Mouse Anti-Human TSH monoclonal antibody, clone 5610

Context: Severe hypothyroidism has profound effects on lipoprotein metabolism including high-density lipoprotein (HDL) cholesterol elevations but effects on HDL function metrics are unknown. Objective: To determine the impact of severe short-term hypothyroidism on HDL particle characteristics, HDL cholesterol efflux capacity (CEC), and HDL antioxidative capacity. Design: Observational study with variables measured during severe short-term hypothyroidism (median TSH 81 mU/L) and after 20 weeks of thyroid hormone supplementation (median TSH 0.03 mU/L) (Netherlands Trial Registry ID 7228). Setting: University hospital setting in The Netherlands. Patients: Seventeen patients who had undergone a total thyroidectomy for differentiated thyroid carcinoma. Main outcome measures: HDL particle characteristics (nuclear magnetic resonance spectrometry), CEC (human THP-1-derived macrophage foam cells and apolipoprotein B-depleted plasma), and HDL anti-oxidative capacity (inhibition of low-density lipoprotein oxidation). Results: During hypothyroidism plasma total cholesterol, HDL cholesterol and apolipoprotein A-I were increased (P = 0.001). HDL particle concentration was unchanged, but there was a shift in HDL subclasses toward larger HDL particles (P < 0.001). CEC was decreased (P = 0.035), also when corrected for HDL cholesterol (P < 0.001) or HDL particle concentration (P = 0.011). HDL antioxidative capacity did not change. Conclusion: During severe short-term hypothyroidism CEC, an important antiatherogenic metric of HDL function, is impaired. HDL cholesterol and larger HDL particles are increased but HDL particle concentration is unchanged. Combined, these findings suggest that HDL quality and quantity are not improved, reflecting dysfunctional HDL in hypothyroidism.

Thyroid disorders are a frequently encountered issue during pregnancy and a cause of maternal and fetal morbidity. In regions like Appalachia that are particularly susceptible to health disparities, descriptive studies are needed to assist in identifying pathologic derangements. We sought to characterize fetal thyroid hormone levels at delivery and investigate whether or not maternal demographic characteristics affect the prevalence of neonatal thyroid disease. A cross-sectional analysis was conducted on 130 pregnant women recruited from the Tri-State region, incorporating areas of Kentucky, Ohio, and West Virginia. Total triiodothyronine (T3) (p= 0.4799), free T3 (p= 0.6323), T3 uptake (p= 0.0926), total thyroxine (T4) (p= 0.8316), free T4 (p= 0.0566), and Thyroid stimulating hormone (TSH) (p= 0.8745) levels were comparable between urban and rural newborns. We found no effect of hypertension status or nicotine levels on fetal umbilical cord thyroid hormone levels. Maternal diabetic status was associated with lower T4 (p= 0.0099) and free T4 (p= 0.0025) levels. Cotinine affected levels of T4 (p= 0.0339). In regard to maternal Body Mass Index (BMI), there was an increase in total T3 as BMI increased (p= 0.0367) and no significant difference in free T3, T3 uptake, T4, free T4, or TSH. There was a negative correlation between TSH and 1 min Apgar scores (p= 0.0058). Lead and cadmium have been implicated to alter TSH levels, but no correlation was found in our study (r(2)= 0.0277). There were no differences in cord blood between urban (37.3 +/- 10.3 fmol/ug DNA) and rural (70.5 +/- 26.8 fmol/ug DNA) benzo(a)pyrene DNA adducts (p= 0.174). Thyroid disorders present a unique opportunity for the prevention of perinatal morbidity and mortality, since maternal treatment, as well as maternal demographic characteristics, can have direct fetal effects.