含吲哚美辛固定式宫内节育器用于人工终止妊娠术后即时放置的临床效果及安全性分析

<正>随着经济的发展和人们生活方式的转变,由于意外怀孕导致的人工终止妊娠手术率有增高的趋势,重复的人工终止妊娠对女性身心健康带来极大的影响。宫内节育器(IUD)属于临床中常用的长效避孕方式,其避孕效果已被广泛认同[1]。人工终止妊娠术后即时放置IUD能够降低二次手术对人体的伤害及痛苦,且并不会增加宫内感染等并发症的发生率[2]。含吲哚美辛固定式IUD属于无支架式含     

不同剂量吲哚美辛对小鼠胚泡着床的影响

吲哚美辛是一种非选择性的前列腺素合成酶抑制剂,国外已有吲哚美辛影响动物着床的报道,在此,进一步观察不同剂量吲哚美辛对小鼠着床的影响,为下一步建立吲哚美辛致小鼠胚泡着床障碍模型奠定基础.     

4%与1%吲哚美辛乳膏的镇痛抗炎作用比较

目的:观察4%与1%吲哚美辛乳膏的镇痛抗炎作用.方法:以1%吲哚美辛乳膏为对比,对几种炎症、疼痛模型考察4%吲哚美辛乳膏的治疗作用.结果:4%吲哚美辛乳膏对甲醛致小鼠足部疼痛、热板法致小鼠足部疼痛、大鼠尾部压痛均有明显镇痛效果,对卡拉胶致大鼠足肿胀和二甲致小鼠耳肿胀有明显抗炎效果.结论:4%吲哚美辛乳膏具有明显的镇痛抗炎药效,优于1%吲哚美辛乳膏.     

三种不同宫腔屏障对宫腔粘连分离术后再粘连的预防效果比较

目的 观察宫腔镜下宫腔粘连分离术(TCRA)后三种宫腔屏障对预防宫腔再次粘连的临床效果.方法 选取2017年5月至2019年5月该院中重度宫腔粘连且有生育要求的患者150例.随机分为球囊组、节育器组、凝胶组,各50例.三组均行TCRA.球囊组在术后宫腔放置COOK球囊.节育器组在术后宫腔放置元宫型含铜含吲哚美辛宫内节育...     

MYCu宫内节育器中吲哚美辛硅橡胶棒的HPLC测定

目的建立高效液相色谱法测定MYCu宫内节育器中吲哚美辛的含量及体外释放量。方法采用C18柱,以甲醇-10mL·L-1醋酸溶液(80∶20)为流动相,检测波长为265nm。结果吲哚美辛进样量在2~184ng之间线性关系良好,平均回收率为100.6%,RSD为0.7%。结论所建立的MYCu宫内节育器中吲哚美辛的含量及体外释放量测定方法简便、准确,可用于质量控制。     

人工流产后即时随机放置吉妮致美临床研究

目的观察吉妮致美于人工流产后即时随机放置的安全性、脱落率、避孕效果、副反应发生率。方法收集观察随访2010年1月至2011年1月本院对停经6—9周,要求终止妊娠同时需避孕的妇女300例,人工流产后即时放置吉妮致美宫内节育器（含吲哚美辛硅橡胶的固定式宫内节育器）,术后定期随访。结果300例累计观察12个月,妊娠率0．66％,脱落率％副反应发生率1．33％因症取出率1．33％。结论人工流产后即时放置吉妮致美宫内节育器安全性高、脱落率低、避孕效果可靠、副反应发生率低。     

大月份人工流产后即时随机放置吉妮致美的临床研究

目的：探讨宫内节育器吉妮致美于大月份人流后即时随机放置的安全性、有效性、不良反应发生情况。方法收集2012年2月~2014年3月期间在本院要求终止妊娠同时需避孕的停经6~10周及10~14周妇女各150例进行临床观察随访,均于人工流产术后马上放置宫内节育器吉妮致美（含吲哚美辛硅橡胶的固定式宫内节育器）,术后给以定期随访。结果300例对象累计观察6个月, A组：脱落率0.67%,不良反应发生率2%,因症取出率0.67%。B组脱落率3.3%,不良反应发生率2.67%,因症取出率1.33%。结论大月份人工流产术后即时放置宫内节育器吉妮致美安全性高、避孕效果确切、不良反应发生率较低,与妊娠9~10周者相比较,大月份人工流产术后放置宫内节育器吉妮致美脱落率较高,达到3.3%。     

吲哚美辛凝胶稳定性研究

目的:考察吲哚美辛凝胶的稳定性.方法:将包装和脱包装的吲哚美辛样品置于高温、高湿、强光环境下,考察其含量变化情况.结果:强光时脱包装吲哚美辛凝胶含量略为下降,高温时(80℃)吲哚美辛凝胶含量下降明显,高湿对吲哚美辛凝胶含量无影响.结论:吲哚美辛凝胶对高温不稳定,对强光略为不稳定,对高湿稳定,提示吲哚美辛凝胶应采用低温避光保存.     

壳聚糖-吲哚美辛缓释微囊药动学研究

目的 研究自制壳聚糖-吲哚美辛微囊的药动学.方法 以市售普通吲哚美辛片剂为参比通过高效液相色谱测定模型动物家兔药时曲线.结果 与普通片剂相比,兔口服壳聚糖-吲哚美辛微囊后,达峰时间明显推迟,且达峰浓度降低(P<0.05);同时药物在兔体内平均驻留时间明显长于普通片(P<0.05);但两制剂的AUC无差异(P>0.05).结论 研制的壳聚糖-吲哚美辛微囊具有较好的缓释效果,且吸收程度与普通吲哚美辛片剂等效.     

药物导电压敏胶的制备及其体外透皮释放试验

目的:考察固化在导电压敏胶中的吲哚美辛在低频脉冲电流作用下的释放现象,试图将透皮给药治疗体系与低频脉冲电刺激相结合来提高疗效。方法:利用紫外光固化技术将吲哚美辛直接固化在导电压敏胶中,通过药物体外透皮释放模型测定吲哚美辛的释放。结果:光引发剂对压敏胶固化有重要影响,使用混合光引发剂有利于固化;压敏胶厚度不宜超过2cm;吲哚美辛药量增加,对预聚体配方的固化及保存有影响,吲哚美辛合适用量约为0.50％。结论:制得了固化良好、具有一定粘性和可多次使用的含药导电压敏胶;低频脉冲电流刺激下(正、负极),压敏胶中吲哚美辛的释放加快。     

武汉市青山区育龄妇女环下移状况分析

目的:了解武汉市青山区育龄妇女宫内节育器下移状况。方法:收集2007年3月~2009年9月青山区计划生育服务站记录的带环育龄妇女资料,采用SPSS13.0软件进行统计分析。结果:带环育龄妇女环下移检出率为2.4%。环下移妇女中,6.5%带器妊娠。出现环下移的妇女年龄主要集中在30~39岁、放环时间主要在10年内、环型以O型环和T型环为主。结论:应加强带环妇女尤其30~39岁年龄段妇女的早期和定期检查。     

痛经康口服液镇痛、抗炎和急性毒性作用研究

目的:研究痛经康口服液的镇痛、抗炎和急性毒性作用。方法:采用醋酸扭体法和热板法观察镇痛作用;采用小鼠耳廓肿胀、毛细血管通透性法观察抗炎作用,采用最大给药量实验研究痛经康口服液对小鼠的急性毒性。结果:痛经康口服液能显著减少小鼠的扭体次数,抑制由二甲苯致小鼠廓肿胀和降低小鼠腹腔毛细血管的通透性,但对热刺激所致小鼠的痛阈值未见明显影响;痛经康口服液在剂量为261g·kg-1时未发现毒性反应。结论:痛经康口服液较为安全且具有明显的镇痛、抗炎作用。     

尾丝对生殖道炎症发病率的影响

目的 了解放置不同宫内节育器（IUD）对患者生殖道感染、盆腔炎发病率的影响.方法 对170例放置有尾丝型IUD的育龄期妇女及170例放置无尾丝型IUD的育龄期妇女进行1年随访,比较两组妇女生殖道感染及盆腔炎发病率.结果 放置有尾丝型IUD妇女生殖道感染及盆腔炎总发病率为2.94％（5/170）;放置无尾丝型IUD妇女总发病率为1.18％（2/170）,不同IUD妇女总发病率差异无统计学意义（x2=1.313,P=0.252＞0.05）,且生殖道感染和（或）盆腔炎均在放置IUD后半年内出现.两组不良反应情况差异无统计学意义（x2=0.080,p=0.777＞0.05）.结论 IUD有无尾丝对妇女生殖道感染及盆腔炎发病无影响,放置IUD时应严格无菌操作,以尽量减少宫腔组织的损伤,减少继发感染.     

雷公藤制剂致肝毒性、生殖毒性和血液系统毒性不良反应回顾性分析

目的：了解雷公藤制剂所致肝毒性、生殖毒性、血液系统毒性不良反应发生的特点和规律,为促进其安全使用提供参考。方法：检索中国生物医学文献数据库、中国期刊全文数据库及中文科技期刊数据库,收集雷公藤制剂引起生殖毒性、肝毒性、血液系统毒性的病例,对其不良反应发生的特点进行归纳总结。结果：共检索到32篇文献,涉及病例43例。其中,致生殖毒性文献6篇,病例8例,主要临床表现为：闭经伴性欲减退,性激素水平下降,功能失调性子宫出血,卵巢、子宫萎缩等;致肝毒性文献7篇,病例10例,主要临床表现为：纳差、乏力、恶心、尿黄、黄疸、全身皮肤黏膜黄染、巩膜黄染、皮疹、发热等;致血液系统毒性文献19篇,病例25例,主要临床表现为：全身不适,腹痛,腹泻,伴发热,重度贫血、鼻出血、皮肤瘀斑等,严重者可致急性再生障碍性贫血,纯红再生障碍性贫血及粒细胞缺乏症、骨髓抑制、类白血病反应等。结论：雷公藤制剂具有肝毒性、生殖毒性和血液系统毒性,应严格掌握其适应证和禁忌证,控制合理的给药时间,小剂量、短期用药,关注配伍减毒和禁忌,选用新剂型如缓释片、双层栓剂等可以在一定程度上减少其不良反应的发生。     

Toxicological review of male reproductive effects and trichloroethylene exposure: Assessing the relevance to human male reproductive health

Effects of trichloroethylene (TCE) on male reproduction and fertility have been studied in mice and rats, and assessed in workers exposed to TCE. Only limited evidence exists for any male reproductive effects in rats or humans. The human studies of TCE male reproductive effects failed to provide much useful information for risk assessment. First, the TCE-specific studies are limited in group size, scope, and typically provide no data on dose, so dose–response assessment is impossible. In other studies, TCE is only one of many solvents identified in the workplace, such that the confounding exposures or lack of evidence of specific exposures make the exposure assessment useless. For TCE risk assessment, one currently must rely upon animal studies as more reliable and useful. The rat studies were generally negative, showing systemic toxicity but little or no male reproductive toxicity. The mouse studies showed various organ effects in the male reproductive system and were typically associated with increased liver weight and kidney toxicity. Enzyme induction and oxidative metabolism appear to be important in the systemic toxicity and may likewise play a role in the reproductive toxicity of TCE. Oxidative metabolites of TCE are formed in the mouse epididymis resulting in epididymal damage, and at systemically toxic high doses, TCE may adversely affect the maturation of sperm and decreasing sperm motility. Protection against systemic toxicity should also protect against adverse effects including male reproductive toxicity.     

Criteria for identifying and listing substances known to cause developmental toxicity under California's Proposition 65

Because of the automatic restrictions and warning requirements imposed on substances identified by the state as "known to cause developmental toxicity," the Expert Committee recommends the use of criteria that emphasize human relevancy, biological plausibility, and evidence in support of a selective, adverse developmental effect at non-maternally-toxic doses. In many instances, data for substances of public concern will be insufficient at present to meet these criteria. The fact that a substance is not listed as "known to cause developmental toxicity" does not create a presumption that the substance is safe. The Expert Committee, therefore, urges that these substances be recommended for further testing and that high priority be given to conducting the necessary tests. The Expert Committee reiterates its concern that substances listed by the SAP be identified according to the toxic endpoints (cancer, male reproductive toxicity, female reproductive toxicity, and/or developmental toxicity) that led to listing. Further, the Expert Committee recommends that the state Health and Welfare Agency institute education programs emphasizing appropriate courses of action for citizens informed of exposures to substances known to the state to cause cancer, birth defects, or reproductive toxicity.     

Developmental toxicity studies in rats and rabbits on 2,4-dichlorophenoxyacetic acid and its forms.

The potential for 2,4-D and its salts and esters to induce developmental toxicity was investigated in rats (8 studies) and rabbits (7 studies). Maternal toxicity associated with exposure was dependent on the dose level expressed as 2,4-D acid equivalents. The severity of the maternal effect was correlated to the 2,4-D acid-equivalent dose, with increasing dose levels that exceeded renal clearance causing increasingly more severe maternal effects. In both species, maternal body weight effects began to be manifested at dose levels of 30 mg 2,4-D acid equivalent/kg/day. At higher dose levels (50-75 mg/kg/day in rats and 75-90 mg/kg/day in rabbits), body weights and feed consumption were more severely affected. At dose levels > or =90 mg/kg/day in rats, clinical signs of toxicity (ataxia, muscular stiffness, and decreased motor activity) and mortality were noted. The no-observed-adverse-effect level (NOAEL) for maternal toxicity in both species across the family of 2,4-D salts and esters was approximately 10 mg/kg/day. Significantly decreased fetal body weights and increased fetal variations were seen in rats only at maternally toxic dose levels in excess of 90 mg/kg/day acid equivalent. At maternally toxic doses in rabbits, embryonal and fetal development were essentially unaffected. There were no effect on maternal reproductive measures such as litter size, resorption rates, or fetal body weights, and there was no evidence of teratogenic activity. In summary, equivalent toxicity of the salts and esters is consistent with rapid and complete metabolic conversion to 2,4-D acid. No adverse fetal effects were noted at dose levels that did not also produce evidence of maternal toxicity or exceed renal clearance of 2,4-D indicating that the developing rat and rabbit fetus were not uniquely sensitive to 2,4-D and its forms.     

15例肿瘤化疗相关性死亡的回顾分析

目的：分析肿瘤化疗相关性死亡的原因和危险因素，总结治疗经验，为临床化疗的选用提供依据。方法：回顾性调查15例经过化疗死亡的病例的临床资料，分析化疗方案、化疗后存活时间、死亡原因和预防方法。结果：15例患者的平均年龄为52．4岁，其中5例使用含多西紫杉醇化疗方案，化疗后存活时间1～29d，平均为16．8d。有5例患者出现Ⅳ度骨髓抑制，其中2例并发肺部感染，4例出现呼吸衰竭。结论：肿瘤化疗相关性死亡与患者的既往病史、年龄和化疗药物等有关。对有肝肺肾病史、年龄〉60岁的患者，避免使用含多西紫杉醇的化疗方案。可能减少肿瘤化疗相关性死亡。     

A two generation reproductive toxicity study with curcumin, turmeric yellow, in Wistar rats.

The reproductive toxicity of curcumin, turmeric yellow, in Wistar rats was studied in order to generate additional relevant toxicity information for the use of curcumin in humans by oral administration. The two generation reproduction study was designed and conducted in accordance with OECD Guideline No. 416 [OECD, 1983. Guidelines for Testing of Chemicals, Guideline No. 416. Two Generation Reproduction Toxicity Study, adopted on 26th May 1983] and in compliance with Good Laboratory Practices (OECD, 1997 Principles of Good Laboratory Practice for the Testing of Chemicals. OECD, C(97)186/Final). The curcumin, mixed in the experimental diet at the concentrations of 1500, 3000 and 10,000 ppm was fed to three groups of rats, i.e., low, mid and high dose groups, and studied for two successive generations. A concurrent control group received experimental diet without the curcumin mixture. There were no treatment related adverse toxicological effects in the parental animals. No gross or microscopic changes were observed in any of the organs. None of the reproductive parameters were affected and there were no effects on the offspring other than a small reduction in pre-weaning body weight gain of the F2 pups at the highest dose level. It was concluded that the no observed adverse effect level (NOAEL) for reproductive toxicity of curcumin, fed in the diet for two successive generations to rats in this study was 10,000 ppm, which is equivalent to 847 and 959 mg/kg bodyweight (bw) per day for male rats and 1043 and 1076 for females for F0 and F1 generations, respectively. This study was the final toxicology study on curcumin reviewed by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) at the 61st Meeting, 2003. The JECFA group considered that the small body weight reduction in the F2 pups of the highest dose group prevented this from being regarded as a no adverse effect level, and so allocated an ADI for curcumin of 0-3 mg/kg bw based on the intake of 250-320 mg/kg bw in the mid-dose group as the NOEL.     

Evaluating the evidence on genotoxicity and reproductive toxicity of carbon black: a critical review

Carbon black is produced industrially by the partial combustion or thermal decomposition of gaseous or liquid hydrocarbons under controlled conditions. It is considered a poorly soluble, low toxicity (PSLT) particle. Recently, results from a number of published studies have suggested that carbon black may be directly genotoxic, and that it may also cause reproductive toxicity. Here, we review the evidence from these studies to determine whether carbon black is likely to act as a primary genotoxicant or reproductive toxicant in humans. For the genotoxicity endpoint, the available evidence clearly shows that carbon black does not directly interact with DNA. However, the study results are consistent with the mechanism that, at high enough concentrations, carbon black causes inflammation and oxidative stress in the lung leading to mutations, which is a secondary genotoxic mechanism. For the reproductive toxicity endpoint for carbon black, to date, there are various lung instillation studies and one short-term inhalation study that evaluated a selected number of reproduction endpoints (e.g. gestational and litter parameters) as well as other general endpoints (e.g. gene expression, neurofunction, DNA damage); usually at one time point or using a single dose. It is possible that some of the adverse effects observed in these studies may be the result of non-specific inflammatory effects caused by high exposure doses. An oral gavage study reported no adverse reproductive or developmental effects at the highest dose tested. The overall weight of evidence indicates that carbon black should not be considered a direct genotoxicant or reproductive toxicant.