderate to severe depression. Examples of tricyclic antidepressants are
amitriptyline (Elavil), protriptyline (Vivactil), desipramine (Norpramin),
nortriptyline (Aventyl, Pamelor), trimipramine (Surmontil), and perphenazine
(Triavil).
Tetracyclic antidepressants are similar in action to tricyclics, but their
structure has four chemical rings. Examples of tetracyclics include maprotiline
(Ludiomil) and mirtazapine (Remeron), a drug that was discussed above
under dual action antidepressants.
TCAs are safe and generally well tolerated when properly prescribed and
administered. However, if taken in over-dose, TCAs can cause life-threatening
heart rhythm disturbances. Some TCAs can also have anti-cholinergic side
effects, which are due to the blocking of the activity of the nerves that
are responsible for control of the heart rate, gut motion, and saliva
production. Thus, some TCAs can produce dry mouth, constipation, and dizziness
upon standing. The dizziness results from low blood pressure that occurs
upon standing (orthostatic hypotension). Anti-cholinergic side effects
can also aggravate narrow angle glaucoma, urinary obstruction due to benign
prostate hypertrophy, and cause delirium in the elderly. TCAs should also
be avoided in patients with seizure disorders and a history of strokes.
Stimulants such as methylphenidate (Ritalin) or dextroamphetamine (Dexedrine)
are used primarily for the treatment of depression that is resistant to
other medications. The stimulants are most commonly used along with other
antidepressants or other medications, such as mood stabilizers, anti-psychotics,
or even thyroid hormone. They are sometimes used alone, but rarely. The
reason they are usually used with other medications for depression is
that unlike the other medications, they induce a rush and a high in both
depressed and non-depressed people. Therefore, the stimulants are highly
addictive drugs.
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Research articles
on Antidepressants Agents |
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Drug Saf. 2005;28(2):137-52.
The safety of newer antidepressants in pregnancy and breastfeeding.
Gentile S.
Department of Mental Health, ASL Salerno 1, District n. 4, Cava de' Tirreni
(Salerno), Italy. salvatore_gentile@aliceposta.it
The pregnancy and postpartum periods are considered to be relatively
high risk times for depressive episodes in women, particularly for those
with pre-existing psychiatric illnesses. Therefore, it may be necessary
to start or continue the pharmacological treatment of depression during
these two timeframes. Hence, the aim of this review is to examine the
effects on the fetus and infant of exposure, through the placenta and
maternal milk, to the following drugs: fluoxetine, fluvoxamine, paroxetine,
sertraline, citalopram, escitalopram, mirtazapine, venlafaxine, reboxetine
and bupropion. The teratogenic risks, perinatal toxicity and effects on
the neurobehavioural development of newborns associated with exposure
through the placenta or maternal milk to these medications need to be
carefully assessed before starting psychopharmacological treatment in
pregnant or lactating women. In spite of the limitations of some of the
studies reviewed, the older selective serotonin-reuptake inhibitors (SSRIs)
[as we await further data regarding escitalopram] and venlafaxine seem
to be devoid of teratogenic risks. By contrast, the data concerning possible
consequences related to exposure to SSRIs via the placenta and breastmilk
on neonatal adaptation and long-term neurocognitive infant's development
are still controversial. Nevertheless, a number of reports have shown
that an association between placental exposure to SSRIs and adverse but
self-limiting effects on neonatal adaptation may exist. In addition, the
information on both teratogenic and functional teratogenic risks associated
with exposure to bupropion, mirtazapine and reboxetine is incomplete or
absent; at present, these compounds should not be used as first-line agents
in the pharmacological treatment of depression in pregnancy and breastfeeding.
Untreated depression is not without its own risks since mothers affected
by depression have a negative impact on the emotional development of their
children and major depression, especially when complicated by a delusional
component, may lead to the mother attempting suicide and infanticide.
Consequently, clinicians need to help mothers weigh the risks of prenatal
exposure to drugs for their babies against the potential risks of untreated
depression and abrupt discontinuation of pharmacological treatment. Given
these situations, we suggest that choosing to administer psychopharmacological
treatment in pregnant or breastfeeding women with depression will result
primarily from a careful evaluation of their psychopathological condition;
currently, the degree of severity of maternal disease appears to represent
the most relevant parameter to take this clinical decision. |
Pharmacoepidemiol
Drug Saf. 2005 Mar 1; [Epub ahead of print] Related Articles, Links
Newer antidepressants in pregnancy and rates of major malformations: a meta-analysis
of prospective comparative studies.
Einarson TR, Einarson A.
Faculty of Pharmacy, Department of Clinical Pharmacology, Faculty of Medicine,
University of Toronto, Ont., Canada.
BACKGROUND: A substantial number of women of childbearing age suffer
from depression. Despite this, relatively little is known about the safety
of antidepressant use during pregnancy. PURPOSE: We conducted a meta-analysis
of prospective comparative cohort studies to quantify the relationship
between maternal exposure to the newer antidepressants and major malformations.
METHODS: We searched Medline, Embase and Reprotox from 1996 to the present
for studies comparing outcomes in first trimester exposures to citalopram,
escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline, reboxetine,
venlafaxine, nefazodone, trazodone, mirtazapine and bupropion to those
of non-exposed mothers. Data were combined using a random effects model;
heterogeneity was tested with chi(2), and publication bias with a funnel
plot and the Begg-Mazumdar statistic. RESULTS: Twenty-two studies were
identified, 15 were rejected (4 reviews, 4 without comparison groups,
2 third trimester exposures, 2 retrospective database studies, 2 case
reports and 1 duplicate); 7 studies (n = 1774) met inclusion criteria.
Effects were not heterogeneous (chi(2) = 2.04, p = 0.92); funnel plot
and test (tau = -0.24, p = 0.45) indicated no publication bias. The summary
relative risk was 1.01 (95%CI: 0.57-1.80). CONCLUSIONS: As a group, the
newer antidepressants are not associated with an increased risk of major
malformations above the baseline of 1-3% in the population. |
Bipolar Disord. 2003
Dec;5(6):421-433.
Antidepressants in bipolar disorder: the case for caution.
Ghaemi SN, Hsu DJ, Soldani F, Goodwin FK.
Bipolar Disorder Research Program, Cambridge Hospital, Cambridge, MA
and Harvard Medical School, Boston, MA, USA Center on Neuroscience, Medical
Progress, and Society and Department of Psychiatry and Behavioral Sciences,
George Washington University, Washington, DC, USA.
The 2002 American Psychiatric Association (APA) guidelines for the treatment
of bipolar disorder recommended more conservative use of antidepressants.
This change in comparison with previous APA guidelines has been criticized,
especially from some groups in Europe. The Munich group in particular
has published a critique of assumptions underlying the conservative recommendations
of the recent APA treatment guidelines. In this paper, we re-examine the
argument put forward by the Munich group, and we demonstrate that indeed,
conceptually and empirically, there is a strong rationale for a cautious
approach to antidepressant use in bipolar disorder, consistent with, and
perhaps even more strongly than, the APA guidelines. This rationale is
based on support for the following four propositions: (i) The risk of
antidepressant induced mood-cycling is high, (ii) Antidepressants have
not been shown to definitively prevent completed suicides and reduce mortality,
whereas lithium has, (iii) Antidepressants have not been shown to be more
effective than mood stabilizers in acute bipolar depression and have been
shown to be less effective than mood stabilizers in preventing depressive
relapse in bipolar disorder and (iv) Mood stabilizers, especially lithium
and lamotrigine, have been shown to be effective in acute and prophylactic
treatment of bipolar depressive episodes. We therefore draw three conclusions
from this interpretation of the evidence: (i) There are significant risks
of mania and long-term worsening of bipolar illness with antidepressants,
(ii) Antidepressants should generally be reserved for severe cases of
acute bipolar depression and not routinely used in mild to moderate cases
and (iii) Antidepressants should be discontinued after recovery from the
depressive episode, and maintained only in those who repeatedly relapse
after antidepressant discontinuation (a minority we judge to represent
only about 15-20% of bipolar depressed patients).
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Acta Psychiatr Scand.
2003 Jul;108(1):24-31.
Antidepressants: psychiatrists' opinions and clinical practice.
Depont F, Rambelomanana S, Le Puil S, Begaud B, Verdoux H, Moore N.
Departments of Pharmacology and Adult Psychiatry, Public Health Research
Institute IFR99, Universite Victor Segalen, Bordeaux, France.
OBJECTIVE: To describe and compare psychiatrists' opinion on antidepressant
drugs and their prescriptions to depressed patients. METHOD: Between January
and September 1999 a representative sample of French psychiatrists was
asked their opinion of the 15 most prescribed antidepressants, and then
to describe the treatments of the current depressive episode of four depressive
patients each, their changes and the reason thereof. RESULTS: A total
of 232 psychiatrists and 935 patients participated. The best ranked antidepressants
were clomipramine, paroxetine and amitriptyline for efficacy, tianeptine,
paroxetine and citalopram for tolerability. In patients, the most often
prescribed were paroxetine, fluoxetine and venlafaxine. Those least often
stopped for intolerance were tianeptine (2.9%), citalopram (5.2%), venlafaxine
(3.3%) and amitriptyline (5.7%) for lack of efficacy. There was no difference
in stopping rates for inefficacy of tricyclics and serotonin-selective
agents. CONCLUSION: The best predictors for the prescribed antidepressants
were the psychiatrists' overall rankings and opinions of the tolerability
of the drug.
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Cochrane Database
Syst Rev. 2003;2:CD003592.
Antidepressants for generalized anxiety disorder (Cochrane Review).
Kapczinski F, Lima MS, Souza N, Js N, Schmitt N, R N.
Department of Psychiatry, Federal University of Rio Grande do Sul - UFRGS,
Departamento de Medicinal Legal e Psiquiatria - HCPA - UFRGS, Rua Ramiro
Barcelos, 2350, Porto Alegre, RS, BRAZIL, 90035-003.
BACKGROUND: Pharmacological treatments have been successfully used to
treat Generalized Anxiety Disorder (GAD). The mainstay for the pharmacological
treatment of GAD in past decades has been the use of benzodiazepine and
non benzodiazepine anxiolytics. Data emerging over the last two decades
have shown that antidepressants may be equally effective to anxiolytics
for treating GAD. The use of antidepressants for treating GAD may be advantageous,
due to the fact that GAD presents a high co morbidity ratio with major
depressive disorder (62%) and dysthymia (37%). OBJECTIVES: To assess the
efficacy and acceptability of antidepressants for treating generalized
anxiety disorder. SEARCH STRATEGY: Cochrane Collaboration Depression,
Anxiety and Neurosis Controlled Trials Register - CCDANCTR (up to May
2002), Anxiety Neurosis (up to May 2002) and Cochrane Controlled Trials
Register (CENTRAL/CCTR) (up to May 2002), MEDLINE (1966 to May 2002),
LILACS (1982 to May 2002); reference searching; personal communication;
conference abstracts and book chapters on the treatment of generalized
anxiety disorder. SELECTION CRITERIA: Randomised controlled trials were
included. Exclusion criteria were: non randomised studies; studies which
included patients with generalized anxiety disorder and another Axis I
co-morbidity. DATA COLLECTION AND ANALYSIS: The data from studies were
extracted independently by two reviewers and relative risks, weighted
mean difference and number needed to treat were estimated. People who
died or dropped out were regarded as having had no improvement. MAIN RESULTS:
Antidepressants (imipramine, venlafaxine and paroxetine) were found to
be superior to placebo in treating GAD. The calculated NNT for antidepressants
in GAD is 5.15. Dropout rates did not differ between antidepressants.
Only one study presented data on imipramine and trazodone. Imipramine
was chosen as the reference drug and, therefore, data on trazodone could
not be included in the meta analysis. Only one study was conducted among
children and adolescents (~~Rynn 2001~~). The latter study showed very
promising results of sertraline in children and adolescents with GAD,
which warrants its replication in larger samples. REVIEWER'S CONCLUSIONS:
The available evidence suggests that antidepressants are superior to placebo
in treating GAD. There is evidence from one trial suggesting that paroxetine
and imipramine have a similar efficacy and tolerability. There is also
evidence from placebo-controlled trials suggesting that these drugs are
well tolerated by GAD patients. Further trials of antidepressants for
GAD will help to demonstrate which antidepressants should be used for
which patients.
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