“…HA was diagnosed when an androgen parameter exceeded the limit of the local laboratory or when hirsutism was presented, but the methods used to test androgens vary greatly around the world, and there is currently no gold standard. LC-MS measurements [23,24] were recently proposed as a reliable measure for androgens, but the high cost and lack of clinical feasibility significantly hinder the clinical application of LC-MS. In addition, the phenotype classification method described in the NIH recommendations was also based on the 2003 Rotterdam criteria [3].…”
This hospital-based observational study aims to estimate differences in metabolic abnormalities between different polycystic ovary syndrome (PCOS) phenotypes and their distribution characteristics. The prevalence of metabolic abnormalities among different PCOS phenotypes, including diabetes mellitus (DM), metabolic syndrome (MS), pre-diabetes mellitus (pre-DM), insulin resistance (IR) and dyslipidemia were compared. A total of 2436 women who were ≥18 years old and who were hospitalized in Sun Yat-Sen University affiliated hospital from 1998 to 2015 in GuangZhou, China, were included in this study. PCOS phenotypes were recorded according to the 2003 Rotterdam criteria, including the polycystic ovary morphology (PCO), hyperandrogenism (HA) and ovulation dysfunction (OD) phenotype (PCO+HA+OD); the ovulation phenotype (PCO+HA); the non-PCO phenotype (HA+OD); and the non-HA phenotype (PCO+OD). Notably, 56% of the patients had the classic phenotype (PCO+HA+OD). Importantly, there was no significant difference in the prevalence of metabolic abnormalities or the distribution characteristics of the metabolic abnormalities among these four PCOS phenotypes. Our study supports the notion that metabolic abnormalities and the distribution characteristics of metabolic abnormalities should not be used to distinguish among the various clinical PCOS phenotypes.
“…HA was diagnosed when an androgen parameter exceeded the limit of the local laboratory or when hirsutism was presented, but the methods used to test androgens vary greatly around the world, and there is currently no gold standard. LC-MS measurements [23,24] were recently proposed as a reliable measure for androgens, but the high cost and lack of clinical feasibility significantly hinder the clinical application of LC-MS. In addition, the phenotype classification method described in the NIH recommendations was also based on the 2003 Rotterdam criteria [3].…”
This hospital-based observational study aims to estimate differences in metabolic abnormalities between different polycystic ovary syndrome (PCOS) phenotypes and their distribution characteristics. The prevalence of metabolic abnormalities among different PCOS phenotypes, including diabetes mellitus (DM), metabolic syndrome (MS), pre-diabetes mellitus (pre-DM), insulin resistance (IR) and dyslipidemia were compared. A total of 2436 women who were ≥18 years old and who were hospitalized in Sun Yat-Sen University affiliated hospital from 1998 to 2015 in GuangZhou, China, were included in this study. PCOS phenotypes were recorded according to the 2003 Rotterdam criteria, including the polycystic ovary morphology (PCO), hyperandrogenism (HA) and ovulation dysfunction (OD) phenotype (PCO+HA+OD); the ovulation phenotype (PCO+HA); the non-PCO phenotype (HA+OD); and the non-HA phenotype (PCO+OD). Notably, 56% of the patients had the classic phenotype (PCO+HA+OD). Importantly, there was no significant difference in the prevalence of metabolic abnormalities or the distribution characteristics of the metabolic abnormalities among these four PCOS phenotypes. Our study supports the notion that metabolic abnormalities and the distribution characteristics of metabolic abnormalities should not be used to distinguish among the various clinical PCOS phenotypes.
“…This method is very accurate, sensitive, and well standardized, as was shown in previous studies (7)(8)(9). Intraassay variation in both the female and male concentration range was 4%.…”
Background: The quality of testosterone assays has been a matter of debate for several years. Known limitations of testosterone immunoassays are the cross-reactivity with other steroids and a high variation in the low concentration range. We hypothesized that one of the additional limitations of testosterone immunoassays is an ineffective displacement of testosterone from its binding protein.
Methods:Thirty samples from women not using oral contraceptives (OAC), 30 samples from women using OAC, and 30 samples from pregnant women were used to measure testosterone by an isotope dilution (ID)-LC-MS/MS method and by 6 commercially available testosterone immunoassays (UniCel
“…In particular, reference ranges are still needed, especially in childhood, since steroid hormones change dramatically with age and pubertal stages and often differ between the sexes [14, 24, 25, 32]. Moreover, a lack of comparability of steroid hormone data due to differences in laboratory methods, even with various LC-MS/MS techniques [9, 33], hampers clinical and basic science studies in endocrine research. Therefore, standardized methods “simplifying” the display and interpretation of complex steroid data could improve diagnosis and research in endocrinology.…”
Background/Aims: The high complexity of pediatric reference ranges across age, sex, and units impairs clinical application and comparability of steroid hormone data, e.g., in congenital adrenal hyperplasia (CAH). We developed a multiples-of-median (MoM) normalization tool to overcome this major drawback in pediatric endocrinology. Methods: Liquid chromatography tandem mass spectrometry data comprising 10 steroid hormones representing 905 controls (555 males, 350 females, 0 to > 16 years) from 2 previous datasets were MoM transformed across age and sex. Twenty-three genetically proven CAH patients were included (21-hydroxylase deficiency [21OHD], n = 19; 11β-hydroxylase deficiency [11OHD], n = 4). MoM cutoffs for single steroids predicting 21OHD and 11OHD were computed and validated through new, independent patients (21OHD, n = 8; adrenal cortical carcinoma, n = 6; obesity, n = 40). Results: 21OHD and 11OHD patients showed disease-typical, easily recognizable MoM patterns independent of age, sex, and concentration units. Two single-steroid cutoffs indicated 21OHD: 3.87 MoM for 17-hydroxyprogesterone (100% sensitivity and 98.83% specificity) and 12.28 MoM for 21-deoxycortisol (94.74% sensitivity and 100% specificity). A cutoff of 13.18 MoM for 11-deoxycortisol indicated 11OHD (100% sensitivity and 100% specificity). Conclusions: Age- and sex-independent MoMs are straightforward for a clinically relevant display of multi-steroid patterns. In addition, defined single-steroid MoMs can serve alone as predictors of 21OHD and 11OHD. Finally, MoM transformation offers substantial enhancement of routine and scientific steroid hormone data exchange due to improved comparability.
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