Generic Strattera is used for treating attention deficit hyperactivity disorder (ADHD).
Other names for this medication:
Also known as: Atomoxetine.
Generic Strattera is used for treating attention deficit hyperactivity disorder (ADHD).
Generic Strattera is a selective norepinephrine reuptake inhibitor. Exactly how Generic Strattera works to treat ADHD is not known. Generic Strattera increases certain chemicals (e.g., norepinephrine) in the brain. This may affect attention span and behavior.
Strattera is also known as Atomoxetine, Attentrol, Tomoxetin, Attentin, Axepta.
Generic name of Generic Strattera is Atomoxetine.
Brand name of Generic Strattera is Strattera.
Take Generic Strattera by mouth with or without food. If stomach upset occurs, take with food to reduce stomach irritation.
Swallow Generic Strattera whole. Do not open or take the capsules apart.
Taking Generic Strattera at the same time each day will help you remember to take it.
If you want to achieve most effective results do not stop taking Generic Strattera suddenly.
If you overdose Generic Strattera and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medication after the expiration date. Keep out of the reach of children.
The most common side effects associated with Strattera are:
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 Strattera if you are allergic to Generic Strattera components.
Do not take Generic Strattera if you're pregnant or you plan to have a baby, or you are a nursing mother.
Do not Generic Strattera if you are taking or have taken a monoamine oxidase inhibitor (MAOI) (e.g., phenelzine) within the last 14 days.
Do not Generic Strattera if you have certain heart problems (e.g., heart defect, heart failure), certain types of irregular heartbeat, severe blood vessel problems, or narrow-angle glaucoma.
Children and teenagers who take Generic Strattera may be at increased risk for suicidal thoughts or actions. Adults may also be affected. The risk may be greater in patients who have had suicidal thoughts or actions in the past. The risk may also be greater in patients who have had bipolar (manic-depressive) illness, or if their family members have had it. Watch patients who take Generic Strattera closely!
Do not try to open the capsules or take them apart. Wash your hands immediately after using Generic Strattera. Do not get Generic Strattera in your eye. It may irritate your eye if you do. If you get Generic Strattera in your eyes or nose, rinse at once with cool water.
Lab tests, including heart rate, blood pressure, and liver function, may be performed while you use Generic Strattera.
Use Generic Strattera with caution in the elderly. They may be more sensitive to its effects, especially dizziness.
Corticosteroids may affect growth rate in children and teenagers in some cases. They may need regular growth checks while they take Generic Strattera.
Generic Strattera should be used with extreme caution in children younger than 6 years old. Safety and effectiveness in these children have not been confirmed.
Sit up or stand slowly, especially in the morning.
Avoid driving machine.
Do not stop taking Generic Strattera suddenly.
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Limited information exists on potentially adverse consequences following pediatric atomoxetine ingestions reported to poison control centers. Using pediatric atomoxetine ingestions reported to Texas poison control centers during 2003-2005, the proportion of cases involving serious outcomes (medical outcomes classified as moderate effects, major effects, death, or judged as potentially toxic exposures) was determined for selected variables and evaluated for statistical significance by calculating the rate ratio (RR) and 95% confidence interval (CI). Of 501 cases identified, 31 (6%) involved serious outcomes. Higher serious outcome rates were found with a maximum dose of >2.8 mg/kg or >200 mg or >4 tablets. Serious outcome rates were also higher if the exposure involved intentional self-harm or the patient was already at or en route to a health care facility when the poison control center was contacted or referred to a health care facility by the poison control center. The severity of the outcome associated with pediatric atomoxetine ingestions was dependent upon the dose and the circumstances of the ingestion (whether intentional self-harm was involved). The management of patients with serious outcomes was more likely to involve health care facilities. This information is useful for creating triage guidelines for the management of pediatric atomoxetine ingestions.
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Sleep disorders centers in a private practice setting and a hospital setting.
Color (C), form (F), and color-form (CF) combination naming were administered to 69 adults during outpatient evaluation, and pre- and posttreatment results were compared for 64 adults.
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Correlation analysis revealed a moderate-to-strong association between changes in the LPS total versus ADHDRS-IV-Parent:Inv total (r: -.68). The LPS Self-control subscale showed higher correlations than the Happy/Social subscale with the symptomatic measures. Regression analysis also showed high sensitivity for functional measures to changes in symptom severity. Stratified analysis of mean changes in ADHDRS-IV-Parent:Inv scores corresponding to standardized changes in LPS functional scores indicated that a threshold reduction of 16-18 points on the ADHDRS-IV-Parent:Inv total score was needed for functional improvements to become evident.
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The persistency rate of ATX was low because it was used for serious cases and MPH included the cases with proven effectiveness and discontinuation. There were also many cases requiring combination therapy. MPH had a high persistency rate for PDD, which did not necessarily mean that it was generally effective.
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These data provide initial evidence that combination use of atomoxetine and olanzapine for the treatment of ADHD and comorbid disruptive behaviors was effective in reducing ADHD symptoms and aggressive behavior in a 10 week treatment period.
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Chronic cerebral hypoperfusion (CCH) is a risk factor for the development of vascular dementia (VaD). CCH participates in a negative role in cognitive impairments. Transient receptor potential vanilloid subtype 1 (TRPV1) participates in cognition, ischemic damage and neuroprotection. Selective norepinephrine transporter (NET) inhibitors have a role in cognitive dysfunction and oxidative stress. The role of TRPV1 and NET in CCH induced VaD is still unknown. The present study has been structured to investigate the role of vanillin; a selective agonist of TRPV1 as well as atomoxetine; a selective NET inhibitor in CCH induced VaD in mice. Permanent bilateral common carotid arteries ligation or two vessel occlusion (2VO) technique was used to induce a stage of chronic cerebral hypoperfusion in mice. 2VO animals have shown significant impairment of locomotion (Actophotometer), motor coordination (Rota rod), learning and memory (Morris water maze). 2VO animals have shown significant reduction in brain catalase, glutathione, and superoxide dismutase, with significant increase in brain infarct size (TTC staining), malondialdehyde and acetyl cholinesterase-AChE activity. Whereas, administration of vanillin as well as atomoxetine has significantly attenuated 2VO induced impaired locomotion, motor coordination, learning and memory, brain damage, brain oxidative stress and higher AChE activity. It may be concluded that 2VO induced CCH has elicited VaD, which was attenuated by vanillin and atomoxetine. Thus, modulators of vanilloid receptors and norepinephrine transporter may be explored further for their benefits in CCH induced VaD.
Several million children and a growing number of adults are currently being treated for attention-deficit hyperactivity disorder (ADHD) worldwide. Concerns have been expressed about possible cardiac effects of the common treatments, namely methylphenidate, amphetamines and atomoxetine. Small increases in mean heart rate (HR) and mean blood pressure (BP) have been reported for all three drugs, but most of the studies have not yielded statistically significant results. These studies also have limitations, particularly regarding the lack of accepted and standardised measurement methods. Several large studies of the very rare phenomenon of sudden death in children have failed to show any convincing association with ADHD treatment. Whether minor increases in HR and BP have a cumulative effect over many years and have a long-term adverse effect on cardiovascular health remains undetermined.
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Results from the GIPD suggest that patient quality of life improves with time on atomoxetine. The effectiveness of atomoxetine in an open-label study was very similar to the effectiveness shown in placebo-controlled trials.
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Atomoxetine (ATX) is a selective norepinephrine reuptake inhibitor approved since 2002 for the treatment of attention deficit hyperactivity disorder (ADHD) in children, adolescents, and adults as an alternative treatment to methylphenidate. Within the framework of a project evaluating the use of alternative biological matrices for therapeutic monitoring of psychoactive drugs in paediatric and non-paediatric individuals, the excretion of ATX and its principal metabolites has been recently studied in oral fluid and hair. The aim of this study was to describe the excretion profile of ATX and its metabolites 4-hydroxyatomoxetine (4-OH-ATX) and N-desmethylatomoxetine (N-des-ATX) in sweat following the administration of different dosage regimens (60, 40, 35, and 18 mg/day) of ATX to six paediatric patients. Sweat patches were applied to the back of each participant and removed at timed intervals. ATX and its metabolites were measured in patches using a previously validated liquid chromatography-tandem mass spectrometric (LC-MS/MS) method. Independently from the administered dose, ATX appeared in the sweat patches 1 h post administration and reached its maximum concentration generally at 24 h. Peak ATX concentrations ranged between 2.31 and 40.4 ng/patch and did not correlate with the administered drug dose, or with body surface area. Total ATX excreted in sweat ranged between 0.008 and 0.121 mg, corresponding to 0.02 and 0.3% of the administered drug. Neither 4-OH-ATX, nor N-des-ATX was detected in either of the collected sweat patches. Measuring ATX in sweat patches can provide information on cumulative drug use from patch application until removal.
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Attainment of a stable dosing regimen was defined as no change in type of drug (including a switch from an immediate release (IR) to a long-acting (LA) formulation), strength, and number of pills per day for five consecutive dispensings. Time to stable dosing regimen was defined as the number of days between the first dispensing for an ADHD drug and the first of five unchanged dispensings.
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The pharmacology, pharmacokinetics, clinical efficacy, safety, drug interactions, dosage and administration, and place in therapy of atomoxetine in the treatment of attention-deficit/hyperactivity disorder (ADHD) are reviewed.
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The clinical presentation of autonomic failure is orthostatic hypotension. Severely affected patients require pharmacological treatment to prevent presyncopal symptoms or frank syncope. We previously reported in a proof of concept study that pediatric doses of the norepinephrine transporter blockade, atomoxetine, increases blood pressure in autonomic failure patients with residual sympathetic activity compared with placebo. Given that the sympathetic nervous system is maximally activated in the upright position, we hypothesized that atomoxetine would be superior to midodrine, a direct vasoconstrictor, in improving upright blood pressure and orthostatic hypotension-related symptoms. To test this hypothesis, we compared the effect of acute atomoxetine versus midodrine on upright systolic blood pressure and orthostatic symptom scores in 65 patients with severe autonomic failure. There were no differences in seated systolic blood pressure (means difference=0.3 mm Hg; 95% confidence [CI], -7.3 to 7.9; P=0.94). In contrast, atomoxetine produced a greater pressor response in upright systolic blood pressure (means difference=7.5 mm Hg; 95% CI, 0.6 to 15; P=0.03) compared with midodrine. Furthermore, atomoxetine (means difference=0.4; 95% CI, 0.1 to 0.8; P=0.02), but not midodrine (means difference=0.5; 95% CI, -0.1 to 1.0; P=0.08), improved orthostatic hypotension-related symptoms as compared with placebo. The results of our study suggest that atomoxetine could be a superior therapeutic option than midodrine for the treatment of orthostatic hypotension in autonomic failure.
For in vivo studies, besipirdine or duloxetine effects on cystometric parameters and striated sphincter electromyographic (SS-EMG) activity were investigated. On the isolated urethra, norepinephrine (NE) concentration-response curves (CRC) were performed in the presence of besipirdine, duloxetine or tomoxetine. Moreover, CRC to HP-748 were constructed in the absence or presence of prazosin. Potency (pEC(50)) and maximal responses (E(max)) were determined.
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A continued improvement of symptoms is expectable until 12 weeks in treatment-naïve ADHD patients treated with atomoxetine as first-line medication. Chief limitations are the small, national sample size and the absence of data beyond the 12-week time-point.
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Atomoxetine was effective for the treatment of ADHD in patients with comorbid ODD. It did not significantly reduce the severity of ODD symptoms, and was well tolerated by the patients.
Data were available for 132 children (ages 5-14), 81.8% of whom had no previous ADHD medication exposure, and 97.0% of whom had started at least one medication. Methylphenidate was used first for 59.8% of children, whereas 33.3% started with an amphetamine product. Of the 47.0% of children who progressed to a second medication trial, 88.7% tried a stimulant from a second class. In total, 19.7% tried atomoxetine, which was typically used as a third stage choice (i.e., after two different stimulant exposures). Stage four to six medications were rarely used, rather stimulants were retried after atomoxetine and/or medication combinations were tried. Symptomatic remission at the end of treatment was achieved by 70.4% and 82.4%, according to parents and teachers respectively, for those with outcome data and who completed treatment. Outcomes for those further along the treatment algorithm were similar to discharges at the beginning of the algorithm.
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To compare the short term efficacy and tolerability of methylphenidate and atomoxetine in children with Attention deficit hyperactivity disorder (ADHD).
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Atomoxetine is cost-effective and may have advantages over stimulants, including benefits to HRQL and no abuse liability and is the only treatment in the UK licensed for continued treatment into adulthood in adolescents who have shown a response from treatment.
To report a case of hepatitis associated with atomoxetine hydrochloride use and to describe the previously-unpublished severe cases of this syndrome.
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The Register was aimed at assessing the benefit-risk profile of the treatment of attention deficit hyperactivity disorder (ADHD) with atomoxetine and methylphenidate.
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A retrospective chart review was conducted to identify major depressive disorder (MDD) patients who had experienced significant symptom improvement (either partial response or remission) following treatment with conventional antidepressants but who were continuing to complain of fatigue. Fourteen such patients (42.2+/-13.4 years of age, five women, baseline HDRS 6.2+/-2.4) with a 17-item Hamilton Depression Rating Scale (HDRS17)<11 who received adjunctive atomoxetine for fatigue were included in the report. Antidepressants augmented were the selective serotonin reuptake inhibitors (SSRIs) (n=11; 78.6%), mirtazapine (n=2, 14.3%), and amitriptyline (n=1, 7.1%).
0.4%; aHR: 7.85, 95% CI: 7.09-8.70), and had a younger mean age at the time of first diagnosis (ADHD: 12.0 years vs.
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Atomoxetine is the first of the group of non-stimulant drugs to be approved by the US Food and Drug Administration to treat this disorder in children, adolescents and adults. Atomoxetine has a direct effect on noradrenalin and dopamine concentrations by exerting a strong and highly selective inhibiting action on the pre-synaptic noradrenalin transporter, with a minimum affinity for other transporters and receptors. After adjustment of the dosage for body weight, the pharmacokinetic parameters are similar across all age and gender groups. Maximal plasma concentration is reached one to two hours after oral administration. Data concerning the effectiveness and safety from the clinical trials and studies reported in the literature are discussed.
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Statistically significantly greater improvement in executive function was observed in young adults with ADHD in the atomoxetine versus placebo group as measured by changes in the BRIEF-A scales.
At the end of the study, it was seen that clinical recovery achieved by ATX and OROS-MPH therapy was associated with improved cognitive processes, and that these agents do not only lead to behavioral changes but also to an improvement in cognitive processes. In addition, improvements in cognitive processes occurred simultaneously with behavioral recovery. Behavior is the result of neurocognitive processes, and further studies on the domains that these drugs affect, or the way in which these agents exert their effects, are needed.
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The locus coeruleus (LC) is the largest norepinephrinergic cell group in the central nervous system and contains a high density of norepinephrine (NE) uptake sites. Alcohol-preferring (AP) rats and high-alcohol-drinking (HAD) rats are selectively bred for high alcohol preference, whereas alcohol-nonpreferring (NP) rats and low-alcohol-drinking (LAD) rats are bred for low alcohol preference. However, it is unknown whether NE uptake sites in the LC are associated with alcohol preference in AP and HAD rats when compared with their respective control rats, NP and LAD rats. This study was designed to examine this question.
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Relevant literature on the long-term (defined as ≥ 12 months) cardiovascular effects of stimulant class medications for ADHD was sought using PubMed searches for clinical literature, epidemiological reports, as well as reviews of post-marketing data and clinical guidelines/consensus statements. Comparison was made to the non-stimulant atomoxetine.
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Doses of methylphenidate (10, 20, and 40 mg) and atomoxetine (20, 40, and 80 mg) were tested once while placebo was tested twice in 12 cigarette smokers. One hour after ingesting drug, participants smoked ad libitum for 4 h. Measures of smoking included total cigarettes, total puffs, and carbon monoxide levels. Snacks and decaffeinated drinks were available ad libitum, and food intake was calculated.
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The objective of this study is to investigate the relative contribution of dopamine (DA) and noradrenaline (NA) to the therapeutic effects of clinically effective drugs in ADHD using rats selected for high impulsivity on the five-choice serial reaction time task (5CSRTT).
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