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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:
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.

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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Use of medications with anticholinergic activity is widespread in older adults. Several studies have highlighted that anticholinergic use may be associated with an increased risk of dementia. The objective of this narrative review is to describe and evaluate studies of anticholinergic medication use and dementia and provide practical suggestions for avoiding use of these medications in older adults. A comprehensive review of the literature, citations from recent reviews and the author's personal files was conducted. Four studies were found that evaluated anticholinergic use and dementia as the primary outcome. Three studies focused on overall anticholinergic medication use and reported a statistically significantly increased risk of Alzheimer's disease or dementia. In one study, dementia risk was primarily found with higher cumulative doses; people using anticholinergic medications at the minimum effective dose recommended for older adults for at least 3 years were at highest risk. In contrast, a study conducted in nursing-home residents with depression did not find that paroxetine [a highly anticholinergic selective serotonin reuptake inhibitor antidepressant, (SSRI)] increased risk for dementia compared with other SSRIs (without anticholinergic activity). Further study is needed to understand the mechanism by which anticholinergic medications may increase risk. In conclusion, there is evidence from three observational studies suggesting that anticholinergic medications may increase dementia risk. Given this potential risk and the myriad of other well-known adverse effects (i.e. constipation, blurred vision, urinary retention, and delirium) associated with anticholinergic medications, it is prudent for prescribers and older adults to minimize use of these medications and consider alternatives when possible.

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The main hypothesis regarding the mechanism of action of antidepressant drugs is monoaminergic and mainly involves two neurotransmitters, serotonin and noradrenaline. Despite the well-recognized therapeutic efficacy of selective serotonin reuptake inhibitors (SSRIs), some disadvantages still occur. For example, they often require 4-6 weeks to achieve clinical benefits in depressed patients. In the past, some molecules that could shorten this long delay of action have been identified. The role of presynaptic autoreceptors - the activation of which leads to an inhibitory feedback control on neurotransmitter synthesis and release - has been extensively studied for antidepressant effects. In our laboratory, we studied the combined effects of an SSRI and a serotonin autoreceptor antagonist of the 5-HT1B subtype using intracerebral in vivo microdialysis in awake, freely moving mice. Important information on SSRIs has been obtained by applying this technique to genetically modified animals, such as constitutive knockout (KO) mice lacking 5-HT1B receptors (5-HT1B KO) generated by homologous recombination: we compared the effects of a combined treatment on extracellular/intrasynaptic levels of serotonin in various nerve terminals area in wild-type control and KO mice. Thus, we found that indirect activation of 5-HT1B autoreceptors limits the effects of SSRIs on dialysate 5-HT levels at serotonergic nerve terminals such as the ventral hippocampus. The study of substance P (neurokinin 1 receptor [R-NK1]) offers another example of the use of KO mice in the development of a new class of antidepressant drugs. NK1 receptor antagonists may display anxiolytic/antidepressant-like properties. The lack of selective compounds for each tachykinin receptor subtype (R-NK 1, R-NK2 or R-NK3) and differences in their affinity between animal species have made R-NK1 KO mice a very useful experimental tool. In collaborative work we found that genetic (R-NK1 KO mice) or pharmacological (GR205171) blockade of R-NK1 is associated with several changes: the increase in cortical 5-HT outflow caused by systemic injection of paroxetine was 4- to 6-fold higher in freely moving R-NK1 KO mice than in wild-type controls. The constitutive lack of NK1 receptors is associated with a functional desensitization of somatodendritic 5-HT1A autoreceptors, resembling that induced by chronic treatment with SSRI antidepressants. These results highlight the link between a neurotransmitter (serotonin) and a neuropeptide (substance P). This genetic strategy allowed us to point out that multiple targets participate to the effects of classical antidepressant drugs within the brain. We hope that, soon, some mice lines (constitutive or tissue specific, conditional rescue mice having alterations of sleep/wakefulness and/or food intake, altered central serotonin and/or noradrenaline neurotransmission, deficit in neurotrophic factors, but increases in intrasynaptic concentrations of substance P) could be a relevant model of the physiopathology of depressive disorders, and could help us understand the appearance of some symptoms. These recent findings suggest that instead of being rejected, the monoaminergic hypothesis of depression should be improved, corrected and completed by studying the role of other neurotransmitter, neuromodulatory compounds (substance P, BDNF [brain-derived neurotrophic factor]). By doing so, it thus could be possible to improve antidepressant drug treatment, i.e. shorten their long delay of action and/or to decrease treatment resistance or improve its tolerance.

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A total of 21 RCTs (4969 participants) were identified. Combined fluoxetine/CBT exhibited the highest efficacy, with fluoxetine alone superior to CBT, paroxetine, sertraline, citalopram, escitalopram, and placebo treatment. Sertraline, paroxetine, escitalopram, and venlafaxine showed superior acceptability to fluoxetine and combined fluoxetine/CBT. Combined fluoxetine/CBT combination was less safe, though CBT was safer than fluoxetine alone. Combined fluoxetine/CBT, fluoxetine, and mirtazapine exhibited the highest efficacy; sertraline, escitalopram, venlafaxine, and paroxetine were the best tolerated; and mirtazapine and venlafaxine were the safest.

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Avoiding the use of clorimipramine, paroxetine, valproate, and atypical antipsychotics during pregnancy is advisable. However, when starting or continuing pharmacological treatment during pregnancy, clinicians should consider not only the intrinsic iatrogenic risk of birth defects or perinatal complications, but also the general safety profile for the expectant mother. Indeed, specific adverse reactions (such as nausea, vomiting, constipation, and excessive weight gain) may aggravate the classic clinical findings of pregnancy, thus indirectly facilitating the occurrence of pregnancy complications and fetal and neonatal problems.

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A review of the consequences of maternal depression on fetal and infant development and the risk and benefits of SSRI use.

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Nearly two thirds of patients with major depressive disorder suffer from a physical illness, and about one fifth of patients with chronic physical illness are depressed. Both of these comorbidities pose diagnostic and therapeutic challenges. Therapeutic effects of antidepressants on pain improvement in patients with chronic physical illnesses and comorbid depression/anxiety have been attributed to the antidepressant or anxiolytic properties of these drugs. However, tricyclic antidepressants have demonstrated analgesic properties in patients with physical illness both with and without depression. The review looks at evidence for the efficacy of the selective serotonin reuptake inhibitor paroxetine on pain in physical illness with and without depression and the mechanisms for the relief of pain and depression.

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Steady-state blood concentrations of (R)- methadone (i.e., the active form), (S)-methadone, and (R,S)-methadone were measured before and after introduction of paroxetine 20 mg/day during a mean period of 12 days in 10 addict patients in methadone maintenance treatment. Eight patients were genotyped as CYP2D6 homozygous extensive metabolizers (EMs) and two patients as poor metabolizers (PMs). Paroxetine significantly increased concentrations of both enantiomers of methadone in the whole group (mean increase for (R)-methadone +/- SD, 26 +/- 32%; range, -14% to +83%, p = 0.032; for (S)-methadone, 49 +/- 51%; range, -29% to +137%, p = 0.028; for (R,S)-methadone, 35 +/- 41%; range, -20% to +112%, p = 0.032) and in the group of eight EMs (mean increase, 32%, p = 0.036; 53%, p = 0.028; and 42%, p = 0.036, for (R)-methadone, (S)-methadone, and (R,S)-methadone, respectively). On the other hand, in the two PMs, (S)-methadone but not (R)-methadone concentrations were increased by paroxetine (mean increases of 36% and 3%, respectively). Paroxetine is a strong CYP2D6 inhibitor, and these results confirm previous studies showing an involvement of CYP2D6 in methadone metabolism with a stereoselectivity toward the (R)-enantiomer. Because paroxetine is a mild inhibitor of CYP1A2, CYP2C9, CYP2C19, and CYP3A4, increase of (S)-methadone concentrations in both EMs and PMs could be mediated by inhibition of any of these isozymes.

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Research suggests high rates of discontinuation of selective serotonin reuptake inhibitors (SSRIs).

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Triiodothyronine (T3) augmentation in treatment-resistant depression had been successfully performed with both tricyclic as well as with SSRI antidepressants. In this paper, the efficacy of addition of moderate dose of l-thyroxine (T4) to serotonergic antidepressants in refractory depression was evaluated.

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The dose regimen for paroxetine in the treatment of depression has been well established through a number of individual dosing studies and analyses from the worldwide clinical data base. The starting dose, which is also the minimal effective dose, is 20 mg/day. For most patients, 20 mg/day will also be the optimal dose. For patients who do not show an adequate therapeutic response within 1 to 3 weeks of initiating therapy, the dose of paroxetine should be increased in 10-mg increments no more often than at weekly intervals to a maximum of 50 mg/day. Medication should be given as a single daily dose, usually in the morning. The therapeutic dose range in the elderly is 20 mg to 40 mg of paroxetine.

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Although paroxetine is a very potent inhibitor of the SERT, paroxetine also Cipro 600 Mg inhibits the NET at serum concentrations > 100 ng/mL. This novel finding may underlie the broad therapeutic utility of paroxetine in mood and anxiety disorders.

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The correlation of clinical Prograf 25 Mg effects with brain drug levels in the paroxetine group suggests that relationships between drug response and brain drug concentrations merit further investigation.

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To assess the efficacy and tolerability of paroxetine 20mg daily, for the treatment of depression and depression Aricept Dose Time associated with anxiety.

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To conduct Strattera Dosage Amounts a comprehensive, systematic review and meta-analysis of the efficacy and tolerability of mirtazapine over other antidepressants in the acute-phase treatment of major depression.

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Healthy (n = 32) and diabetic Hytrin Brand Name (n = 32) rats were further divided into 2 groups of saline or paroxetine administration.

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It is uncertain as to what short-term outcomes predict long- Aldactone Drug Interactions term treatment compliance and outcomes in patients with MDD.

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A case history is presented of a 35-year-old man who was referred because of his desire for amputation of his left leg, without sexual connotations. Abilify Drug Price The course of a combined cognitive behavioural psychotherapy with SSRI treatment is described.

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Major depressive disorder is often associated with elevated glucocorticoid levels, Naprosyn Generic which in turn suppress cell proliferation and neurogenesis in the hippocampus. Increasing evidence supports that antidepressants induce hippocampal neurogenesis and this induces speculation that decrease in hippocampal neurogenesis has causal relationship with depression. There is, however, a lack of information about neurogenic effects of antidepressants on the subventricular zone, which is another CNS region with continuous neurogenesis throughout adulthood. In the present study, we investigated whether corticosterone and the SSRI paroxetine, have effects on SVZ cell proliferation.

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A sensitive, robust, and selective liquid chromatographic-tandem mass spectrometric method Vigrx Negative Reviews (LC-MS/MS) was developed and validated for paroxetine quantification in human EDTA plasma.