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目的:观察继发于感染的双侧附睾梗阻性无精子症患者的附睾病理特征,分析可能的病理生理机制以便寻找可能的治疗靶点。方法:2015年3~12月,收集既往有附睾感染史的不育就诊者11例,年龄28~53岁。通过精液常规、精液离心检查筛选确诊为无精子症患者,行生殖激素、精浆生化、阴囊超声检查,初步确定系附睾梗阻性无精子症者,进行手术探查,观察附睾大体病理特征并采集图像;切取病变处附睾组织,行病理切片观察。结果:病变附睾大体标本观察示,附睾管积水样改变是主要的病理特征;病理切片观察,附睾管管腔结构完整,管腔内充盈扩张,腔内未见精子。大多数病例管壁间未见炎性细胞浸润,以无纤维化为主。少数病程较长患者除附睾管扩张外,可见腔内组织细胞浸润、间质纤维组织增生或间质纤维透明变性,散在淋巴细胞、嗜酸性细胞浸润。结论:继发于感染的附睾梗阻性无精子症患者病变附睾的病理解剖学特征主要为附睾管积水,以及造成的腔内梗阻,其具体机制有待进一步研究。
OBJECTIVE: To observe the epididymal pathological features of patients with bilateral epididymal esophageal obstruction secondary to infection and to analyze possible pathophysiological mechanisms in search of possible therapeutic targets. Methods: From March to December 2015, 11 infertility patients with past history of epididymitis were collected, aged from 28 to 53 years. The patients were diagnosed as azoospermia by sperm routine examination and semen centrifugation screening. The reproductive hormones, seminal plasma biochemistry and scrotal ultrasound examination were performed to identify the patients with epididymal obstructive azoospermia. Surgical exploration was performed to observe the gross pathological features of the epididymis and to collect the images Cut the epididymal lesions at the pathological section. Results: The gross epididymal specimens showed that the changes of epididymal water samples were the main pathological features. The pathological findings of the epididymal canal showed that the structure of the epididymal canal was intact, the cavity was filled and dilated, and no sperm was found in the cavity. In most cases there was no infiltration of inflammatory cells in the wall, with no fibrosis. In addition to a small number of patients with longer duration of epididymal tube expansion, we can see intraluminal tissue cell infiltration, interstitial fibrosis or interstitial fibrinous degeneration, scattered in lymphocytes, eosinophil infiltration. Conclusion: The pathological anatomy of epididymal epididymis in patients with epididymal epididymis secondary to infection of epididymis is mainly caused by epididymal fluid and intracavitary obstruction. The exact mechanism remains to be further studied.