前列腺增生——前列腺增生的病因学研究进展

前列腺增生症(benign prostate hyperplasia，BPH)是导致老年男性下尿路症状(lower urinary tractsymptoms，LUTS)的主要原因之一。尽管自从1960年以来，人们一直致力于前列腺增生症病因学的研究，然而到目前为止，BPH的发病机制仍未完全阐明。关于BPH的发病机制，目前主要有以下几种学说：激素一内分泌学说、生长因子学说、上皮一间质细胞相互作用学说、细胞凋亡与基因调控学说等。     

前列腺增生的病因学研究进展

关于前列腺增生(BPH)的病因迄今还未完全阐明。 BPH的发生需具备两个基本条件;①正常睾丸存在;②年老。在BPH的病因上有一点是明确的,即内分泌的影响。根据有三:①在青春期前去势者不发生BPH;②BPH病人去势术后增生腺体缩小;③动物实验投用某些性激素可复制BPH。兹就近年来BPH的研究进展,简述以下两种学说。     

前列腺增生症的病因学及新进展

前列腺增生症是老年男性常见病 ,其病因尚不清楚。本文就前列腺增生症的病因从激素内分泌、生长因子、上皮 -间质细胞相互作用、细胞凋亡等方面作一综述。     

前列腺增生症的病因学及新进展

前列腺增生症是老年男性常见病，其病因尚不清楚。本文就前列腺增生症的病因从激素内分泌、生长因子、上皮-间质细胞相互作用、细胞凋亡等方面作一综述。     

Madigan前列腺增生切除术

为了提高前列腺增生症的手术治疗效果，采用Ｍａｄｉｇａｎ手术治疗前列腺增生症患者２５例。１５例尿道完整，１０例损伤尿道缝合修复；术后出血少、恢复快；随访４～２５个月，无尿道狭窄、尿失禁等并发症。对手术优点、术中注意事项及适应证的选择进行了讨论。     

良性前列腺增生症病因学研究进展（下）

7导管系统作用前列腺是一个分泌腺作，其分泌卢物通过导管系统转运输送到尿道，可以从尿道中的导管开口处追踪每个导管系统。人前列腺由30多个导管系统构成。在小气腹例前列腺，每叶由8个导管系统构成，但其构成要比人的相应部位简单得多。对小鼠前列腺的研究表明，根据导管系统至尿道部管口的距离可将其分为近端、中段和远端三个区域。在远端区，其上皮细胞形状呈柱状，细胞有丝分裂活跃；在中段区，细胞形状屯呈高柱状，但有丝分裂是静止的，只有这个区的细胞有分泌功能，细胞死亡在上面两个区都不明显；在近端区，细胞呈低立方形或扁平形…     

纤维增生型前列腺增生症

对收治的４６例以纤维组织增生为主的ＢＰＨ作Ｂ超、尿动力学、手术、病理等资料的研究，提示此类ＢＰＨ腺体增大不明显，质硬，下尿路梗阻程度及膀胱功能受损较严重。对碱性成纤维生长因子（ｂＦＧＦ）、纤维连接蛋白（ＦＮ）与纤维化性ＢＰＨ的关系进行讨论。提出此类ＢＰＨ的诊断及鉴别诊断，认为以ＴＵＲＰ术为最佳疗法。     

良性前列腺增生的微创治疗

良性前列腺增生（BPH）是老年男性最常见疾病之一,随着人们寿命的延长,其发病逐年增多。由于BPH的发病机制目前尚未完全清楚,其药物治疗效果不甚理想。微创治疗因其损伤小、恢复快,疗效好,而被广泛应用。传统TURP治疗BPH已有70余年历史,一直被业界作为BPH手术治疗的“金标准”。     

PSA对前列腺增生间质细胞的生长抑制作用

目的探讨前列腺特异性抗原（ＰＳＡ）对前列腺间质细胞的生长调控作用。方法原代培养前列腺间质细胞，分别用ＰＳＡ（１μｇ／ｍｌ），β型转化生长因子（ＴＧＦβ１，５ｎｇ／ｍｌ）、ＰＳＡ＋ＴＧＦβ１及无血清培养液处理，分别于第１～４天作ＭＴＴ试验测定细胞生长曲线。用不同剂量的ＰＳＡ处理细胞，观察其细胞生长与凋亡的反应。结果ＰＳＡ组的活细胞密度比同期对照组减少２０．４％～４９．５％，ＴＧＦβ１无明显影响，ＰＳＡ＋ＴＧＦβ１在前３天与ＰＳＡ组差异无显著性，第４天则为０．０３６±０．００４，明显低于ＰＳＡ组（０．０５５±０．０１０），Ｐ＜０．０５。随着ＰＳＡ浓度的升高，ＭＴＴ试验显示的活细胞密度逐渐减少，Ｅｌｉｓａ实验显示细胞凋亡指数逐渐增加。结论ＰＳＡ对前列腺间质细胞有抑制生长和诱导凋亡的作用。     

良性前列腺增生合并慢性前列腺炎的研究进展

良性前列腺增生(BPH)和慢性前列腺炎(CP)均为男性常见病、多发病,且BPH多可合并CP。本文就BPH合并CP的流行病学、发病因素以及临床特点等进行了综述。患BPH或CP之一的患者比普通人群有更高的几率患另一种疾病。炎症可能参与了BPH的发生,合并有CP的BPH患者在年龄、前列腺重量、体积、症状评分特别是疼痛评分等方面均高于单纯BPH患者,差别有统计学意义。在治疗上对选择性α1受体阻滞剂、5α还原酶抑制剂、抗生素和超声微泡等的应用进行了阐述。     

Benign prostatic hyperplasia and prostate carcinoma in native Africans

OBJECTIVE: To study the factors associated with morbidity and mortality in benign prostatic hyperplasia (BPH) and carcinoma of the prostate in native Africans. PATIENTS AND METHODS: A prospective study was conducted from 1993 to 1998 at the Ahmadu Bello University Teaching Hospitals, Zaria, Nigeria. During this 5-year period 686 patients were investigated and treated for symptoms and signs of prostatism. They were followed up for a mean (range) of 19.5 (1-60) months. RESULTS: BPH was found in 588 and clinical carcinoma in 98 patients. Adequate results, including a histological diagnosis, were available for 640 patients; there were 545 patients with BPH and 95 patients with histologically diagnosed prostate cancer. Treatment consisted of open prostatectomy for BPH, and subcapsular orchidectomy and/or open bladder-neck wedge resection for patients with prostate cancer and bladder neck obstruction. Within 6 months of surgery, four of 545 (0.7%) patients with BPH and 25 of 95 (26. 3%) with prostate cancer had died. Two-thirds of the patients with cancer presented with paraparesis or paraplegia. CONCLUSIONS: BPH and prostate cancer cause significant morbidity and mortality in African men. There is a need for health education about the early recognition of symptoms. Provision of facilities for transurethral prostatectomy would minimize the complications of surgery and ensure better use of the meagre resources available for health care.     

Benign prostatic hyperplasia

The aetiological background of benign prostatic hyperplasia (BPH) is still obscure, though new information is steadily gained. In the context of pathomorphogenesis, major importance seems to be attributable to fibromuscular (stromal) tissue, since evidence has been produced to significant decline in glanduloparenchymal area relative to the normal overall volume of the prostate. Urine flow measurement has proved to be the most important screening test. Accurate presurgical determination of size of a hyperplastic prostate is not possible unless ultrasound is used. The hydrodynamic effects on the urinary bladder are recordable by means of combined flow and pressure measurement. Therapeutic medication is merely symptomatic, since no causative pharmacotherapy has so far become available. Transurethral prostatectomy is the optional approach to the majority of patients with prostatic symptoms. Postoperative complaints call for high-accuracy elucidation, since strictures and stones have frequently developed unnoticed.     

Benign prostatic hyperplasia

Male lower urinary tract symptoms (LUTS) have a multifactorial aetiology and are not simply solely due to bladder outflow obstruction (BOO) from benign prostatic hyperplasia (BPH). Other causes of LUTS include bladder dysfunction, malignant prostatic disease, urethral disease and medical conditions such as polyuria. Complications from BPH include acute urinary retention, urinary tract infection and haematuria. Following investigation, men are treated with medical therapy for BPH using α-blockers and 5α-reductase inhibitors. Some men undergo surgery for their symptoms and this can be in the form of open prostatectomy, transurethral resection of the prostate (TURP) and a variety of laser ablating and enucleating techniques.