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Background: The association of subclinical hypothyroidism (SCH) with insulin resistance, metabolic syndrome (MS), and coronary atherosclerosis is uncertain., Objective: To investigate the role of increased intrahepatic fat in the association of SCH with insulin resistance, MS, and coronary atherosclerosis., Design, Patients, and Methods: We conducted a cross-sectional study in a sample of 753 subjects (46% males) aged 35-70 years with no history of diabetes, renal, hepatic, thyroid, or coronary heart disease, and were participants of the Genetics of Atherosclerotic Disease study. SCH was defined as a high serum TSH level with normal free thyroxine concentration. Fatty liver (FL), coronary artery calcification (CAC), and abdominal visceral adipose tissue were assessed by computed tomography. Cross-sectional associations of SCH with and without FL, with MS, insulin resistance, and subclinical atherosclerosis defined as a CAC score >0, were examined in logistic regression models., Results: SCH was observed in 17.7% of the population studied. The prevalence of FL was similar in both euthyroid and SCH subjects (31.8 vs 27.8%, P=0.371). SCH plus FL subjects were heavier and had more metabolic abnormalities compared with SCH plus normal liver subjects. In multivariate-adjusted logistic regression analyses, SCH plus FL was associated with MS (odds ratio (OR): 2.73, 95% CI: 1.26-5.92), insulin resistance (OR: 4.91, 95% CI: 1.63-14.75), and CAC score >0 (OR: 3.05, 95% CI: 1.20-7.76). SCH without FL showed no associations., Conclusion: SCH with FL is associated with increased odds of MS, insulin resistance, and CAC, independent of potential confounders., (© 2014 European Society of Endocrinology.)

Objective: Premature atherosclerosis in patients with SLE is partially explained by traditional risk factors; therefore, we aimed to identify lupus-related risk factors for coronary artery calcifications., Methods: An inception cohort of 139 lupus patients (93% females) was screened for coronary artery calcifications using Multidetector CT, after 5.1 years of follow-up. Clinical and immunological variables and cardiovascular risk factors were assessed longitudinally. Also, 100 age- and sex-matched healthy subjects were studied. Correlates for calcifications were analysed in lupus patients, including levels of lipids and inflammatory molecules in samples obtained at enrolment, mid-term follow-up and at screening., Results: At enrolment, lupus patients were 27.2 (9.1) years of age and with a disease duration of 5.4 (3.8) months. Calcifications were detected in 7.2% of patients and 1% of controls [unadjusted odds ratio (OR) 7.7, 95% CI 1.05, 336.3, P = 0.02]. In lupus, calcifications were detected since the age of 23 years and from 3 years of diagnosis. Patients with calcifications were older, post-menopausal, and had higher levels of serum apolipoprotein B and Framingham risk scores (P < 0.05). Lupus-related factors identified included age at diagnosis, IgG aCLs, cumulative lupus activity, length of moderate/severe activity and cumulative dose of prednisone and CYC (P < 0.05). Use of anti-malarials was protective (P = 0.006). Logistic regression analysis showed as predictors of calcification: disease duration (OR 15.1, 95% CI 2.6, 87.2), age at enrolment (OR 8.5, 95% CI 1.7, 43.0) and SLEDAI 2000 update (SLEDAI-2K) mean area under the curve (OR 12.3, 95% CI 2.5, 61.8). Longitudinal analyses of lipids and inflammatory molecules did not differ between patients., Conclusions: Disease activity is a potentially modifiable risk factor for coronary artery calcifications in SLE. Therefore, management of traditional risk factors plus tight control of lupus activity, including the use of anti-malarials, is recommended.