Functional Ovarian Hyperandrogenism/Minority Adolescents

描述（由申请人提供）：功能性卵巢高雄激素血症 (FOH)多囊卵巢综合征（PCOS）的病因有哪些？ 不同程度的排卵功能障碍， 高雄激素血症和临床上明显的高雄激素血症。生化 高雄激素血症和高雄激素血症的临床标准还没有 这是针对大量少数民族女性青少年人口确定的。的 研究的具体目的是：1）确定 FOH/PCOS的临床表现和生化决定因素， 主要为加勒比-西班牙裔和非洲裔美国人的临床样本 女性青少年; 2）建立规范的生化决定因素， 该人群的高雄激素血症; 3）确定临床相关因素 青春期女孩高雄激素血症;和4），以确定是否青少年 患有FOH/PCOS的女性比正常体重匹配的青少年更有可能 有糖尿病家族史，高血压， 血压或心血管疾病，或有显着较高的葡萄糖， 胰岛素比率。假设如下：1）睾酮和 月经周期异常受试者的雄烯二酮水平和/或 高雄激素血症的物理证据将显着大于 那些月经周期正常，没有身体证据的人 高雄激素血症; 2）临床和历史特征的组合可能是 用于开发可预测血清雄激素水平的模型;以及3） 患有FOH/PCOS的受试者比正常受试者更有可能 加勒比-西班牙裔，有糖尿病危险因素的证据 糖尿病和心血管疾病，并有显着较高的葡萄糖 胰岛素的比例。将连续招募250名12至21岁的女性 来自多个临床站点的患者;患有慢性疾病或 活性药物将被排除在外。受试者将完成一份问卷， 了解月经和家族史的特征，并进行体检。 检查以评估高雄激素血症的临床体征。血清水平 空腹游离和总睾酮，雄烯二酮，促黄体激素， 卵泡刺激素、胰岛素、17-OH孕酮和葡萄糖将被 测定了确定血清雄激素水平与临床 根据FOH/PCOS的特征，所有受试者将在临床上分为三组 将在这些组中比较不同的类别和雄激素水平， 使用ANOVA。高雄激素血症将被定义为上述两个标准差 正常受试者的平均睾酮和雄烯二酮水平 月经周期和没有高雄激素血症的身体证据（I类）。 高雄激素血症的临床预测模型将使用 雄激素测量的多元线性回归分析。病例对照 将进行研究，以确定青少年受试者之间的差异 有无FOH/PCOS。更好地理解化学和生物技术 少数民族青少年FOH/PCOS的临床特征将有助于 制定早期治疗方法和预防后期严重 这种疾病的自然进展导致的健康问题。

DESCRIPTION (provided by applicant): Functional Ovarian Hyperandrogenism (FOH), also called Polycystic Ovarian Syndrome (PCOS) consists of a spectrum of dysfunction with varying degrees of ovulatory dysfunction, hyperandrogenemia, and clinically evident hyperandrogenism. The biochemical and clinical criteria for hyperandrogenemia and hyperandrogenism have not yet been determined for a large ethnic minority female adolescent population. The specific aims of the study are: 1) to determine the relationship between the clinical presentation and the biochemical determinants of FOH/PCOS in a clinical sample of predominantly Caribbean-Hispanic and African-American female adolescents; 2) to establish norms for the biochemical determinants of hyperandrogenemia in this population; 3) to determine the clinical correlates of hyperandrogenemia in adolescent girls; and 4) to determine if adolescent females with FOH/PCOS are more likely than normal, weight-matched adolescents to be Caribbean-Hispanic, to have a family history of diabetes, high blood pressure or cardiovascular disease, or to have significantly higher glucose to insulin ratios. The hypotheses are as follows: 1) the testosterone and androstenedione levels in subjects with menstrual cycle abnormalities and/or physical evidence of hyperandrogenism will be significantly greater than in those with normal menstrual cycles and no physical evidence for hyperandrogenism; 2) a combination of clinical and historical features may be used to develop a model that can predict serum androgen levels; and 3) subjects with FOH/PCOS will be more likely than normal subjects to be of Caribbean-Hispanic descent, to have evidence of risk factors for diabetes mellitus and cardiovascular disease, and to have significantly higher glucose to insulin ratios. 250 females aged 12 to 21 will be consecutively recruited from several clinical sites; girls with chronic illnesses or on hormonally active drugs will be excluded. Subjects will complete a questionnaire to elicit features of menstrual and family history and will undergo a physical examination to evaluate for clinical signs of hyperandrogenism. Serum levels of fasting free and total testosterone, androstenedione, luteinizing hormone, follicle stimulating hormone, insulin, 17-OH progesterone, and glucose will be measured. To determine the association of serum androgen levels with clinical features of FOH/PCOS, all subjects will be clinically stratified into three different categories and androgen levels will be compared among these groups, using ANOVA. Hyperandrogenism will be defined as two standard deviations above the mean testosterone and androstenedione levels in subjects with normal menstrual cycles and no physical evidence of hyperandrogenism (category I). A clinical prediction model for hyperandrogenemia will be developed using multiple linear regression analyses for androgen measures. A case-control study will be performed to determine differences between adolescent subjects with and without FOH/PCOS. Improved understanding of the boichemical and clinical features of FOH/PCOS in minority adolescents will facilitate the development of earlier treatment modalities and prevention of later serious health problems that result from the natural progression of this disorder.