Carlo Cappelli, Mario Rotondi, Ilenia Pirola, Barbara Agosti, Annamaria Formenti, Emanuela Zarra, Umberto Valentini, Paola Leporati, Luca Chiovato and Maurizio Castellano
A retrospective study to evaluate the changes in TSH concentrations in diabetic patients treated or not treated with metformin and/or l-thyroxine (l-T4).
Three hundred and ninety three euthyroid diabetic patients were divided into three groups on the basis of metformin and/or l-T4 treatment: Group (M−/L−), 119 subjects never treated with metformin and l-T4; Group (M+/L−), 203 subjects who started metformin treatment at recruitment; and Group (M+/L+), 71 patients on l-T4 who started metformin recruitment.
The effect of metformin on serum TSH concentrations was analyzed in relation to the basal value of TSH (below 2.5 mIU/l (Q1) or between 2.51 and 4.5 mIU/l (Q2)). In patients of group M+/L+, TSH significantly decreased independently from the basal level (Q1, from 1.45±0.53 to 1.01±1.12 mU/l (P=0.037); Q2, from 3.60±0.53 to 1.91±0.89 mU/l (P<0.0001)). In M+/L− group, the decrease in TSH was significant only in those patients with a basal high-normal serum TSH (Q2: from 3.24±0.51 to 2.27±1.28 mU/l (P=0.004)); in M−/L− patients, no significant changes in TSH levels were observed.
In patients of group M+/L− showing high-normal basal TSH levels, a significant decrease in TSH was observed independently from the presence or absence of thyroid peroxidase antibodies (AbTPO; Q2 AbTPO +: from 3.38±0.48 to 1.87±1.08 mU/l (P<0.001); Q2 AbTPO −: from 3.21±0.52 to 2.34±1.31 mU/l (P<0.001)).
These data strengthen the known TSH-lowering effect of metformin in diabetic patients on l-T4 treatment and shows a significant reduction of TSH also in euthyroid patients with higher baseline TSH levels independently from the presence of AbTPO.
Roberta Ricotti, Arianna Solito, Elena Mariotti Zani, Marina Caputo, Giulia Genoni, Francesco Barone-Adesi, Valentina Mancioppi, Emanuela Agosti, Gianluca Aimaretti, Simonetta Bellone and Flavia Prodam
Data on metabolic impairments in Cushing’s syndrome and GH deficiency all suggest that the relationship between cortisol and GH/IGF-I axis in obesity may have a role in the related diseases. However, studies focusing only on one of these hormones are often controversial in paediatrics. We aimed to explore the simultaneous relationship between cortisol and IGF-I with the metabolic alterations in paediatric obesity.
Retrospective cross-sectional study in a tertiary care center. We recruited 876 (441 males and 435 females) overweight and obese children and adolescents. A complete clinical and biochemical evaluation including OGTT was performed. Cortisol and IGF-I SDS were divided in quartiles and then crossed to explore the reciprocal influence of high/high, low/low, and high/low levels of each one on the metabolic alterations of obesity.
Subjects in the higher quartiles of IGF-I-SDS and cortisol had an increased risk of hypertension, hypercholesterolemia, high levels of triglycerides, and reduced HDL cholesterol. Diversely, lower IGF-I-SDS quartiles were associated with higher blood glucose, insulin, insulin resistance, and reduced insulin sensitivity levels with the rise of cortisol quartiles.
We observed that apart from glucose metabolism that is associated with low IGF-I and high cortisol levels, the other parameters known to be associated with increased cardiovascular risk were related to high levels of both IGF-I and cortisol, even if within normal range. Cortisol and IGF-I play a complex role in the comorbidities of obesity, and the evaluation of both variables could clarify some of the discordant results.