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Women receiving antidepressants during pregnancy and their neonates were studied. Cord and maternal drug concentrations were measured at birth and in the neonates plasma on day 3. Neonates were also assessed using a range of neurobehavioral tests and compared to controls.
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Findings provide new insights into a melancholic profile of reduced ability to function interpersonally or effectively deal with one׳s emotions. This distinctly poorer capacity for social skills remained post-treatment. The pre-treatment profile may account for some of the difficulty in achieving remission or response with treatment.
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In the asymptomatic phase of the disease, panic disorder patients present a particular neurotic/anxious personality pattern. This pattern, although altered in the presence of acute symptoms, could be a focus of research.
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Apathy has a significant negative impact on the quality of life. It can be a part of other axis I and axis III disorders such as depression. It has also been reported as a treatment emergent side effect of SSRI drugs. A 48 year old male with diagnosis of personality change due to medical condition and depressive symptoms was started on Sertraline. Although his depressive symptoms, impulse control and his irritability improved significantly he became quite apathetic. This responded positively to a reduction in the dose of sertraline. Since apathy can be a residual symptom of depression it may be a valid consideration to increase the dose of the SSRI. However if apathy was not a significant part of depressive syndrome prior to SSRI treatment then antidepressant treatment emergent apathy needs to be considered and one option is to reduce the dose of the SSRI. Other options appear to be addition of other pharmacological agents such as stimulants, dopamine agonists, acetylcholinesterase inhibitors and NMDA antagonists.
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In the present study, we investigated whether restoring descending noradrenergic inhibitory tone can attenuate pain in a PD rat model, which was established by stereotaxic infusion of 6-hydroxydopamine (6-OHDA) into the bilateral striatum (CPu). PD rats developed thermal and mechanical hypersensitivity at the 4th week after surgery. HPLC analysis showed that NE content, but not dopamine or 5-HT, significantly decreased in lumbar spinal cord in PD rats. Additional noradrenergic depletion by injection of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) aggravated pain hypersensitivity in PD rats. At the 5th week after injection of 6-OHDA, systemic treatment with pharmacological norepinephrine (NE) precursor droxidopa (L-DOPS) or α2 adrenoceptor agonist clonidine significantly attenuated thermal and mechanical pain hypersensitivity in PD rats. Furthermore, application of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) reuptake inhibitors duloxetine, but not 5-HT selective reuptake inhibitors sertraline, significantly inhibited thermal and mechanical pain hypersensitivity in PD rats. Systemic administration of Madopar (L-DOPA) or the D2/D3 agonist pramipexole slightly inhibited the thermal, but not mechanical, hypersensitivity in PD rats. Thus, our study revealed that impairment of descending noradrenergic system may play a key role in PD-associated pain and restoring spinal noradrenergic inhibitory tone may serve as a novel strategy to manage PD-associated pain.
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Sertraline (Zoloft) is a selective serotonin reuptake inhibitor that is commonly used in adults in the treatment of mood and anxiety disorders. Whereas it also is used to treat these illnesses in children, it is not currently approved by the Food and Drug Administration for use in this population. Sertraline use has been increasing secondary to its efficacy and its more tolerable side effect profile than the tricyclic antidepressants. It is also much safer in overdose than the tricyclic antidepressants. Although there have been numerous reports of sertraline overdose in adults, reports in the pediatric population are much less common. We review the literature regarding sertraline overdose in children, describe a case of sertraline ingestion in a 22-month-old infant, and discuss the treatment of such an overdose.
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Ceriodaphnia dubia were tested to evaluate the acute and chronic interactive effects of diphenhydramine and sertraline. Observed effects were compared with 2 reference toxicity models, the concentration addition model and the independent action model. Results indicate that the 2 drugs exhibit additive toxicity in C. dubia. In some cases, individually sublethal concentrations of the chemicals resulted in 100% mortality when combined, demonstrating the potentially severe impact of trace environmental contaminants.
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We examined the effects of inhibition of MAPK kinase (MEK) in mouse behavioral models for depression including interactions with effects of antidepressant drugs. We also assessed the behavioral consequences of a heterozygous gene deletion for BDNF combined with MEK inhibition or stress.
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Current data suggest that monoamines, acetylcholine, amino acids, cortisol, thyroid hormones, and melatonin may be involved in the pathophysiology of bipolar disorder (BPD). Any neuropsychological or pharmacologic factor causing a disturbance in these neurochemicals may trigger manic/hypomanic switching. Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD, but only recently have the traditional antidepressants been systematically studied. Paroxetine, 20 mg/d, monotherapy in treatment of acute, relatively "pure" bipolar I and II depression, and fluoxetine monotherapy in bipolar II depression conferred a similar risk as placebo for TEM. Paroxetine or bupropion adjunctive therapy to mood stabilizer(s) had a similar risk as placebo for treatment of TEM in real world patients with bipolar depression during continuation treatment. Venlafaxine was shown to have an increased risk of TEM compared with bupropion and sertraline. The evolving literature continues to support the role of mood stabilizers in preventing future mood episodes of BPD.
Intervening in depression and/or low perceived social support within 28 days after myocardial infarction (MI) in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial did not increase event-free survival. The purpose of the present investigation was to conduct post hoc analyses on sex and ethnic minority subgroups to assess whether any treatment subgroup is at reduced or increased risk of greater morbidity/mortality.
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Varicella is largely a childhood disease, with more than 90% of cases occurring in children younger than 10 years. The primary infection is characterized by generalized vesicular dermal exanthemas, which are extremely contagious. Secondary bacterial infection and varicella pneumonia, usually seen in the immunocompromised or adult populations, may have high morbidity and mortality. Varicella in childhood is a generally benign and self-limited disorder; however, severe, life-threatening neurological complications may occur. We report a previously healthy eight-year-old boy who presented with acute hemiplegia and obsessive-compulsive disorder secondary to a lesion in lentiform nuclei associated with a history of recent varicella infection. The child was treated with sertraline for obsessive-compulsive disorder symptoms and made a full recovery.
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It is hoped that this practical commentary on research design, execution, analysis, and reporting, based on specific examples, will benefit researchers, authors, readers, and reviewers more than guidance delivered in the form of general advice.
T3 augmentation resulted in improvement of mood scores. The responders' rate of 42% in our study is comparable to the response rates reported using T3 or lithium to augment tricyclic antidepressants or other combination strategies used to treat resistant depression. Even though one patient withdrew prematurely due to side effects, the remaining 11 patients tolerated the addition of T3 very well. With the availability of T3, a viable, safe, inexpensive and effective augmentation treatment, the recent trend of replacing T3 with other novel strategies appears unwarranted.
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In both placebo- and sertraline-treated groups, most patients displayed minor fluctuations in antipsychotic serum levels over 6 weeks. There was no clinical evidence of drug interactions in the sertraline-treated group.
Major depression is a common diagnosis in older individuals. The authors present preliminary findings on the response to sertraline in depressed elderly patients with and without dementia. Previous research on antidepressant treatment in elderly patients suggests that it is effective in treating depression. The authors followed depressed patients with and without dementia. Treatment response was more marked in the subgroup without dementia, but there was no statistically significant difference in response between the two subgroups. Depressed elderly patients with dementia may improve on antidepressant treatment, although treatment response may be less robust than in depressed patients without dementia.
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The proposed method was successfully applied to the analysis of commercial tablets and the results obtained were in good agreement with those obtained using the reference method. Furthermore, the method was applied for the determination of SER in spiked and real human plasma. The mean % recovery (n = 3) was 94.33 ± 1.53 and 92.00 ± 2.65, respectively. A proposal of the reaction pathway was postulated.
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Cytochrome P450 2B6 (CYP2B6) is involved in the metabolism of drugs such as bupropion, efavirenz, propofol, and selegiline, among others. More than 200 commonly prescribed drugs and other xenobiotics were examined for their ability to inhibit CYP2B6-mediated bupropion hydroxylase activity. Thirty compounds were found exhibiting greater than 50% inhibition at 30 microM. Inhibitors of CYP2B6 were identified from a wide variety of therapeutic classes. The 2 platelet aggregation inhibitors, clopidogrel and ticlopidine, were both identified as potent inhibitors (IC50 = 0.0206 and 0.149 microM, respectively). Other inhibitors (IC50 < 1 microM) included clotrimazole, itraconazole, sertraline, and raloxifene. These in vitro data were used along with clinical pharmacokinetic information in the prediction of potential drug-drug interactions that could occur by inhibition of CYP2B6. Although few drugs tested are expected to cause drug interactions, clopidogrel and ticlopidine were identified as being of concern as potential inhibitors of clinical relevance. These findings are discussed in context to potential drug interactions that could be observed between these agents and drugs for which CYP2B6 is involved in metabolism.
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This case draws attention to REM sleep behaviour disorder and its potential interaction with depression and cognitive impairment, producing symptoms which can be mistaken for early dementia. The diagnosis of REM sleep behaviour disorder is easily missed, and it requires careful history-taking and sleep investigation in all suspected sufferers. Associated neurological, sleep and psychiatric conditions (including depression and cognitive impairment) may confound the diagnosis.
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The aim of the study was to evaluate the comparative risk of self-harm associated with the use of different antidepressants.
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The initial treatment of obsessive-compulsive disorder (OCD) has generally been limited to serotonergic agents, cognitive-behavioral therapy (CBT), or a combination of the two. These findings were supported by the POTS study for OCD in children and adolescents. However, treatment with serotonergic agents or CBT can take several weeks before benefit is seen; severe cases of OCD may require more immediate treatment.
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Both sertraline and amitriptyline are suitable for the treatment of Major Depression; sertraline is comparable to amitriptyline with regard to efficacy, and offers the additional benefit of a more favorable safety profile.
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The findings suggest that fibromyalgia, in contrast to major depression, may not be accompanied by activation of cell-mediated immunity.
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Glossodynia is chronic pain localized around the tongue, with no perceivable organic abnormalities. In the fields of oral and maxillofacial surgery, it is categorized as an oral psychosomatic disease. In contrast, psychiatric nosology classifies glossodynia as a pain disorder among somatoform disorders, per the DSM-IV. The patient was a 71-year-old woman who developed symptoms of glossodynia, specifically a sore tongue. In the decade before she presented to us, she had had bizarre symptoms of oral cenesthopathy such as the sensation that her teeth had become 'limp and floppy' and that she needles in her mouth. Treatment was attempted using several psychotropic drugs, but no satisfactory response was noted. Because the patient was referred to our outpatient clinic, we tried psychotropic therapy again. Additionally, valproic acid, tandospirone and sertraline were administered (in this order), but the patient still showed no response. However, when sertraline was changed to milnacipran, all symptoms disappeared in a short period. We suggest that a small dose of milnacipran can be effective for controlling oral cenesthopathy as well as glossodynia.
Like major depression, dysthymia has been associated with elevated production of interleukin-1 (IL-1 beta) in mitogen-stimulated lymphocytes. In the present investigation, we assessed whether the elevated IL-1 beta production in dysthymic patients would normalize following treatment with sertraline.
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To characterize the safety profile of dapoxetine in PE treatment and to report the incidence, severity, and type of adverse events.
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Several case reports have indicated that the selective serotonin re-uptake inhibitor (SSRI) fluoxetine increases phenytoin blood levels when given concurrently. The mechanism of this drug-drug interaction has been attributed to inhibition of CYP2C9-catalyzed hydroxylation of phenytoin to its major oxidative metabolite in humans, para-hydroxyphenyl phenyl hydantoin (HPPH). With a bank of human liver microsomes (HLM), four SSRIs (fluoxetine, norfluoxetine, sertraline, and paroxetine) were tested for inhibition of HPPH formation. Initially, the K(m) and V(max) values of phenytoin hydroxylation to HPPH were determined in the individual HLM samples. The average K(m) (n=8) was 9.7+/-2.9 microM. The V(max) varied fivefold, with an average value of 113+/-53 pmol HPPH/min/nmol CYP450. All of the SSRIs inhibited HPPH formation; resulting Ki values were 31.1+/-10.1 microM (fluoxetine) (n=5), 51.1+/-9.4 microM (norfluoxetine) (n=3), 52.2+/-21.5 microM (sertraline) (n=3), and 80.0+/-7.2 microM (paroxetine) (n=3). Sulfaphenazole (10 microM), utilized as a positive control for inhibition of HPPH formation, inhibited phenytoin hydroxylation (>95%) in all HLM samples. Diclofenac hydroxylation to 4'-OH diclofenac, a specific marker for CYP2C9 activity, was determined in HLM1-HLM6 and was highly correlated with HPPH formation in HLM1-HLM6, indicating that phenytoin hydroxylation in human liver microsomes is largely due to CYP2C9. This work presents direct evidence that the effect of fluoxetine on phenytoin blood levels may be explained by inhibition of CYP2C9-catalyzed phenytoin hydroxylation. In light of typical SSRI blood levels observed in patients, this study also suggests that the risk of a SSRI-phenytoin interaction is highest with fluoxetine and norfluoxetine, and less likely with sertraline and paroxetine.