前列腺癌根治术后膀胱颈部与精囊侵犯的预后比较

目的 比较前列腺癌根治性切除术后膀胱颈部与精囊侵犯患者的预后. 方法 回顾性分析2002年1月至2008年12月我院接受耻骨后前列腺癌根治性切除术的42例患者,年龄59～78岁,平均70.3岁.42例患者分为pT4a组(膀胱颈部侵犯的患者17例)和pT3b组(单侧或双侧精囊侵犯的患者25例).术后分别采取辅助治疗,定期门诊随访,以术后血清前列腺特异抗原(PSA)连续2次大于0.2 μg/L定义为生化复发,术后随访至发生生化复发的时间或随访至截止日期未发生生化复发的时间定义为无生化复发生存时间. 结果 两组患者术后随访50～122个月,17.6％(3/17)膀胱颈部侵犯者术后发生生化复发,24.0％(6/25)精囊侵犯者发生生化复发,两组比较差异无统计学意义(P＞0.05). 结论 前列腺癌根治术后辅助内分泌治疗能明显延长膀胱颈部侵犯与精囊侵犯的前列腺癌患者无生化复发生存期,但两组无生化复发生存率无差别,可考虑降低膀胱颈部侵犯在TNM系统中的分期.     

一期经尿道浅表膀胱癌并增生前列腺切除术后肿瘤复发情况观察

47例初发浅表膀胱癌伴良性前列腺增生患者分为A、B两组。A组21例,仅行经尿道膀胱肿瘤电切术（TURBt）;B组26例,一期行经尿道膀胱肿瘤＋前列腺电切术（TURBt＋P）。两组均给予吡喃阿霉素早期膀胱灌注配合术后常规灌注。随访3 a肿瘤复发率,A组33.3%,B组8.3%,两者相比P〈0.05。复发肿瘤均不位于前列腺窝。认为与单行TURBt相比,TURBt＋P治疗浅表膀胱癌合并良性前列腺增生,能有效解除下尿路梗阻,减少肿瘤术后复发。     

TUR-BT联合TUPKP治疗表浅性膀胱癌合并良性前列腺增生的疗效及安全性

目的 探讨同期行经尿道等离子双极膀胱肿瘤电切术(TUR-BT)联合经尿道前列腺等离子双极电切术(TUPKP)治疗表浅性膀胱癌(SBC)合并良性前列腺增生(BPH)的疗效及安全性.方法 选择SBC合并BPH患者39例,随机分为TUR-BT联合TUPKP组20例(A组)、单纯TUR-BT组19例(B组).观察两组术前、术后最大尿流率(MFR)、平均尿流率(AFR)、国际前列腺症状评分(IPSS)、残余尿量(RU)、生活质量评分(QOL)以及术后肿瘤复发率.结果 术后随访9～54个月,A组术后1例发生非原手术区域膀胱肿瘤复发,其MFR、AFR较术前明显升高(P均＜0.05),IPSS、RU、QOL明显降低(P均＜0.05).B组术后6例发生非原手术区域膀胱肿瘤复发,其MFR、AFR、IPSS、RU、QOL手术前后比较P均＞0.05.两组术后肿瘤复发率比较差异有统计学意义(P＜0.05).结论 TUR-BT联合TUPKP治疗SBC合并BPH能有效解除下尿路梗阻,减少肿瘤术后复发,疗效确切,安全可行.     

两种方法治疗浸润性膀胱癌的近期临床效果及远期生存率比较

目的：观察保留膀胱的综合疗法及根治性膀胱切除术治疗浸润性膀胱癌的近期临床效果、远期生存率,为膀胱癌的临床治疗提供依据。方法对2007年10月～2010年10月采用局部肿瘤切除术＋化疗（保留组）及根治性膀胱切除术（全切组）治疗的59例浸润性膀胱癌患者的临床资料进行回顾性分析,比较两组近期临床效果、远期生存率,采用Cox回归分析法分析预后影响因素。结果两组均无围手术期死亡病例,保留组出血量少于全切组,手术时间、住院时间、留置导尿管时间及膀胱冲洗时间均短于全切组,并发症发生率显著低于全切组（P均＜0．05）;两组5年生存率无显著差异（P﹥0．05）。结论与根治性膀胱切除术比较,保留膀胱的综合疗法对浸润性膀胱癌的远期肿瘤学根治效果相似,且具有患者创伤小、术后恢复快及生存质量高等优点,值得临床借鉴。     

吡柔比星联合IFN-α黏膜下注射加膀胱灌注防治浅表性膀胱癌术后复发(附33例报告)

68例浅表性膀胱癌患者随机分为A、B两组。A组33例术中予吡柔比星＋IFN-α黏膜下多中心注射,术后定期膀胱灌注;B组35例仅在术后定期行吡柔比星＋INF-α膀胱灌注。随访1～3a,A组复发率9．09％（3／33）,B组25.71％（9／35）,P〈0.05。认为吡柔比星与IFN-α术中黏膜下多中心注射加术后定期膀胱灌注预防浅表性膀胱癌术后复发疗效显著。     

膀胱癌合并前列腺增生症同期手术对癌复发的影响

目的观察膀胱癌合并前列腺增生症（BPH）同期手术对癌复发的影响,为手术模式的选择提供参考依据。方法检索膀胱癌合并BPH患者手术治疗的文献报道,比较同期膀胱癌和前列腺切除术（研究组）与单纯膀胱癌切除术（对照组）对膀胱癌合并BPH患者术后癌复发的影响,采用Meta分析法对所有符合纳入标准的研究结果进行分析,计算研究组相对对照组癌复发危险的优势比（OR）,评价两种手术模式对膀胱癌复发的影响。结果符合纳入标准的文献共8篇,总样本量为358例,其中研究组194例,癌复发43例;对照组164例,癌复发59例。合并OR=0．52,95％可信区间为0．32—0．84。结论膀胱癌合并BPH患者同期行膀胱癌和前列腺切除术可以降低术后癌复发。     

表阿霉素局部应用预防膀胱癌术后复发44例临床观察

44例膀胱癌经尿道膀胱肿瘤电切术（TURBt）或膀胱部分切除术后,用表阿霉素（EPI）（1g／L）行膀胱灌注,保留1h,每周1次,连用8周,而后每月1次,连用10个月。随访12～24个月,有8例复发,1a复发率为15．9％（7／44）,2a复发率为18．2％（8／44）;高级别膀胱癌患者在复发组所占百分比为87．5％（7／8）,未复发组为33．3％（12／36）,两者相比,P〈0．05;浸润性膀胱癌患者在复发组所占百分比为75．O％（6／8）,未复发组为19．4％（7／36）,两者相比,P〈0．01;不良反应发生率为11．4％（5／44）。认为膀胱癌术后膀胱灌注EPI对预防膀胱癌复发效果满意,不良反应少。     

肌层浸润性膀胱癌化疗研究进展

膀胱癌是临床上泌尿系统中最常见的恶性肿瘤,2008年全世界新发膀胱癌386 300例,有150200例死于膀胱癌[1].在男性肿瘤中,膀胱癌的发病率和病死率分别居于第7位和第9位.膀胱癌可分为非肌层浸润性膀胱癌（NMIBC）、肌层浸润性膀胱癌（MIBC）和转移性膀胱癌,其中20％ ～ 30％的新发病例是MIBC[2].MIBC的治疗以根治性膀胱切除、盆腔淋巴结清扫为主,术后复发率高达30％～45％,5年生存率为45％～66％[3].其中部分患者,特别是老年患者,伴有严重的心肺疾患,以及有些患者因畏惧根治性膀胱全切术后生活质量下降,拒绝行根治性膀胱全切术.MIBC仅手术治疗效果不理想,临床往往会辅以放、化疗为主的治疗手段.现就MIBC的主要化疗方案作一综述.     

膀胱移行细胞癌伴前列腺腺癌的诊断与治疗（附6例报告）

目的提高膀胱移行细胞癌伴前列腺腺癌的诊治水平。方法对6例膀胱移行细胞癌伴前列腺腺癌患者的临床资料进行分析。结果6例中以膀胱肿瘤首诊4例,其中1例于术后19个月死于肿瘤转移,余3例随访22～58个月,平均35个月,1例无瘤生存,1例术后18个月出现肿瘤复发,另1例带瘤生存。以前列腺腺癌首诊的2例,分别随访20个月和46个月,均曾出现膀胱癌复发而行手术治疗,目前无瘤生存。结论血清PSA测定、直肠指诊、经直肠前列腺B超榆查＋活检及膀胱镜检查是诊断膀胱移行细胞癌伴前列腺腺癌的主要方法,其中治疗方案应根据膀胱癌的分期来确定,根治性膀胱前列腺切除是影响预后的重要因素。     

尿膀胱肿瘤抗原测定在膀胱癌术后复发监测中的应用

目的评估尿膀胱肿瘤抗原(BTA)测定在膀胱癌术后复发监测中的应用价值。方法分别收集膀胱癌术后复发组(n=67)、未复发组(n=61)及正常对照组(n=50)的受试者尿液,用酶联免疫吸附实验(ELISA)法测定各样本BTA含量。复发患者行手术治疗,标本送病理检查观察其肿瘤病理分级与临床分期情况。结果膀胱癌术后复发组BTA水平明显高于正常对照组和术后未复发组,差异均有统计学意义(P <0. 05)。膀胱癌术后复发组BTA水平随病理分级增加而升高(P <0. 05)。BTA总敏感性为83. 8%,其中G1级63. 6%,G2～G3级92. 3%。特异性为88. 5%。结论尿BTA测定在膀胱癌术后复发监测中有较高临床价值,合理运用能减少膀胱镜检查次数,减轻患者痛苦。     

Inflammation and prostate cancer

There is emerging evidence that prostate inflammation may contribute to prostatic carcinogenesis. Chronic inflammation has been associated with the development of malignancy in several other organs such as esophagus, stomach, colon, liver and urinary bladder. Inflammation is thought to incite carcinogenesis by causing cell and genome damage, promoting cellular turnover, and creating a tissue microenvironment that can enhance cell replication, angiogenesis and tissue repair. Epidemiological data have correlated prostatitis and sexually transmitted diseases with an increased risk of prostate cancer and intake of anti-inflammatory drugs and antioxidants with a decreased risk. Evidence from genetic and molecular studies also support the hypothesis that prostate inflammation and/or infection may be a cause of prostate cancer. In 1999 De Marzo et al proposed that proliferative inflammatory atrophy (PIA) is a precursor to PIN and cancer. Further research will provide opportunities for the discovery and development of strategies for treatment and prevention of prostate cancer.     

Obesity and prostate cancer

The relationship between obesity and prostate cancer is currently a hotly debated topic, but despite the number of publications devoted to the topic, the actual nature of the relationship remains uncertain. Obesity has been shown to have a direct relationship with the incidence of prostate cancer in a number of studies but an equal number of studies have shown no association. The relationship is further obscured with recent findings that obesity in younger obese men may actually be protective against prostate cancer. Confounding factors include the lack of correlation of body mass index (BMI) as a measure of central obesity and the lack of consistency in timing of BMI measurements, i.e. before or after diagnosis and in young or advanced adulthood. Evidence for increased BMI as a risk factor for prostate cancer is unclear, but less ambiguous is the mounting substantiation that obesity is associated with prognostically worse disease, poorer post-surgical outcomes and increased prostate cancer mortality, irregardless of margin status. From a biologic perspective, one can put forth a number of potential mechanisms by which obesity might promote prostate cancer and/or prostate cancer progression including; low levels of testosterone, increased levels of estrogen, co-existing diabetes or metabolic syndrome, increased circulating insulin-growth factor-one (IGF-1), increased levels of leptin, decreased levels of adiponectin and increased dietary saturated fats. Evidence for the association of these factors with prostate cancer are examined herein. The timing of serum measurements is crucial in elucidating whether these factors have causative influence on prostate cancer or rather are produced by the prostate cancer cells and are better understood as markers of disease. The interaction between obesity and prostate cancer is important to clarify because it will have impact on the prevention, prognostication and treatment of prostate cancer. Future study with careful attention to avoid the methodological pitfalls of the past need be accomplished to bear out the nature of the interaction of obesity and prostate cancer.     

Oestrogens and prostate cancer

Androgens are essential for stimulating normal development, growth and secretory activities of the prostate whereas oestrogens are generally regarded as inhibitors of growth. Evidence for the local synthesis of oestrogens includes the detection of aromatase mRNA and protein in the stroma of human non-malignant tissues and in malignant tissue, where it is detected in epithelial tumour cells. As well, aromatase activity was measured by biochemical assay and protein was detected in prostatic non-malignant and tumour cell lines. Taken together with the identification of direct oestrogenic actions on the prostate, these results suggest that alterations in local oestrogen synthesis may have significant consequences in malignancy of these organs. Genetically modified mouse models were studied in order to evaluate the action of oestrogens alone or in combination with androgens on the prostate gland. Hypogonadal (hpg) mice are deficient in gonadotrophins and androgens but showed direct proliferative responses to oestradiol. The responses were characterised by discrete lobe-specific changes including smooth-muscle regression, fibroblast proliferation, inflammation, and basal epithelial cell proliferation and metaplasia. The aromatase knockout (ArKO) mouse, deficient in oestrogens due to a non-functional aromatase enzyme, developed prostatic hyperplasia during the lifelong exposure to elevated androgens, however, no malignant changes were detected in the prostate at any time. In contrast, combined androgen and oestrogen treatment has been shown to induce prostatic dysplasia and adenocarcinoma. These results demonstrate that malignant changes to the prostate gland are dependent upon both androgenic and oestrogenic responses and that neither hormone alone is sufficient to evoke aberrant patterns of growth, resulting in malignancy.     

Coagulopathy in prostate cancer

Patients with metastatic hormone-refractory prostate carcinoma may have dramatic and life-threatening coagulation complications from their disease. We report here the case of a man with relapsing disseminated intravascular coagulation, and review the different coagulation disorders that may occur during prostatic carcinoma evolution. We focus mainly on disseminated intravascular coagulation (DIC), the most frequent coagulation complication. Other coagulopathies associated with prostate cancer are thrombocytopenic thrombotic purpura, thrombosis, Trousseau's syndrome and acquired factor VIII inhibitor development.     

Screening for prostate cancer

Epidemiologically, screening is justified by the importance of the disease and the lack of prospects for primary prevention, but evidence from natural history is unhelpful since men are more likely to die with, rather than from, prostate cancer. The available screening tests do not always detect men whose lesions could result in future morbidity or mortality. Evidence is limited for the benefits of treatment for localised cancers detected through screening, whereas the evidence for harm is clear. Observational evidence for the effect of population screening programmes is mixed, with no clear association between intensity of screening and reduced prostate cancer mortality. Screening for prostate cancer cannot be justified in low-risk populations, but the balance of benefit and harm will be more favourable after risk stratification. Prostate cancer screening can be justified only in research programmes designed to assess its effectiveness and help identify the groups who may benefit.     

Aromatase and prostate cancer

The normal growth and development of the prostate requires the presence and action of androgens, which are also known risk factors in the origins of benign and malignant prostate disease. Paradoxically, the incidence of prostate disease increases with age when serum androgen levels are in decline and emerging evidence suggests that estrogens may also be important in the normal prostate, as well as in the etiology of prostate disease. Both estrogen receptor subtypes are present in the prostate, demonstrating that the gland responds directly to estrogens. Recent data suggests that estrogens play a role in prostate disease and has demonstrated that high doses of estrogens induce premalignant dysplasia and in combination with high doses of androgens, malignancy. The production of estrogens from androgens is mediated by the aromatase enzyme, the aberrant expression of which plays a critical role in the disease process in other tissues, most notably the breast. The prostate expresses aromatase within the stroma of benign tissue, while in malignancy there is an induction of epithelial expression with altered promoter utilisation. Although the presence of aromatase in the prostate and its aberrant expression in prostate cancer is significant, its role and contribution to prostate carcinogenesis remains unclear. Transgenic mouse models lacking aromatase (ArKO) and over-expressing aromatase (AROM+) have provided an ideal means to examine aromatase expression in the prostate. Studies using these animals may lead to a better understanding of the role that aromatase--and therefore estrogen--plays in the development and progression of prostate disease.