ECE2014 Poster Presentations Thyroid (non-cancer) (125 abstracts)
1Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milano, Italy; 2Metabolic Medicine, Policlinico di Monza, Monza, Italy; 3UO Endocrinologia e Malattie Metaboliche, Fondazione IRCCS Ca Granda-Ospedale Maggiore, Milano, Italy.
Hypothyroidism is a risk factor for obesity, central adiposity and ectopic fat accumulation. To assess whether this risk could be detected also in stable patients taking regularly the LT4 replacement therapy we assessed retrospectively the prevalence of metabolic syndrome (ATP III definition) and calculated the fatty liver index (FLI) and the visceral adiposity index (VAI) in patients attending our Outpatient Endocrinology Clinic because of known primary acquired hypothyroidism undergoing LT4 replacement therapy on a regular basis (n=997) and used as control group patients with stable euthyroid multi-nodular goitre (MNG; n=502). Hypothyroid patients were younger (56±15 vs 60±14 years; P<0.001), and showed higher BMI (28.7±6.4 vs 27.2±5.3 kg/m2; P<0.001) and FLI (58±31 vs 49±32; P=0.02) but no difference in VAI (4.6±3.1 vs 4.6±3.5) and prevalence of the metabolic syndrome (47 vs 47%), neither in the prevalence of type 2 diabetes (11 vs 11%) and known CVD (11 vs 12%) when compared to MNG patients. The actual BMI was directly associated with the duration of LT4 replacement therapy also when adjusted for age, sex and average TSH levels (R=0.30; ρ=0.03). No difference in metabolic syndrome, FLI and VAI was detected when the comparison between groups was adjusted for age, sex and BMI. In conclusion, hypothyroid patients regularly undergoing LT4 replacement therapy showed higher BMI regardless of age, sex and TSH levels in comparison with MNG patients. In contrast, no difference in the prevalence of the metabolic syndrome and in surrogate biomarkers of fatty liver and visceral adiposity was observed when the analysis was adjusted for the different age and BMI. The isolated finding of higher BMI may be due to an initial weight gain associated to the diagnostic-related delay in beginning LT4 therapy but also to persistent subtle defects of energy metabolism not fully reverted by the LT4 therapy.