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Paxil (Paroxetine)

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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:
Aropax, Casbol, Deroxat, Divarius, Eutimil, Frosinor, Motivan, Parotur, Paroxat, Paroxetina, Paroxetinum, Pexep cr, Pexeva, Sereupin, Seroxat, Tagonis, Xet

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Also known as: Paroxetine.


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.


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.


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.


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.


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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We first compared 70 initially unmedicated MDD-patients with 51 age- and gender-matched controls at study-entry, regarding salivary cortisol and erythrocyte membrane FAs [omega-3 docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), FA-chain length, -unsaturation and -peroxidizability]. Subsequently, we treated patients with 6 weeks 20mg/day selective serotonin reuptake inhibitor paroxetine. After 6 weeks, we continued this treatment in responders (i.e. showing ≥50% decrease in Hamilton depression rating scale-score), and randomized non-responders to a 6-week, double-blind, placebo-controlled dose-escalation up to 50mg/day. We repeated cortisol and FA-measures in patients after 6 and 12 weeks.

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The effects of paroxetine on steady-state plasma concentrations of risperidone and its active metabolite 9-hydroxyrisperidone (9-OH-risperidone) were studied in 10 patients with schizophrenia or schizoaffective disorder. Patients stabilized using risperidone therapy (4-8 mg/d) also received paroxetine (20 mg/d) for 4 weeks. During paroxetine administration, mean plasma concentrations of risperidone increased significantly (P < 0.01), whereas levels of 9-OH-risperidone decreased slightly but not significantly. After 4 weeks of paroxetine treatment, the sum of the concentrations of risperidone and 9-OH-risperidone (active moiety) increased significantly by 45% (P < 0.05) over baseline. The mean plasma risperidone/9-OH-risperidone ratio was also significantly modified (P < 0.001) during paroxetine treatment. The drug combination was generally well tolerated with the exception of one patient who developed Parkinsonian symptoms in the second week of adjunctive therapy. In this patient total plasma levels of risperidone and its active metabolite increased by 62% during paroxetine co-administration. The authors' findings indicate that paroxetine, a potent inhibitor of CYP2D6, may impair the elimination of risperidone, primarily by inhibiting CYP2D6-mediated 9-hydroxylation and to a lesser extent by simultaneously affecting the further metabolism of 9-OH-risperidone or other pathways of risperidone biotransformation. Careful clinical observation and possibly monitoring of plasma risperidone levels may be useful whenever paroxetine is co-administered with risperidone.

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Women in their reproductive years are at risk of experiencing depressive and anxiety disorders. As such, it is likely that pregnant women will undergo treatment with antidepressants. We review the risk of adverse birth outcomes and neonatal complications subsequent to antidepressant use in pregnancy. An inconsistent literature shows that antidepressant exposure is associated with shortened gestations and diminished fetal growth; these effects are small. Transitory neonatal signs are seen in some neonates after exposure to antidepressants in utero. No specific pattern of malformations has been consistently associated with antidepressants, with the possible exception of paroxetine and cardiac malformations. There is inconclusive evidence of a link between antidepressants in late pregnancy and persistent pulmonary hypertension in the newborn. Extensive study finds that antidepressants cannot be considered major teratogens. It is likely that confounding factors contribute to a number of the adverse effects found to be associated with antidepressant use in pregnancy.

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A gas chromatographic-mass spectrometric (GC-MS) method in positive ion chemical ionization mode in combination with a solid phase extraction was optimized for new-generation antidepressants and their metabolites in postmortem blood, brain tissue, and hair. Twelve antidepressants and their active metabolites (i.e., mirtazapine, viloxazine, venlafaxine, citalopram, mianserin, reboxetine, fluoxetine, fluvoxamine, sertraline, maprotiline, melitracen, paroxetine, desmethylfluoxetine, desmethylmianserin, desmethylmirtazapine, desmethylsertraline, desmethylmaprotiline, desmethylcitalopram, and didesmethylcitalopram) could be quantified. In this article, in addition to the validation of the GC-MS method, four postmortem cases are discussed to demonstrate the usefulness of the described method in forensic toxicology. In these cases, sertraline, fluoxetine, citalopram, and trazodone in combination with their active metabolites were quantified. Blood concentrations ranged from subtherapeutic to toxic concentrations, while brain to plasma ratios ranged from 0.8 to 17. Hair concentrations ranged from 0.4 to 2.5 ng/mg depending on the compound and hair segment.

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A Web-based method is described for rapidly and objectively obtaining patient views on the effects and side-effects of treatment with antidepressants. The method entails a systematized search of many URLs (Uniform Resource Locators, or Web page addresses), using keywords and phrases to extract the named drug and symptom that are reliably relevant to the medication being taken by the individual reporting the experience online. Unwanted medical conditions (e.g., cancer) are excluded.

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Recent studies have implicated brain‐derived neurotrophic factor (BDNF) in the pathophysiology of depression and in the activities of antidepressant drugs. Serum BDNF levels are lower in depressed patients and increase in response to antidepressant medications; however, no studies have examined the association between plasma concentrations of antidepressant drugs and plasma BDNF levels. We assessed plasma BDNF levels and paroxetine concentrations in 45 patients with major depression who were being treated with paroxetine. Plasma samples were collected between 10:00 h and 12:00 h at baseline and after 1, 2 and 6 weeks of treatment. The BDNF level and paroxetine concentration of each sample were measured via enzyme immunoassay and high‐performance liquid chromatography, respectively. Plasma BDNF levels increased after 2 and 6 weeks of paroxetine treatment. Plasma BDNF levels were significantly lower in men than in women. Changes in plasma BDNF level were correlated with plasma drug concentration after 2 (r = 0.309, p < 0.05) and 6 weeks (r = 0.329, p < 0.05) but not correlated with plasma drug concentration after 1 week (r = 0.284, ns). Multiple regression analysis confirmed that this change was only significantly correlated with plasma paroxetine concentration after 2 (standardised beta = 0.343, p < 0.05) and 6 weeks (standardised beta = 0.375, p < 0.05). These results suggest that paroxetine treatment increases plasma BDNF levels and that plasma paroxetine levels play an important role in changes in plasma BDNF levels.

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Drug-free depressed outpatients (n=49; both sexes; aged 25-55 years), received paroxetine (20 mg/day). We quantified SERT occupancy with iodine-123-labeled 2beta-carbomethoxy-3beta-(4-iodophenyl)-tropane single-photon emission computed tomography imaging at baseline and after 6 weeks; we genotyped 5-HTTLPR (S, L(G), L(A)).

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These data suggest that suppression of serotonin (but not noradrenaline or dopamine) reuptake by SSRIs and SNRIs modifies circadian locomotor activity rhythms in hamsters. Further, they support the notion that an inhibitory influence upon the early-morning light-induced advance in circadian activity contributes to the therapeutic effects of serotonin uptake inhibitors in certain depressed patients.

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Paroxetine controlled release (CR) is approved for the treatment of major depressive disorder (MDD) in the dosage range of 25 to 62.5 mg daily. However, lower daily doses (12.5 mg and 25 mg) of this formulation have not been investigated in the treatment of MDD. If the 12.5-mg and 25-mg doses are found to be efficacious, these lower doses may well convey a superior tolerability profile for paroxetine CR in the treatment of MDD.

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This prospective study of women who gave birth at our tertiary center from 2000 to 2007 yielded 235 women who reported first-trimester SSRI use during pregnancy. All newborns born during the study period and found to have a persistent cardiac murmur on day 2 or 3 of life were referred for examination by a pediatric cardiologist and by echocardiography. The findings were compared between the newborns who were exposed to SSRIs and those who were not.

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paxil generic equivalent 2016-07-18

Bulimic status was associated with markedly reduced density of paroxetine-binding sites, modest Flomax Generic Equivalent blunting of m-CPP stimulated PRL response, and greater nausea following m-CPP. Biological variables did not co-vary with most psychopathological or eating-symptom indices. However, there were inverse associations (in bulimic women only) between scores indicating impulsivity (largely 'unreflectiveness') and density of platelet 5-HT uptake sites.

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The occurrence of pharmaceuticals in source waters is increasing. Although UV advanced oxidation is known to be an effective barrier against micropollutants, degradation rates are only available for limited amounts of pharmaceuticals. Therefore, the degradation of a large group of pharmaceuticals has been studied in this research for the UV/H2O2 process under different conditions, including pharmaceuticals of which the degradation by UV/H2O2 was never reported before (e.g., metformin, paroxetine, pindolol, sotalol, venlafaxine, etc.). Monochromatic low pressure (LP) and polychromatic medium pressure (MP) lamps were used for three different water matrices. In order to have well defined hydraulic conditions, all experiments were conducted in a collimated beam apparatus. Degradation rates for the pharmaceuticals were determined. For those compounds used in this research that are also reported in literature, measured degradation results are in good agreement with literature Cymbalta Cost Help data. Pharmaceutical degradation for only photolysis with LP lamps is small, which is increased by using a MP lamp. Most of the pharmaceuticals are well removed when applying both UV (either LP or MP) and H2O2. However, differences in degradation rates between pharmaceuticals can be large. For example, ketoprofen, prednisolone, pindolol are very well removed by UV/H2O2, whereas metformin, cyclophosphamide, ifosfamide are very little removed by UV/H2O2.

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Duloxetine (Cymbalta) is an orally administered, selective serotonin and noradrenaline reuptake inhibitor (SNRI) that has been approved for the Astelin Generic Otc treatment of major depressive disorder (MDD). Based on a considerable body of evidence, duloxetine at dosages ranging from 40 to 120 mg/day was effective in the short- and long-term treatment of MDD. Significant improvements versus placebo in core emotional symptoms as well as painful physical symptoms associated with depression, were seen in most, but not all, appropriately designed studies; results of meta-analyses suggested that improvements in these efficacy measures were apparent after 1-2 weeks' treatment with the highest recommended dosage of 60 mg once daily. Short-term (< or =15 weeks) administration of duloxetine at fixed or flexible dosages between 60 and 120 mg/day was noninferior to paroxetine 20 mg once daily, noninferior or inferior to escitalopram 10-20mg once daily, and had a similar global benefit-risk (GBR) profile to that of venlafaxine extended-release (XR) 150-225 mg/day in the treatment of MDD. Longer-term (6-8 months) treatment with duloxetine was similar in efficacy to paroxetine and escitalopram. Duloxetine is generally well tolerated, although it may be appropriate to avoid initiating treatment with the 60 mg/day dosage, as this has been associated with a higher discontinuation rate due to adverse events in some (but not all) comparative studies with escitalopram and venlafaxine XR. Definitive comparisons are awaited, although duloxetine seemingly provides a useful alternative to SSRIs and other SNRIs for the treatment of MDD. It also appears to be an attractive option for MDD patients presenting with painful physical symptoms.

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Measures of serum sodium could be Uroxatral Buy ascertained in only a subpopulation.

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Risks of persistent pulmonary hypertension of the newborn associated with early and late exposure to SSRIs during pregnancy and adjusted for important maternal and pregnancy Anafranil Online Order characteristics. Comparisons were made between infants exposed and not exposed to SSRIs.

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Antidepressants, more specifically SSRIs, represent one example of a widely prescribed class of medications in pregnant women for which less than adequate pregnancy data have been available since the first drug in this class was marketed 20 years ago. Moreover, findings from studies performed after Cardura Generic Name 2005, when health governmental authorities issued warnings regarding first trimester exposure to paroxetine and the risk of cardiac malformations, may be the result of detection bias if physicians were investigating more their pregnant patients that used paroxetine than the others.

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The Seroquel Generic Cost prevalence rate of weight gain was 55.2%; 40.6% of the patients had a weight gain of 7% or more compared to the baseline. Overall, antidepressant use was significantly related to increased body weight. Specifically, citalopram, escitalopram, sertraline, paroxetine, venlafaxine, duloxetine and mirtazapine, but not fluoxetine, were associated with significant weight gain. Multivariate logistic regression analysis indicated that lower education status, lower body mass index at the onset of antidepressant use and family history of obesity were independent predictors of weight gain ≥7% compared to the baseline.

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The positive motivational effects of a range of antidepressants/neurotransmitter reuptake inhibitor compounds were studied using conditioned place preference. These agents included amitriptyline (2.5-10 mg/kg), venlafaxine (5 and 10 mg/kg), sibutramine (5 and 10 mg/kg), fluoxetine (2.5-10 mg/kg), paroxetine (5-15 mg/kg) and sertraline (2.5-10 mg/kg). Male Wistar rats were place conditioned in a three-compartment box to vehicle or drug alternately for 8 days using a 30-min pretreatment time. Control animals received vehicle only. Cocaine (5 mg/kg) was used as a positive control for the procedure. Significant place preference (P<0.05) was observed with paroxetine (15 mg/kg), fluoxetine (5 and 10 mg/kg), sertraline (2.5-10 Avodart Generic Brand mg/kg) and cocaine. Venlafaxine and sibutramine, serotonin/noradrenaline reuptake inhibitors, produced no place conditioning, while the highest dose of the tricyclic antidepressant, amitriptyline (10 mg/kg), produced signs of place aversion. The role of serotonin in reward pathways and differences in serotonin, noradrenaline and dopamine reuptake-inhibiting properties of these compounds may explain why only the serotonin-selective reuptake inhibitors produced place preference in this study.

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Up to a third of elderly patients with major depressive disorder are treatment resistant, yet little objective evidence is available to guide the clinician in managing these patients. We report here our experience with elderly Hytrin Generic Name subjects with prospectively defined treatment-resistant depression in 2 separate research studies: one entailing an augmentation strategy, the other a change to venlafaxine extended release (XR).

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Data obtained from this study revealed that the aqueous root extract of L. cupanioides restored sexual competence in sexually impaired rats possibly by increasing sexual drive through enhanced reproductive hormones concentration, particularly testosterone, thus supporting the folkloric claim of the plant for the management of sexual disorder in males.

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In vivo extracellular unitary recordings, in vitro 3H-5-hydroxy-tryptamine (5-HT) uptake, and 3H-paroxetine binding assays were used to assess the effect of acute and long-term administration of the 5-HT reuptake inhibitor paroxetine on the neuronal 5-HT transporter in the rat dorsal hippocampus. Recovery time of the firing activity of CA3 hippocampus pyramidal neurons following microiontophoretic application of 5-HT was used as an index of in vivo reuptake activity. In a first series of experiments, the acute intravenous administration of paroxetine and 5-HT denervation with the neurotoxin 5,7-dihydroxytryptamine produced a marked prolongation of the suppressant effect of 5-HT, indicating that reuptake into 5-HT terminals plays a significant role in terminating the action of microiontophoretically applied 5-HT. In a second series of experiments, rats were treated with paroxetine (10 mg/kg/d, s.c.) for 2 or 21 d. In both treatment groups, there was a marked prolongation of the effect of microiontophoretically applied 5-HT; however, in rats treated for 2 d, the prolongation was significantly greater than that observed in rats treated for 21 d. After the 21 d treatment with paroxetine and a 48 hr washout, the prolongation of the effect of microiontophoretically applied 5-HT by acute intravenous paroxetine was significantly reduced, suggesting a decrease in the number of 5-HT carriers. In keeping with this interpretation, following the same treatment regimen, there was a 50% and 60% reduction of the in vitro 3H-5-HT uptake in hippocampal and dorsal raphe slices, respectively, and a reduced effectiveness of paroxetine in blocking 3H-5-HT uptake in both regions. The determination of the binding parameters of 3H-paroxetine revealed that, in rats treated for 21 d with paroxetine (10 mg/kg/d, s.c.), following a 48 hr washout Kd values were unchanged but Bmax values were reduced by 70% and 60% in hippocampal and cortical membranes, respectively.

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Mean change in the primary efficacy measure was greater with escitalopram 10 and 20 mg than with placebo; 10 mg was more efficacious than paroxetine. Paroxetine was superior to placebo on some secondary measures, at some time points. Compared with placebo, more patients withdrew because of adverse events with escitalopram 20 mg and paroxetine.