These results confirm that human thyrocytes secrete CXC chemokines and demonstrate that the secretion of CXCL8 and CXCL10 is sustained by specific proinflammatory cytokines or their combination, which ultimately determines the nature of the infiltrating lymphocytes in human thyroid diseases. These results indirectly support a major role for CXCL10 in thyroid autoimmunity whereas CXCL8 might be involved in tumor-related inflammation.

Introduction: Combination therapy with both basal insulin (BI) and glucagon-like peptide-1 receptor agonists (GLP-1RAs) is an effective treatment in patients with uncontrolled type 2 diabetes mellitus (T2DM). The recent development and release of a fixed-ratio combination of slow-release insulin degludec and the GLP-1RA liraglutide (IDegLira) represents an improvement to this therapy. We have conducted a real-world evidence study in Italian patients with T2DM to evaluate whether the encouraging clinical trial results obtained with IDegLira, which became available in Italy in January 2018, can be confirmed in Italian clinical practice. Methods: This was a multicenter, retrospective, observational study in patients with T2DM treated with IDegLira from January to December 2018. Prior to the initiation of IDegLira therapy, patients were treated with BI with or without one or more concomitant oral antidiabetic drugs (BOT group) or according to the basal bolus protocol (BI and rapid-acting insulin treatment; BB group).

Morbid obesity is associated with a high rate of raised serum TSH associated with normal free thyroid hormones. The body repercussions of this thyroid abnormality, suggesting subclinical hypothyroidism, are still debated. In particular, it is unclear whether the raised serum TSH of obesity results in changes of circulating lipids typically observed in hypothyroidism. Aim of this study was to evaluate the impact of a raised serum TSH on the lipid profile in morbid-obese and non-obese patients. Serum TSH, FT4, FT3, Tg-Ab, TPO-Ab and lipids were measured in 55 morbid-obese (BMI > 40 kg/m(2)) and 55 non-obese (BMI < 30 kg/m(2)) patients with a raised serum TSH. Despite similar serum levels of TSH, FT4 and FT3, morbid-obese patients displayed significantly lower mean levels of total cholesterol (200.8 ± 35.6 vs. 226.9 ± 41.4 mg/dl, p < 0.001) and a significantly lower prevalence of hypercholesterolemia (50.9 vs. 72.7 %, p < 0.01) when compared with non-obese patients. Morbid-obese patients also had lower mean serum HDL cholesterol and higher serum triglycerides. The impact of a raised serum TSH on the lipid profile differs in morbid-obese compared to non-obese patients, suggesting that obese patients might not be truly hypothyroid. Measuring total cholesterol could be a helpful tool for deciding whether a morbid-obese patient with a raised serum TSH should be given levothyroxine treatment.

Basedow's disease (BD) owes its name to the German physician Karl Adolph von Basedow, who described in 1840 the clinical picture of exophthalmic toxic goitre. More than one century after the seminal paper of Karl von Basedow, the ultimate cause of BD remains to be fully elucidated. In the last years, evidence was accumulated indicating that BD is a polygenic and multifactorial disease that develops as a result of a complex interplay between genetic susceptibility and environmental and endogenous factors, which leads to the loss of immune tolerance to thyroid antigens and in particular to the TSH receptor. Our aim is to review the current knowledge on the pathogenesis of BD. To this purpose, we will firstly focus our attention on the role of genetic factors (the HLA complex, the genes encoding for thyroglobulin, the TSH receptor, CD40, CTLA-4 and PTPN22), and of environmental factors (iodine, infections, psychological stress, gender, smoking, thyroid damage, vitamin D, selenium, immune modulating agents) as possible causes of BD. Taking advantage of the experimental animal models of BD, we will then focus on the immunological mechanisms leading to the loss of tolerance in BD. The pathogenic role played by the chemokine system will be also reviewed.