前列腺液16srDNA表达与慢性前列腺炎／慢性骨盆疼痛综合征疗效的关系

目的：探讨前列腺液16srDNA的表达与慢性前列腺炎／慢性骨盆疼痛综合征（CP／CPPS，Ⅲ型前列腺炎）疗效的关系。方法：选择符合美国国立卫生研究院（NIH）诊断标准的CP／CPPS患者70例．其中ⅢA型36例，ⅢB；型34例。门诊行前列腺液常规镜检和细菌、支原体，衣原体病原学检查，并对前列腺液中的16srDNA进行PCR检测，参考病原学结果实施抗生素为主的综合治疗。以慢性前列腺炎症状指数（NIH-CPSI）为疗效指标进行治疗前后疗效比较。结果：CP／CPPS抗生素治疗组中，16srDNA阳性者治疗显效率（81．4％）明显高于16srDNA阴性者（63％）（P〈0．01）。16srDNA阴性的ⅢA组总显效率较ⅢB；组低（P〈O．05），而16srDNA阳性的 两组间比较差异无统计学意义（P〉0．05）。结论：前列腺液16srDNA的表达与CP／CPPS的疗效有相关性，16srDNA的表达对前列腺炎的分型可能有一定参考意义。     

前列腺液16s rDNA检测在慢性前列腺炎诊治中的临床意义

目的探讨前列腺液16s rDNA检测对慢性前列腺炎的临床诊断和治疗意义。方法选择符合美国国立卫生研究院（NIH）诊断标准的Ⅱ型前列腺炎和Ⅲ型前列腺炎患者67例。常规前列腺液镜检和细菌、支原体、衣原体检查，并对前列腺液中的16s rDNA进行PCR检测，治疗全部采用以抗生素为主的综合治疗。以慢性前列腺炎症状指数（NIH-CPSI）为疗效指标，治疗4周后进行疗效比较。结果Ⅱ、ⅢA和ⅢB型前列腺炎16s rDNA阳性率分别为100％（11／11）、62．5％（20／32）、66．7％（16／24）。Ⅱ型前列腺炎治疗显效率100％；在Ⅲ型前列腺炎中，ⅢA、ⅢB组无差异，而16s rDNA阳性组治疗总显效率（80．0％）明显高于16s rDNA阴性组（52．4％）（P〈0．05）。结论前列腺液16s rDNA表达与前列腺炎的疗效有良好的相关性，可作为Ⅲ型前列腺炎选用抗生素治疗的依据，并对前列腺炎分型有一定参考价值。     

慢性前列腺炎患者前列腺液16S rDNA检测的临床意义

目的:探讨慢性前列腺炎患者前列腺液16S rDNA检测的临床意义。方法:对116例慢性前列腺炎患者前列腺液采用PCR方法检测其16S rDNA,比较不同亚型前列腺炎的16S rDNA阳性率并分析其相关性。结果:29例Ⅱ型前列腺炎前列腺液16S rDNA PCR均阳性,阳性率100%;87例Ⅲ型前列腺炎前列腺液16S rDNA PCR阳性71例,阳性率82%,其中ⅢA型前列腺炎前列腺液PCR阳性率94%(45/48),ⅢB型前列腺炎前列腺液PCR阳性率67%(26/39)。结论:16S rDNA的检测可能成为慢性前列腺炎分型的一个指标。     

有关慢性前列腺炎及慢性盆腔疼痛综合征的新认识

慢性前列腺炎 (CP)及慢性盆腔疼痛综合征(chronicpelvicpainsyndrome ,CPPS)为泌尿外科常见疾病。由于病因不明 ,疗效不够满意 ,给患者身心健康带来一定的影响。 2 0 0 2年 12月美国《Urology》发表了NIH近年来有关本病的研究报道[1] ,认为可作为诊断、处理本病的参考。有关CP/CPPS的主要问题为非细菌性前列腺炎 ,Ⅲ型又分为ⅢA及ⅢB亚型 ,前列腺液中白细胞常增高者为ⅢA ,白细胞正常者为ⅢB ,患者的主要症状为阴茎、尿道、会阴部疼痛。近来一组多中心的协作研究表明前列腺液中白细胞的多少与症状无关 ,对选择治疗和预测疗效无明显…     

前列腺按摩液pH测定在慢性前列腺炎中的临床应用价值

Ⅲ型前列腺炎，即慢性非细菌性前列腺炎/慢性盆底疼痛综合征(CP/CPPS)在各型前列腺炎中发病率最高、争议最多且疗效最不确定，按前列腺按摩液中白细胞数量，又分为炎症性(ⅢA)和非炎症性(ⅢB)两个亚型。但研究表明，白细胞数与症状程度不相关，提示除白细胞和细菌的因素外，还有其他引起CPPS症状的因素存在，     

性激素与慢性无菌性前列腺炎/慢性盆底疼痛综合征关系的研究进展

1995年美国国立卫生研究院(NIH)对前列腺炎症候群重新分类,Ⅲ型即为慢性无菌性前列腺炎/慢性盆底疼痛综合征(Chronic prostatitis/chronic pelvic pain syndrome,CP/CPPS)[1],传统分类的慢性无菌性前列腺炎属于ⅢA型,前列腺痛属ⅢB型[2].     

慢性前列腺炎/慢性骨盆疼痛综合征治疗新进展

慢性前列腺炎(CP)尤其是慢性前列腺炎/慢性骨盆疼痛综合征(CP/CPPS)(Ⅲ型)的发病机制至今尚不完全清楚,人群发病率可达2.5%~16.0%,为50岁以下男性最常见的泌尿外科疾病。20世纪90年代以来,在美国国立卫生研究院慢性前列腺炎协作研究网(NIH-CPCRN)、国际前列腺炎协作网(IPCN)等国际研究机构的协调下,各国研究者对CP的病因、诊断、治疗等诸方面进行了较以往更大规模的深入研究。CPPS是CP中最常见的也是疗效最差的一种类型,本文综述了近几年来CP/CPPS治疗新进展,探讨了其目前治疗所面临的主要问题及可能的原因,并对CP/CPPS治疗的前景予以展望。     

对CP/CPPS患者临床症状和生活质量的前瞻性研究

慢性前列腺炎（CP）／慢性盆腔疼痛综合征（CPPS）的临床特征主要表现为前列腺慢性疼痛。但是,与慢性细菌性前列腺炎不同,CP／CPPS并没有可证明的感染来解释其临床表现,抗生素也不能改善其症状。根据目前普遍接受的前列腺炎分类方法,大部分CP／CPPS患者可以被归类为Ⅲ型CP／CPPS。这一类型前列腺炎又包括炎症性CP／CPPS（ⅢA）和非炎症性CP／CPPS（ⅢB）。ⅢA患者精液、前列腺按摩液或尿三杯中可查到较多的白细胞,而ⅢB的情况则相反。在美国,尽管尚缺乏基于流行病学资料而得出的发病程度和发病率情况,但一些研究表明：无论种族或年龄,有超过10％成年人患有CP／CPPS。而且,目前尚无针对绝大部分患者一的有效治疗手段。     

细胞因子及热休克蛋白在慢性前列腺炎患者精浆中的含量及其临床意义

目的:探讨慢性细菌性前列腺炎以及慢性前列腺炎/慢性骨盆疼痛综合症(CP/CPPS)患者精浆中肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)以及热休克蛋白70(HSP70)的含量及临床意义。方法:采用酶联免疫吸附测定法(ELISA)对36例慢性细菌性前列腺炎(Ⅱ型)、43例炎症型慢性非细菌性前列腺炎即炎症型慢性骨盆疼痛综合征(ⅢA型)、46例非炎症型慢性非细菌性前列腺炎即非炎症型慢性骨盆疼痛综合征(ⅢB型)患者及25例健康志愿者精浆中TNF-α、IL-1β以及HSP70含量进行测定分析,并将HSP70的表达与慢性前列腺炎症状评分进行相关性分析。结果:慢性细菌性前列腺炎患者精浆中细胞因子(TNF-α、IL-1β)以及HSP70含量明显高于CP/CPPS患者及正常对照组。CP/CPPSⅢA型患者精浆中IL-1β的含量明显高于CP/CPPSⅢB型患者及正常对照组。CP/CPPS患者精浆中HSP70的含量明显低于正常对照组。慢性细菌性前列腺炎患者精浆中HSP70的含量与CPSI评分呈显著负相关。结论:精浆中HSP70的含量能够作为评价慢性细菌性前列腺炎病情程度的分子生物学指标。IL-1β能够作为CP/CPPS分型诊断指标。对于慢性细菌性前列腺炎患者,HSP70具有细胞保护功能。CP/CPPS患者精浆中HSP70表达的抑制可能与T细胞功能受损有关。     

巨噬细胞炎性蛋白-1α在前列腺按摩液中的表达及意义

目的:检测前列腺按摩液(EPS)中巨噬细胞炎性蛋白-1α( MIP-1 α)的mRNA和蛋白表达水平,探讨其在慢性前列腺炎分型中的意义.方法:50例临床诊断的慢性前列腺炎患者,其中慢性细菌性前列腺炎(CBP)16例,慢性非细菌性前列腺炎/慢性骨盆疼痛综合征(CPPS) 23例,分为ⅢA型11例,ⅢB型12例.无症状性炎症性前列腺炎Ⅳ型11例.收集EPS.同时选取15例健康自愿者做正常对照.RT-PCR法扩增MIP-1α mRNA,统计分析各组mRNA表达差异.ELISA法检测MIP-1α的蛋白表达水平,统计分析各组EPS的MIP-1α浓度差异.结果:RT-PCR半定量分析显示,MIP-1α mRNA在CPPSⅢA组和CPPSⅢB组的表达显著高于其他各组(P＜0.05).ELISA分析显示,MIP-1α蛋白浓度在CPPSⅢA组[(1 174.3±89.2) pg/ml]和CPPSⅢB组[(842.3±76 2)pg/ml]也显著高于正常组[ (198.0±37.8) pg/ml]、CBP组[(347.0 ±61.6) pg/ml]及Ⅳ型组[(292.0±56.4) pg/ml](P＜0.05).结论:从mRNA和蛋白水平检测EPS中MIP-1α可能有助于慢性前列腺炎的分型诊断.     

前列腺灌注管加压灌注药物治疗慢性前列腺炎

目的：观察应用前列腺灌注管加压灌注药物治疗慢性前列腺炎的效果。方法：对１７６例慢性前列腺炎患者经尿道置入前列腺灌注管加压灌注药物并联合多功能前列腺治疗仪治疗。结果：１７６便中治愈１３４例,好转３２例,有效率９４．３％。治疗后随访６￣１８个月,８例复发。结论：应用前列腺灌中压灌注药物并联合多功能前列腺治疗仪治疗慢性前列腺炎具有疗效好,副作用少的优点,是治疗慢性前列腺炎可供选择的有效方法之一。     

Etiologic theories of chronic prostatitis/chronic pelvic pain syndrome

The etiology of chronic prostatitis/chronic pelvic pain syndrome is unknown. Whereas infection causes category I and II prostatitis, the evidence for an ongoing infection in category III patients is lacking. Immunologic, neurologic, and psychologic factors likely play a role in the development and maintenance of symptoms in these men. The traditional concept of pain as a simple response to a noxious stimulus has some merit, but modern research indicates that the response is much more complex, and we must look at a patient’s physiology and psychology to be able to interpret each individual’s pain response. It is some advance in the field to realize that we probably need to look beyond the prostate and address the entire biopsychosocial problem to be able to offer successful treatment to these men.     

Rights of chronic renal failure patients undergoing chronic dialysis therapy.

The Patient Advocacy Committee of the International Federation of Kidney Foundations (IFKF) has developed a document proposing a set of rights for individuals with end stage renal failure (ESRF). These rights have been approved by the Board of Directors of the IFKF. Twenty rights have been developed and are organized into the following categories: (i) need of treatment and choice of patients; (ii) treatment of ESRF by haemodialysis; (iii) treatment of ESRF by peritoneal dialysis; and (iv) renal transplantation. It is the hope of this Committee and the IFKF that this document will provide a stimulus to more scientific inquiry and discussion as to what rights do patients possess with regard to treatment of chronic kidney disease, regardless of where they live or what may be their economic, social, ethnic or political status.     

Role of bacteria in chronic prostatitis/ chronic pelvic pain syndrome

Throughout the past century, we have refined our understanding of prostatitis, moving from using a primarily clinical definition to considering it as a complex inflammatory condition. The inconsistency in identifying uropathogens in patients with symptoms of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) has led to controversy in therapeutic management. There is compelling evidence that the normal prostate has minimal inflammation and no bacteria. Clinicians using the Meares/Stamey criteria identified uropathogens localized to the prostate in only 6% to 8% of CP/CPPS patients. This suggests that bacteria may have a role in less than 10% of men with CP/CPPS. That some patients respond to antimicrobials could suggest that eradication of bacteria reduces symptoms. However, the beneficial effect of antimicrobial drugs may not be due to their antibacterial action, but to their anti-inflammatory action. The normal prostate shows minimal inflammation, but only 50% of CP/CPPS patients exhibit prostatic leukocytosis. Prudence demands that we examine the function of the white blood cells—the cytokines produced. Several basic science advances allowed new avenues of research regarding the detection of molecular evidence of causative uropathogens. New research brings new controversy and unexpected findings, but further refines our understanding of the immune system and the CP/CPPS disease process.     

Risks of chronic metabolic acidosis in patients with chronic kidney disease

Risks of chronic metabolic acidosis in patients with chronic kidney disease. Metabolic acidosis is associated with chronic renal failure (CRF). Often, maintenance dialysis therapies are not able to reverse this condition. The major systemic consequences of chronic metabolic acidosis are increased protein catabolism, decreased protein synthesis, and a negative protein balance that improves after bicarbonate supplementation. Metabolic acidosis also induces insulin resistance and a decrease in the elevated serum leptin levels associated with CRF. These three factors may promote protein catabolism in maintenance dialysis patients. Available data suggest that metabolic acidosis is both catabolic and anti-anabolic. Several clinical studies have shown that correction of metabolic acidosis in maintenance dialysis patients is associated with modest improvements in nutritional status. Preliminary evidence indicates that metabolic acidosis may play a role in beta2-microglobulin accumulation, as well as the hypertriglyceridemia seen in renal failure. Interventional studies for metabolic acidosis have yielded inconsistent results in CRF and maintenance hemodialysis patients. In chronic peritoneal dialysis patients, the mitigation of acidemia appears more consistently to improve nutritional status and reduce hospitalizations. Large-scale, prospective, randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in maintenance hemodialysis patients. To avoid adverse events, an aggressive management approach is necessary to correct metabolic acidosis. Clinicians should attempt to adhere to the National Kidney Foundation Kidney Disease Outcome Quality Initiative (K/DOQI) guidelines for maintenance dialysis patients. The guidelines recommend maintenance of serum bicarbonate levels at 22 mEq/L or greater.     

慢性胰腺炎的分期探讨

目的 建立一种慢性胰腺炎分期系统并据此分析临床病例.方法 分析国内外慢性胰腺炎分期方式,提出临床实用的分期系统,据此对连续89例病人病情进行归纳分析.结果 该系统对形态学改变、疼痛、并发症及功能异常进行组合,构成四个阶段:Ⅰ、Ⅱ、Ⅲ和Ⅳ期各占1.1%、39.3%、44.9%和14.6%,疼痛发生率87.6%,并发症发生率46.1%.结论 该系统评价指标客观、实用,并可据分期选择治疗方式.     

Quercetin for chronic prostatitis/chronic pelvic pain syndrome

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common condition with a heterogeneous origin that responds best to multimodal therapy. The bioflavonoid quercetin has antioxidant and antiinflammatory effects that have proven useful for treating this condition. Using the clinical phenotype system UPOINT, quercetin can be helpful for those with organ-specific complaints (bladder or prostate) and pelvic floor spasm. This article discusses the current understanding of CP/CPPS and how treatment with quercetin can be used alone or as part of multimodal therapy.     

Pathophysiology of chronic pancreatitis

Although the most common causes of chronic pancreatitis have not changed, it has become clear that a host of modifying biochemical, inflammatory, neural, and genetic deviations allows the disease to progress. Alterations in biochemical composition allow calcific stone formation, whereas various toxins, cytokines, and neuropeptides contribute to the progression of fibrosis and pain production. The basic cellular structure contributing to fibrosis of the pancreas has been elucidated and factors responsible for its activation delineated. Of most importance is the recent recognition of a set of genetic mutations that results in several aberrations of normal pancreatic physiology, which, in conjunction with other inciting insults or by themselves, allow the disease to begin and progress.