Bierhoff E, Vogel J, Benz M, Giefer T, Wernert N, Pfeifer U
Department of Pathology, Rheinische Friedrich Wilhelms University, Bonn, Germany.
Eur Urol. 1996;29(3):345-54. doi: 10.1159/000473774.
Stromal nodules from benign prostatic hyperplasia (BPH; n = 375 from autopsy, n = 100 from biopsy specimens) were investigated with regard to cytoskeletal components, topography, vascularization, leukocytic infiltrates, and proliferative activity.
The nature of stromal nodules was studied by histopathology and immunohistochemistry, using antibodies against alpha-actin, desmin, myosin, vimentin, BMA-120, factor VIII, CD3, CD4, CD20, CD34, CD45RO, CD68, PCNA, and MiB1.
The findings lead to an extended classification of stromal nodules in BPH: immature mesenchymal (IM; 8.8%), fibroblastic (FB; 65.2), fibromuscular (FM; 21.6), and smooth muscular (SM; 4.4%). The different types occurred in all age decades in a similar distribution (FB > FM > IM > SM). Topographical studies (modified zonal subdivision of McNeal) revealed stromal nodules predominantly in the transitional zone (n = 286), less in the central zone (n = 78), occasionally in the peripheral zone (n = 11), and predominantly in the periurethral (n = 287) and less in the intermediate (n = 84) and subcapsular (n = 4) regions. The different types of nodules presented a distinct vascular pattern. FB, FM, and SM nodules showed significantly increased diffuse infiltrates of T lymphocytes-mainly T helper cells (mean 73%)-and an increase of B lymphocytes. Proliferative activity in the nodules was not observed. Stromal nodules were not observed in normal nonhyperplastic prostates; they only occurred in combination with hyperplastic nodular glandular proliferates.
The findings are suggestive of a maturational sequence of stromal nodules in BPH and of a possible significance of immunocompetent cells in the development of stromal nodules and further suggest that both stroma and epithelium of the prostate respond with nodular hyperplasia to the stimulus, which causes BPH.
对良性前列腺增生（BPH）的基质结节（尸检获取375个，活检标本获取100个）进行细胞骨架成分、拓扑结构、血管生成、白细胞浸润及增殖活性方面的研究。
通过组织病理学和免疫组织化学研究基质结节的性质，使用抗α-肌动蛋白、结蛋白、肌球蛋白、波形蛋白、BMA-120、因子VIII、CD3、CD4、CD20、CD34、CD45RO、CD68、增殖细胞核抗原（PCNA）和MiB1的抗体。
这些发现导致了BPH中基质结节的扩展分类：未成熟间充质型（IM；8.8%）、成纤维细胞型（FB；65.2%）、纤维肌型（FM；21.6%）和平滑肌型（SM；4.4%）。不同类型在所有年龄段的分布相似（FB>FM>IM>SM）。拓扑学研究（麦克尼尔改良的分区细分法）显示，基质结节主要位于移行区（n = 286），中央区较少（n = 78），偶尔位于外周区（n = 11），主要位于尿道周围（n = 287），中间区较少（n = 84），包膜下区最少（n = 4）。不同类型的结节呈现出独特的血管模式。FB、FM和SM结节显示T淋巴细胞（主要是辅助性T细胞，平均73%）的弥漫性浸润显著增加，B淋巴细胞也增加。未观察到结节中的增殖活性。在正常未增生的前列腺中未观察到基质结节；它们仅与增生性结节状腺增生同时出现。
这些发现提示BPH中基质结节存在成熟序列，免疫活性细胞在基质结节形成过程中可能具有重要意义，并进一步表明前列腺的基质和上皮均对导致BPH的刺激以结节性增生作出反应。
