前列腺癌去雄激素治疗不良反应的预防和处理

目的观察去雄激素治疗前列腺癌的不良反应,并探讨其预防和治疗。方法回顾性分析1998年7月-2006年1月112例去雄激素治疗晚期前列腺癌的临床资料。结果112例患者中,97例完成了不良反应的调查。随访3-36月,去雄激素治疗后潮热、性功能障碍、病理性骨折发生率分别为46％、75％、4％;患者潮热、精神疲乏、四肢乏力、纳差症状明显加重(P<0．05);性功能明显减退(P<0．05)。12例潮热症状严重者使用抗抑郁药博乐欣(25mg,tid)1-2周症状减轻。7例有骨转移性疼痛或严重骨质疏松患者,应用唑来膦酸4mg静脉滴注,每45d一次,骨痛症状缓解。结论去雄激素对前列腺癌患者生活质量有一定影响。博乐欣可减轻患者潮热症状,唑来膦酸可预防和治疗去雄激素相关的骨质疏松并发症。     

前列腺特异抗原和高分子量细胞角蛋白改良免疫组织化学染色法对前列腺癌的诊断作用

目的 探讨前列腺特异抗原(PSA)和高分子量细胞角蛋白(CK34βE12)改良免疫组织化学染色法对前列腺癌鉴别诊断的作用。方法 对52例疑难病例采用改良免疫组织化学染色法检查。即在同一切片的一侧贴附可靠的阳性对照组织，应用微波处理，尽可能保存和修复抗原，在显微镜下严格控制显色等方法以达到最佳染色效果。结果3例前列腺不典型腺瘤样增生(AAH)、37例前列腺上皮内瘤(PIN)高表达PSA与CK34βE12；3例前列腺导管内癌也表达PSA及CK34βE12；9例前列腺腺癌仅表达PSA无CK34βE12表达；10例膀胱移行上皮癌均不表达PSA与CK34βE12。结论 PSA和CK34βE12的改良免疫染色可以作为前列腺癌鉴别诊断的工具之一，对指导临床治疗可发挥重要作用。     

转化生长因子在前列腺增生中作用的研究

目的：探讨转化生长因子α(TGF-α)和转化生长因子β(TGF-β)在良性前列腺增生症组织中的表达及意义。方法：利用免疫组织化学方法研究TGF-α和TGF-β在40例BPH组织和5例正常前列腺组织中的表达。结果：TGF-α在BPH组织上皮和间质中的表达强阳性率均高于正常前列腺组织(P＜0．01)。且TGF-α在BPH组织上皮组织的表达明显高于其在间质中的表达(P＜0．01)。TGF-β在BPH组织上皮和间质中的表达明显高于正常前列腺组织(P＜0．01)。且TGF-β在BPH组织间质中的表达明显高于其在上皮组织中的表达(P＜0.01)。结论：TGF-α在前列腺组织中表达增高，尤其在腔上皮细胞的胞浆中高度表达，TGF-β在前列腺包织中表达增高，尤其在间质组织中的过度表达，提示其可能直接或间接参与了前列腺间质细胞的分化和增殖，参与了BPH的病理过程。     

输精管结扎干扰前列腺增生过程的机制探讨——精浆睾酮双氢睾酮的放射免疫测定

本文应用放射免疫测定的方法检测了13例输精管结扎后(平均15.3年,平均年龄50岁)的男性精浆双氢睾酮和睾酮的浓度,另取同年龄组男性13例作为对照。结果表明,精浆睾酮在结扎组(374.54p/ml)和正常对照组(315.64Pg/ml)中没有明显差异,而结扎组精浆中双氢睾酮(46.21pg/ml)却明显低子对照组(184.27pg/ml(p<0.01)。作者认为,输精管结扎对精浆DHT有长期影响,这可能是其对前列腺增生过程产生抑制作用的原因之一。     

性激素受体及相关生长因子在前列腺基质细胞中的表达

目的：探讨前列腺基质增生的发病机制与性激素以及相关生长因子的关系。方法：应用RT－PCR的方法研究了在人前列腺不同细胞类型中Smoothelin的表达，研究了雄、雌激素受体及相关生长因子在前列腺基质细胞中的表达，以及它们在前列腺基质细胞分化中表达的变化。结果：Smoothelin是前列腺平滑肌细胞特异性的标记蛋白；雄激素受体（AR）、碱性成纤维细胞生长因子（bFGF)、角化细胞生长因子（KGF）主要在前列腺成纤维细胞中表达，而雌激素受体（ER）、转移生长因子β1（TGFβ1）主要在平滑肌细胞中表达。结论：前列腺基质增生与雌激素受体和转移生长因子β1的过度表达密切相关。     

Nuclear p53 Overexpression in Bladder, Prostate, and Renal Carcinomas

Background :
The aim of this study was to examine nuclear p53 overexpression in transitional cell carcinoma of the bladder, adenocarcinoma of the prostate, and renal cell carcinoma.
Methods :
Forty-four pathologic specimens from 39 bladder cancer patients, 41 prostatic adenocarcinoma, and 39 renal cell carcinoma specimens were analyzed immunohistochemically with D07 monoclonal antibody to detect the expression of the mutant p53 gene. Overexpression was said to occur when the number of positively-stained tumor nuclei were≥ 10% in each specimen. p53 overexpression was correlated with the clinical and histopathological features of these cancers.
Results :
Nuclear p53 overexpression occurred in 18.2% of transitional cell bladder cancer specimens, 12.2% of prostate cancer specimens, and 17.9% of renal cell cancer specimens. Statistical analyses showed that grade, vascular invasion, and necrosis in bladder cancer, a high Gleason score in prostate cancer, and the 1-year mortality rate in renal cancer were significantly related with p53 nuclear overexpression (P<0.05).
Conclusion :
Using the D07 monoclonal antibody, nuclear p53 overexpression is relatively uncommon in urologic malignancies, and moderately correlates with several histopathological and clinical features of urologic malignancies.     

乳舒胶囊镇痛、抗炎作用研究

目的：研究乳舒胶囊(RS)的镇痛、抗炎药效。方法：采用RS灌胃给药后，分别用甩尾法、热板法、扭体法研究RS对乳腺增生模型大鼠及小鼠的镇痛作用，分别用二甲苯法、琼脂法研究RS抑制小鼠耳廓炎症及大鼠慢性炎症性肉芽肿的作用。结果：乳舒胶囊能提高乳腺增生模型大鼠和小鼠的痛阈值、能减少醋酸致扭体疼痛小鼠的扭体次数、延长其发生扭体的潜伏期，有明显的镇痛作用；还可以抑制琼脂所致的大鼠肉芽肿和二甲苯致小鼠耳肿胀，有明显的抗炎作用。结论：乳舒胶囊镇痛、抗炎作用明显、疗效确切。     

万艾可治疗ED时对BPH引起LUTS改善的研究

目的 :探索、研究万艾可在治疗阴茎勃起功能障碍 (ED)时对由良性前列腺增生 (BPH)引起的下尿路症状(LUTS)的影响。　方法 :32例ED同时伴有BPH的研究对象 ,采用IIEF 5问卷表和IPSS评分表 ,在服用万艾可前和服药后 6个月分别各填写一次 ,应用单因素方差分析对所得到的前后评分进行统计学分析。结果 :在服药前32例ED中 ,轻、中、重分别为 14、13、5例 ,BPH中轻、中、重分别为 3、15、14例 ;服药后IIEF 5评分平均上升4 2 .36 % ,IPSS评分平均下降 2 0 .14 % ,两者在统计学上都有显著性差异 ,P <0 .0 1。　结论 :在治疗中老年性ED合并BPH中 ,应用万艾可既能治疗ED ,取得完美的性生活 ,又能达到改善由BPH引起的LUTS。万艾可是一治疗ED有效的药物 ,但对于前列腺基质平滑肌亦有辅助性松弛作用 ,因此也有助于BPH时LUTS的缓解。     

Nodular hyperplasia surrounding fibrolamellar carcinoma

We report a case of acetaminophen-induced liver necrosis in a 14-year-old girl. At autopsy, a 9 cm subcapsular nodule was present in the right lobe of the liver which showed distinct zonation: a central greyish white area of fibrolamellar carcinoma with a peripheral fleshy, tan-coloured rim ranging from 1 to 2 cm in thickness. This peripheral zone consisted of nodular, hyperplastic parenchyma resembling the changes seen in focal nodular hyperplasia, and stood out from the adjacent necrotic parenchyma. The sparing of this zone from the deleterious effects of acetaminophen provides indirect evidence of a predominantly arterial rather than portal blood supply to this region. The arterial supply was most probably derived from the tumour vasculature and may explain the parenchymal hyperplasia sometimes reported adjacent to a fibrolamellar carcinoma. Awareness of this phenomenon is essential when evaluating a needle biopsy, as sampling of this region may lead to a false negative diagnosis.     

Direct injections of calcitriol into enlarged parathyroid glands in chronic dialysis patients with severe parathyroid hyperfunction

Summary: Severe secondary hyperparathyroidism in chronic dialysis patients has been recently treated by supraphysiological concentration of calcitriol achieved through pulse therapy. However, there are many patients resistant to this therapy, who usually have larger parathyroid gland(s). to overcome this resistance, calcitriol was injected directly into the enlarged glands under ultrasonographic guidance. We injected 70–90% of the calculated gland volume of calcitriol solution (1 μg/mL) into the glands of 7 patients three times per week for 2 weeks. the parathyroid hormone (PTH) levels decreased significantly after 2 weeks of direct injections of calcitriol. Following a further 4 weeks of calcitriol pulse therapy, PTH levels remained suppressed and serum alkaline phosphatase activity and the volume of parathyroid glands also decreased. During the long-term follow up, five patients remained well controlled with calcitriol pulse therapy, while two patients needed ethanol injections to control hyperparathyroidism. Although we could not completely rule out a toxic effect of the vehicle, direct injection of calcitriol into parathyroid glands may be another treatment option for chronic dialysis patients. Our data further support the important role of resistance of parathyroid cells to calcitriol in the pathogenesis of parathyroid hyper function in uraemic patients.