Objective To systematically evaluate the effectiveness and safety of fluoxetine in treating premature ejaculation (PE). Methods All randomized controlled trials (RCTs) on fluoxetine treating PE published from July 1996 to May 2012 were collected in the following databases: MEDLINE, EMbase, PubMed, Ovid, The Cochrane Central Register of Controlled Trials, CBM and CKNI. According to the inclusion and exclusion criteria, literature screening, data extraction and quality assessment were conducted independently by two reviewers. Then meta-analysis was performed using RevMan 5.0 software. Results A total of 6 RCTs involving 221 patients were included finally. The results of meta-analysis showed that, as for effectiveness, there was no significant difference in the intravaginal ejaculatory latency time (IELT) between the two groups before the treatment (WMD=–0.21, 95%CI −4.79 to 4.37, P=0.93), but the IELT of the fluoxetine group was obviously longer than that of the control group after the treatment, with a significant difference (WMD=134.54, 95%CI 79.78 to 189.30, Plt;0.000 01). The results of sensitivity analysis indicated that the IELT of the fluoxetine group was longer than that of the control group, with a significant difference (WMD=155.19, 95%CI 130.64 to 179.75, Plt;0.000 01). As for safety, the fluoxetine group was higher in the incidence of adverse reaction than the control group, with a significant difference (OR=5.49, 95%CI 2.43 to 12.38, Plt;0.000 1). Conclusion Current evidence indicates that fluoxetine can improve the symptoms of PE patients, obviously prolong the IELT, and improve the quality of sexual life; and it is tolerable to patients with mild adverse reactions and is suitable for long-term intake. For the limited quantity of the included studies, we herein believe that, to obtain more evidence, it is necessary to further confirm the diagnosis and therapeutic criteria of PE, to design and conduct more multicenter and large scale clinical studies by adopting the internationally recognized indexes, and to perform a long-term follow-up．
Objective To assess the efficacy and safety of mirtazapine and fluoxetine on depression. Methods We searched The Cochrane Library (Issue 2, 2009), MEDLINE (1980 to Dec.2008), EMbase (1980 to Dec.2008), CBM (1980 to Dec.2008), VIP (1980 to Dec.2008), CNKI (1980 to Dec.2008) and Wanfang database (1980 to Dec.2008) to search randomized controlled trials (RCTs) comparing mirtazapine with fluoxetine for depression. The quality of the included trials was assessed and meta-analysis was conducted by RevMan 5.0 software. Results Five RCTs involving 695 patients were included. The results of meta-analyses showed that: (1) After one-week treatment and two-week treatment, effectiveness of the mirtazapine group was significantly higher than that of the fluoxetine group [one-week treatment: RR=2.00, 95%CI (1.30, 3.10), P=0.002; two-week treatment: RR=1.49, 95%CI (1.08, 2.06), P=0.02]. But after six-week treatment, there was no significant difference of the efficacy between the mirtazapine and the fluoxetine groups with RR=1.21 and 95%CI 0.89 to 1.63 (P=0.23), and the cure rate of the mirtazapine group was a little higher than that of the fluoxetine group with RR=1.40 and 95%CI 1.09 to 1.80 (P=0.009). (2) Side reaction: The somnolence and weight gain rates of the mirtazapine group was higher than those of the fluoxetine group with RR=1.78 and 95%CI 1.18 to 2.70 (P=0.006) and RR=5.91 and 95%CI 2.21 to 15.83 (P=0.000 4). But fluoxetine more easily induced nausea and insomnia with RR=0.47 and 95%CI 0.31 to 0.71 (P=0.000 3); RR=0.39 and 95%CI 0.17 to 0.89 (P=0.03) than mirtazapine. And the other common side reactions were all not significantly different between the two groups (Pgt;0.05). Conclusion Mirtazapine is more effective than fluoxetine and works faster. Mirtazapine could more easily induce somnolence and weight gain, and is with lower nausea or insomnia rate when compared with fluoxetine. And there is no significant difference in comparison of other common side reactions.
Objective To evaluate the effectiveness and safety of both olanzapine combined with fluoxetine (combination therapy) and fluoxetine (monotherapy) for refractory depression. Methods According to the computer retrieval from PubMed (1966 to September 2009), Cochrane Library (Issue 3, 2009), EMbase (1974 to September 2009), SCI (1974 to September 2009), CNKI (1994 to September 2009), CBM (1978 to September 2009), CSJD (1989 to September 2009) and Wanfang Database (1997 to September 2009), and the manual retrieval from related journals and conference proceedings were conducted, to include randomized controlled trials of comparison in between olanzapine combined with fluoxetine and fluoxetine in treating refractory depression. We collected the valid data after assessing the methodology quality of included studies on the basis of Jadad scoring standard, and conducted meta-analysis with RevMan 5.0 software. Results A total of 7 studies with 1 230 patients were included. The meta-analysis showed that, there was no significant difference between two groups about the scores of HAMA (Hamilton Anxiety Scale) at the end of the 1st week, but the olanzapine combined with fluoxetine in trial group was much better for relieving anxiety situation compared to fluoxetine in control group at the end of the 2nd, 4th, 8th and 12th week. In accordance with the scores of CGI (Clinical Global Impression Scale), there was no significant difference at the end of 2nd and 4th week after treatment, but there was a significant difference at the end of 8th and 12th week. As to the changes of MADRS (Montgomery and Asberg Depression Rating Scale), the trial group was much distinct than control group at the end of the 1st, 2nd, 4th and 8th week. In summary, the clinical effect of trial group was superior to that of control group, and there was no significant difference in adverse reactions between two groups (RR=1.10, 95%CI 0.99 to 1.23). Conclusion Current evidence shows that, the clinical effect and safety of olanzapine combined with fluoxetine in treating refractory depression is obviously superior to that of fluoxetine.
Objective To evaluate the therapeutic effect and safety of Bupropion hydrochloride sustained-release tablets in the treatment of depression. Methods A total of 48 patients meeting the diagnostic criteria of depression of CCMD-3 were randomly treated with Bupropion hydrochloride sustained-release tablets or Fluoxetine tablets for 42 days. Hamilton depression rating scale, Hamilton anxiety rating scale, clinical global impression and treatment emergent symptom scale were used to evaluate the therapeutic effect. Blood routine test, urine routine test and electrocardiogram were examined before and after the treatment. Results The effective rate of Bupropion hydrochloride sustained-release tablets [83% (20/ 24) ] was higher than that of Fluoxetine tablets [63% (15/ 24)], with a P value of 0.104. The incidence of adverse reactions was 46% (11/24) in both groups. Conclusion The therapeutic effect of Bupropion hydrochloride sustained-release tablets on depression is similar to that of Fluoxetine tablets, with mild adverse reactions to both treatments.
Objective To determine whether fluoxetine, a commonly used selective serotonin reuptake inhibitors (SSRIs), could exacerbate bleeding in a intracerebral hemorrhage (ICH) mouse model. Methods Forty two 12-14 month old female specific pathogen free C57BL/6 mice were selected. Mice were randomly divided into fluoxetine group (fluoxetine pre-treatment) and control group, with 21 mice in each group. After treated with fluoxetine for 7 days, ICH was induced by injecting collagenase Ⅶ-S into the right striatum of middle-aged female mice. Effects of fluoxetine on exacerbating bleeding were evaluated by a combination of histologic, molecular, cellular, and behavioral assessments. Results On the third day after ICH, the hemorrhage volumes of the control group and fluoxetine group were (4.59±1.80) mm3 and (6.09±1.08) mm3, respectively. In middle-aged female mice subjected to collagenase-induced ICH, fluoxetine pre-treatment significantly exacerbated neurological deficit, cerebral hemorrhage volume, myelin damage, hemoglobin and iron deposition, neuronal degeneration, and brain edema (P<0.05). Although there was no significant difference in tail bleeding time between the two groups, fluoxetine pre-treatment might increase tail bleeding time [(276.73±211.06) vs. (438.00±236.79) s; t=−1.686, P=0.055]. Conclusions The use of fluoxetine and more generally of SSRIs, which inhibits platelet aggregation, may exacerbate bleeding after ICH. Thus, patients with depression after ICH may avoid concomitant use of such drugs when choosing an antidepressant.