脊髓损伤患者勃起功能障碍的治疗

大多数脊髓损伤(SCI)的男性患者存在不同类型及程度的勃起功能障碍(ED),这主要取决于SCI的部位和严重程度。SCI康复期,部分男性患者可恢复残留的性功能。SCI后ED的治疗包括心理治疗、口服PDE5抑制剂、海绵体注射血管活性药物(ICI)、经尿道给药、真空勃起装置(VED)及阴茎缩窄环、阴茎假体植入手术、骶神经调节等,首选口服PDE5抑制剂治疗。高位SCI患者口服PDE5抑制剂,可能获得较好的疗效;而低位的SCI患者,采用ICI或者联合治疗的效果较好。     

负压勃起装置治疗前列腺癌根治术后的勃起功能障碍

目的:探讨负压勃起装置(VED)治疗前列腺癌根治术(RP)后勃起功能障碍(ED)的有效性和安全性。方法:开放性RP术后ED患者6例,3例于术后3个月内(A组),3例于术后12个月以上(B组)分别进行VED康复治疗,比较两组在VED治疗前,治疗后3个月和6个月的IIEF-5评分的差异,治疗6个月后的阴茎长度和周径变化的差异。评价VED应用的安全性,以及患者和性伴侣的满意度。结果:6例患者VED治疗后3个月和6个月的IIEF-5平均评分均较治疗前提高(P<0.05)。A组患者VED治疗后3个月IIEF-5评分(8.7±0.6)分,治疗后6个月IIEF-5评分(13.0±1.0)分,均高于B组患者[(6.7±0.6)分;(8.3±1.5)分](P<0.05)。VED治疗后6个月,A组患者阴茎长度缩短(0.4±0.1)cm,周径缩短(0.2±0.1)cm,B组患者阴茎长度缩短(1.7±0.4)cm,周径缩短(0.9±0.3)cm,两组相比均有显著差异(P<0.05)。VED治疗后6个月的患者及性伴侣性生活满意率分别为83.3%和50.0%。VED治疗期间,1例患者诉阴茎皮肤发暗,2例诉性交僵硬麻木感,其余无明显不良反应。结论:RP术后ED患者早期进行VED康复治疗,能显著改善勃起功能,减少阴茎萎缩。     

非性交勃起在勃起功能障碍患者阴茎康复中的应用

勃起功能障碍(ED)是临床上常见的一种男科疾病,有研究显示40~70岁的男性ED患病率约52%,且日益趋向年轻化。目前认为,缺氧是ED的独立危险因素,其导致ED的机制复杂多样。近年来,阴茎康复理念备受重视,这一理念的引导实施是通过增加海绵体组织氧供,降低组织纤维化和凋亡以促进勃起功能恢复正常。而针对增加海绵体组织氧供的一些非性交勃起手段,如行为治疗、药物治疗、真空负压吸引装置治疗、海绵体内注射治疗等,可在一定程度上模拟男性正常自然性交勃起,帮助患者进行有效的阴茎康复锻炼。本文就目前非性交勃起治疗在阴茎康复中的应用作一论述。     

体外冲击波治疗勃起功能障碍及阴茎硬结症的研究进展

阴茎海绵体血管内皮受损、血管舒缩功能障碍、血流量不足是引起勃起功能障碍(ED)的重要病因。目前对ED的治疗主要应用5-型磷酸二酯酶抑制剂(PDE5I),但对部分ED患者无效。由阴茎硬结病(PD)引起的ED除使用PDE5I,还可采取手术、电疗等物理疗法,但疗效难以保证。近年发现低强度体外冲击波治疗(LI-ESWT)能促进血管再生,提高阴茎海绵体血流量,有望成为治疗ED和PD的一项有效的新方法。     

服用小剂量他达那非对动脉性勃起功能障碍患者临床疗效的观察

目的:观察服用小剂量磷酸二酯酶-5(PDE5)抑制剂他达那非对动脉性勃起功能障碍(ED)患者的疗效。方法:对43例动脉性ED患者采用了疗程为4周的隔日小剂量(5 mg)晚餐后口服他达那非的用药方案,在治疗前后进行IIEF-5评分同时用彩色多普勒超声联合阴茎血管活性药物前列腺素(PGE-1)注射实验,检测阴茎双侧海绵体动脉的收缩期最大流速(PSV)。结果:经统计学分析,IIEF-5评分以及阴茎双侧海绵体动脉的PSV在治疗4周后有显著提高(P<0.05)。结论:口服小剂量他达那非能有效提高动脉性ED患者阴茎海绵体动脉的收缩期最大流速,改善患者的勃起质量。     

男性盆腔部位肿瘤术后的阴茎康复

常见的男性盆腔部位肿瘤包括前列腺癌,膀胱癌和直肠癌,上述肿瘤患者在接受根治性手术后的阴茎勃起功能障碍(ED)发生率为25%~100%。造成术后ED的最大原因是神经血管束的受损,由此造成阴茎海绵体组织供氧减少,阴茎发生纤维化。术后早期的阴茎康复疗法能促进患者改善或恢复勃起功能。本文就目前男性盆腔部位肿瘤术后的阴茎康复做一综述。     

根治性前列腺切除术后勃起功能障碍不同治疗方案的Meta分析

目的系统评价不同治疗方案对根治性前列腺切除术后勃起功能障碍(ED)的疗效。方法检索The CochraneLibrary、PubMed、EMbase、中国知网、维普以及万方数据库,检索时间从建库至2018年4月,纳入根治性前列腺切除术后ED不同治疗方案的临床研究,文献数据采用RevMan 5.3软件进行统计学分析,并行发表偏倚风险评估。结果共11篇随机对照研究及5篇病例对照研究纳入本项研究,累计病例2 012例。Meta分析结果显示,5型磷酸二酯酶抑制剂(PDE5-Is)对患者满意改善程度显著优于对照组[OR=1.73,95%CI(1.34,2.23),P0.01]。各亚组分析结果显示:真空负压勃起装置(VED)对患者满意度改善无显著疗效[OR=1.51,95%CI(0.76,3.00),P=0.24];阴茎海绵体药物注射前列腺素E1(PGE1)对患者满意度改善效果显著[OR=8.50,95%CI(3.09,23.42),P0.01]。偏倚分析显示纳入的研究结果无明显发表偏移。结论对于根治性前列腺切除术后ED患者,采用PDE5-Is可显著改善ED症状;而对于疗效不佳的患者,选择联合治疗是适宜之选。     

他达拉非治疗ED的概述

勃起功能障碍(ED)是男科常见病、多发病,PDE5抑制剂能竞争性抑制PDE5而抑制cGMP的水解,提高阴茎海绵体平滑肌细胞内cGMP浓度,达到治疗ED的效果。他达拉非可使阴茎海绵体内cGMP水平提高,从而导致勃起。他达拉非可有效改善各种病因和各种程度ED患者的勃起功能;其具有以下特点:有效时间长,安全性高,易于被患者及性伴侣接受,增强性自信、性自尊,性体验更加自然。使患者从生理、心理上最大程度的得到治疗,有效提高性生活质量。因此他达拉非在ED患者的治疗中值得推广。     

脂肪源性干细胞治疗勃起功能障碍的研究进展

勃起功能障碍(erectile dysfunction,ED)是男性常见疾病,直接影响患者的生活质量.近年来,人们对阴茎勃起机制和ED病理生理学的研究取得一定进展,有了许多治疗ED的方法,如:口服磷酸二酯酶5型(phosphodiesterase 5,PDE5)抑制剂、阴茎海绵体内注射血管活性药物及阴茎假体植入[1]等.     

阴茎海绵体动态测压及造影的检查流程和临床应用

目的:探讨阴茎海绵体动态测压及造影(DICC)的操作流程及其在静脉型勃起功能障碍(VED)诊断中的价值。方法:临床行彩色多普勒超声检查筛选阴茎海绵体注射试验(ICI)阴性、高度怀疑VED的103例ED患者,对其进行DICC,对比观察检查结果维持灌注速度(FTM)和海绵体压力衰退值(PD)。结果:21例检查结果正常,其余VED患者根据其FTM和PD分为可疑静脉漏(5例)及轻度(39例)、中度(25例)、重度(13例)静脉漏;仅4例出现阴茎皮下血肿,3~5 d后均消失,无其他并发症发生。结论:DICC诊断VED微创、可靠、安全、可重复性高,可依据其检查结果将患者做进一步分类。     

Neurogenic erectile dysfunction

Neurogenic erectile dysfunction is a consequence of alterations in neural pathways, autonomic, somatic, the combination of both or brain components that induce erection. This review aims to explain the physiopathological mechanisms of the most frequent neurological alterations causing erectile dysfunction and sexual disorders.     

Primary erectile dysfunction

We evaluated 67 patients 18 to 60 years old (mean age 28.5 years) with primary erectile dysfunction (absence of full sustained erections since early childhood or puberty) using a multidisciplinary approach. Organic causes of the erectile dysfunction were found in 57 of the 67 patients (85 per cent): 12 (18 per cent) had neurological, 35 (52 per cent) arteriogenic and 35 (52 per cent) venogenic abnormalities. Psychogenic factors were diagnosed in 11 patients (16 per cent), while in 4 (6 per cent) a classification was not possible. Concomitant psychogenic abnormalities were found in 39 of the 57 patients (68 per cent) with organic primary erectile dysfunction. Our results suggest that primary erectile dysfunction is caused mainly by organic factors. However, for successful therapy the frequent secondary psychogenic abnormalities must be considered.     

Vascular erectile dysfunction

Vascular etiology is present in up to 60% of the patients with erectile dysfunction (ED). Both small vessel disease, such as that in diabetes mellitus, and arteriosclerosis of bigger size arteries, as in hypertension, cause arterial insufficiency and erectile dysfunction. Tobacco smoking alters the arterial hemodynamics in the penis, causing erectile dysfunction in a high percentage of advanced age smokers: pelvic arteries fibrosis and stenosis accelerates the existing arteriosclerosis. Venous occlusive dysfunction may be due to the decrease of corpora cavernosa compliance or tunica albuginea inherent anomalies. Vascular endothelial growth factor may play a role in the modulation of vascularization of the normal penile architecture. Various events, all of them important, may cause erectile dysfunction. Moreover, no cause can participate independently. A cascade of situations (including psychological factors as well as organic) may lead to erectile dysfunction. A continuous understanding of organic causes of erectile dysfunction will allow physicians to discover treatments for their correction, as well as to give confidence to the patient.     

Neurologic erectile dysfunction

Neurologic erectile dysfunction presents a diagnostic and treatment challenge to the internist and urologist. Multiple chronic disease modalities and traumatic etiologies exist. Education regarding these conditions and a detailed and thorough history and office work-up are the best resources for the clinician. Treatment can follow the model of proceeding from the least to most invasive procedure (process of care), taking into account patient and partner satisfaction. Because the psychology of grief and loss may enter into treatment of some neurologic conditions (e.g., erectile dysfunction after radical retropubic prostatectomy, spinal cord injury, or chronic diseases), a whole-patient approach encompassing psychotherapy is warranted.     

Imaging for erectile dysfunction

Radiological imaging in the field of erectile dysfunction has diminished in importance over the past 5 years with the advent of new therapies. However, in selected cases, Doppler scanning continues to have a role, and current research is aimed at optimizing the results of the tests. In addition, the new techniques of functional magnetic resonance imaging and positron emission tomography scanning are beginning to offer new insights into the central mechanisms which control erections.     

Hyperlipidemia and erectile dysfunction

We have done consecutive studies to investigate the effects of impaired lipid metabolism on the contractile and relaxation response of cavernous smooth muscles and to elucidate its pathogenesis: 1 ) incidence of hyperlipidemia in impotent patients; 2) erection response to intmcavemous injection of papaverine in impotent patients with hyperlipidemia; 3) relaxation responses of isolated cavemosal smooth muscles to endothelium-independent and endothelium-dependent vasodilators in impotent patients with hypercholesterolemia or hypertriglyceridemia; 4) involvement of superoxide radical in the impaired endothelium-dependent relaxation of cavernous smooth muscle in hypercholesterolemic rabbits; 5) effects of isolated lipoproteins and triglyceride, combined oxidized LDL plus triglyceride, and combined oxidized LDL plus HDL on contractile and relaxation response of rabbit cavernous smooth muscles; 6) involvement of e-NOS in the impaired endothelium-dependent relaxation of cavernous smooth muscle in hypercholesterolemic rabbit. Hypercholesterolemia may cause impairment of endothelium-dependent relaxation. Oxidized LDL is the major causative cholesterol of the impaired relaxation response. A chain reaction, the production of superoxide radicals and functional impairment of eNOS may be a major cause of the functional impairment in the early stages of hypercholesterolemia.