1例无脑儿脑垂体形态学探讨

目的：外表畸形与内脏畸形常并存，本文旨在探索两者之间有何相关因素。方法：取正常胎儿脑垂体和无脑儿脑垂体组织，用Helly液固定，制成石蜡切片，用HE等染色作组织学观察。结果：无脑儿腺细胞分化晚，TSH细胞多，功能旺盛，甲状腺发达，无ACTH细胞和赫令氏体异常，肾上腺萎缩。结论：内分泌紊乱是导致内脏畸形的原因。     

妊娠期甲状腺功能减退症的药物治疗

妊娠期胎儿甲状腺激素的来源人类甲状腺在孕第三周开始发育,甲状腺组织在孕第45至50天合并并移行至最终的位置,孕第70天后甲状腺基本发育完全。自妊娠11周起,胎儿的下丘脑和垂体开始分泌促甲状腺激素释放激素(TRH)和促甲状腺激素(TSH),甲状腺组织亦具备了摄碘能力。尽管自妊娠12周起,胎儿甲状腺开始分泌甲状腺     

孕妇妊娠早期甲状腺过氧化物酶抗体与促甲状腺激素的关系以及妊娠结局

目的探究孕妇妊娠早期甲状腺过氧化物酶抗体(TPOAb)与促甲状腺激素(TSH)的关系以及妊娠结局。方法选取2014年10月~2015年10月我院接收的60例孕周为16~24周的孕妇进行研究。血清中TSH采用免疫发光分析法测定,TPOAb采用电化学发光免疫分析法测定。记录孕妇血清中的促甲状腺激素(TSH)与抗甲状腺过氧化物酶抗体(TPOAb)水平,以及TPOAb阴性、TPOAb阳性孕妇的TSH水平,记录TPOAb阴性、TPOAb阳性孕妇的先兆流产率、先兆早产率、早产率等不良妊娠发生率。结果 60例孕妇中,TSH水平正常的孕妇28例,占46.7%,TSH水平异常的孕妇32例,占53.3%;TPOAb阳性孕妇有27例,占45.0%;TPOAb阴性孕妇有33例,占55.0%。其中TSH水平异常患者的TPOAb阳性有22例(68.75%),TSH水平正常患者的TPOAb阳性有5例(17.86%),TSH水平不同患者的TPOAb阳性发生率比较,差异明显(P0.05);根据TPOAb阳性组与阴性组孕妇血清中TSH水平得出,阳性组(27/60),阴性组(33/60),33例TPOAb阴性孕妇仅有3例TSH异常,因此,TPOAb阳性组与阴性组孕妇血清中TSH异常水平比较,差异具有统计学意义(P0.05);TPOAb阳性组产妇的先兆流产率、先兆早产率、早产率等不良妊娠发生率(40.7%)明显高于TPOAb阴性组,差异具有统计学意义(P0.05)。结论 TPOAb和TSH的检测可以提高甲状腺功能紊乱的检测率,TPOAb阳性的孕妇甲状腺紊乱显著增多,对胎儿的发育以及孕妇的生命健康意义明显,值得在临床上大力应用推广。     

妊娠期亚临床甲状腺功能减退症的研究进展

甲状腺素(T4)是维持机体正常生长、发育不可缺少的激素,特别是对骨和脑的发育尤为重要.因此,如果妊娠期间发生甲状腺功能减退症(简称甲减)就会对母体和胎儿造成不同程度的危害.妊娠期亚临床甲减(subclinical hypothroidism,SHT)是妊娠期最常见的一种甲状腺功能异常,是指促甲状腺素(thyroid stimulating hormone,TSH)高于正常范围,而血清游离甲状腺索(free thyroxine,FT4)与游离三碘甲状腺原氨酸(free triiodothyronine,FT3)在正常范围内.     

花都地区孕妇早中晚期甲状腺功能变化研究

目的研究花都地区孕妇早中晚期甲状腺功能变化。方法选择广州市花都区的孕妇作为观察组,进一步分为早期妊娠组、中期妊娠组、晚期妊娠组,选择非孕妇女作为对照组,检测甲状腺功能指标三碘甲状腺原氨酸(TT3)、总甲状腺素(TT4)、游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)及促甲状腺激素(TSH)的水平。结果早期妊娠组孕妇的甲状腺功能指标TT3、TT4、FT3、FT4与对照组的差异无统计学意义(P0.05),TSH水平低于对照组、差异有统计学意义(P0.05);中期妊娠组和晚期妊娠组TT3、TT4、FT3、FT4水平均低于对照组,TSH水平高于对照组、差异有统计学意义(P0.05)。结论妊娠早期孕妇甲状腺功能无明显变化,妊娠中晚期时甲状腺激素水平显著降低,需要在临床中采取检查措施以及时发现、进而保证胎儿的正常发育。     

促甲状腺素和甲状腺过氧化物酶抗体在孕期筛查中的价值

目的：通过检测孕妇体内促甲状腺素(TSH)与甲状腺过氧化物酶抗体(TPOAb)的水平,探讨其在筛查孕妇发生甲状腺功能紊乱中的价值与意义。方法孕妇588例,甲状腺功能紊乱组79例;甲状腺功能正常组509例(高龄孕妇组88例,正常孕妇组421例),采用微粒子化学发光法分别检测并比较受试者的TSH、TPOAb水平。结果与甲状腺功能正常组相比,甲状腺功能紊乱组血清TSH与TPOAb水平高,差异具有统计学意义(P<0.05);正常孕妇组与高龄孕妇组比较,差异无统计学意义(P>0.05)。结论甲状腺功能检测指标TSH和TPOAb可以作为孕妇产前筛查的检测指标,预测孕妇发生甲状腺功能异常的风险。     

妊娠中期单纯性甲状腺自身抗体阳性及单纯性低甲状腺素血症对妊娠结局的影响

目的 分析甲状腺过氧化物酶抗体(TPOAb)在妊娠中晚期的患病率及滴度的变化特点,探讨妊娠中期单纯性TPOAb阳性和单纯性低甲状腺素(T4)血症对妊娠结局的影响。方法 选择2015年5月至10月在南京医科大学附属妇产医院产科产前门诊接受孕期检查的孕20～27周妊娠妇女2 300例,作为TPOAb阴性(-)组,用于制定妊娠中期甲状腺功能正常值的参考范围,其中甲状腺功能正常者2 075例,作为甲状腺功能正常组;妊娠中期TPOAb阳性孕妇167例,作为TPOAb阳性(+)组;采用化学发光免疫法分别于孕20～27周、孕30～34周及孕36～40周序贯检测孕妇血清促甲状腺激素(TSH)、游离甲状腺素(FT4)、TPOAb,追踪记录孕期病情变化直至分娩。结果 妊娠中期FT4的参考值为9.82～16.77 pmol·L-1、TSH的参考值为0.60～4.88 mIU·L-1;TPOAb(+)组亚临床甲减发病率较TPOAb(-)组高(7.7% vs.2.48%,P＜0.05);与孕20～27周组相比较,孕30～34周组和孕36～40周组TPOAb阳性发病率均明显下降(P＜0.01);以孕20～27周组的111例TPOAb阳性者为观察对象,三个时期TPOAb滴度呈进行性下降;单纯性TPOAb(+)者149例,单纯性低甲状腺素(T4)血症者111例,单纯性TPOAb(+)组与甲状腺功能正常组比较,妊娠期糖尿病、妊娠期高血压疾病、胎膜早破、羊水异常、胎位异常、胎盘异常、脐带异常、妊娠丢失、早产、胎儿窘迫、新生儿窒息、胎儿发育异常、胎儿生长受限、巨大儿、有指征剖宫产、产后出血发病率均差异无统计学意义(P＞0.05),单纯性低T4组与甲状腺功能正常组比较,妊娠期糖尿病、巨大儿发病率及有指征剖宫产发生率明显升高(分别为P＜0.01、P＜0.05、P＜0.01),余各指标比较均差异无统计学意义(P＞0.05)。 结论 TPOAb阳性率及滴度随孕周增加均呈逐渐下降趋势,妊娠中期单纯性TPOAb阳性不增加不良妊娠结局及并发症的发生率,单纯性低T4血症与妊娠期糖尿病、巨大儿发病率及有指征剖宫产发生率升高有关。     

超声检查在早期胎儿中枢神经系统畸形中的筛查

目的:探讨超声检查在孕早期胎儿中枢神经系统畸形中的筛查诊断价值。方法:应用超声诊断仪对2915例孕11~14周孕妇进行彩色多普勒超声检查,重点观察胎儿中枢神经系统发育情况,对中枢神经系统结构异常的胎儿建议引产终止妊娠。结果:2915例11~14孕周孕妇共发现胎儿中枢神经系统畸形12例,检出率0.41%(12/2915),所有胎儿畸形均引产后病理检查予以证实。12例胎儿中枢神经系统畸形中,无脑儿例(41.67%),其次是脑膨出3例(25.00%)、开放性脊柱裂、2例(16.67%),脉络丛囊肿、前脑无裂畸形各1例(8.33%)。结论:超声检查能早期发现胎儿神经系统畸形,及时采取干预措施,有利于落实优生优育政策。     

子痫前期孕妇及新生儿甲状腺相关激素水平的变化研究

目的:研究子痫前期孕妇的甲状腺功能变化及对胎儿发育的影响.方法:采用病例对照研究方法,检测子痫前期(pre-eclamptic,PE)患者及新生儿促甲状腺激素(TSH)、总甲状腺素(TT4)、游离甲状腺素(FT4)、总三碘甲腺原氨酸(TT3)、游离三碘甲腺原氨酸(FT3)水平,入院时采用B超检测胎儿发育状况,进行胎儿生物物理4项评分(BPS).结果:轻度PE、重度PE患者TSH水平均有显著性升高,胎儿BPS分值均显著性降低,轻度PE患者FT3、FT4水平降低,重度PE患者仅FT4水平降低.重度PE组新生儿各项激素水平均低于对照组.结论:子痫前期伴有甲状腺功能的改变,对胎儿发育产生不利影响.     

妊娠与巴塞多氏病

妊娠与较轻的巴塞多氏病有许多共同点,所以后者在合并妊娠时易被遗漏,即妊娠时伴有心慌、多汗、轻度的甲状腺肿大,脉搏快、无月经等,检查证实血中T_4、T_3值增高,甲状腺放射性碘吸收率增高(现在已禁止使用),BMR值增高等,妊娠时血中FT_4、FT_3等值可能在正常范围里可能低值,因血中TSH在正常范围用血中FT_4、FT_3值增高,TSH降低,TRAb阳性的指标鉴别巴塞多氏病比较容易。 抗甲状腺制剂疗法,因为药物可通过胎盘,可能对胎儿有影响。一般每日药量PTU20mg以下,如MM120g以下对胎儿的智力发育无影响,抗甲状腺给药量尽可能的少,PTU每日给药量已超过300mg,在妊娠中期或妊娠后期应该施行手术疗法。 妊娠时使用放射性碘疗法,因碘的胎盘透过性及甲状腺积集而禁忌使用。而无机碘可抑制胎儿的甲状腺功能,引起甲状腺肿大,压迫胎儿气管,可造     

Paroxetine for the treatment of depression: a critical update

Disorders of thyroid function are common among women of childbearing age. It is known that thyroid physiology normally alters during gestation. Clinicians, often, overlook thyroid dysfunction in pregnant women because of nonspecific symptoms and the hypermetabolic state of normal pregnancy. After all, the clinician must consider thyroid dysfunction as a possibility in pregnant women and differentiate normal physiological changes from thyroid disease. Abnormalities of maternal thyroid function can affect the fetus directly or indirectly. The fetal thyroid begins to produce thyroid hormones after the first trimester, so the critical thyroid hormones for fetal brain development must be supplied by the mother. It is of interest how sensitive the fetus is to decreases in circulating maternal thyroid hormones and in maternal thyrotoxicosis. Over recent years there has been an expansion of knowledge regarding thyroid disease in pregnancy and subsequently controversies about management of thyroid disease in pregnancy. This review focuses on maternal overt and subclinical hypothyroidism in pregnancy, suggesting guidelines for appropriate treatment for this disease due to its frequency, especially the subclinical manifestation, and the controversy that exists. It also reviews the complications in mother and fetus when hypothyroidism is untreated. On the other hand, with respect to other differing opinions, some recommendations should be given by the authors about supplying thyroxin to pregnant women with thyroid disease other than hypothyroidism.     

Recommendations for thyroxin therapy during pregnancy

Disorders of thyroid function are common among women of childbearing age. It is known that thyroid physiology normally alters during gestation. Clinicians, often, overlook thyroid dysfunction in pregnant women because of nonspecific symptoms and the hypermetabolic state of normal pregnancy. After all, the clinician must consider thyroid dysfunction as a possibility in pregnant women and differentiate normal physiological changes from thyroid disease. Abnormalities of maternal thyroid function can affect the fetus directly or indirectly. The fetal thyroid begins to produce thyroid hormones after the first trimester, so the critical thyroid hormones for fetal brain development must be supplied by the mother. It is of interest how sensitive the fetus is to decreases in circulating maternal thyroid hormones and in maternal thyrotoxicosis. Over recent years there has been an expansion of knowledge regarding thyroid disease in pregnancy and subsequently controversies about management of thyroid disease in pregnancy. This review focuses on maternal overt and subclinical hypothyroidism in pregnancy, suggesting guidelines for appropriate treatment for this disease due to its frequency, especially the subclinical manifestation, and the controversy that exists. It also reviews the complications in mother and fetus when hypothyroidism is untreated. On the other hand, with respect to other differing opinions, some recommendations should be given by the authors about supplying thyroxin to pregnant women with thyroid disease other than hypothyroidism.     

Motility and stereotyped behaviour induced by amphetamine and apomorphine on hypophysectomized and on thyroidectomized rats.

The reduction of the hypermotility and stereotyped behaviour induced by amphetamine and apomorphine was used as a criterion for the effectiveness of neuroleptics. Considering the impact of neuroleptics on the hypophysis as well as the relationship between the hypophysis and the thyroid, motility and stereotyped behaviour induced by amphetamine and apomorphine was studied in both hypophysectomized and thyroidectomized rats. In the hypophysectomized rat, amphetamine-induced hypermotility, observed between 1 and 3 hours after administration, was almost 3 times greater than in normal animals. Thyroidectomy resulted in a reversal of the motility effect induced by amphetamine. The stereotyped behaviour induced by apomorphine was practically abolished in both hypophysectomized and thyroidectomized animals.     

Studies on the intracerebral metabolism of anticonvulsant drugs--I. Perfusion of primidone through the isolated brain of the rat

Primidone and phenobarbital (each 85 nmoles/ml were separately perfused through the isolated brain of the rat. After 5 min of perfusion similar amounts of primidone and phenobarbital were taken up into the brain; for both drugs the concentration ratio between brain and perfusion medium was about 0.2. However, after 2 hr of perfusion the mean concentration ratio for primidone was about 0.55; for phenobarbital it was about 0.9 thus indicating a better uptake of phenobarbital. In two regions (hypophysis, mesencephalon) the concentration of phenobarbital was significantly higher than in perfusion medium. During 2 hr of perfusion of primidone, substantial quantities of phenobarbital and PEMA were formed amounting to 1400 pmoles for each metabolite. The highest concentration of the metabolites was found in septum, hypothalamus, hypophysis and mesencephalon. The in situ metabolism of primidone in the intact brain was demonstrated for the first time.     

Natural variations in brain phenylethanolamine-N-methyltransferase activity during different phases of the oestrous cycle: effect of chronic dexamethasone treatment

The activity of phenylethanolamine-N-methyltransferase (PNMT) was studied in the hypothalamus, hypophysis, striatum and the rest of the brain during the four different phases of the oestrous cycle of the rat. The oestrous phase was marked by high level of enzyme activity in all the regions except the hypophysis. The hypophysis showed maximum increase in activity at the metoestrous phase of the oestrous cycle. Chronic treatment of rats with dexamethasone for 10 days led to decreased level of PNMT activity in the hypophysis, hypothalamus and the rest of brain. These decreases were important in the hypothalamus and the hypophysis which represented only 25 and 20% of the control activity after dexamethasone administration.     

Mode of action: developmental thyroid hormone insufficiency--neurological abnormalities resulting from exposure to propylthiouracil

Because thyroid hormone is essential for normal brain development before and after birth, environmental chemicals that interfere with thyroid hormone signaling can adversely affect brain development. Adverse consequences of thyroid hormone insufficiency depend both on severity and developmental timing, indicating that environmental antithyroid factors may produce different effects at different developmental windows of exposure. Mechanistic studies can provide important insight into the potential impact of chemicals on human thyroid function, but relevance to humans must be systematically evaluated. This kind of analysis depends on data sets that include information about animals and humans. The drug 6-n-propyl-2-thiouracil (PTU) is used in animals to experimentally manipulate serum thyroid hormone levels, and in humans to treat patients, including pregnant women, with Graves' disease. A systematic analysis of the mode of action (MOA) of PTU in rats and in humans discloses similar modes of action. While the analysis predicts that PTU doses that produce thyroid hormone insufficiency in humans would adversely affect the developing brain, careful monitoring of PTU administration in pregnant and lactating humans keeps infant serum thyroid hormone levels within the normal range.     

Mode of Action: Developmental Thyroid Hormone Insufficiency—Neurological Abnormalities Resulting From Exposure to Propylthiouracil

Because thyroid hormone is essential for normal brain development before and after birth, environmental chemicals that interfere with thyroid hormone signaling can adversely affect brain development. Adverse consequences of thyroid hormone insufficiency depend both on severity and developmental timing, indicating that environmental antithyroid factors may produce different effects at different developmental windows of exposure. Mechanistic studies can provide important insight into the potential impact of chemicals on human thyroid function, but relevance to humans must be systematically evaluated. This kind of analysis depends on data sets that include information about animals and humans. The drug 6-n-propyl-2-thiouracil (PTU) is used in animals to experimentally manipulate serum thyroid hormone levels, and in humans to treat patients, including pregnant women, with Graves' disease. A systematic analysis of the mode of action (MOA) of PTU in rats and in humans discloses similar modes of action. While the analysis predicts that PTU doses that produce thyroid hormone insufficiency in humans would adversely affect the developing brain, careful monitoring of PTU administration in pregnant and lactating humans keeps infant serum thyroid hormone levels within the normal range.     

Ability of the Hershberger assay protocol to detect thyroid function modulators

In vivo screening methods for detection of thyroid function modulators are now under development in many research laboratories. We assessed the applicability of the Hershberger assay protocol to screen for thyroid function modulators. In experiment 1, castrated male BrlHan WIST@Jcl (GALAS) rats were administered a potent thyroid peroxidase inhibitor, 3-amino-1,2,4-triazole (AT), in doses of 0, 40, 200, and 1,000 mg/kg/day with gravimetric endpoint, and in experiment 2, castrated and intact male rats were administered in doses of 0, 40, and 200 mg/kg/day, with quantification of the extent of hypertrophy of the thyroid epithelium, to assess the effects of castration, by gavage to 8-week-old for 10 consecutive days. At necropsy of both experiments, the thyroid glands and hypophysis were collected and fixed with 10% neutral-buffered formalin. To avoid crushing during weighing because of their fragility, the thyroid glands and hypophysis were weighed approximately 24 h after fixation with 10% neutral-buffered formalin. All animals were sacrificed approximately 24 h after the final dose. In experiment 2, the thyroid glands of all animals were stained with hematoxylin and eosin for histological examination and morphometry of follicular epithelial height. In experiment 1, absolute and relative thyroid weights in all of the AT groups were statistically increased in a dose-dependent manner, regardless of the testosterone propionate (TP)-injection. In experiment 2, the results showed a significant increase in thyroid weight in the 200 mg/kg groups of both castrated and intact rats. Hypophyseal weight was unaltered by AT, but comparison of vehicle-treated groups showed that the hypophyseal weight of the castrated rats was greater than that of the intact rats. Enlarged thyroid glands were observed in the AT-treated rats at necropsy. Histological examination of the thyroid glands of all the AT-treated animals showed hypertrophy and hyperplasia of the follicular epithelial cells, and the height of follicular epithelium of the thyroid glands increased in a dose-dependent manner in both the castrated and intact rats. In experiment 1, assessment of the (anti-) androgenic action of AT in seminal vesicle weight revealed a significant increase in the 200 and 1,000 mg/kg + TP groups in a dose-dependent manner. These results suggest that the effect of AT can be detected by the Hershberger assay 10-day administration protocol and may be useful for screening for thyroid function modulators regardless of whether the animals have been castrated.