Tsujimoto Yuichi, Takayama Hitoshi, Nonomura Norio, Okuyama Akihiko, Aozasa Katsuyuki
Department of Pathology, Osaka University Medical School, Suita, Osaka, Japan.
Prostate. 2002 Sep 1;52(4):279-87. doi: 10.1002/pros.10116.
Postatrophic hyperplasia (PAH) is one of the patterns of prostatic atrophy but has been regarded as a precursor of prostatic cancer (PCA) because of its possible increase in proliferative activity compared with simple atrophy and morphologic mimicry of PCA.
Radical prostatectomy specimens obtained from 28 patients with PCA were analyzed by histologic and immunohistochemical methods by using 34 beta E12 and Ki-67 as primary antibodies. Tissue from PAH, PCA, high-grade prostatic intraepithelial neoplasia (HGPIN), a possible precursor of PCA, and benign hyperplasia were microdissected and p53 gene mutations were examined by the polymerase chain reaction-single strand conformation polymorphism method followed by direct sequencing.
Histologically, PAH consists of compactly arranged small acini with irregular atrophic-appearing contours, mimicking PCA. PAH lesions were detected in 7 (25%) of 28 cases with PCA: multifocal in 6 of 7 (85.7%) cases, maximum size of lesions ranged from 0.3 to 2.3 mm. Mild nuclear enlargement and small nucleoli were observed in all cases. Capsular or perineural invasion, crystalloids, and mitotic figures were not found in any case. Inflammatory changes and fibrosis near PAH were found in 100% and 71% of cases, respectively. PAH involved non-transition zone in all cases and occasionally involved transition zone. Forty-three percent of PAH lesions were in proximity (<2 mm) to PCA. None of the clinical and pathologic factors examined were correlated with the presence of PAH. Immunohistochemical analysis by using 34 beta E12 revealed intact basal cells. Proliferative activity defined by positive rate for labeling with MIB-1 antibody was intermediate between benign prostatic hyperplasia and HGPIN. The frequency of p53 mutations in PAH lesions was 5.3%, which was similar to that in HGPIN lesions (4.2%). Benign glands never showed mutations.
These findings suggested that PAH might be a precursor for PCA.
萎缩后增生（PAH）是前列腺萎缩的一种类型，但因其与单纯萎缩相比增殖活性可能增加以及在形态学上与前列腺癌（PCA）相似，一直被视为前列腺癌的前驱病变。
采用组织学和免疫组织化学方法，以34βE12和Ki-67作为一抗，对28例前列腺癌患者的根治性前列腺切除术标本进行分析。对PAH、PCA、高级别前列腺上皮内瘤变（HGPIN，PCA的一种可能前驱病变）和良性增生组织进行显微切割，采用聚合酶链反应-单链构象多态性方法检测p53基因突变，随后进行直接测序。
组织学上，PAH由紧密排列的小腺泡组成，轮廓呈不规则萎缩状，类似PCA。28例PCA患者中有7例（25%）检测到PAH病变：7例中有6例（85.7%）为多灶性，病变最大直径为0.3至2.3毫米。所有病例均观察到轻度核增大和小核仁。所有病例均未发现包膜或神经周围侵犯、类晶体和有丝分裂象。分别有100%和71%的病例在PAH附近发现炎症改变和纤维化。所有病例中PAH均累及非移行区，偶尔累及移行区。43%的PAH病变与PCA相邻（<2毫米）。所检查的临床和病理因素均与PAH的存在无关。使用34βE12进行免疫组织化学分析显示基底细胞完整。以MIB-1抗体标记阳性率定义的增殖活性介于良性前列腺增生和HGPIN之间。PAH病变中p53基因突变频率为5.3%，与HGPIN病变（4.2%）相似。良性腺体未发现突变。
这些发现提示PAH可能是PCA的前驱病变。
