内分泌治疗高龄中晚期前列腺癌患者临床疗效及安全性研究

目的探讨高龄中晚期前列腺癌内分泌治疗的临床疗效及安全性。方法回顾性分析北部战区总医院2008—2018年采用内分泌治疗的78例高龄中晚期前列腺癌患者的临床资料。根据治疗方法的不同将其分为A组(n=31)与B组(n=47)。A组采用常规双侧睾丸切除去势术联合比卡鲁胺治疗,B组采用戈舍瑞林联合比卡鲁胺治疗。比较两组患者的中位无进展生存期(PFS)、中位总生存期(OS)及治疗相关的不良反应。结果 A、B两组患者的中位PFS、中位OS比较,差异均无统计学意义(P>0.05)。两组患者乳房胀痛、乳房发育、潮热、骨质疏松方面药物不良反应的发生率比较,差异均无统计学意义(P>0.05);B组乏力、肝酶异常的发生率显著高于A组,两组间比较,差异均有统计学意义(P<0.05)。结论在高龄中晚期前列腺癌患者中,戈舍瑞林联合比卡鲁胺治疗方案可取得与手术去势联合比卡鲁胺治疗同样的疗效,不良反应均可耐受,可作为临床治疗高龄中晚期前列腺癌的方案之一。     

前列腺癌9例根治术前辅助治疗效果分析

1995年始,我们应用促性腺激素类似物(LHRH-A)和抗雄性激素药物,对前列腺癌9例根治术前辅助治疗,有效地缩小了前列腺和病灶体积,并降低了切缘肿瘤的阳性率。1　临床资料1.1　一般情况　本组年龄59～69岁,平均63.8岁。辅助治疗前均经活检确诊为前列腺癌。临床分期为B1期5例,C2期4例。B超测量前列腺体积为32.3±21.7cm3,病灶体积为1.2±0.8cm3。前列腺特异性抗原(PSA)为33.8±15.9mg/L。Gleason评分为4.8±1.5分。1.2　用药方法　均应用醋酸亮丙瑞林(日本武田制药公司生产)3.75mg,皮下注射,1次/28d。氟硝丁酰胺(美国先灵葆雅制药厂生产)2…     

注射用炎琥宁治疗小儿急性上呼吸道感染50例疗效观察

目的:比较炎琥宁与病毒唑对小儿急性上呼吸道感染的疗效.方法:将100例急性上呼吸道感染的患儿随机分为治疗组(炎琥宁组50例)和对照组(病毒唑组50例).治疗组对症治疗后给予静脉滴注注射用炎琥宁10 mg/(kg*d),1～2次/d,3～5 d为1个疗程;对照组对症治疗后给予静脉滴注病毒唑10～15 mg/(kg*d),1～2次/d,3～5 d为1个疗程.结果:治疗组总有效率为98%,对照组为86%,两组比较,差异有显著性(P＜0.05).结论:注射用炎琥宁治疗小儿急性上呼吸道感染,可以显著缩短病程及缓解症状,防止并发症的发生,且疗效确切,优于病毒唑注射液.     

丙戊酸钠治疗癫痫持续状态的疗效及安全性

目的:评估丙戊酸钠(VPA)快速静滴控制癫痫持续状态(SE)的有效性及安全性.方法:60例SE患者随机分为治疗组和对照组各30例,对照组安定首剂10 mg静脉注射,随后以(1.5～2.0)μg/(kg·min)的速度微泵持续静注安定;治疗组首剂给丙戊酸钠注射剂(10～15)mg/kg,在3～5 min内静脉注射,而后以(0.5～1)mg/(kg·h)持续静脉滴注,根据病情调整滴注速度.结果:治疗组总有效率83.3%,对照组为66.7%,治疗组的有效率高于对照组(P＜0.05).治疗组癫痫完全控制时间(29.01±10.84)s明显短于对照组癫痫完全控制时间[(34.93±10.54)s](P＜0.05).结论: 快速静脉使用VPA治疗癫痫持续状态起效快,作用强,安全有效.     

炔雌醇环丙孕酮片联合坤泰胶囊治疗多囊卵巢综合征患者的疗效及对其内分泌与排卵的影响

目的 探讨炔雌醇环丙孕酮片联合坤泰胶囊治疗多囊卵巢综合征(polycystic ovarian syndrome,PCOS)患者的临床疗效与对其内分泌与排卵的影响.方法 将收治的94例PCOS患者分为两组,对照组47例,只口服炔雌醇环丙孕酮片,观察组47例,采用炔雌醇环丙孕酮片与坤泰胶囊联合治疗,比较两组患者的治疗效果、生殖内分泌的各项指标与排卵情况.结果 观察组治疗有效率高达95.7%,对照组治疗有效率为74.5%(P<0.05).结论 在多囊卵巢综合征患者的临床治疗中,应用炔雌醇环丙孕酮片与坤泰胶囊联合治疗,疗效确切,对患者生殖内分泌与排卵的改善具有积极效果.     

丙戊酸钠注射液联合左乙拉西坦治疗难治性癫痫持续状态的临床观察

目的探讨丙戊酸钠注射液联合鼻饲左乙拉西坦治疗难治性癫痫持续状态(RSE)的疗效及安全性。方法对2010年1月—2012年8月连续登记的48例经地西泮静滴、苯巴比妥肌内注射治疗未能控制的RSE患者,其中25例单独使用丙戊酸钠注射液(丙戊酸钠组),23例应用丙戊酸钠注射液联合鼻饲左乙拉西坦(联合治疗组)。两组丙戊酸钠注射液使用方法均首剂为10～15 mg/kg,在3～5 min内静脉注射,而后以0.5～1 mg/(kg.h)持续静脉滴注。联合治疗组中鼻饲左乙拉西坦中位剂量为1 000 mg(范围:500～3 000 mg)。结果丙戊酸钠组总有效率为60.0%,联合治疗组为95.7%,两组比较,差异有统计学意义(P<0.05)。联合治疗组及丙戊酸钠组有效患者均在1 h内癫痫持续状态(SE)得到控制,然而丙戊酸钠组有40%在其后72 h仍间断癫痫发作,而联合治疗组仅4.3%在其后72 h见癫痫发作。两组治疗前后的血、尿常规、肝肾功能、凝血功能、心电图无明显变化。结论丙戊酸钠注射液联合鼻饲左乙拉西坦治疗RSE安全有效,且起效快、作用强、控制时间长。     

醋酸奥曲肽不同给药方式治疗胃溃疡合并失血性休克疗效对比

【摘要】 目的 对比分析醋酸奥曲肽不同给药方式治疗胃溃疡合并失血性休克的临床效果。 方法 选取2019年7月至2021年7月辽宁省人民医院收治的 90 例胃溃疡合并失血性休克患者作为研究对象, 按照不同给药方式将其分为观察组 (45 例) 和对照组 (45 例), 观察组患者予以静脉滴注注射用埃索美拉唑钠联合皮下注射注射用醋酸奥曲肽治疗, 对照组患者予以静脉滴注注射用埃索美拉唑钠联合持续静脉泵注注射用醋酸奥曲肽治疗, 对比观察两组患者血红蛋白水平、胃液 pH 值、止血时间、输血量与不良反应发生情况。结果 治疗 14 d后, 观察组患者血红蛋白水平与胃液 pH 值均明显高于对照组 (t =6.037、14.956, P 均 <0.001)。观察组患者止血时间及输血量与对照组无明显差异 (t =0.445、0.373, P =0.657、0.710)。治疗期间, 观察组患者不良反应发生率为 6.67%, 与对照组患者的不良反应发生率 11.11%无明显差异 (χ 2 =0.549, P =0.459)。 结论 皮下注射与持续静脉泵注注射用醋酸奥曲肽治疗胃溃疡合并失血性休克的止血效果虽相当, 但皮下注射更有利于提高血红蛋白水平与胃液 pH 值。     

注射用醋酸卡泊芬净与更昔洛韦存在配伍禁忌

<正>遵医嘱为一肾移植术后肺部感染患者静滴0.9%氯化钠100 ml+注射用醋酸卡泊芬净(商品名:科塞斯)50 mg,液体滴完后,换上0.9%氯化钠250 ml+注射用更昔洛     

干扰素加激素治疗散发性脑炎19例疗效分析

病例选择 根据临床诊断标准,随机选择散发性脑炎(下称散脑)住院患者19例,试用干扰素加激素治疗(一组);另选同时期住院的散脑患者27例,单用激素治疗作对照(二组)。 治疗方法 一组患者,用人(脐)白细胞干扰素5ml(浓度8,000u/ml)肌注,1次/日,用药5～35天(一般15天),同时加用激素(方法同二组)。二组患者,用地塞米松10～20mg静滴,1次/日,连用7～10天,后改强的松口服,30～40mg/日,病情好转后逐步减量。     

甾体激素对致死剂量照射小鼠骨髓移植疗效的影响(摘要)

Laca纯系成年雌雄小鼠,受了~(60)Coγ线950rad(剂量率82R/min)一次全身照射后,移植5×10~6同系而性别不同的小鼠骨髓细胞,60天活存率54.4％,照射对照组于12～15天内全部死亡。在移植前3天或移植后即刻分别肌肉注射0.25mg和0.05mg 3,17β棕榈酸椎二醇(简称“棕二”)或0.5mg丙酸睾丸酮(简称“丙睾”),可使活存提高到76.2％～86.4％。对造血组织脾脏,也有促进其恢复重量的趋势。若单纯应用“棕二”或“丙睾”对950rad照射小鼠未见有明显的防治作用。     

Growth hormone and athletes

Growth hormone is a powerful anabolic hormone that affects all body systems and plays an important role in muscle growth. It is released from the anterior pituitary in response to a variety of stimuli including exercise, sleep, stress, and the administration of a variety of drugs and amino acids. Serum levels are variable and are dependent on such factors as age, sex, body composition and level of fitness. Animal experiments have shown that growth hormone can partially reverse surgically induced muscle atrophy and weakness. Growth hormone administration to normal animals leads to muscle hypertrophy, but this muscular growth is not accompanied by increased strength. Growth hormone excess leads to acromegaly, a disease with significant morbidity, including a myopathy in which muscles appear larger but are functionally weaker. Although there is no scientific evidence documenting an improvement in athletic performance following growth hormone supplementation, it is reported that this practice is becoming more widespread among athletes wishing to avoid detection with current doping control measures. There are anecdotal reports that athletes are injecting cadaveric or biosynthetic forms of growth hormone, both of which are associated with potentially serious complications. In addition, some athletes are ingesting drugs and amino acids in the belief that their endogenous growth hormone secretion will be increased. There have been no scientific studies on the effects of growth hormone supplementation, and the anecdotal reports have been equivocal, with some individuals reporting spectacular results while others report no change. Despite the lack of valid evidence for its efficacy and its potentially serious side effects, it has been predicted that growth hormone use may increase. Growth hormone use and abuse has the potential to dramatically change the future conduct of athletics and may prove to be a threat to the concept of fair competition.     

Involvement of endogenous growth hormone-releasing hormone (GHRH) in the exercise-related response of growth hormone

The aim of this study was to investigate the involvement of endogenous growth hormone-releasing hormone (GHRH) in the growth hormone (GH) release during strenuous exercise (EX). Eight healthy male subjects (age: 22.1 +/- 0.8 yr, body mass index: 22.2 +/- 0.9 kg/m 2, .VO 2 max: 52.2 +/- 0.5 ml/min/kg [mean +/- SEM]) were exposed to incremental EX until volitional exhaustion (cycle ergometry), and in random order to a maximally stimulating bolus injection of 100 microg GHRH, or to combined administration of 100 microg GHRH and EX (GHRH+EX). Serial blood samples in the fasted state were taken immediately before the start of each trial, and at appropriate intervals over 2 h. Total GH availability was calculated as area under the response curve (AUC), corrected for differences in baseline values. The results showed that peak serum GH levels to GHRH alone and EX alone were not significantly different: 41.5 +/- 9.0 microg/l and 64.1 +/- 8.1(mean +/- SEM). Peak GH level to GHRH+EX was 156.1 +/- 19.9 microg/l, which was significantly greater than to either stimulus alone (p < 0.02) or additively (105.6 +/- 17.1 microg/l, p < 0.02). AUC's to GHRH alone and EX alone were not significantly different (3242 +/- 839 vs. 2472 +/- 408 microg/l x 120 min). AUC to GHRH+EX (7807 +/- 1221 microg/l x 120 min) was greater than to either stimulus alone (p < 0.02) or additively (5714 +/- 1247 microg/l x 120 min, p < 0.02). This indicates a potentiating (synergistic) effect between GHRH and EX. We postulate that GH responses to strenuous EX are only partially due to maximal GHRH activation. Next to complete inhibition of hypothalamic somatostatin activity, which is achieved by strenuous exercise, activation of endogenous GH-releasing peptides, such as Ghrelin, must be operative.     

Growth hormone responses during strenuous exercise: the role of GH-releasing hormone and GH-releasing peptide-2

PURPOSE AND METHODS: This study was designed to investigate the role of two effective releasers of growth hormone (GH): GHRH and GHRP-2 during exercise (EX). Eight healthy male subjects (ages: 22 +/- 1.2 (mean +/- SD) yr, BMI: 22.5 +/- 2.2 kg x m(-2)) were exposed to maximally stimulating dose of 100 microg GHRH iv, and 200 microg GHRP-2 iv, during incremental EX on a cycle ergometer to exhaustion. GH responses after EX alone were compared with the responses after the combined administration of the same EX plus GHRH, EX plus GHRP-2, and EX plus GHRH plus GHRP-2. Blood samples were obtained in the fasted state at intervals for 2 h postexercise and the area under the GH response curve (AUC) was calculated by trapezoidal integration. RESULTS: Significant differences (P < 0.003) were observed between the AUCs after administration of EX alone (mean +/- SEM): 2,324 +/- 312 microg x L(-1) 120 min, after EX plus GHRH: 6,952 +/- 1,083, after EX plus GHRP-2: 14,674 +/- 2,210, and after the combination EX plus GHRH plus GHRP-2: 17,673 +/- 1,670. However, AUCs after each combination did not differ significantly from those after arithmetical addition of each separate stimulus, indicating that the mechanisms of the respective stimuli do not interact. Linear regression analysis on mean GH responses between 20 and 30 min after the start of EX showed that EX alone and GHRH alone explain about 59% (adj. R2) of the GH response to the combination EX plus GHRH. The ratio of the respective regression coefficients (GHRH vs EX) was about 2:1 (instead of 1:1), indicating that EX seems to potentiate the activity of GHRH. GHRH alone and EX alone also explained about 74% of the response to the combination EX plus GHRP-2. In the latter response, a synergistic action of GHRP-2 on GHRH could be observed. CONCLUSIONS: The data indicate that under strenuous EX conditions, endogenous GHRH activity causes a further increase of GH release. A GHRP-2 mediated mechanism in the central neuroendocrine regulation acts as a "booster," possibly by stimulating the effects of GHRH and/or an unknown hypothalamic factor, as well as by stimulating the pituitary GH release directly.