环境内分泌干扰物对儿童生长发育与健康的影响

保护儿童免受化学毒物的危害是对现代社会的一大挑战。当今世界 ,儿童有接触近 15 0 0 0种大量生产的化学合成物质的危险[1 ] 。其中许多化学物质广泛分布于环境之中。半数以上的这些化学物质从未进行过潜在毒理试验 ,其对儿童的潜在危险大多不清楚。处于生长发育阶段的儿童 ,环境化学毒物尤其是环境内分泌干扰物肯定对其健康和生长发育产生潜在的不良影响。因此 ,研究环境内分泌干扰物与儿童的健康和生长发育的关系 ,对保护儿童的健康具有重要意义。1.环境内分泌干扰物 :环境内分泌干扰物 (EndocrineDisruptors EndocrineDisruptingChemi…     

环境内分泌干扰物与kisspeptin系统

环境内分泌干扰物( environmental endocrine disruptors,EED)对性发育的影响越来越受到关注。 Kisspeptin系统是EED干扰下丘脑-垂体-性腺轴新靶点。 EED的雌激素特性使其能够对kisspeptin系统产生影响,从而导致一系列改变,如青春启动时间改变、生育障碍及代谢紊乱。目前主要对三种干扰kisspeptin信号传导途径的EED进行了研究,包括双酚A、多氯联苯和植物雌激素染料异黄酮。     

应重视环境内分泌干扰物所致的儿童性发育异常

当前的正常儿童已较普遍地暴露于环境内分泌干扰物（EEDs）中,而EEDs与儿童性发育异常的发病有密切关系,是其重要的致病因素之一,应引起足够重视。尽快完善相关产业及环保方面的政策法规,从源头上杜绝这些有害物质造成的环境污染;另一方面应积极制定适合国情的有效防治方案,包括采用药物进行治疗干预。已证实恰当的中药治疗方案对EEDs的拟雌激素活性具有显著的拮抗作用。所用中药可通过对靶器官上雌激素受体、雌激素合成酶及生长因子的调节作用,发挥其对EEDs拟雌激素活性的拮抗作用。     

性早熟病因的研究进展

性早熟是发于儿童的一种生长发育异常性疾病.多科研究表明,其发病因素是多方面的,是以遗传为基础,遗传因素和环境因素相互作用的结果,现对性早熟的病因在遗传、环境、营养方面的进展作如下综述.     

环境内分泌干扰物与儿童性分化、性发育异常

环境内分泌干扰物是普遍存在于环境中的一类外源性化学物质,这些物质可干扰体内天然激素的合成、释放、转运、与受体结合、代谢及清除等各个方面,干扰正常激素维持体内平衡和调节发育过程的作用.环境内分泌干扰物被证实是引起儿童性分化、性发育异常的重要致病因素.环境内分泌干扰物可扰乱下丘脑-垂体-性腺轴,干扰雄激素的生物合成、转运、...     

儿童性早熟与社会暴露

性早熟(precocious puberty)是指女孩在8岁前、男孩9岁(或9岁半)前出现第二性征、世界各国对性早熟的界定还有很大分歧，我国目前还没有这方面的调查统计资料，适合当代社会的性早熟的年龄划分还需要进一步的调查研究、性早熟按下丘脑-垂体-性腺轴(HPGA)功能是否提前发动分为两大类：一类是中枢性性早熟(CPP，或称真性、GnRH依赖性．完全性性早熟)；另一类是外周性性早熟(PPP，或称假性、     

滋肾阴泻相火中药对环境内分泌干扰物染毒大鼠卵巢雌激素合成相关酶表达的影响

目的观察滋肾阴泻相火中药对壬基酚(NP)及双酚A(BPA)染毒大鼠卵巢雌激素合成相关系列酶基因及蛋白表达水平的影响,探讨所用中药拮抗环境内分泌干扰物(EEDs)拟雌激素活性的作用机制。方法 3周龄雌性SD大鼠30只,分为染毒组、治疗组及对照组。染毒组单纯喂饲NP或NP与BPA联合喂饲,治疗组以滋肾阴泻相火中药与染毒物同时喂饲,对照组喂饲溶剂玉米油,疗程15 d。疗程结束时,检测其子宫湿质量及脏器系数,测定其卵巢类固醇急性调节蛋白(StAR)、胆固醇侧链裂解酶(CYP11A1)、芳香化酶(CYP19al)、17-羟类固醇脱氢酶(17-HSD)、17al羟化酶(CYP17al)、3-羟类固醇脱氢酶(3-HSD)的基因表达水平和StAR、CYP11A1、CYP19al蛋白表达水平,进行各组间相互对比。结果染毒组与对照组比较,子宫湿质量、脏器系数增加,卵巢StAR、CYP11A1、CYP19al的基因及蛋白表达水平均明显上调(Pa<0.05),17-HSD、CYP17al、3-HSD的mRNA水平差异无统计学意义;而治疗组与染毒组比较子宫湿质量、脏器系数降低,StAR、CYP11A1的基因及蛋白表达水平均显著下调(Pa<0.05),CYP19al、17-HSD、CYP17al、3-HSD的mRNA水平差异无统计学意义。结论 NP及BPA可诱导卵巢雌激素合成相关酶的表达,促进自身雌激素的生物合成,而中药治疗干预可显著拮抗染毒物质的这种诱导作用,明显抑制染毒动物自身雌激素的生物合成。这可能是中药有效拮抗EEDs拟雌激素活性的主要作用机制之一。     

环境内分泌干扰物对性激素合成相关酶基因调控网络的不良影响

环境内分泌干扰物(environmental endocrine disruptor,EED)是具有干扰机体内分泌系统的一类外源性化学物质.研究表明性激素合成相关酶基因是EED的重要靶点.性激素合成与代谢的失衡可致机体生殖障碍、性分化、性发育异常及某些癌症的发病风险增加等.其中类固醇合成急性调节蛋白、芳香化酶等是性激素合成的限速酶及关键酶,这些酶及蛋白又受一系列转录因子及信号通路的调控.基于在性激素合成中的特殊作用,这些酶、转录因子及信号通路等组成的基因调控网络与EED之间的关系备受关注.遗传背景的差异性可影响机体对EED的敏感性.该文就近年来性激素合成相关酶基因的调控以及EED对其产生的不良影响作一综述.     

环境内分泌干扰物与青春期发育异常

环境内分泌干扰物(EEDs)对儿童健康的影响日益引起关注.该文对EEDs的种类、作用机制及其所引起的青春期发育异常进行综述,提出EEDs特别是环境雌激素能够在儿童出生前或出生后进入机体,引致生殖系统功能紊乱,严重时可造成青春期发育异常,从而对儿童生理、心理健康造成不良影响.     

儿童性早熟的研究进展

性早熟是一种生长发育异常,表现为青春期特征提前出现。近年来本病的发生率显著增高,已成为最常见的小儿内分泌疾病之一。复旦大学公共卫生学院儿童少年卫生学教研室与复旦大学儿科医院联合进行的临床流行病学调查显示,目前上海地区儿童性早熟的患病率约为100/万。     

儿童性早熟药物治疗进展

性早熟包括中枢性性早熟(CPP)和外周性性早熟(PPP)2种.1个月缓释型促性腺激素释放激素类似物(GnRHa)是CPP的标准治疗药物,较长时间缓释型GnRHa的疗效与1个月缓释型相近,而有较好的发展前景;重组人生长激素(rhGH)或氧雄龙不推荐常规用于接受GnRHa治疗的CPP患儿.PPP的治疗要根据性别、病因、药物机制等个体化,确切疗效需要更多中心观察;继发性CPP需联合应用GnRHa.     

真性性早熟患儿骨代谢改变和干预策略

真性性早熟是由于下丘脑 垂体 性腺轴提前发动所致。治疗首选长效促性腺激素释放激素类似物 (GnRHa) ,它对遏制真性性早熟患儿的过早发育和提高最终身高已被公认。但GnRHa治疗后会减少患儿的骨密度 ,明显抑制患儿成骨细胞及破骨细胞的功能活动 ,从而对骨密度峰值的取得起负面影响。而钙剂、维生素D的摄入 ,生长激素的应用及体育锻炼可预防和治疗GnRHa应用后引起的骨密度下降 ,使患儿顺利达到骨密度峰值。该文就GnRHa治疗对真性性早熟患儿骨密度、骨代谢生化指标的变化及临床干预措施进行综述 ,力求能够早期预防和治疗 ,以减少对患儿生长发育的不良影响 ,提高人口素质。     

Body Proportions in Precocious Puberty

ABSTRACT. Sitting height (SH) and sub-ischial leg length (SLL) were measured in 10 boys and 16 girls with precocious puberty; the patients were aged from 1.5 to 13.4 years at the time. Standard deviation scores (SDS) calculated for chronological age and bone age showed higher scores for SH than for SLL in all but two patients, both girls: the differences between the SDS for SH and SLL were more marked in the boys. The findings indicate that growth of the trunk is usually greater than growth of the legs in precocious puberty, particularly in boys.     

Isosexual Precocious Puberty in Girls

ABSTRACT. This paper reviews the clinical findings, pituitary gonadotrophin reserve and plasma oestradiol, neurological findings and pelvic ultrasound appearance in 47 girls with precocious puberty starting before the age of 7 years. Of the 39 girls who had air encephalograms or cranial CT scans, 19 showed intracranial abnormalities (hamartomas 11; hydrocephalus 5; optic glioma 2; arachnoid cyst 1). There was no significant difference in the peak serum luteinizing hormone and follicle-stimulating hormone responses to intravenous gonadotrophin stimulating hormone in girls with and without intracranial lesions. Pelvic ultrasound examination showed development of the ovaries, uterus, and vagina similar to that seen in normal puberty. Treatment with cyproterone acetate (50-100 mg/day) in 26 girls resulted in arrest of breast development and suppression of menstruation, but a definite effect on growth was not documented.     

Laughing Seizures and Precocious Puberty

Penfold, J. L, Manson, J. I. and Caldicott, W. M. (1978). Aust. Paediatr. J., 14, 185–190. Laughing seizures and precocious puberty. (Case report and review of the literature.) A girl with laughing seizures and precocious puberty is presented in detail. She appears unique in having a congenital cardiac lesion in addition to a hypothalamic hamartomatous malformation. Nine other children with laughing seizures and sexual precocity have been reported previously and their clinical features and investigations are summarised. Relevant findings of the series include a very young age of onset of precocity, difficulty in localising a cerebral lesion in almost a third of the children, high incidence of mental retardation and poor response to anticonvulsant therapy. Psychosexual problems were surprisingly minimal. Cyproterone acetate appears to be the most promising drug in suppressing premature hypothalamic-pituitary activity.     

促性腺激素释放激素类似物在儿童中枢性性早熟中的应用

中枢性性早熟(CPP)是常见的儿科内分泌疾病,其危害是成年身高减损、性征提前出现及心理问题.3～4周缓释型促性腺激素释放激素类似物(GnRHa)是目前国际上公认的治疗CPP的药物.快速进展型CPP是GnRHa的应用指征.近30 a的应用经验证明,GnRHa能有效抑制骨龄进展,在使线性生长减慢的同时,可有效改善成年身高,不良反应少,对成年后生殖轴功能、骨健康及身体成分等无明显负性影响.     

Oncologic Causes of Precocious Puberty

Tumors are rare, but well-documented causes of precocious puberty in both sexes. The therapeutic and prognostic implications of a diagnosis of cancer require that the presence of a neoplastic process be ruled out in any case of precocious puberty. Granulosa-cell tumor of the ovary and Leydig-cell tumor of the testis are the most frequent gonadal tumors inducing precocious pseudopuberty in the two sexes. Adrenal tumors sustain a variety of endocrine syndromes, the most frequent one being virilization with or without hypercortisolism. Pure feminizing adrenal neoplasms have been described.

For reasons not yet well understood, hypothalamochiasmatic glioma (β-HCG) secreting tumors have almost never been described in association with female precocious puberty. Among these neoplasia, pineal germ-cell tumor inducing sexual maturation must be included.

Hypothalamochiasmatic glioma and chraniopharyngioma are the two cerebral tumors capable of inducing true precocious puberty. Even if equally distributed between both sexes, these tumors interfere with sexual maturation less frequently in girls than in boys.

Hypothalamic hamartoma is considered a benign tumor, since it does represent a space-occupying mass. It more correctly could be called a malformation if its histologic characteristics are recalled. This cerebral lesion is now frequently described in children with true precocious puberty, probably because of improved diagnostic imaging methods.