Despite the use of intensified LLT, many FH patients continue to experience high plasma LDL-C levels and, consequently, do not achieve recommended treatment targets. Type of LDL-receptor mutation, use of ezetimibe, coexistent diabetes, and ASCVD status can bear significantly on the likelihood of attaining LDL-C treatment goals.

OBJECTIVEHyperglycemia may increase mortality in patients who receive total parenteral nutrition (TPN). However, this has not been well studied in noncritically ill patients (i.e., patients in the nonintensive care unit setting). The aim of this study was to determine whether mean blood glucose level during TPN infusion is associated with increased mortality in noncritically ill hospitalized patients.RESEARCH DESIGN AND METHODSThis prospective multicenter study involved 19 Spanish hospitals. Noncritically ill patients who were prescribed TPN were included prospectively, and data were collected on demographic, clinical, and laboratory variables as well as on in-hospital mortality.RESULTSThe study included 605 patients (mean age 63.2 ± 15.7 years). The daily mean TPN values were 1.630 ± 323 kcal, 3.2 ± 0.7 g carbohydrates/kg, 1.26 ± 0.3 g amino acids/kg, and 0.9 ± 0.2 g lipids/kg. Multiple logistic regression analysis showed that the patients who had mean blood glucose levels >180 mg/dL during the TPN infusion had a risk of mortality that was 5.6 times greater than those with mean blood glucose levels <140 mg/dL (95% CI 1.47–21.4 mg/dL) after adjusting for age, sex, nutritional state, presence of diabetes or hyperglycemia before starting TPN, diagnosis, prior comorbidity, carbohydrates infused, use of steroid therapy, SD of blood glucose level, insulin units supplied, infectious complications, albumin, C-reactive protein, and HbA1c levels.CONCLUSIONSHyperglycemia (mean blood glucose level >180 mg/dL) in noncritically ill patients who receive TPN is associated with a higher risk of in-hospital mortality.

Background/Aims: Obesity has been associated with hypothyroidism and impaired insulin sensitivity. However, few studies have specifically addressed the association between insulin sensitivity and thyroid function. Our aim was to look for a relation between these 2 factors in a sample of obese males. Methods: One hundred and forty-four euthyroid male obese patients – mean age 42.6 years, mean body mass index (BMI) 41.8 – were enrolled in this cross-sectional study. The hospital study protocol at entrance included baseline serum thyroid-stimulating hormone (TSH), insulin and glucose concentrations. Data were studied using an age-adjusted simple and multivariate linear regression analysis with TSH as the dependent and insulin and BMI as the independent variables. Results: Mean TSH and insulin were 1.6 and 21.2 mU/l, respectively. It was found that their relationship follows a regression model: TSH = 1.725–0.019 (age) + 0.003 (insulin) + 0.017 (BMI). Further data showed a positive correlation between BMI and TSH (r = 0.22; p < 0.05), as well as between serum baseline insulin (>10 mU/l) and TSH concentration (r = 0.27; p < 0.05). This association was stronger in patients with higher insulin values (>21.2 mU/l; r = 0.40; p < 0.01). However, negative correlations between age and insulin (r = –0.14; not significant) and age and TSH (r = –0.35; p < 0.05) were observed. Conclusions: In obese males, insulin resistance is significantly related with impairment of thyroid function, and this situation seems to be attenuated with age.

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Morbid obesity is frequently associated with abnormal LVM, particularly in patients with OSA; this association is independent of HT, BMI, body composition, and other clinical factors, supporting a direct role of OSA on LVM in morbid obesity. This suggests that OSA and LVM might be taken as predictors of the cardiovascular risk in these patients.

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