Disease relevance of Aropax

• CONCLUSIONS: In patients with malignant melanoma, pretreatment with paroxetine appears to be an effective strategy for minimizing depression induced by interferon alfa [1].
• Paroxetine controlled release in the treatment of menopausal hot flashes: a randomized controlled trial [2].
• Comparison of paroxetine and nortriptyline in depressed patients with ischemic heart disease [3].
• The cost-effectiveness of psychotherapy and paroxetine for severe irritable bowel syndrome [4].
• Hyperglycemia associated with paroxetine [5].

Psychiatry related information on Aropax

• CONCLUSIONS: Paroxetine is an effective treatment for patients with generalized social phobia [6].
• CONCLUSIONS: Paroxetine showed moderate benefit for depressive symptoms and mental health function in elderly patients with dysthymia and more severely impaired elderly patients with minor depression [7].
• INTERVENTIONS: Patients were randomly assigned to receive paroxetine (n = 137) or placebo (n = 140), starting at 10 mg/d and titrated to a maximum of 40 mg/d, or problem-solving treatment-primary care (PST-PC; n = 138) [7].
• For dysthymia, paroxetine improved mental health functioning vs placebo among patients whose baseline functioning was high (difference in mean [SE] change in SF-36 mental component scores, 5.8 [2.02]; P =. 01) or intermediate (difference in mean [SE] change in SF-36 mental component scores, 4.4 [1.74]; P =.03) [7].
• Adult night terrors and paroxetine [8].

High impact information on Aropax

• CONCLUSIONS: The SSRI antidepressants paroxetine, fluoxetine, and sertraline were similar in effectiveness for depressive symptoms as well as multiple domains of health-related quality of life over the entire 9 months of this trial [9].
• Paroxetine treatment of generalized social phobia (social anxiety disorder): a randomized controlled trial [6].
• CONCLUSION: Venlafaxine ER is effective in the short-term treatment of generalized social anxiety disorder, with efficacy and tolerability comparable to paroxetine [10].
• Effects of the serotonin transporter gene promoter polymorphism on mirtazapine and paroxetine efficacy and adverse events in geriatric major depression [11].
• Unique directional changes in frontal cortex, cingulate, and hippocampus with CBT relative to paroxetine may reflect modality-specific effects with implications for understanding mechanisms underlying different treatment strategies [12].

Chemical compound and disease context of Aropax

• We report that administration of paroxetine, a widely prescribed antidepressant drug that acts by inhibiting reuptake of the neurotransmitter serotonin, suppresses the neurodegenerative process and increases the survival of huntingtin mutant mice, an animal model of Huntington's disease (HD) [13].
• CONCLUSIONS: For some patients taking sertraline and paroxetine who experience sexual dysfunction side effects, brief drug holidays may allow for significant improvement in sexual functioning without a significant return of depressive symptoms [14].
• Pindolol potentiation of paroxetine for generalized social phobia: a double-blind, placebo-controlled, crossover study [15].
• The clinical significance of this action on norepinephrine uptake is currently unknown, but this action may contribute to the broad therapeutic efficacy of paroxetine in the treatment of depression, panic disorder, social anxiety disorder, posttraumatic stress disorder, and generalized anxiety disorder [16].
• OBJECTIVE: This study compared the efficacy and safety of paroxetine and imipramine with that of placebo in the treatment of bipolar depression in adult outpatients stabilized on a regimen of lithium [17].

Biological context of Aropax

• METHODS: Maximal number of platelet tritiated paroxetine binding sites (Bmax) and dissociation constant (Kd) values were measured in patients with personality disorder (n = 24) and healthy volunteers (n = 12) [18].
• CONCLUSIONS: Normalization of platelet activation is associated with paroxetine treatment of patients with depression [19].
• Here we show that 3 structurally distinct SSRIs--fluoxetine, paroxetine, and citalopram--act directly on Burkitt lymphoma (BL) cells to trigger rapid and extensive programmed cell death [20].
• Side effect severity in paroxetine-treated patients with the C/C genotype was also greater [21].
• OBJECTIVE: The purpose of this study was to determine the extent of infant medication exposure through breast-feeding during maternal treatment with paroxetine [22].

Anatomical context of Aropax

• Levels of mRNA for the SERT in the raphe nucleus were also unaltered by chronic paroxetine treatment [23].
• 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 [24].
• RNA-injected Xenopus oocytes accumulate 5HT, and paroxetine or desipramine inhibit this uptake [25].
• Chronic administration of selective serotonin reuptake inhibitor (SSRI) paroxetine modulates human motor cortex excitability in healthy subjects [26].
• Paroxetine in breast milk [27].

Associations of Aropax with other chemical compounds

• OBJECTIVE: To determine if the 5HTTLPR polymorphism influences the efficacy and tolerability of mirtazapine and paroxetine hydrochloride, 2 frequently prescribed antidepressants with differing pharmacologic profiles, in geriatric depression [11].
• Our results indicate that the SSRIs fluoxetine, sertraline, and paroxetine decrease the K(m) of the conversion of 5alpha-dihydroprogesterone to allopregnanolone by human 3alpha-HSD type III 10- to 30-fold [28].
• Surprisingly, the effects of the selective serotonin reuptake inhibitors (SSRIs) fluoxetine, sertraline, and paroxetine were also absent or severely attenuated in the Dbh(-/-) mice [29].
• CONCLUSIONS: During treatment with clinical doses of paroxetine or citalopram, approximately 80% of 5-HTT receptors are occupied [30].
• METHOD: A double-blind, placebo-controlled, crossover design was used to compare addition of 5 mg of pindolol t.i.d. or placebo for 4 weeks to a steady paroxetine dose [15].

Gene context of Aropax

• RESULTS: Survival analysis showed discontinuations due to paroxetine-induced side effects were strongly associated with the HTR2A C/C genotype [21].
• Furthermore, paroxetine lowered expression of the platelet activation marker CD63 in response to two different concentrations of thrombin receptor-activating peptide (P < .01) [31].
• Paroxetine substantially inhibits CYP2D6 but doses not appear to inhibit any other CYP enzyme [32].
• Determinants of interindividual variability and extent of CYP2D6 and CYP1A2 inhibition by paroxetine and fluvoxamine in vivo [33].
• We identified a paroxetine-treated mother and her infant who were both CYP2D6 poor metabolizers, as well as a citalopram-treated mother with CYP2C19 poor metabolizer status, but the serum drug levels of their infants were still either undetectable (paroxetine) or low (citalopram) [34].

Analytical, diagnostic and therapeutic context of Aropax

• METHODS: In a double-blind study of 40 patients with malignant melanoma who were eligible for high-dose interferon alfa therapy, we randomly assigned 20 patients to receive the antidepressant paroxetine and 20 to receive placebo [1].
• METHODS: This was a placebo-controlled multicenter study comprising a single-blind acute treatment phase (12 weeks) and a randomized, double-blind maintenance treatment phase (24 weeks) for patients who had responded to paroxetine during the acute phase [35].
• Compared with placebo, paroxetine treatment significantly (P<.001) improved the symptoms of social anxiety as shown on the Liebowitz Social Anxiety Scale, Social Phobia Inventory, Sheehan Disability Scale, Symptom Checklist-90 score, and EuroQol visual analogue scale, indicating decreased disability and increased well-being [35].
• CONCLUSION: Paroxetine had no influence on fatigue in patients receiving chemotherapy [36].
• In a double-blind, placebo controlled and crossover study, 19 subjects received daily 20 mg paroxetine or placebo, respectively, over a period of 30 days separated by a wash-out period of 3 months [37].

References