雄激素去除治疗对老年前列腺癌和前列腺增生患者血清骨代谢的影响

目的 探讨不同雄激素去除治疗对老年前列腺癌、前列腺增生患者血清骨代谢的影响.方法 检测前列腺癌行药物去势(A组,20例)或手术去势(B组,20例)和前列腺增生(C组,40例)用非那雄胺治疗的老年患者治疗前及治疗1年后血清睾酮(T)、骨钙素(OC)、总Ⅰ型前胶原氨基端肽(tPINP)、Ⅰ型胶原羧基端肽(β-CTX)、甲状旁腺激素(PTH)、钙(Ca)、磷(P)水平.同期体检正常的老年男性40例为对照(D组).结果 治疗前,四组骨代谢相关指标差异均无统计学意义(P＞0.05).治疗1年后,A、B组的tPINP和β-CTx均高于D组(P＜0.05),但C组与D组相仿(P＞0.05);A、B组的T均低于D组(P＜0.01).结论 检测血清tPINP和β-CTx可以帮助临床评估雄激素去除治疗的老年前列腺癌患者骨代谢的变化.非那雄胺对于老年前列腺增生患者血清骨代谢指标水平无明显影响.     

放疗对前列腺癌患者细胞雄激素受体的影响

目的 观察放疗对前列腺癌细胞雄激素受体的影响.方法 培养人前列腺癌细胞株LNCap及CWR22R,每个细胞株各分为两组,即放疗组及非放疗组,培养第3天,每组3个培养皿分别加入75%乙醇1nm（EtoH组,作为阴性对照）,比较放疗本身对细胞株ARmRA的影响）;加入DHT（二氢睾酮）1 nm及10 nm,DHT分别相当去势及正常睾酮水平.培养至第5天,放疗组进行放射治疗,剂量为2.7 Gy/min,持续3 min,放疗后24 h收集细胞;非放疗组不作放射治疗,RT-PCR方法比较每个细胞株组雄激素受体（AR）,PSA表达的改变,并重复试验3次.结果 放射治疗前后,EtoH组的ARmRNA,PSAmRNA差异无统计学意义,DHT1组ARmRNA,PSAmRNA显著下降（P〈0.01）,而DHT10组ARmRNA表达则显著上升（P〈0.01）,PSAmRNA轻度升高（P〉0.05）.结论在睾酮达去势水平的前列腺癌细胞,放疗有效;而在正常睾酮水平的前列腺癌细胞,放疗效果不佳.AR下降可作为放疗有效性的较灵敏指标.     

前列腺癌患者能补充雄激素吗

前列腺癌是雄激素依赖性肿瘤,因此,去雄激素治疗就成为前列腺癌一项很重要的治疗方案。睾丸切除术或者化学去势（化疗）是最简便有效的方法。现在提出“前列腺癌患者能够补充雄激素吗”的问题,人们一定会感到很诧异,或许有人会认为是在饮鸩止渴呢。     

药物治疗对初诊甲亢患者骨密度和骨代谢标志物的影响

目的探讨初诊甲亢患者药物治疗对患者骨密度和骨代谢标志物的影响。方法抽取我院2015年2月至2017年2月收治的80例甲状腺功能亢进症(简称甲亢)患者为观察组研究对象,另再设我院接受检查的80例健康者为对照组,观察组实施药物治疗,检测治疗前后股骨颈骨密度(股骨颈BMD)、血清碱性磷酸酶(ALP)、促甲状腺激素(TSH)、β-特殊胶原序列(β-CTX)、游离甲状腺素(FT4)和血清骨钙素(N-MID),并予以对比分析。结果对照组股骨颈BMD为(0.89±0.14)g/cm~2,与观察组的(0.62±0.13)g/cm~2相比,差异有统计学意义(P <0.05),观察组治疗前后股骨颈BMD差异有统计学意义(P <0.05);对照组血清ALP、β-CTX、N-MID等指标明显低于观察组,差异存在统计学意义(P <0.05);治疗后,上述指标明显下降,相比于治疗前,差异有统计学意义(P <0.05)。结论药物治疗初诊甲亢患者效果明显,可降低骨代谢标志物水平,防止骨折疏松。     

循证护理对前列腺癌去雄激素治疗后不良事件的影响

目的探讨循证护理对前列腺癌去雄激素治疗后不良事件的影响。方法将接受去雄激素治疗的前列腺癌患者80例随机分为循证组和常规组,每组40例。对2组不良事件的发生情况及治疗依从性进行比较。结果循证组不良事件发生率低于常规组,治疗依从性高于常规组,差异均有统计学意义（P〈0.05）。结论运用循证护理可减轻前列腺癌去雄激素治疗后的不良事件,提高前列腺癌患者的生活质量。     

循证护理对前列腺癌去雄激素治疗后不良事件的影响

目的 探讨循证护理对前列腺癌去雄激素治疗后不良事件的影响.方法 将接受去雄激素治疗的前列腺癌患者80例随机分为循证组和常规组,每组40例.对2组不良事件的发生情况及治疗依从性进行比较.结果 循证组不良事件发生率低于常规组,治疗依从性高于常规组,差异均有统计学意义(P<0.05).结论 运用循证护理可减轻前列腺癌去雄激素治疗后的不良事件,提高前列腺癌患者的生活质量.     

去雄激素治疗前列腺癌不良反应的护理干预

目的 探讨去雄激素治疗前列腺癌患者不良反应的护理方法及效果.方法 选取42例接受去雄激素治疗的前列腺癌患者为研究对象,随机分为两组,实验组21例给予护理干预,对照组21例给予常规护理方法.对两组患者的遵医行为、生活自理能力、生活质量进行比较分析.结果 两组患者的遵医行为、生活自理能力、生活质量均有显著差异,实验组患者的遵医行为、生活自理能力、生活质量评分均高于对照组.结论 科学的护理可减轻不良反应对患者生活质量的负性影响,确保内分泌治疗的顺利进行.     

降钙素序贯治疗对男性中老年人骨代谢的影响

目的 探讨降钙素序贯治疗对低转换率低骨量病人骨代谢的影响.方法 选取28例男性骨质疏松症或骨量减少病人进行治疗研究.所有病人均接受降钙素治疗,同时基础服用钙尔奇D 600 mg/d.降钙素治疗剂量:第一周20 U肌肉注射,隔日1次,第二周开始20 U肌肉注射,每周2次直至第24周.在开始治疗前、治疗第12周及第24周分别检测血清骨钙素(BGP)、尿1型胶原纤维N端多肽(NTX)及C端多肽(CLP).应用SPSS10.0软件包对三批均数分别进行t-test.结果 有20例完成全程治疗,年龄(63.25±14.62)岁,骨质疏松症15例,骨量减少病人5例.8例不同时期退出治疗,年龄(60.89±9.56)岁.治疗12周病人尿NTX明显下降(P＜0.05),BGP未出现明显降低.24周NTX继续维持低水平,同时BGP不仅与12周相比明显提高(P＜0.01),而且与治疗前相比亦出现明显提高(P=0.05).结论 小剂量降钙素序贯治疗(24周)对骨吸收代谢有持续的抑制作用,未出现明显的逃逸现象.同时,适当长的治疗周期对骨合成代谢有一定的促进作用.     

液相色谱质谱方法对前列腺癌患者治疗前后血清中代谢组学的研究

目的:观察前列腺癌患者治疗过程中代谢物的变化,找寻其与前列腺癌患者治疗的关系,从而为前列腺癌的早期诊断和发病机制研究提供一个新的思路。方法:超高效液相色谱单级四级杆飞行时间串联质谱联用仪分别对临床四组受试者血清标本进行分析。结果:与正常组比较,前列腺癌未治疗组标志物分布有显著性差异(P<0.05);前列腺癌治疗好组标志物分布有显著性差异(P<0.05);前列腺癌治疗差组标志物分布有显著性差异(P<0.05),两治疗组间标志物分布分布有显著性差异(P<0.05)。结论:研究发现共同参与了胆固醇代谢的三个有意义的代谢产物(脱氧胆酸、甘氨鹅脱氧胆酸和二十二碳五烯酸),它们可能在去势抵抗型前列腺癌转变中发挥重要作用。     

最大限度雄激素阻断治疗晚期前列腺癌的护理

前列腺癌是男性常见的恶性肿瘤之一,由于其普查工作滞后,早期诊断率较低,患者就诊时已失去了前列腺癌根治术的机会,故大多数选择最大限度雄激素阻断治疗,那么如何加强此类患者的护理管理就显得尤为重要。     

Effect of androgen deprivation therapy in the thyroid function test of patients with prostate cancer

We have assessed the effect of androgen deprivation therapy (ADT) in the thyroid function test in prostate cancer patients. Serum levels of tri-iodothyronine (T3), thyroxine (T4), free thyroxine (FT4) and thyroid-stimulating hormone (TSH) were determined in a cross-sectional study that included 279 patients diagnosed with prostate cancer. A subset of 96 patients free of prostate-specific antigen relapse after radical prostatectomy became a control group and 183 patients under continuous ADT formed the study group. Sixty-four patients out of the study group were treated with luteinizing hormone-releasing hormone (LHRH) agonist and 119 with LHRH agonist plus bicalutamide. The average time of ADT was 42.5 months (3-218). Results were as follows. Mean T3 level was 122.7 ng/dl (72.6-213.0) in the control group and 123.8 ng/dl (64.4-228.2) in patients under ADT, p=0.472. Mean T4 level was 7.66 (1.81-4.30) and 7.66 microg/dl (3.60-13.30), respectively, p=0.884. Mean TSH level was 1.58 (0.44-11.70) and 1.81 mU/dl (0.15-6.58), respectively, p=0.007. Mean FT4 level was 1.24 (0.80-1.90) and 1.18 ng/dl (0.80-1.90), respectively, p=0.018. No statistically significant differences between the T3, T4, TSH and FT4 serum levels were detected according to the modality of ADT. The serum level of TSH was higher than 5 mU/l in six patients (2.1%); however, all cases had a normal FT4 serum level. This mild hypothyroidism was detected in two of the 96 patients of the control group (2.1%) and in four of the 183 under ADT (2.2%). Our data show that ADT seems to alter the thyroid function test. A statistically significant increase in TSH serum level and a decrease in FT4 serum level were detected in patients under ADT. However, only a mild hypothyroidism was detected in about 2% of the patients with prostate cancer, independently of ADT.     

前列腺癌去势疗法与糖尿病相关性的Meta分析

目的 探讨去势疗法是否会增加前列腺癌（PCa）患者罹患糖尿病的风险。方法 系统检索Medline、Embase、Cochrane Library Central关于去势疗法（ADT）应用于PCa并报道该治疗与糖尿病相关性的临床试验研究,对文献进行数据提取及Meta分析。结果 共8项临床研究,涉及65 695名应用ADT及91 893名未应用去势疗法（non-ADT）的PCa患者纳入分析。应用ADT的患者其糖尿病的发病率较non-ADT者高出39%[RR=1.39,95%CI（1.27~1.53）,P<0.01];亚组分析发现,不同的ADT对糖尿病发病率亦有不同的相关性,促雄性激素释放激素抑制剂能明显增加PCa患者罹患糖尿病的风险[RR=1.45,95%CI（1.36~1.54）,P<0.01];促雄性激素释放激素抑制剂联合口服抗雄性激素药物[RR=1.40,95%CI（1.01~1.93）,P<0.01],以及睾丸切除术也可明显增加糖尿病患病的风险[RR=1.34,95%CI（1.20~1.50）,P<0.01],而单纯服用抗雄性激素的药物则与糖尿病无明显相关性[RR=1.33,95%CI（0.75~2.36）,P=0.33]。结论 ADT可明显增加PCa罹患糖尿病的风险,提示临床应用该疗法需考虑采取相应的预防措施。     

Management of the side effects of androgen deprivation therapy in men with prostate cancer

Background: Androgen deprivation therapy is the foundation of the medical management of prostate cancer. Androgen deprivation therapy offers improved efficacy when used with local therapy such as external beam radiation therapy and substantial palliation in the metastatic setting. Objective: The adverse events of androgen deprivation therapy include hot flashes, decreased bone mineral density, metabolic changes and gynecomastia. Each of these is described as well as their individual management. Method: The medical literature pertaining to androgen deprivation therapy and its adverse events was reviewed with pertinent publications highlighted. Results: Despite the long history of androgen deprivation therapy use in prostate cancer, ongoing work continues to identify and define the adverse events better. For each complication and particularly with regard to metabolic syndrome, recent efforts continue to characterize the problem and its rational management.     

Effect of adjuvant androgen deprivation on thyroid function tests in prostate cancer patients

Androgen deprivation (AD) used in the treatment of prostate cancer is known to alter concentrations of sex hormones and their binding globulins. Less is known as to its effect on thyroid hormones. In this prospective study the effects of AD on thyroid function were clarified. Levels of serum thyroid stimulating hormone (TSH), free thyroxine (FT4) and thyroid binding globulin concentrations were measured in prostate cancer patients treated with either radical radiotherapy and androgen deprivation for 12 months (AD) or radical radiotherapy alone (RT). Measurements were made at baseline, and at 3, 6 and 12 months. At baseline and at 3 months the results of thyroid function tests did not differ significantly between groups. A significant decline in serum testosterone in the AD group was accompanied by a significant decline in FT4 at 6 and 12 months, while no significant changes in thyroid function were observed in the RT group. The decline in FT4 among AD patients did not evoke a normal TSH response. Prolonged use of AD hampers the interpretation of thyroid test results. This finding has substantial implications for the follow-up of patients in hormonally treated prostate cancer.     

Toremifene--a promising therapy for the prevention of prostate cancer and complications of androgen deprivation therapy

Deregulation of the estrogen axis in humans prompts a series of tissue-specific events. In the breast and prostate, alterations in estrogen signalling lead to genotypic and phenotypic molecular alterations that result in dysplastic cellular appearance, deregulated cell growth and carcinoma. In bone, decreased estrogen leads to increased osteoclastogenesis and bone resorption, decreased bone mineral density and a significant fracture risk. Toremifene is a selective estrogen receptor modulator that exerts pharmacological activity in the breast, bone and prostate. An intense interest in developing this agent for prostate cancer chemoprevention is based on the reduction of premalignant and malignant prostate lesions in a transgenic model of prostate cancer. Biological and clinical activity was demonstrated in Phase II trials by the prevention of progression to prostate cancer in men with high-grade prostate intraepithelial neoplasia and through suppression of bone turnover biomarkers and increased bone mineral density in men on androgen deprivation therapy for prostate cancer.     

Bisphosphonates to prevent osteoporosis in men receiving androgen deprivation therapy for prostate cancer

Osteoporosis is an important complication of androgen deprivation therapy for prostate cancer. Androgen deprivation therapy either by bilateral orchiectomies or treatment with a gonadotropin-releasing hormone agonist decreases bone mineral density (BMD) and increases the risk of fracture. Dietary factors and lifestyle may contribute to bone loss. There are limited prospective data about treatment or prevention of osteoporosis in men with prostate cancer and many recommendations are based on studies of postmenopausal osteoporosis. Lifestyle modification including smoking cessation, moderation of alcohol consumption, and regular weight bearing exercise should be encouraged. Supplemental calcium and vitamin D are recommended. Additional treatment may be warranted for men with osteoporosis, fractures, or high rates of bone loss during androgen deprivation therapy. Recent studies have evaluated the efficacy of bisphosphonates to prevent bone loss during androgen deprivation therapy. Pamidronate (pamidronic acid), a second-generation bisphosphonate, prevents bone loss in the hip and spine during androgen deprivation therapy. Zoledronic acid, a more potent third-generation bisphosphonate, not only prevents bone loss but also increases BMD in the hip and spine. Alendronate (alendronic acid) is approved for the treatment of osteoporosis in men although its efficacy and that of other oral bisphosphonates has not been evaluated in men receiving androgen deprivation therapy. Additional prospective studies are needed to evaluate the long-term effects of bisphosphonates on fracture risk and disease-related outcomes.     

Androgen deprivation therapy for prostate cancer

Androgen deprivation continues to play a crucial role in the treatment of advanced and metastatic prostate cancer. In the 65 years since its use was first described, urologists and medical oncologists have developed new and innovative ways to manipulate the hypothalamic-pituitary-gonadal axis with the goal of alleviating symptoms and prolonging the life of men with prostate cancer. Despite the successes that androgen deprivation therapy has brought, each method and regimen possesses unique benefits and burdens, of which the clinician and patient must be cognizant. This review discusses the first-line androgen deprivation methods and regimens presently in use with special attention paid to their side effects and the management of them, as well as the question of when to initiate androgen deprivation therapy.