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Cymbalta

Generic Cymbalta is an effective medication with highly developed components which is taken in treatment of serious depression and all symptoms connected with depression. Generic Cymbalta is an antidepressant in a group of drugs called selective serotonin and norepinephrine reuptake inhibitors (SSNRIs). Generic Cymbalta affects chemicals in the brain that may become unbalanced and cause depression.

Other names for this medication:
Ariclaim, Delok, Deloxi, Duloxetin, Duloxetina, Duloxetinum, Duxetin, Duzela, Xeristar, Yentreve

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Also known as: Duloxetine.

Description

Generic Cymbalta is developed by medical scientists to treat major depressive disorder and general anxiety disorder. It is an antidepressant in a group of drugs called selective serotonin and norepinephrine reuptake inhibitors. Generic Cymbalta affects chemicals in the brain that may become unbalanced and cause depression.

Generic Cymbalta is also used to treat a chronic pain disorder called fibromyalgia, treat pain caused by nerve damage in people with diabetes (diabetic neuropathy) and to treat chronic musculoskeletal pain, including discomfort from osteoarthritis and chronic lower back pain.

Dosage

Take Generic Cymbalta with a full glass of water with or without food.

It is recommended to take Generic Cymbalta at the same time each day.

Do not crush, chew, break, or open a delayed-release capsule. Swallow the tablet whole.

If you want to achieve most effective results do not stop using Generic Cymbalta suddenly.

Overdose

If you overdose Generic Cymbalta and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at a room temperature between 4 and 30 degrees C (39 and 86 degrees F) away from moisture, light and heat. Throw away the after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Cymbalta 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 Cymbalta if you are allergic to Generic Cymbalta components.

Do not take Generic Cymbalta if you're pregnant or you plan to have a baby, or you are a nursing mother. This medication can cause birth defects. Tell your doctor right away if you become pregnant during treatment.

Be very careful with Generic Cymbalta if you're pregnant or you plan to have a baby. Do not take Generic Cymbalta if you are breast-feeding.

Do not take Generic Cymbalta together with thioridazine (Mellaril), or an MAO inhibitor such as furazolidone (Furoxone), isocarboxazid (Marplan), phenelzine (Nardil), rasagiline (Azilect), selegiline (Eldepryl, Emsam, Zelapar), or tranylcypromine (Parnate). A dangerous drug interaction could occur, leading to serious side effects. You must wait at least 14 days after stopping an MAO inhibitor before you can take Generic Cymbalta. After you stop taking Generic Cymbalta, you must wait at least 5 days before you start taking an MAOI.

Generic Cymbalta can be not safety for children and people younger than 18 years old.

Do not take Generic Cymbalta if you have any of these conditions:liver or kidney disease, seizures or epilepsy, a bleeding or blood clotting disorder, glaucoma, bipolar disorder (manic depression), a history of drug abuse or suicidal thoughts.Be careful if you drive or do anything that requires you to be alert. Generic Cymbalta may impair your thinking or reactions.

Avoid alcohol.

It can be dangerous to stop Generic Cymbalta using suddenly.

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Generalized anxiety disorder (GAD), a prevalent and chronic illness, is associated with dysregulation in both serotonergic and noradrenergic neurotransmission. Our study examined the efficacy, safety, and tolerability of duloxetine hydrochloride, a dual reuptake inhibitor of serotonin and norepinephrine, for short-term treatment of adults with GAD. In a 10-week, double-blind, progressive-titration, flexible-dose trial, 327 adult outpatients with a DSM-IV-defined GAD diagnosis were randomized to duloxetine 60-120 mg (DLX, N=168) or placebo (PLA, N=159) treatment. The primary efficacy measure was mean change from baseline to endpoint in Hamilton Anxiety Scale (HAMA) total score. Secondary outcome measures included response rate (HAMA total score reduction > or =50% from baseline), Clinician Global Impression-Improvement (CGI-I) scores, and Sheehan Disability Scale (SDS) scores. Patients who received duloxetine treatment demonstrated significantly greater improvement in HAMA total scores (P=.02); a higher response rate (P=.03), and greater improvement (P=.04) than patients who received placebo. Duloxetine-treated patients were also significantly more improved than placebo-treated patients on SDS global functional (P<.01) and work, social, and family/home impairment scores (P<.05). The rate of discontinuation due to adverse events (AEs) was higher for the duloxetine group compared with the placebo group (P=.002). The AEs most frequently associated with duloxetine were nausea, dizziness, and somnolence. Duloxetine was an efficacious, safe, and well-tolerated treatment that resulted in clinically significant improvements in symptom severity and functioning for patients with GAD.

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There were 13 reviews of variable quality. Quality assessment of studies included in the reviews and their findings were adequately tabulated in all but four reviews. Meta-analysis of data was carried out in six reviews. Pelvic floor muscle training (PFMT) and other physical treatments, estrogens and duloxetine were better than no treatment in SUI. Based on the assessment as per GRADE system, only 2/13 (15.4%) reviews were deemed to be of high quality, 8/13 (61.5%) of moderate quality and 3/13 (23.1%) of low quality. The case for recommendation of PFMT and duloxetine was strong.

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In AERS all antidepressants had some degree of association with hepatic injury, in that at least one hepatic event was disproportionately represented for each drug. Signals were detected for duloxetine cases analyzed against full and antidepressant-only backgrounds. These signals corresponded to labeled events or events investigated during ongoing surveillance. Using a duloxetine fatal-case series, disproportional representation of clinically serious events was detected relative to both backgrounds, but the signals were refuted upon independent expert panel case review. The Aperio study showed no difference in hepatic injury between duloxetine and venlafaxine initiators after proper control for baseline risks, suggesting differential prescribing of duloxetine, perhaps preferentially as second-line therapy in some initiators.

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Data were analysed from all placebo-controlled trials of duloxetine completed as of December 2008. The 52 studies included 17,822 patients (duloxetine n = 10,326; placebo n = 7496) with major depressive disorder, generalized anxiety disorder, diabetic peripheral neuropathic pain, fibromyalgia, osteoarthritis knee pain (OAKP), chronic lower back pain and lower urinary tract disorders. The main outcome measures were rates of treatment-emergent adverse events (TEAEs) and adverse events reported as the reason for discontinuation.

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The available evidence shows that there does not seem to be any difference in efficacy between duloxetine and other oral pharmacological therapies, providing a valuable alternative for this disabling condition.

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In this randomized double-blind trial, adult nondepressed patients with a non-neuropathic CLBP and a weekly mean of the 24-hour average pain score>or=4 at baseline (0-10 scale) were treated with either duloxetine or placebo for 13 weeks. The dose of duloxetine during first 7 weeks was 60 mg once daily. At week 7, patients reporting<30% pain reduction had their dose increased to 120 mg. The primary outcome measure was the Brief Pain Inventory (BPI) 24-hour average pain rating. Secondary measures included Roland-Morris Disability Questionnaire-24; Patient's Global Impressions of Improvement; Clinical Global Impressions-Severity (CGI-S); BPI-Severity and -Interference (BPI-I); and weekly means of the 24-hour average pain, night pain, and worst pain scores from patient diaries. Quality-of-life, safety, and tolerability outcomes were also assessed.

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Tamsulosin is the main etiological agent involved in IFIS. However several cases of IFIS, supposedly secondary to drugs of different groups have recently been reported in the literature. The authors use this case report as a means to discuss why most of these cases should be considered anecdotal evidence.

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In depressed patients tricyclic antidepressants and selective serotonin and noradrenaline reuptake inhibitors can reduce not only depressive, but also painful physical symptoms. We investigated whether under treatment with duloxetine pain improves earlier than mood.

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Recent reviews have questioned whether the serotonin-norepinephrine reuptake inhibitor (SNRI) desvenlafaxine succinate offers any practical clinical advantages over existing SNRIs. The following case is one instance where it appears that this SNRI offers unique safety and benefit. Presented is a case report of a patient with Gilbert's syndrome, longstanding social phobia, and more recent depressive disorder not Luvox Cost otherwise specified, who was found to have elevated liver transaminases when prescribed both duloxetine and venlafaxine. The patient subsequently responded to desvenlafaxine but without liver abnormalities. In this patient with Gilbert's Syndrome, desvenlafaxine's lack of metabolism through the cytochrome P450 (CYP) 2D6 pathway may explain the avoidance of these abnormalities and thus suggests a possible therapeutic role for this SNRI in similarly susceptible patients.

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A significant group by time interaction was identified in the anterior default mode network in which MDD patients showed increased connectivity with Cymbalta Generic Brand treatment, while there were no significant changes in healthy participants. In the emotional Stroop task, increased posterior cingulate activation in MDD patients normalized following treatment. No significant group by time effects were observed for happy or sad facial processing, including in amygdala responsiveness, or in regional cerebral volumes. Reduced baseline resting state connectivity within the orbitofrontal component of the default mode network was predictive of clinical response. An early increase in hippocampal volume was predictive of clinical response.

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We evaluated all completed duloxetine trials in MDD with data lock by February 2, 2004. We compared incidence of suicide-related events with duloxetine versus placebo in controlled trials Compare Buspar Prices , using Mantel-Haenszel incidence difference (MHID) and exposure time-adjusted rate difference (MHRD) methods, and analyzed changes in Hamilton Depression Scale (HAMD) Item-3 (suicidality) scores.

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