Endocrine Abstracts

Autoimmune thyroiditis is a common disease with different clinical aspects. It has not been established whether a rapid cellular destruction, with evolution towards hypothyroidism, may be associated with specific clinical phenotypes. To clarify this point, we studied 386 consecutive patients affected by autoimmune thyroiditis diagnosed within the previous 3 years: 193 patients (170 female and 23 males, age range 57.5±12.8, Group 1) were treated with L-thyroxine since they had clinical or subclinical (TSH≧4 μU/ml) hypothyroidism; and 193 patients (167 females and 26 males, age range 49±15.9, Group 2) were not submitted to drug therapy (TSH range 0.7–3.0 μU/ml). All patients underwent an accurate medical history to assess the presence of metabolic and thyroid diseases in the family and associated diseases (hypertension, hypercholesterolemia, type 2 diabetes, and obesity), and were submitted to thyroid ultrasound and serum determination of TSH, free T₃, free T₄, Tg-Ab, and TPO-Ab. Comparison between Group 1 and Group 2 showed that type 2 diabetes, hypercholesterolemia, and hypertension were significantly more frequent in Group 1 than in Group 2 (P<0.01). Moreover, the proportion of obese patients was 45.6% (88/193) in Group 1 and 22.3% (43/193) in Group 2 (χ²=23.3992; P<0.0001). In addition, comparison of BMI in the two groups showed mean BMI values of 31.10±0.62 in Group 1 and of 28.62±0.65 in Group 2 (P<0.001). To evaluate the relationship between obesity and the need of L-thyroxine therapy (started when TSH≥4 μU/ml), a multiple regression logistic model, with stepwise selection, was applied. The need of L-thyroxine therapy was significantly associated with obesity (P<0.001), as well as with the family history of obesity (P<0.0001) and of type 2 diabetes (P=0.0016). Our study indicates that obesity and related metabolic abnormalities are associated with evolution of thyroid autoimmunity towards hypothyroidism and need of L-thyroxine therapy. This link may be potentially due to i) reduced thyroid hormones favouring fat mass accumulation, and/or ii) Th1 cytokines (e.g. TNFα, IL-1β, IFNγ), that are increased in obesity, promoting thyroid cell destruction and metabolic abnormalities.