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PE Patient (pe + patient)
Selected AbstractsPhosphodiesterase 5 inhibitors in the treatment of premature ejaculationINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 5 2006W. F. Wang Summary To date, there is no FDA-approved therapy for premature ejaculation (PE). Recently, phosphodiesterase 5 inhibitors (PDE5 -Is) have been demonstrated to have encouraging results in the treatment of PE by a few studies. The aim of this review was to assess the updated manuscripts and thereafter present the practical recommendations and possible mechanisms concerning PDE5 -Is for treating PE. Using MEDLINE, we searched and assessed the peer manuscripts published from 1 January 1996 to 1 September 2005 about PDE5 -Is for treating PE. The results show that the number of patients in all the reports is very few and most of the studies do not employ double-blinded and placebo-controlled tests, though they are prospective and randomized. Therefore, the results and conclusions might be biased. PDE5 -Is are suggested to be used in PE with old age or associated with erectile dysfunction (ED), or to be employed alone or in combination with selective-serotonin reuptake inhibitors (SSRIs) when SSRIs fail to treat PE; behavioural therapy is proposed to be used for preventing the recurrence of PE following withdrawal of PDE5 -Is. In addition, for the PE patient with a definite aetiological cause, the aetiology should be cured first, if PE still exists, followed by PDE-Is prescription. Possible mechanisms that are involved include relaxing the smooth muscles of vas deferens, seminal vesicle, prostate and urethra; decreasing the central sympathetic output; inducing peripheral analgesia; prolonging the duration of erection; and increasing confidence, the perception of ejaculatory control, overall sexual satisfaction, and decreasing the post-orgasmic refractory time to achieve a second erection after ejaculation. Well-designed multicentre studies are urgently warranted to further elucidate the efficacies and safety as well as mechanisms of PDE5 -Is in the treatment of PE. [source] Urologist Practice Patterns in the Management of Premature Ejaculation: A Nationwide SurveyTHE JOURNAL OF SEXUAL MEDICINE, Issue 1 2008Alan Shindel MD ABSTRACT Introduction., Contemporary U.S. urologist's "real world" practice patterns in treating premature ejaculation (PE) are unknown. Aim., To ascertain contemporary urologist practice patterns in the management of PE. Method., A randomly generated mailing list of 1,009 practicing urologists was generated from the American Urologic Association (AUA) member directory. A custom-designed survey was mailed to these urologists with a cover letter and a return-address envelope. Responses were compared with the AUA 2004 guidelines for the treatment of PE. Main Outcome Measures., The survey assessed several practice-related factors and asked questions of how the subject would handle various presentations of PE in their practice. Results., Responses from practicing urologists totaled 207 (21%). Eighty-four percent of the respondents were in private practice and 11% were in academics. Most urologists (73%) saw less than one PE patient per week. On-demand selective serotonin reuptake inhibitor (SSRI) therapy was the most commonly selected first line treatment (26%), with daily dosing a close second (22%). Combination SSRI therapy, the "stop/start" technique, the "squeeze" technique, and topical anesthetics were favored by 13, 18, 18, and 11% of the respondents, respectively. If primary treatment failed, changing dosing of SSRIs, topical anesthetics, and referral to psychiatry were increasingly popular options. Ten percent of urologists would treat PE before erectile dysfunction (ED) in a patient with both conditions, with the remainder of the respondents treating ED first, typically with a phosphodiesterase type 5 inhibitor (78% of total). Fifty-one percent of urologists report that they would inquire about the sexual partner, but only 8, 7, and 4% would evaluate, refer, or treat the partner, respectively. Conclusions., The majority of our respondents diagnose PE by patient complaint, and treat ED before PE, as per the 2004 PE guidelines. Very few urologists offer referral or treatment to sexual partners of men suffering from PE. Additional randomized studies in the treatment of PE are needed. Shindel A, Nelson C, and Brandes S. Urologist practice patterns in the management of premature ejaculation: A nationwide survey. J Sex Med 2008;5:199,205. [source] Role of EG-VEGF in human placentation: Physiological and pathological implicationsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 8b 2009Pascale Hoffmann Abstract Pre-eclampsia (PE), the major cause of maternal morbidity and mortality, is thought to be caused by shallow invasion of the maternal decidua by extravillous trophoblasts (EVT). Data suggest that a fine balance between the expressions of pro- and anti-invasive factors might regulate EVT invasiveness. Recently, we showed that the expression of the new growth factor endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is high in early pregnancy but falls after 11 weeks, suggesting an essential role for this factor in early pregnancy. Using human villous explants and HTR-8/SVneo, a first trimester extravillous trophoblast cell line, we showed differential expression of EG-VEGF receptors, PKR1 and PKR2, in the placenta and demonstrated that EG-VEGF inhibits EVT migration, invasion and tube-like organisation. EG-VEGF inhibitory effect on invasion was supported by a decrease in matrix metalloproteinase (MMP)-2 and MMP-9 production. Interference with PKR2 expression, using specific siRNAs, reversed the EG-VEGF-induced inhibitory effects. Furthermore, we determined EG-VEGF circulating levels in normal and PE patients. Our results showed that EG-VEGF levels were highest during the first trimester of pregnancy and decreased thereafter to non-pregnant levels. More important, EG-VEGF levels were significantly elevated in PE patients compared with age-matched controls. These findings identify EG-VEGF as a novel paracrine regulator of trophoblast invasion. We speculate that a failure to correctly down-regulate placental expression of EG-VEGF at the end of the first trimester of pregnancy might lead to PE. [source] Gene expression in chorionic villous samples at 11 weeks' gestation from women destined to develop preeclampsiaPRENATAL DIAGNOSIS, Issue 10 2008Antonio Farina Abstract Objective To evaluate the direct alterations in mRNA expression among chorionic villous samples from 11 weeks' pregnant women who would develop preeclampsia (PE) later in the pregnancy. Method Case-control study encompassing five women destined to develop PE [cases matched 1:5 for gestational age (GA) with 25 controls]. We quantified mRNA expression on tissue samples from chorionic villous sampling (CVS) of normal and PE patients. We then assessed mRNA expressions of vascular endothelial growth factor (VEGFA), VEGFA receptor 1 (Flt-1), endoglin (Eng), placental growth factor (PlGF), transforming growth factor-,1 (TGF-,1), heme oxygenase-1 (HO-1) and superoxide dismutase (SOD). Data were analyzed by nonparametric rank analysis. Results For all the mRNA species considered in this study, all the mean observed ranks in the PE group were significantly altered compared to the rank expectation among controls. mRNA for Eng and TGF-,1 were the markers with the highest degree of aberration in PE, in respect to controls. The results are consistent with those already reported for the corresponding circulating proteins. mRNA for HO-1 and SOD were instead associated with the lowest aberration. Conclusion It is assumed that the pathogenesis of PE is associated with pathophysiological alterations to trophoblasts in early gestation. Our study has directly proved that gene expressions relating to angiogenesis or oxidative stress are altered in the first trimester trophoblasts that go on to develop PE later. These results would put the basis for a possible screening method for PE by using residual CVS. Copyright © 2008 John Wiley & Sons, Ltd. [source] |