营养性疾病

北京市大兴区青少年肥胖及超重现状调查；小儿肥胖对肾脏的影响；合理营养干预为主治疗肥胖病伴高血压患儿的研究；青少年肥胖与代谢综合征关系的研究；单纯性肥胖儿童脂代谢与LEPR及ApoE基因多态性的相关性研究；单纯性肥胖儿童与脂肪肝的关系；大连市城区7岁以下儿童单纯性肥胖状况分析；儿童肥胖与睡眠及相关激素的关系。     

儿童单纯性肥胖症的病因及预防

儿童单纯性肥胖症患病率不断上升,其已成为危害儿童健康的重要公共卫生学问题之一.针对儿童期单纯性肥胖症的病因及预防做了简要综述.其病因复杂多样,肥胖具有家族聚集性,同时不良的饮食行为和不良的生活方式以及睡眠不足均可导致超重、肥胖的发生;高出生体质量和心理压力大也是后天发生儿童单纯性肥胖症的危险因素.给予肥胖儿童合适的家庭指导、采用灵敏度高的筛检方法及时将肥胖及超重儿童筛查出来以及对孕期的饮食指导,均可降低儿童单纯性肥胖症的发生.     

儿童单纯性肥胖与纤维蛋白原及其Bβ-148C/T基因多态性的关系研究

探讨儿童单纯性肥胖与纤维蛋白原（Fg）及其Bβ-148C/T基因多态性的关系， 为儿童单纯性肥胖的防治提供理论依据。方法　选取2004年6月至2007年9月华北煤炭医学院附属医院单纯性肥胖儿童及正常对照组儿童各106例，抽取空腹静脉血5 mL，测定Fg水平和分子功能；采用聚合酶链反应及限制性酶切方法对Fg Bβ-148C/T位点的基因型进行测定。结果　单纯性肥胖儿童血浆Fg水平及分子功能明显高于健康对照组（ P < 0.05） ， 儿童单纯性肥胖T等位基因频率明显高于健康对照组 （P < 0.05） ，而且儿童单纯性肥胖组CT与TT基因型个体的血浆Fg水平及Fg单体聚合速度（FMPV）明显高于CC基因型组（P < 0.05）。结论　儿童肥胖能引起血浆Fg水平增高，分子功能增强，FgBβ-148C/T基因多态性通过影响Fg水平及单体聚合速率可能为儿童单纯性肥胖的一个累效基因。     

儿童单纯性肥胖研究现状

国内外儿童单纯性肥胖症的发病率在快速增长,世界卫生组织宣布儿童肥胖已成为保健的首要问题。近年来中国儿童少年肥胖检出率明显增高,长此以往将严重影响儿童少年的健康状况和身体素质,并增高成人慢性病的患病风险。本文就近年来儿童单纯性肥胖的情况做一综述,指出儿童单纯性肥胖的发生因素,防治重点,望引起关注。     

0～3岁儿童单纯性肥胖调查及影响因素分析

目的:探讨南宁市江南区0～3岁儿童单纯性肥胖状况及主要影响因素,为制定预防儿童肥胖提供科学依据。方法:对2010年1月至12月来我院儿保门诊体检的0～3岁儿童5071名作为调查对象,对其父母进行现场问卷,分析儿童单纯性肥胖的影响因素。结果:0～3岁单纯性肥胖检出率为4.99%,0～1岁肥胖发生率最高为6.28%;男童的检出率高于女童,且差异均有显著性意义;危险因素提示儿童父母患肥胖症、高出生体重、进餐速度、喜食肉食等为肥胖主要因素。结论:单纯性肥胖发生率与儿童的年龄及性别、高出生体重、遗传、不良的饮食行为等因素有关,1岁以内是肥胖干预的第一关键期,肥胖的控制应从婴幼儿期甚至孕期就开始。     

儿童单纯性肥胖症预防文献分析简

目的 汇总分析1986/2013有关儿童肥胖症预防的文献,寻找儿童单纯性肥胖症预防方法,为临床应用提供依据.方法 查阅中国知网收集1986/2013发表在国内期刊上有关儿童肥胖症预防的文献,制定纳入、排除标准,进行文献筛选归纳分析,由此探讨儿童单纯性肥胖症早期预防的方法.结果 共下载符合要求的文献共144篇,除实验及理论性文章,符合要求的文献共59篇.分析得出合理膳食、适宜的运动能有效控制少年儿童单纯性肥胖的发生.结论 儿童单纯性肥胖可以通过合理饮食、适当运动、改善生活习惯进行早期预防.     

营养性疾病

重庆地区0～18岁儿童营养问题调查；遵义市7岁以下儿童营养不良流行病学调查分析；新生儿佝偻病骨代谢转换生化标志物检测的意义；烟台市幼儿单纯性肥胖相关因素的分析；乌鲁木齐市3—7岁集体儿童单纯性肥胖的检出率及影响因素分析.     

肥胖儿童骨密度变化及其影响因素分析

分析肥胖儿童骨密度（BMD）及其影响因素,为早期预防骨质疏松提供科学依据。方法　2007年1—12月从长沙市开福区5所小学7～12岁学龄儿童中 ,按照体质指数（BMI）法诊断单纯性肥胖,随机抽取119例单纯性肥胖儿童及103名正常儿童。采用双能X线骨密度仪（DEXA）全身扫描,测量BMD和身体成分。结 果　单纯性肥胖儿童的身高、体重、BMI、腰围和腰臀比均显著高于正常儿童。单纯性肥胖儿童的各部位瘦组织含量（LM）、脂肪组织含量（FM）、体脂百分比（ PBF）及躯干脂肪组织百分比均显著高于正常儿童,但四肢FM百分比却显著低于正常儿童。肥胖儿童各部位BMD和骨矿物质含量（BMC）均大于正常儿童。控制FM后 ,BMD（或BMC）与LM呈显著正相关：控制LM后,BMC与FM亦呈正相关。多元逐步回归分析显示,影响儿童BMD的主要因素是LM。 结论　肥胖儿童BMD高于正常儿童 ,LM对儿童成长中骨的BMD起重要作用。     

血清胰岛素浓度的变化与肥胖儿童生长关系的探讨

目的探讨单纯性肥胖儿童的生长与其血清胰岛素(Ins)、胰岛素样生长因子 1(IGF 1)、胰岛素样生长因子结合蛋白 3(IGFBP 3)浓度的关系。 方法2004 03中山大学附属二院对31例单纯性肥胖儿童及48例同龄正常儿童的生长参数及空腹Ins、IGF 1、IGFBP 3浓度进行测定，并进行比较及相关性分析。 结果肥胖组血清Ins、IGFBP 3浓度显著高于对照组(P<005,P<001)，而两组间IGF 1差异则无显著性意义，血清Ins浓度与BMI、IGFBP 3呈正相关，肥胖儿童身高SDS与1NS、IGF 1正相关。 结论肥胖儿童存在有非生长激素(GH)依赖性生长的代偿机制。其中高胰岛素血症可能参与了这一过程，它既可以通过增加IGFBP 3的合成来间接提高IGF 1的生物活性，又可以直接发挥促生长作用。     

综合干预对单纯性肥胖儿童治疗效果分析

目的：探讨综合干预对单纯性肥胖儿童的治疗效果。方法：于石家庄市城区11所幼儿园体检中选取4～6岁单纯性肥胖儿童132例中自愿采取综合干预的患儿40例为研究组,给予饮食、运动、心理、家庭综合干预,观察干预前后效果,同时与未进行干预的肥胖儿童30例（对照组）进行对比。结果：经过综合干预后研究组在体重方面控制良好,与对照组比较,差异显著（P〈0.05）,有统计学意义;在身高方面差异不显著（P〉0.05）,无统计学意义。经过干预研究组显效25例,有效12例,总有效率为92．5％,与对照组的总有效率53．57％相比,差异显著（χ^2=13．872,P〈0.01）。经过干预后肥胖儿童不良生活行为得到改善。结论：从学龄前肥胖儿童开始,加强单纯性肥胖儿童的早期预防和治疗,制定个体化综合干预措施,对家长及老师进行肥胖相关知识的健康教育,帮助儿童形成良好的行为习惯,减轻体重,降低儿童单纯性肥胖的发生。     

早孕期甲状腺过氧化物酶抗体阳性对甲状腺功能的影响

目的：探讨妊娠8~12周甲状腺过氧化物酶抗体(TPOAb)阳性对甲状腺功能的影响。方法：对2010年9月至2011年6月北京友谊医院产科门诊行产前检查的611例无甲状腺疾病高危因素的健康初产妇,于妊娠8~12周进行甲状腺功能[促甲状腺激素(TSH)、游离四碘甲状腺原氨酸(FT4)]和TPOAb的检测,通过制定早孕期甲状腺功能正常参考区间,分析TPOAb阳性切割值、阳性率及对TSH、FT4的影响。结果：(1)妊娠8~12周TPOAb中位数值及变化范围为38.9(6.4~>1300)mU/L。(2)通过建立妊娠8~12周人群特异参考标准,以第90百分位计算TPOAb阳性切割值为206.77 mU/L,TPOAb阳性率为10.8%(66/611)。(3)回归分析显示：TPOAb滴度与TSH呈正相关,与FT4呈负相关,P值均为0.000。妊娠8~12周TPOAb阳性妇女TSH中位数值较TPOAb阴性者升高0.4 mU/L,前者TSH异常升高的风险是后者的4.4倍。结论：妊娠8~12周TPOAb阳性率为10.8%,通过建立妊娠期人群特异甲状腺功能参考标准和TPOAb阳性切割值,可避免过高估计TPOAb的阳性率。TPOAb阳性孕妇发生TSH异常升高的风险明显增加。     

Thyroid Doppler ultrasonography and resistive index in the evaluation of the need for ablative or antithyroid drug therapy in Graves' hyperthyroidism.

BACKGROUND AND PURPOSE: Graves' disease (GD) is the most common hyperthyroid disorder, but the therapeutic strategy for choosing between medical or ablative therapy has not been standardized. Thyroid hypervascularity is an important diagnostic feature in GD. This study collected Doppler ultrasonography data from patients with GD, Hashimoto's thyroiditis, and simple goiter to develop a hemodynamic index for use in the evaluation of when antithyroid drugs (ATDs) should be withdrawn or ablative therapy given in GD. MATERIAL AND METHODS: Thyroid Doppler ultrasonography was used to measure the resistive index (RI) and pulsatility index (PI) in various thyroid diseases. We studied 88 patients, including 13 untreated GD patients, 14 euthyroid GD patients after withdrawal of ATDs for more than 12 months, 14 euthyroid GD patients with normal thyroid stimulating hormone (TSH) concentrations after regular ATD treatment for 12 months (well controlled), 16 hyperthyroid GD patients with undetectable TSH concentrations after regular ATD treatment for more than 12 months (poorly controlled), 13 Hashimoto's thyroiditis patients, and 18 patients with simple goiters. RESULTS: The PI and RI were significantly different between patients with untreated (median PI/RI 1.36/0.79) or medically well-controlled (median PI/RI 0.66/0.51) GD, but no significant differences in PI and RI were found between patients with untreated or medically poorly controlled (median PI/RI 1.24/0.74) GD. An RI cut-off of at least 0.7 with undetectable TSH was found to be suggestive of the need for ablative therapy in GD patients who had received regular ATD treatment for more than 12 months, because of its statistically high sensitivity and specificity in all untreated and poorly controlled GD patients. An RI of less than 0.6 with normal TSH was suggestive of the need for withdrawal of ATDs in GD patients receiving regular medical treatment, because of its statistically high sensitivity and specificity in all treated euthyroid GD patients. CONCLUSIONS: This study has developed an RI-derived hemodynamic index that determines the need for ablative or ATD therapy in patients with GD. A large-scale, prospective study is needed to confirm its clinical value.     

Effect of long-term hormone substitution therapy on serum TSH level in postmenopausal women

OBJECTIVE: Dysfunction's of the thyroid gland are one of the most important endocrinological diseases. We report serum TSH levels in postmenopausal women before and during long-term hormone replacement therapy. MATERIAL AND METHODS: 107 postmenopausal patients participated in this study. Criteria for inclusion were: no known thyroid dysfunction and request for hormone replacement. Before starting therapy TSH serum levels were measured in each patient. If basal levels were within normal range TSH serum levels were reported over 4 years of hormone replacement therapy. RESULTS: More than 10% of the postmenopausal women showed pathological TSH-levels without clinical symptoms requiring further diagnostic. During subsequent treatment cycles (4 years) serum TSH in euthyroid patients did not show significant changes. Women using hormone replacement therapy developed no new manifestation of thyroid disease. CONCLUSION: In euthyroid women using long-term hormone replacement therapy are no changes in thyroid function caused by hormone replacement therapy to expect.     

The role of hCG in regulation of the thyroid gland in normal and abnormal pregnancy.

There is strong evidence that at least some forms of hCG can interact with and stimulate the thyroid both in vitro and in vivo. Changes in thyroid tests are sufficiently common in normal pregnancy for us to regard them as physiologic. The evidence that hCG is the agent responsible for these changes remains largely circumstantial but is now supported by an increasing body of evidence from laboratory studies. Trophoblastic tumors secrete variant forms of hCG that can stimulate the thyroid, but we do not know if they have any role in the extreme examples of thyroid stimulation encountered in normal pregnancy. Preparations of hCG from pregnancy urine bind to thyroid membranes from a wide variety of species, but they do not activate adenylate cyclase in all assay systems. The enzyme in human thyroid cells or membranes is, at best, only weakly stimulated by hCG. There are ample in vitro data that hCG can stimulate the thyroid, but studies using human thyroid cells have yielded conflicting results. The most direct evidence comes from the study of thyroid tests in normal pregnancy. In early pregnancy, when hCG concentrations are highest, free thyroid hormones are increased and serum TSH concentration is decreased. An inverse correlation exists between serum hCG and TSH concentrations, but hCG generally correlates poorly with individual thyroid tests. An activity in pregnancy serum related to hCG is able to stimulate FRTL-5 cells and may account for the changes in thyroid function observed in pregnancy. Structural considerations, along with data from biologic assays and sensitive thyroid function tests, suggest that hCG has significant thyroid-stimulating activity. This information suggests that the thyroid may be under dual control from both hCG and TSH in early pregnancy.     

Thyroid function and postmenopause

There is an increasing prevalence of high levels of thyroid stimulating hormone (TSH) with age - particularly in postmenopausal women - which are higher than in men. The incidence of thyroid disease in a population of postmenopausal women is as follows: clinical thyroid disease ,about 2.4%; subclinical thyroid disease ,about 23.2%. Among the group with subclinical thyroid disease ,73.8% are hypothyroid and 26.2% are hyperthyroid. The rate of thyroid cancer increases with age. The symptoms of thyroid disease can be similar to postmenopausal complaints and are clinically difficult to differentiate. There can also be an absence of clinical symptoms. It is of importance that even mild thyroid failure can have a number of clinical effects such as depression ,memory loss ,cognitive impairment and a variety of neuromuscular complaints. Myocardial function has been found to be subtly impaired. There is also an increased cardiovascular risk ,caused by increased serum total cholesterol and low-density lipoprotein cholesterol as well as reduced levels of high-density lipoprotein. These adverse effects can be improved or corrected by L-thyroxine replacement therapy. Such treatment has been found to be cost-effective. With time ,overt hypothyroidism can develop. Therefore ,routine screening of thyroid function in the climacteric period to determine subclinical thyroid disease is recommended. Hormone replacement therapy (HRT) in women with hypothyroidism treated with thyroxine causes changes in free thyroxine and TSH. Increased binding of thyroxine to elevated thyroxine-binding globulin causes an elevation of TSH by feedback. Since adaptation is insufficient ,there is an increased need for thyroxine in these women taking HRT. TSH levels should be controlled at 12 weeks after the beginning of therapy. At higher age the need for iodine and thyroxine is decreased. Therefore ,therapy has to be controlled. For bone metabolism thyroid hormones play a dominant role. While there are only marginal differences between hypothyroid patients and euthyroid controls ,there are large differences for hyperthyroid patients. Previous thyrotoxicosis and subsequent long-lasting L-thyroxine treatment are together associated with reduction in femoral and vertebral bone density in postmenopausal women. In these cases HRT is important for the control of bone loss.     

Thyroid disease]

The incidence of pregnant women with thyroid dysfunction has been reported to be around 0.1-0.4%. Graves' disease accounts for more than half of these disorders. The main cause of thyroid disease in pregnancy and puerperium is autoimmune dysfunction. Whether there may be goitre or exophthalmus present, clinical signs as inappropriate weight gain, high systolic pressure, palpitation (greater than or equal to 110/min), emotional lability, fatigue, acceleration of suppression of the Achilles' tendon reflex should induce changes in the biochemical thyroid function tests. Parameters for the diagnosis and management for hyperthyroidism are serum levels of free T4 and TSH, while those of T3, reverse T3, and TSH are for hypothyroidism. Serum anti-microsomal antibodies and anti-thyroglobulin antibodies which have no effect on the fetus are also good markers for severity. The transplacental transfer of maternal TSH receptor antibodies consisting of stimulatory and inhibitory immunoglobulins and maternal thyroid-binding inhibiting immunoglobulins play roles in the development of transient neonatal hyper- or hypothyroidism. Fetal control is achieved by optimal maternal management. Untreated hyperthyroidism may be associated with fetal malformations. This risk may be reduced by antithyroid drug treatment of up to 150 mg/day of propylthiouracil which has less chance of placental passage and less secretion into the mother's milk than methyl-mercapto-imidazol. Maternal thyroid function should be kept in the upper limit of normal range, taking into consideration the fetal dysfunction induced by over-administration of the drug which passes through placenta. Children of hypothyroid women taking inadequate replacement therapy manifested lower IQ values compared to the progeny of euthyroid or hypothyroid women taking adequate therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thyroid function and postmenopause.

There is an increasing prevalence of high levels of thyroid stimulating hormone (TSH) with age - particularly in postmenopausal women - which are higher than in men. The incidence of thyroid disease in a population of postmenopausal women is as follows: clinical thyroid disease, about 2.4%; subclinical thyroid disease, about 23.2%. Among the group with subclinical thyroid disease, 73.8% are hypothyroid and 26.2% are hyperthyroid. The rate of thyroid cancer increases with age. The symptoms of thyroid disease can be similar to postmenopausal complaints and are clinically difficult to differentiate. There can also be an absence of clinical symptoms. It is of importance that even mild thyroid failure can have a number of clinical effects such as depression, memory loss, cognitive impairment and a variety of neuromuscular complaints. Myocardial function has been found to be subtly impaired. There is also an increased cardiovascular risk, caused by increased serum total cholesterol and low-density lipoprotein cholesterol as well as reduced levels of high-density lipoprotein. These adverse effects can be improved or corrected by L-thyroxine replacement therapy. Such treatment has been found to be cost-effective. With time, overt hypothyroidism can develop. Therefore, routine screening of thyroid function in the climacteric period to determine subclinical thyroid disease is recommended. Hormone replacement therapy (HRT) in women with hypothyroidism treated with thyroxine causes changes in free thyroxine and TSH. Increased binding of thyroxine to elevated thyroxine-binding globulin causes an elevation of TSH by feedback. Since adaptation is insufficient, there is an increased need for thyroxine in these women taking HRT. TSH levels should be controlled at 12 weeks after the beginning of therapy. At higher age the need for iodine and thyroxine is decreased. Therefore, therapy has to be controlled. For bone metabolism thyroid hormones play a dominant role. While there are only marginal differences between hypothyroid patients and euthyroid controls, there are large differences for hyperthyroid patients. Previous thyrotoxicosis and subsequent long-lasting L-thyroxine treatment are together associated with reduction in femoral and vertebral bone density in postmenopausal women. In these cases HRT is important for the control of bone loss.     

Thyroid disease in pregnancy

Thyroid testing during pregnancy should be performed on symptomatic women or those with a personal history of thyroid disease. Overt hypothyroidism complicates up to 3 of 1,000 pregnancies and is characterized by nonspecific signs or symptoms that are easily confused with complaints common to pregnancy itself. Physiologic changes in serum thyroid-stimulating hormone (TSH) and free thyroxine (T(4)) related to pregnancy also confound the diagnosis of hypothyroidism during pregnancy. If the TSH is abnormal, then evaluation of free T(4) is recommended. The diagnosis of overt hypothyroidism is established by an elevated TSH and a low free T(4). The goal of treatment with levothyroxine is to return TSH to the normal range. Overt hyperthyroidism complicates approximately 2 of 1,000 pregnancies. Clinical features of hyperthyroidism can also be confused with those typical of pregnancy. Clinical hyperthyroidism is confirmed by a low TSH and elevation in free T(4) concentration. The goal of treatment with thioamide drugs is to maintain free T(4) in the upper normal range using the lowest possible dosage. Postpartum thyroiditis requiring thyroxine replacement has been reported in 2% to 5% of women. Most women will return to the euthyroid state within 12 months.     

Changes in thyroid status in pregnant women treated with ritodrine

In a clinical study of 17 pregnant women treated with ritodrine, a beta 2-sympathomimetic agent used for tocolysis, thyroid hormone status was assessed longitudinally. This was done in order to verify the hypothesis that an increase in T3 levels could result from adrenergic stimulation, since propranolol, a beta blocking agent, has proved to decrease T3 levels in man. Indeed, a statistically significant increase in T3 serum concentration and in T3/T4 ratio was found on the second day after the start of treatment with ritodrine (p less than 0.02 and less than 0.01 respectively). After discontinuation of treatment a decrease in T3 serum levels, compared to both treatment and pretreatment levels, was observed. The free T4 concentration showed a significant drop after the first week of treatment (p less than 0.01), but no changes were found in T4 and TSH levels. It was concluded that the beta 2-mimetic-mediated changes in thyroid status provide one more reason for restriction of the use of beta-mimetic drugs in hyperthyroidic patients and might offer an additional explanation for the undesirable chronotropic cardiac side-effects of the therapy.