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Paxil (Paroxetine)
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Paxil

Generic Paxil is a medication with highly developed components which is taken in treatment of serious disorders such as panic and social anxiety disorders, female premenstrual dysphoric disorder, post-traumatic stress disorder and depression. Generic Paxil acts as an anti-depression remedy. Generic Paxil operates by giving brains balance and mental stability.

Other names for this medication:

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Paroxetine

 

Also known as:  Paroxetine.

Description

Generic Paxil is found by professionals of medicine to combat mental dangerous disorders (depression, panic and social anxiety disorders, female premenstrual dysphoric disorder, and post-traumatic stress disorder). Target of Generic Paxil is to control and keep brain's balance.

Generic Paxil operates by giving brains balance and mental stability.

Paxil is also known as Paroxetine, Pari, Pexep, Parolin, Seroxat.

Generic Paxil is selective serotonin reuptake inhibitor (SSRI).

Generic name of Generic Paxil is Paroxetine.

Brand names of Generic Paxil are Paxil CR, Pexeva, Paxil.

Dosage

Generic Paxil is available in tablets (10 mg, 20 mg, 30 mg, 40 mg) and oral suspension. You should take it by mouth with meals of without it.

It is better to take Generic Paxil every day at the same time for nearly 4 weeks.

Generic Paxil cannot be given to patients under 18 years.

Take Generic Paxil and remember that its dosage depends on health state of patients.

For depression

Normal starting dose is 25 mg once a day.

For panic and social anxiety disorders

Normal starting dose is 12.5 mg once a day.

For aged people or patients with kidney or liver problems

Normal dose is 12.5 mg once a day.

If you want to achieve most effective results do not stop taking Generic Paxil suddenly.

Overdose

If you overdose Generic Paxil and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Paxil overdosage: seizures, confused mental state, coma, tremor, nausea, blurred vision, retching, sweating, decreased urination, aggression, rapid heartbeat.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Paxil are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Paxil if you are allergic to Generic Paxil components.

Be careful with Generic Paxil if you are pregnant, planning to become pregnant, or are breast-feeding.

Do not take Generic Paxil if you take medications as isocarboxazid (Marplan); monoamine oxidase inhibitors as MAOIs (rasagiline (Azilect)); pimozide (Orap); tranylcypromine (Parnate), phenelzine (Nardil), selegiline (Eldepryl, Emsam); thioridazine (Mellaril).

Do not take it if you are under 18.

Be careful with Generic Paxil if you suffer from liver or kidney disease, manic depression, seizures, epilepsy, suicidal thoughts.

Be careful with Generic Paxil if you take medications as blood thinner as warfarin (Coumadin); naproxen (Aleve, Naprosyn); phenothiazine as prochlorperazine (Compazine), chlorpromazine (Thorazine), fluphenazine (Prolixin), mesoridazine (Serentil); St. John's wort, tramadol (Ultram); tryptophan; aspirin; lithium (Lithobid, Eskalith); nabumetone (Relafen); ibuprofen (Advil, Motrin); risperidone (Risperdal); indomethacin; almotriptan (Axert), frovatriptan (Frova), sumatriptan (Imitrex), naratriptan (Amerge), rizatriptan (Maxalt), or zolmitriptan (Zomig); atomoxetine (Strattera); etodolac (Lodine); heart rhythm medication as flecainide (Tambocor) or propafenone (Rhythmol); diclofenac (Voltaren); cimetidine (Tagamet); amitriptyline (Elavil), citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac, Sarafem), fluvoxamine (Luvox), imipramine (Tofranil), nortriptyline (Pamelor), or sertraline (Zoloft); piroxicam (Feldene).

Try to be careful with Generic Paxil usage in case ever had drug abuse.

Avoid alcohol.

Try to avoid machine driving.

It can be dangerous to stop Generic Paxil taking suddenly.

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Rats pretreated with tranylcypromine and given clomipramine, developed head and body twitches, forelimb flexor-extensor movements and wet dog shakes, phenomena which failed to develop when pretreatment incorporated p-chlorophenylalanine (PCPA) but were unabated when this included alpha-methyl-p-tyrosine (AMPT). Locomotor activity, itself enhanced by tranylcypromine, was further and significantly elevated compared to saline, by clomipramine or imipramine in grouped rats (n = 3) but not in single or paired rats; desipramine lacked such action. This effect of clomipramine was prevented when PCPA was incorporated into the pretreatment and that of imipramine by including PCPA or AMPT. Brain monoamine oxidase (MAO) A inhibition was 92% and that of MAO B, 80%. Cortical hydroxytryptamine (5-HT) and noradrenaline concentrations as well as hypothalamic 5-HT, were significantly elevated by tranylcypromine, as was dopamine in the striatum, nucleus accumbens and tuberculum olfactorium. Hyperthermia developed in tranylcypromine pretreated rats given paroxetine or fluoxetine. Myoclonic phenomena were elicited by paroxetine, fluoxetine, clomipramine or imipramine in nialamide pretreated rats but these were less intense than in rats pretreated with phenelzine or tranylcypromine. Fatalities were fewer than in rats pretreated with tranylcypromine or phenelzine. Brain MAO A inhibition was 92% and that of MAO B, 69%.

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There is some empirical evidence that selective serotonin reuptake inhibitors reduce suicidal ideas faster than other antidepressants. These findings are well in line with the theory of a serotonergic hypofunction in suicidal patients. To test this hypothesis the data of a 6-week double-blind control-group study comparing paroxetine versus amitriptyline were analyzed with respect to suicidality. The global antidepressive efficacy was comparable under dosages of 30 mg paroxetine or 150 mg amitriptyline per day. A differentiated analysis failed to confirm the hypothesis of a faster reduction of suicidal cognitions by paroxetine.

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As adults age, many changes in functioning occur, and dementia and/or depression may develop. Medications used to manage dementia and depression include selective serotonin reuptake inhibitors. The challenge for nurses is recognizing which behaviors, signs, and symptoms are the result of the dementia or depression and which are the result of the drug therapy. The purpose of this article is to present information to increase awareness of the complexities of care for older adults with dementia and/or depression and identify possible implications for practicing nurses.

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Both enantiomers abolished the acute MDMA-induced hyperthermia and attenuated the subsequent neurotoxic loss of 5-HT, 5-HIAA and [3H]-paroxetine binding. When rats given the enantiomer plus MDMA were warmed to keep their rectal temperature elevated to near that of animals given only MDMA, the neuroprotective effect of (S)-(-)-AR-A008055 was still seen, while the effect of (R)-(+)-AR-A008055 was abolished. Protection was also seen when (S)-(-)-AR-A008055 (50 mg/kg) was given, a dose which produced only a modest attenuation of MDMA-induced hyperthermia.

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Numerous attempts have been made to develop suitable radiolabeled tracers for positron emission tomography or single photon emission computed tomography imaging of the serotonin transporter (SERT), but most often, negative outcomes are reported. The aim of this study is to define characteristics of a good SERT radioligand and to investigate species differences. We examined seven different selective serotonin reuptake inhibitors (SSRIs) and that except for one all have been previously tested as emission tomography ligands. The outcome of the ligands as emission tomography tracers was compared in relation with receptor density (Bmax) and/or ligand affinity (Kd) in rat and monkey cerebrum and cerebellum (reference region) membranes. [3H]-(S)-Citalopram and [3H]-(+)-McN5652 display statistically significantly lower affinity, whereas [3H]paroxetine displays statistically significantly higher affinity for SERT in monkey cortex when compared with the rat cerebrum. The affinity of [3H]MADAM, [123I]ADAM, and [11C]DASB for SERT obtained with rat cerebrum and monkey cortex are similar. In monkey cortex, Kd and Bmax could not be determined with [3H]fluoxetine. Of the seven SSRIs, [3H]-(S)-citalopram, [3H]MADAM, and [11C]DASB displayed significant specific binding to SERT in monkey cerebellum, with Bmax cortex:cerebellum ratios being 17, 3, and 4, respectively. In rat brain tissue the ratios were 12, 6, and 3, respectively. In conclusion, it can be estimated that imaging of the human SERT in a high-density region requires radioligands with Kd values between 0.03 and a maximum of 0.3 nM (at 37 degrees C). The differential specific cerebellar binding raises the question of the suitability of cerebellum as a reference region for nonspecific binding.

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26 suicides and 330 episodes of self-harm were identified within 120 days of an antidepressant prescription. On univariate analysis the association, expressed as OR (95% CI), between selective serotonin reuptake inhibitors (SSRIs) and self harm and suicide were 2.26 (1.27-4.76) and 1.92 (0.77-4.83), respectively. When corrected for the confounding effects of age, gender and depression/suicidal ideation there was an association between SSRIs and self harm, OR 1.66 (95% CI 1.23-2.23), but not for suicide, 1.28 (0.38-4.35). Paroxetine was a significant risk factor for suicide on univariate analysis, 4.23 (1.19-14.95), but not when corrected for age, gender and depression/suicidal ideation, 2.76 (0.30-24.87).

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An open, non-comparative 7 week study entered 60 patients (mean age 36.6 +/- 3.22 years) with panic disorders and agoraphobias with panic disorders. Paroxetin was given in a single daily dose 20-60 mg/day in the morning. The results were assessed by Hamilton and Sihan scales, scale of clinical impression, by reduction of panic attacks.

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Human immunodeficiency virus-infected patients have an increased risk for depression. Despite the high potential for drug-drug interactions, limited data on the combined use of antidepressants and antiretrovirals are available. Theoretically, ritonavir-boosted protease inhibitors may inhibit CYP2D6-mediated metabolism of paroxetine. We wanted to determine the effect of fosamprenavir-ritonavir on paroxetine pharmacokinetics and vice versa and to evaluate the safety of the combination. Group A started with 20 mg paroxetine every day for 10 days; after a wash-out period of 16 days, subjects received paroxetine (20 mg every day) plus fosamprenavir-ritonavir (700/100 mg twice a day) from days 28 to 37. Group B received the regimens in reverse order. On days 10 and 37, pharmacokinetic curves were recorded. Twenty-six healthy subjects (18 females, 8 males) were included. Median (range) age and weight were 44.4 (18.2 to 64.3) years and 68.8 (51.0 to 89.4) kg. Three subjects were excluded (two because of adverse events; one for nonadherence). Addition of fosamprenavir-ritonavir to paroxetine resulted in a significant decrease in paroxetine exposure: the geometric mean ratios (90% confidence intervals) of paroxetine plus fosamprenavir-ritonavir to paroxetine alone were 0.45 (0.41 to 0.49) for the area under the concentration-time curve from 0 to 24 h (AUC(0-24)), 0.49 (0.45 to 0.53) for the maximum concentration of the drug in plasma (C(max)), and 0.75 (0.71 to 0.80) for the apparent elimination half-life (t(1/2)). The free fraction of paroxetine showed a median (interquartile range) increase of 30% (18 to 42%) after the addition of fosamprenavir-ritonavir. The AUC(0-12), C(max), C(min), and t(1/2) of amprenavir and ritonavir were similar to those of historical controls. No serious adverse events occurred. Fosamprenavir-ritonavir reduced total paroxetine exposure by 55%. This is partly explained by protein displacement of paroxetine. We think that this interaction is clinically relevant and that titration to a higher dose of paroxetine may be necessary to accomplish the needed antidepressant effect.

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The cumulative percentage of responders receiving milnacipran reached over 80% after 4 weeks, but it did reach this level for fluvoxamine or paroxetine until after 6 weeks.

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To test the hypothesis that in patients with major depressive disorder (MDD), the response for specific Hamilton Depression Rating Scale items will differ for duloxetine compared with selective serotonin reuptake inhibitors (SSRIs) and that patterns of response will differ based on symptom severity at baseline.

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A solid state electrochemical method for screening different families of adulterant chemicals illegally added to commercial phytotherapuetic formulations is described. The proposed method, based on the voltammetry of microparticles approach, permits a fast and sensitive way to distinguish between anorexics (amfepramone, fenproporex, sibutramine), benzozodiazepinic anxiolytics (clonazepam, flurazepam, alprazolam, midazolam, medazepam, chlordiazepoxide, diazepam), antidepressants (bupropione, fluoxetine, sertraline, paroxetine), diuretics (hydrochlorothiazide, furosemide, chlortalidone, amiloride, spironolactone), and hypoglycemics (glimepiride, chlorpropamide, glibenclamide) based on characteristic voltammetric signals recorded on solid micro- or nanosamples attached to graphite electrodes immersed into aqueous electrolytes.

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All cases of adverse drug reactions (ADRs) involving sexual disorders, spontaneously reported to the French Pharmacovigilance Database from 1 January 1985 to December 2009, were reviewed. Cases of sexual disorders in SRI users were described. We calculated the rate of reported sexual disorders as a percentage of the total ADRs reported for each drug. The association between reported cases and the use of SRIs was assessed using reporting odds ratios (ROR) with 95 % confidence intervals (CIs).

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The majority of opioid dependent patients suffer from various psychiatric and somatic comorbid diseases like mood and anxiety disorders, psychotic diseases, personality disorders, HIV infection, Hepatitis B and C. If medical treatment is needed, grouping active substances to FDA Pregnancy Categories (A, B, C, D or X) may be helpful. The majority of substances reported here only fulfill the FDA-categories C or D, which means that they could have teratogenic effects, but with probably different rank order. First of all, referring to mood, personality and anxiety disorders, the focus should be laid on non-pharmacological treatment by offering psychotherapeutic and supporting psychosocial interventions to the patients. However, opioid dependent pregnant patients who suffer from severe diseases such as psychosis, bipolar affective disorder or severe depression, may need psychoactive medication like antipsychotics, antidepressants or mood stabilizers to prevent them from harm caused by psychotic ideas and actions and/or suicidality. However these medications may comprise fetal risks, especially when taken together, and therefore should only be used when benefit and risks are considered together with patients and their relatives. It is important to avoid acute or renewed psychiatric decompensation. We present the current differentiated knowledge for therapy of opioid dependent patients with antipsychotics, antidepressants (e.g. higher fetal risk in case of treatment with fluoxetine and paroxetine) or mood stabilizers. All of them should only be used after considering benefit and risks. During pregnancy, there should not be switched between different antidepressant drugs. Referring mood stabilizers, the intake of valproic acid should be avoided in pregnancy or at least, dosage should be kept as low as possible since severe teratogenetic effects are known. In addition the specific drug treatment of HIV and hepatitis B during pregnancy is described. During childbirth HIV-infected patients should receive zidovudine intravenously to prevent vertical transmission. Co-infection with hepatitis C cannot be treated during pregnancy, since interferons are associated with a severe risk of fetal malformations and ribavirin has teratogenic effects; for this reason interferon therapy should be started after delivery.

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In a previous investigation, we observed altered expression of sepiapterin reductase (SPR) in cultured neural cells chronically exposed to paroxetine. SPR is an enzyme, which catalyzes the final step in the synthesis of tetrahydrobiopterin (BH4). BH4 is an essential cofactor for synthesis of many neurotransmitters including serotonin. Given the pivotal role of SPR in neurotransmitter production, we sought to test the hypothesis that SPR would influence susceptibility to mood disorders and patient response to antidepressants.

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Previously it was found that both acute and chronic antidepressant pre-treatment enhanced the locomotor hyperactivity induced by a challenge injection of the non-competitive NMDA receptor antagonist, dizocilpine (MK-801). In the present study the effects of acute and chronic antidepressant administration on phencyclidine (PCP)-induced locomotor hyperactivity were examined. Phencyclidine (PCP), a non-competitive NMDA receptor antagonist increased locomotor activity in rats. Fluoxetine given acutely increased and prolonged the PCP-induced locomotor hyperactivity, while citalopram, sertraline and paroxetine had no effect on the PCP-induced behavioural effect. Repeated treatment with fluoxetine, citalopram and paroxetine increased the PCP-induced locomotor hyperactivity. In contrast, chronic sertraline administration attenuated the locomotor response to a PCP challenge. These results indicate that these antidepressants which are presumed to have a similar pharmacological profile, differ in their ability to alter PCP-induced hyperactivity. Whether these differences have any bearing on the therapeutic or adverse effects of these drugs remains to be shown.

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Ten publications, comprising a total of 2,046 patients, evaluated the efficacy of four SSRIs (fluoxetine, paroxetine, sertraline and citalopram) in child and adolescent depression. It is noted that an additional 6 trials (with a total of 1,234 patients) were not reported by the industry because of a lack of efficacy or problematic side effects, including suicidal behaviors. Meta-analyses revealed no data supporting the use of SSRIs, except for fluoxetine. To formulate recommendations for clinical practice, it is necessary to examine specific issues such as (1) the link between SSRIs, depression and suicidal risk; (2) SSRI age-related specific effects, and (3) the high placebo response in child and adolescent depression.

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The effect of sibutramine and dexfenfluramine on 5-HT re-uptake sites, labelled with [(3)H]paroxetine, have been determined in various rat brain regions. In addition, the ability of fluoxetine and sibutramine to protect against the changes in [(3)H]paroxetine binding produced by dexfenfluramine was examined. Sibutramine (9 mg/kg, p.o.) and dexfenfluramine (1, 3 and 10 mg/kg, p.o.) were administered twice daily (before 09.00 h and after 16.00 h) for four days, followed by a 14 day drug-free period. In the protection studies, fluoxetine (10 mg/kg, i.p.) and sibutramine (9 mg/kg, p.o.) were given 1 h prior to dexfenfluramine (10 mg/kg, p.o.) using the same dosing regimen as described above. Sibutramine (9 mg/kg, p.o.; three times its ED(50) to inhibit food intake at 2 h) had no significant effect on the number or affinity of 5-HT re-uptake sites the brain regions studied. In contrast, dexfenfluramine at an equivalent dose (3 mg/kg, p.o.) significantly decreased the number of 5-HT re-uptake sites in frontal cortex (by 35%), hippocampus (by 47%) and hypothalamus (by 27%). This effect was dose-dependent with marked decreases (by 58-84%) in the number of sites following 10 mg/kg, p.o. These effects were not associated with changes in binding affinity. Fluoxetine (10 mg/kg, i.p.) completely blocked the effect of dexfenfluramine (10 mg/kg, p.o.) without having any significant effect alone. Sibutramine (9 mg/kg, p.o.) also blocked the effects of dexfenfluramine, although the reversal was only partial in frontal cortex, hippocampus and hypothalamus. Thus sibutramine, unlike dexfenfluramine, does not alter brain 5-HT re-uptake sites. Furthermore, sibutramine and fluoxetine protect against the deficits in 5-HT re-uptake sites produced by dexfenfluramine. These data provide further evidence that sibutramine is a 5-HT re-uptake inhibitor and it does not have neurotoxic potential.

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Seventeen (45%) subjects had "much" or "very much" improvement and achieved at least a 40% decrease in their total Yale-Brown Obsessive Compulsive Scale (Y-BOCS) score. Responders had lower obsessive-compulsive scores on the Symptom Checklist 90-Revised, had a lower checking score on the Maudsley Obsessive-Compulsive Inventory, were less likely to have had prior drug therapy, and in general suffered more obsessive-compulsive symptoms. They were significantly less likely to have hoarding obsessions and corresponding compulsions. The latter finding was confirmed using multiple regression analysis.

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The agents p-chlorophenylalanine (PCPA) and p-chloroamphetamine (PCA) deplete brain serotonin (5-HT) levels by two different mechanisms; PCPA inhibits the enzyme tryptophan hydroxylase, whereas PCA has a neurotoxic action on certain 5-HT neurons. The parameters of [3H]paroxetine binding to homogenates prepared from the cerebral cortex of rats treated with PCPA, PCA, or saline; vehicle were investigated. The tissue concentrations of 5-HT and 5-hydroxyindole-3-acetic acid (5-HIAA) were also determined by HPLC in the same brain samples. After PCPA treatment, neither the maximum binding capacity (Bmax) nor the dissociation constant (KD) of [3H]paroxetine for the 5-HT uptake recognition site differed from controls despite a substantial reduction in the concentration of 5-HT and 5-HIAA. In contrast, significant changes in both the Bmax and KD values were observed in the cerebral cortex of rats treated with PCA. Furthermore, [3H]paroxetine binding and tissue concentrations of 5-HT and 5-HIAA were measured in the following different regions of the rat brain: cingulate, parietal, and visual cortical areas; dorsal and ventral hippocampus; rostral and caudal halves of neostriatum; ventral mesencephalic tegmentum; and midbrain raphe nuclei region after administration of PCPA, PCA, or saline vehicle. There was an excellent correlation between regional 5-HT levels and specific [3H]paroxetine binding in control and PCA-treated rats although this correlation was lost after PCPA treatment. Under these conditions, the 5-HT innervation remains unchanged whereas the concentration of 5-HT and 5-HIAA is greatly reduced. Thus, [3H]paroxetine binding appears to provide a reliable marker of 5-HT innervation density within the mammalian CNS.

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Pharmacy claims data from a commercial managed care health plan covering 19,000 lives and national drug data were used to compile a list of frequently prescribed medications. Excluding medications in which packaging, formulation, and potential adverse pharmacologic outcomes prohibited splitting, we performed a cost analysis of medications amenable to splitting.

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Sexual dysfunction is a common adverse effect of antidepressant treatment. Physicians should monitor their patients for antidepressant-induced sexual adverse effects, as these may affect compliance with therapy and ultimate treatment success. In addition to the consequences for patient health and well-being, managed-care organizations should be concerned with sexually related adverse effects of antidepressants, insofar as additional healthcare resources may be required to treat depressed patients in whom these adverse effects arise.

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Since 2003, fewer children and adolescents have been prescribed antidepressants in primary care. However, fluoxetine and non-SSRI antidepressant prevalences have not risen, implying that they are not prescribed as alternative treatments. This study shows that the CSM advice has had a significant effect in reversing the rising prevalence of antidepressant prescribing to children and adolescents in primary care.

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We examined the role of 5-hydroxytryptamine(2C) (5-HT(2C)) receptors in marble-burying behavior in mice. When administered alone, the selective 5-HT(2C) agonist WAY161503 (3 mg/kg) inhibited marble-burying behavior. Moreover, the selective 5-HT(2C) antagonist SB242084 (3 mg/kg) reversed the inhibition of marble-burying behavior by 2,5-dimethoxy-4-iodoamphetamine (DOI) (1 mg/kg) or WAY161503 (3 mg/kg). Similarly, SB242084 (1 mg/kg) reversed the inhibition of marble-burying behavior by fluvoxamine (30 mg/kg) or paroxetine (3 mg/kg). These results suggest that 5-HT(2C) receptors play a role in marble-burying behavior in mice.

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Depression is a serious and widespread emotional disorder among the elderly. This study compared the efficacy and safety of bupropion sustained release (SR) with the selective serotonin reuptake inhibitor paroxetine in the treatment of major depression in elderly outpatients.

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A total of 100 normally potent men suffering from PE were enrolled in a randomized single-blinded comparative study of fluoxetine, paroxetine and escitalopram Patients were randomized into 3 treatment groups. Group 1 comprised 33 men who received fluoxetine 20 mg daily, group 2 comprised 37 men who received escitalopram 10 mg and group 3 comprised 30 men who received paroxetine 20 mg daily. All drug regimens were given in early morning dose and continued for 4 weeks.

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Our results suggest that SPS can reproduce behavioral alteration similar to that observed in patients with PTSD, and this elevated fear response can be alleviated by the chronic administration of PRX at doses producing clinically relevant serum concentrations.

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A .6 mg/kg dose of methylphenidate improves stopping performance and directly targets a stop-related brain mechanism that has been reported before to be compromised in a group of ADHD patients. This mechanism was not influenced by acute serotonergic reuptake inhibition.

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Sixty-five patients prescribed benzodiazepines from prescription day 1 were analyzed for the primary outcome. The percentage of benzodiazepine users was significantly lower in the mirtazapine than in the SSRIs group at weeks 6, 12, and 24 (21.4 vs. 81.8 %; 11.1 vs. 85.7 %, both P < 0.001; and 12.5 vs. 81.8 %, P = 0.0011, respectively). No between-group difference was observed in HDRS score changes. Serum proBDNF levels were significantly decreased (χ(2) = 8.5, df = 3, P = 0.036) and serum mature BDNF levels were temporarily significantly decreased (F = 3.5, df = 2.4, P = 0.027) in the responders of both groups at week 24.

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The syntheses of some 3-substituted-2-(4-methyl-1-piperazinyl)-4-phenylquinolines are reported. The title compounds were tested for their potential activities on 5-HT receptor subtypes and 5-HT uptake site; compounds 4b-d showed micromolar affinity for 5-HT3 and 5-HT uptake site.

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Data from 22 randomized, controlled trials comparing escitalopram with SSRIs, SNRIs, or placebo in the treatment of adult MDD or GAD were included. Both last observation carried forward (LOCF) and repeated measurements (MMRM) were used to analyze the sleep item of the Montgomery Åsberg Depression Rating Scale (MADRS) or Hamilton Anxiety Rating Scale (HAM-A) after 8 weeks of treatment. Sleep-related treatment-emergent adverse events were also compared across groups.

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paxil 30mg dose 2017-07-23

Co-administration of multiple oral doses of 20 mg paroxetine once daily with a single oral dose of the 0.4 mg tamsulosin HCl capsule increased the adjusted geometric mean (gMean) values of C(max) and AUC(0,∞) of tamsulosin by factors of 1.34 (90% CI 1.21, 1.49) and 1.64 (90% CI 1.44, 1.85), respectively, and increased the terminal half-life (t(1/2) ) of tamsulosin HCl from 11.4 h to 15.3 h. Co-administration of multiple oral doses of 400 mg buy paxil ketoconazole once daily with a single oral dose of the 0.4 mg tamsulosin increased the gMean values of C(max) and AUC(0,∞) of tamsulosin by a factor of 2.20 (90% CI 1.96, 2.45) and 2.80 (90% CI 2.56, 3.07), respectively. The terminal half-life was slightly increased from 10.5 h to 11.8 h. These pharmacokinetic changes were not accompanied by clinically significant alterations of haemodynamic responses during orthostatic stress testing.

paxil recommended dosage 2016-05-31

Compared to controls, patients buy paxil showed higher FA-chain length, FA-unsaturation and FA-peroxidation, and more negative relationships of FA-unsaturation and FA-peroxidation with cortisol. Moreover, these negative relationships were associated with paroxetine nonresponse. Nonresponse was also associated with low DHA, which was related to low fatty fish intake. Furthermore, early responders showed initial low FA-chain length, FA-peroxidation and EPA that increased during the study, while non-responders exhibited opposite patterns.

paxil off brand 2016-09-21

Personality disorder status led to differential response at 16 weeks; 66% v. 44% (antidepressants v. cognitive therapy respectively) for people with personality disorder, and 49% v. 70% (antidepressants v. cognitive therapy respectively) for people without personality disorder. For people with personality disorder, sustained response rates over the 12-month follow-up were nearly identical (38%) in the prior cognitive therapy and continuation-medication treatment arms. People with personality disorder withdrawn from medication evidenced the lowest sustained response rate ( buy paxil 6%). Despite the poor response of people with personality disorder to cognitive therapy, nearly all those who did respond sustained their response.

paxil oral suspension 2015-03-04

Recent studies suggest that buy paxil serotonergic functioning may be aberrant in patients with social phobia. Capacity of the serotonin (5-HT) transporter, as determined by 3H-paroxetine binding, was measured in 18 drug-free patients with generalized social phobia and compared to 15 drug-free patients with panic disorder and 23 healthy control subjects. The density (Bmax) and affinity (1/Kd) of 3H-paroxetine binding sites was similar in all three groups. To the extent that the serotonin transporter in platelets and neurons is comparable, these findings suggest that this aspect of serotonergic function is normal in patients with social phobia.

paxil generic equivalent 2015-01-14

Each of the groups of rats buy paxil was treated for 14 days with one of the following: an antidepressant drug (desipramine, paroxetine, venlafaxine, or tianeptine); a mood stabilizer (lithium or carbamazepine); or 8 hours' partial sleep deprivation. Thyroid hormone concentrations were quantified in homogenates, nuclei, mitochondria, synaptosomes, myelin, and microsomes in 11 rat brain areas.

paxil 30mg reviews 2016-05-25

Although stimulants as the treatment of choice are widely prescribed in ADHD, little is known about their long-term neurobiological effects. Hence, for the first time the present study examined the long-term effects of chronic methylphenidate (MPH) administration on striatal 5-hydroxytryptamine transporter (5-HTT) densities in an animal model of ADHD. First, it compared the normal development of striatal 5-HTT densities of spontaneously hypertensive rats (SHR) as an animal model of ADHD and Wistar Kyoto (WKY) rats as controls; binding of the highly selective ligand of 5-HTT [(3)H]paroxetine was determined on membrane preparations of the striatum of SHR and WKY rats on postnatal days 25, 50, and 90, i.e. from the time of weaning until adulthood. Second, the long-term effect of chronic administration of 2 mg/kg per day MPH at two different developmental stages (days 25-39 or 50-64) on the striatal 5-HTT density was examined in both rat strains at day 90. Long-term effects of MPH treatment on striatal 5-HTT density in adulthood could be ruled out in both healthy (WKY) and "ADHD" rats (SHR). But a higher striatal 5-HTT density in older SHR versus WKY rats might indicate ADHD specific changes in the 5-HT system that needs further buy paxil investigation not only in animals.

paxil reviews 2016-05-14

All these women had significant improvements in the HAMA, HAMD, CGI, and PRISM calendar. The rate of response to paroxetine treatment lay between 50% and 78.6% in the continuous-treatment group, and 37.5-93.8% in the intermittent-treatment group, as determined at the study end-point. Limitations of the present study included the open- buy paxil label design and the incorporation of a limited sample size.

paxil dosage reduction 2015-06-14

The aim of this study was to evaluate the potential of hair analysis to monitor medication adherence in headache patients undergoing chronic therapy. For this purpose, the following buy paxil parameters were analyzed: the detection rate of 23 therapeutic drugs in headache patients' hair, the degree of agreement between the self-reported drug and the drug found in hair, and whether the levels found in hair reflected the drug intake reported by the patients.

paxil maximum dosage 2015-09-17

Individuals with current or past depression are often smokers who are more nicotine dependent, more likely to suffer buy paxil from negative mood changes after nicotine withdrawal, and more likely to relapse to smoking after quitting than the general population, which contributes to their higher morbidity and mortality from smoking-related illnesses. It remains unclear what interventions can help them to quit smoking.

paxil cr generic 2016-11-16

Serotonin released from platelets has been suggested as one substance causing the vasospasm following subarachnoid hemorrhage. We studied whether such serotonin is able to buy paxil constrict pial vessels.

paxil 20 tablet 2016-10-06

The elderly frequently use psychoactive drugs including alcohol (ethanol), benzodiazepines and opioid analgesics, which have a propensity to cause abuse and dependence. Theoretically, the changes in pharmacokinetics of these agents in the elderly may modify their abuse and dependence potential. In the elderly, blood alcohol concentrations following an oral dose are higher, alcohol withdrawal syndrome follows a more severe and protracted clinical course and requires treatment with higher doses of chlordiazepoxide than needed for buy paxil younger adults. However, there is no direct evidence that supports an increased direct abuse and dependence potential of alcohol because of its altered kinetics in the elderly. In the case of oxidatively metabolised benzodiazepine, both age-related pharmacokinetics and pharmacodynamic changes may increase their clinical effects in the elderly. The hypothesis that benzodiazepines have an increased abuse and dependence potential in the elderly has not been tested. Many of the benzodiazepines (e.g. alprazolam, triazolam and midazolam) are metabolised by the cytochrome P450 (CYP)3A subfamily. The pharmacokinetics of these agents may be modified by inhibition of CYP3A due to concurrently administered medications such as selective serotonin reuptake inhibitors. Unfortunately, data on the direct measures of abuse and dependence potential of benzodiazepines are not available in the elderly. Thus, a conclusive statement on the contribution of age-related pharmacokinetic changes to benzodiazepine abuse and dependence cannot be made at the present time. The clinical effects of codeine do not appear to change with age. Codeine is O-demethylated to its active metabolite morphine by the genetically polymorphic CYP2D6 isozyme. The activity of this isozyme is unaltered by age, gender or smoking habits; however, it is subject to potent inhibition by some of the frequently used medications in the elderly, such as the antidepressants paroxetine and fluoxetine. This may result in an impairment in O-demethylation of codeine to morphine and may lead to a decrease in the abuse and dependence potential of codeine. Conversely, those with a very rapid CYP2D6 catalytic activity may have an increased potential for codeine abuse and dependence. The clinical significance of age-related pharmacokinetic changes should be evaluated within the context of clinical practice. Most physicians are inclined to prescribe lower doses to the elderly, which may offset the potential impact of altered pharmacokinetics on the abuse and dependence potential of psychoactive agents. In summary, the available data are not sufficient for a definitive conclusion on whether the pharmacokinetic changes in the elderly translate to an increase in the abuse and dependence potential of alcohol, benzodiazepines or opioids. In particular, the data on age-associated changes in direct measures of abuse potential of these agents are missing. Future comparative systemic pharmacokinetic-pharmacodynamic studies assessing pertinent outcome measures on abuse and dependence potential of commonly used psychoactive drugs are required to resolve the ongoing controversy on risk factors for drug abuse and dependence in the elderly.

common dosage paxil 2015-07-21

Intent-to-treat analyses revealed that both groups improved from pretreatment to posttreatment. Although the treatment group improved more than the control group on most measures, few differences were statistically significant. For the primary outcome, 57.1% of participants in the treatment arm buy paxil had at least a 50% reduction in HAM-D score, compared with 40% in the control group (nonsignificant). Treatment effects were greater among the participants who completed the study; 78.6% of completers had a treatment response compared with 42.1% of controls (P=.073).

paxil online pharmacy 2016-12-26

A retrospective drug utilization analysis was conducted to compare concomitant use buy paxil of anxiolytics and hypnotics among patients who received selective serotonin reuptake inhibitors (SSRIs). Data were extracted from an administrative prescription claims database. Patients must have been 18 to 64 years of age, without antidepressant, anxiolytic, or hypnotic use before SSRI therapy initiation, and without the use of antidepressants, other than the original SSRI, after SSRI therapy initiation. The study sample included 117,319 patients. Concomitant anxiolytic use for the total sample was 9.8%. Concomitant anxiolytic use rates for the comparison groups were: fluoxetine, 9.5%; paroxetine, 11.4%; and sertraline, 9.5%. Concomitant hypnotic use for the total sample was 2.8%. Concomitant hypnotic use rates for the comparison groups were: fluoxetine, 2.5%; paroxetine, 3.5%; and sertraline, 2.8%. The majority of concomitant anxiolytic and hypnotic use was initiated on the same day as SSRI therapy initiation. The anxiolytic and hypnotic concomitant use rates for fluoxetine and sertraline patients were significantly lower than the concomitant use rates for paroxetine patients. An understanding of the clinical, quality-of-life, and economic implications of the concomitant use differences will require further study.

paxil 60 mg 2016-11-14

We present preliminary data on the efficacy of paroxetine, as compared with nortriptyline, in preventing or delaying relapse and recurrence of major depression in elderly patients. Following double-blind, acute-phase pharmacotherapy, 25 patients (mean age = 72.5 years) began open-trial continuation Atarax Maximum Dosage treatment with paroxetine (mean dose = 24.5 mg/day), and 15 patients (mean age = 77.5 years) received nortriptyline (mean dose = 51.3 mg/day; mean blood level = 85.5 ng/mL). Over an 18-month period, paroxetine and nortriptyline have shown comparable efficacy in preventing or delaying relapse and recurrence, with 80% to 90% of patients remaining well. These data suggest that paroxetine holds promise for long-term maintenance treatment in patients in their 70s and older with depression; however, further controlled evaluation is necessary.

paxil good reviews 2016-10-28

The effects of paroxetine (20 and 40 mg/day) and amitriptyline (75 mg/day, used as an active control) on car driving and psychomotor function were compared with those of placebo in a double-blind, crossover study employing 16 healthy subjects. Performance testing occurred on the first and last day of each 8-day treatment series. Side-effects, sleep Betnovate Buy Online duration and sleep quality were rated daily. Amitriptyline produced severe drowsiness and strikingly impaired performance on nearly every test on the first day but its effects were practically gone after 1 week of treatment. Paroxetine 20 mg, the usual antidepressant dose, had no effect on performance. Paroxetine 40 mg did not affect road tracking but slightly impaired performance in some psychomotor tests in a persistent manner. Paroxetine had no effect on sleep following the 20 mg dose but reduced quality following the 40 mg dose. Side-effects that the administered drugs have in common were milder during paroxetine than amitriptyline treatment. However, some dose-related side-effects (e.g. nausea and delayed ejaculation) were only reported during paroxetine treatment.

paxil high dose 2016-11-06

In this prospective study, Personality Disorders (PersD) were Effexor 900 Mg evaluated in patients with Panic Disorder (PD), before and after one year of pharmacotherapy to verify whether personality characteristics changed after treatment.

paxil highest dosage 2015-10-28

A right-handed 55-year-old Benicar Maximum Dosage man who was a heavy smoker was admitted to the hospital after a right hemiplegia of sudden onset. Clinical examination revealed a right global hemiplegia including the face and a right hemihypoesthesia. Cerebral CT scan and MRI showed an infarct in the retrolenticular part of the posterior limb of the left internal capsule extending upward into the posterior paraventricular corona radiata region. Transesophageal echocardiography revealed an atrial septal aneurysm of 15-mm excursion without associated patent foramen ovale. From the first day of admission, the patient exhibited very frequent and intense fits of pathological crying. Their persistence led to initiation of treatment with the selective serotonin reuptake inhibitor paroxetine on day 30. Complete and immediate resolution of pathological crying occurred 24 hours after onset of therapy. Follow-up examination at day 90 confirmed the absence of relapse of pathological crying.

paxil dosage amounts 2016-05-12

Systematically to assess symptoms and effects on Cymbalta Capsule Image daily functioning related to interruption of SSRI therapy.

paxil drug class 2015-07-29

During remission of depression, five outpatients noticed an increase of libido experienced as strange to them, i.e. preoccupation with sexual thoughts, first appearance of promiscuity, of unsafe sexual intercourse, and of excessive Cordarone 900 Mg pursuit of pornography, respectively, during administration, change in dose or discontinuation of SSRI.

paxil drug 2016-07-14

There were significant relationships between daily affect and events reported in the daily diary for the sample as a whole, with no differences between groups in mean slopes of positive or negative affect across the length of the study Strattera Generic Version . There were no differences between groups in affective variability. However, the SSRI group, but not the placebo group, demonstrated a significant drug-dependent decrease in negative affect related to negative events. There were no other observed group differences on any other measure.

paxil dosage levels 2016-10-12

In Tobin v. SmithKline Beecham Pharmaceuticals a jury in the U.S. District Court for the District of Wyoming found that the medication Paxil "can cause some individuals to commit homicide and/or suicide," and that it was a legal cause of the deaths in this case. A motion was recently put before the United States District Court for the District of Utah to adopt the findings of the Tobin case--via the application of collateral estoppel--to a case involving an individual's suicide while prescribed Paxil. This article summarizes these two cases, as reflected in court documents, and comments on limitations of common causality assertions.

paxil medicine 2016-12-02

Using a linear multilevel model analysis, we found that the discontinued group had significantly higher scores on the Cornell scale after 25 weeks than the continuation group (difference -2.89 (95% confidence interval -4.76 to -1.02); P=0.003). We saw a similar result in the mean total score for the neuropsychiatric inventory after 25 weeks, but this difference was non-significant (-5.96 (-12.35 to 0.44); P=0.068). We confirmed these results by non-response analysis (>30% worsening on the Cornell scale)--significantly more patients worsened in the discontinuation group than in the continuation group (32 (54%) v 17 (29%); P=0.006). We found no significant differences between the groups for secondary outcomes. Forty seven (37%) patients withdrew from the study early.

paxil positive reviews 2016-03-17

The literature was searched to identify randomised, double-blind, placebo-controlled trials of SSRIs in the treatment of major depression. Efficacy outcomes were response to treatment and change in depressive symptoms. Reporting of adverse events was used as an indicator of tolerability. Random effects meta-analyses were used to calculate pooled estimates. Meta-regression analyses were performed to investigate the association between adverse events and efficacy. Potential mediation was investigated with the Baron & Kenny approach.

paxil and alcohol 2015-05-19

Thirty-four patients with primary premature ejaculation were randomly assigned to receive 20 mg or 40 mg daily of paroxetine for 7 weeks in a double-blind fixed-dose trial after an initial dose of 20 mg/day in the first week. Patients and their female partners were interviewed separately. In the group receiving 20 mg, one of two capsules consisted of placebo and in the group receiving 40 mg, both capsules contained active drug.

paxil 20 mg 2015-09-25

Clinical trials with antidepressant drugs often fail to detect drug effect, even with drugs that are known to be efficacious. In a previous publication, we showed that a model-based approach is required to address some of the existing challenges in the design of clinical trial protocols. Here, we illustrate how the implementation of an interim analysis (IA) may help to identify studies that are headed for failure, early in the trial before completion of treatment. In contrast to traditional IA procedures, an adaptive Bayesian approach is proposed to optimize the timing of analysis and decision criteria for futility and efficacy, taking into account enrollment rate and treatment response at intermediate visits in the trial. Validation procedures involving re-enrollment of patients confirmed the performance of the method. Our findings reveal that optimization of the timing and decision criteria at the interim stage is critical for the accuracy of the conclusions about treatment efficacy or futility.

paxil dosage forms 2017-08-13

Study A: Geometric mean AUC0-36 for BCQB alone and co-administered with paroxetine were 474.3 and 631.3pgh/ml, respectively. The geometric mean ratio (GMR) of AUC0-36 was 1.33 (1.13-1.46), 90% C.Is, and was out the predefined bioequivalence interval (90% C.Is, 0.80-1.25). Geometric mean Cmax were 187.0 and 181.2pg/ml. Study B: The GMR of AUC0-36 was 0.98 (0.90-1.07), 90% C.Is for BCQB, and the GMR of AUC0-72 was 0.98 (0.87-1.11), 90% C.Is for roxithromycin. Both GMRs were within the predefined bioequivalence interval (90% C.Is, 0.80-1.25). Other pharmacokinetic parameters were within the predefined interval. No serious adverse events were reported and no significant clinical changes were observed in laboratory test results, vital signs and ECGs in any of the studies. All treatments were well tolerated.

paxil 70 mg 2016-03-17

To report a case of excessive sweating probably caused by paroxetine, review the literature on antidepressant-induced sweating, and provide recommendations for the management of antidepressant-induced sweating.

paxil 10mg medication 2016-09-12

Randomized controlled clinical trials have demonstrated that escitalopram is efficacious in a range of mood and anxiety disorders, but the individual trials are insufficiently large to allow a full exploration of its tolerability.