No abstract

Background and purpose: Metabolic syndrome (MetS) is a disorder associated with an increased risk of cardiovascular disease. The frequency of each component of MetS in Turner syndrome (TS) subjects is high. An elevated incidence of hearing loss has also been reported in TS. Sensorineural hearing loss (SNHL) affects at least half of young women with TS. The association between MetS and SNHL has not been previously considered in TS. The aim of this study is to evaluate the association between these two conditions. Patients and Methods: Cross-sectional anthropometric, cardio-metabolic and audiological data were obtained from a cohort consisting of unrelated TS subjects (>20 years of age; n = 93). Metabolic syndrome was defined according to the International Diabetes Federation criteria. Types and severity of hearing loss were based on the American Speech Hearing Association guidelines. Results: Hearing loss was detected in 74% of ears from adult TS subjects and SNHL was observed in half of our TS subjects. The prevalence of MetS in TS subjects with or without SNHL was 64% and 11%, respectively (P < 0.05). After adjusting for age, MetS was related to a ninefold increase in the odds of SNHL. This odds increased in a stepwise manner as the number of MetS components increased. Conclusion: MetS and its individual components were associated factors for SNHL in TS subjects. A reduction in the number and severity of the components of MetS might potentially contribute to decreasing the progression of SNHL at younger ages, but further studies will be needed to explain the underlying pathological mechanism connecting MetS and SNHL.

This is the first study to assess CoQ10 levels in amniotic fluid during pregnancy in which levels were significantly lower among those delivering preterm. More research is warranted in this regard.

Preeclampsia is a common (approximately 7% of all pregnancies) disorder of pregnancy in which the normal hemodynamic response to pregnancy is compromised. Despite many years of intensive research, the pathogenesis of preeclampsia is still not fully understood. The objective of the present study was to investigate the levels of coenzyme Q(10) (CoQ(10)) in placental tissue compared to maternal and umbilical cord levels both during normal pregnancy and in those complicated with preeclampsia. Pregnant women (n = 30) and women with preeclampsia (n = 30) were included. Maternal, newborn cord blood levels and placental content of coenzyme Q(10) were measured by high performance liquid chromatography (HPLC). Plasma coenzyme Q(10) levels were significantly higher in normal pregnant women than in women with preeclampsia. CoQ(10) content in placenta from women with preeclampsia (mean 0.28 SEM 0.11 nmol/mg protein) was significantly higher compared to normal pregnancy (mean 0.09 SEM 0.01 nmol/mg protein; p = 0.05). Levels of CoQ(10) in cord blood from normal pregnant women (mean 0.30 SEM 0.05 micromol/l) were significantly lower than in preeclamptic women (mean 4.03 SEM 2.38 micromol/l). In conclusion, these data indicate a possible involvement of CoQ(10) in preeclampsia that might bear deep physiopathological significance and deserve to be further elucidated.

Objective: To assess insulin sensitivity and pancreatic β-cell function in an adult population of Ecuadorian individuals with Turner syndrome (TS). Design and Methods: This was a cross-sectional correlational study conducted in TS subjects (>20 years old; n = 38). A standard 2-h oral glucose tolerance test was performed in both women with TS and the reference group. Glucose, lipids, insulin, and C-peptide concentrations were measured. Homeostasis Model Assessment (HOMA) of Insulin Resistance, Quantitative Insulin Sensitivity Check Index, McAuley, Matsuda, and Belfiore indices were calculated to evaluate the degree of insulin resistance (IR). The pancreatic β-cell function was assessed using HOMA-β, basal C-Peptide Index (CPI), and CPII at 120 ′. Results: A higher prevalence of impaired glucose tolerance was found in TS subjects compared with the reference group. Although significant differences were found for glucose concentrations at 60 ′ and 120 ′ (but not at 0 ′), only the baseline insulin concentrations differed significantly between the two groups. The values of the IR indices were statistically different between study and reference groups. A significant number of TS subjects diagnosed with IR were differently classified according to the index applied. The concentrations of C-peptide at 0 ′ and 120 ′ of TS subjects were similar to those of the control group. In contrast, the CPI and CPII values in the study group were significantly lower than those in the control group. Conclusion: It is impossible to select the best surrogate method for the assessment of IR in women with TS. The CPI and CPII values could be preferable to other indices to assess the pancreatic β-cell function in TS subjects. Our findings suggest that IR and pancreatic β-cell dysfunction could be independent events in women with TS, and both conditions seem to be caused by the disease per se. Our results imply that early screening and intervention for TS would be therapeutic for TS women.