Pontari Michel A, Ruggieri Michael R
Department of Urology, Temple University School of Medicine, 3401 N. Broad Street, Philadelphia, PA 19140, USA.
J Urol. 2004 Sep;172(3):839-45. doi: 10.1097/01.ju.0000136002.76898.04.
We reviewed the current literature on mechanisms involved in the pathogenesis of prostatitis/chronic pelvic pain syndrome (CPPS).
A literature review for the years 1966 to 2003 was performed using the MEDLINE database of the United States National Library of Medicine.
National Institutes of Health categories I and II prostatitis result from identifiable prostatic infections, whereas patients with category IV are asymptomatic. The majority of symptomatic cases are category III or chronic prostatitis (CP)/CPPS. The etiology of CP/CPPS is unknown. The traditional marker of inflammation, namely white blood cells in prostatic fluids, does not correlate with the predominant symptom of pelvic pain. An imbalance toward increased proinflammatory and decreased anti-inflammatory cytokines has been implicated and a few studies have shown some correlation of this with pelvic pain. The imbalance in some men may result from polymorphisms at the cytokine loci. An autoimmune process may be involved and experimental evidence indicates that this can be under hormonal influence. Recent findings include possible defects in the androgen receptor. The prostate may not even be the source of the symptoms. Pelvic pain also correlates with the neurotrophin nerve growth factor implicated in neurogenic inflammation and central sensitization. Finally, psychological stress may produce measurable biochemical changes and influence the other processes. The role of normal prostatic bacterial flora in inciting the inflammatory response has also been reconsidered.
The symptoms of CP/CPPS appear to result from an interplay between psychological factors and dysfunction in the immune, neurological and endocrine systems.
我们回顾了目前关于前列腺炎/慢性盆腔疼痛综合征（CPPS）发病机制的文献。
使用美国国立医学图书馆的MEDLINE数据库对1966年至2003年的文献进行了回顾。
美国国立卫生研究院分类中的I型和II型前列腺炎是由可识别的前列腺感染引起的，而IV型患者无症状。大多数有症状的病例属于III型或慢性前列腺炎（CP）/CPPS。CP/CPPS的病因尚不清楚。传统的炎症标志物，即前列腺液中的白细胞，与盆腔疼痛的主要症状无关。促炎细胞因子增加和抗炎细胞因子减少的失衡被认为与此有关，一些研究表明这与盆腔疼痛有一定相关性。一些男性的这种失衡可能是由于细胞因子基因座的多态性。可能涉及自身免疫过程，实验证据表明这可能受激素影响。最近的研究结果包括雄激素受体可能存在缺陷。前列腺甚至可能不是症状的来源。盆腔疼痛还与参与神经源性炎症和中枢敏化的神经营养因子神经生长因子有关。最后，心理压力可能会产生可测量的生化变化并影响其他过程。正常前列腺细菌菌群在引发炎症反应中的作用也已被重新审视。
CP/CPPS的症状似乎是心理因素与免疫、神经和内分泌系统功能障碍之间相互作用的结果。
