Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2009) 20 P141

ECE2009 Poster Presentations Thyroid (117 abstracts)

Thyrotropin suppression by metformin in a cohort of patients with differentiated thyroid cancer in follow-up

Roberto Citarrella , Luciana Puleo , Francesco Chiofalo , Lucia Smeraldi , Miriam Nucera & Pierina Richiusa


Endocrinology Section of Universitary Policlinic, Palermo, Italy.


Background: It has been reported that metformin might modify thyroid hormone economy. This farmacological tool appears very useful in patients with differentiated thyroid cancer usually receiving high Levo-tiroxine (L-T4) doses to suppress thyrotropin (TSH). In those patients that after five years of follow-up showed no persistence of disease, it’s useful to abolish the iatrogenic hyperthyroid condition.

Objective: To evaluate metformin efficacy to suppress TSH.

Methods: From a population of patients with differentiated thyroid cancer in follow-up we selected a cohort of 30 long-standing subjects (mean age: 48.1±9.52; F/M: 24/6) in which oral glucose tolerance test documented an insulin-resistance syndrome. Patients were in L-T4 substitutive/suppressive therapy at the dose of 2.2–3 mcg/pro kg body weight. BMI, TSH, FT4 were measured at baseline, after two and four months. At baseline L-T4 therapy was reduced to 2 mcg/pro kg body weight, aimed to reduce subclinical hyperthyroidism, and after two months metformin 500 mg tid was introduced.

Results: At the study start patients showed undosable TSH (0.22±0.20); in this stage L-T4 therapy was reduced to 2 mcg/pro kg body weight. Two months after reduction of oral L-T4 therapy TSH levels were in the normal range (0.96±0.62) showing statistical difference from baseline (P=0.003). After four months TSH levels were suppressed (0.21±0.29) showing significant difference from the value obtained after two months of L-T4 reduction (P=0.03) but not from baseline (P=ns). There was no change in FT4.

Conclusions: Initiation of treatment with metformin caused suppression of TSH to subnormal levels without clinical symptoms of hyperthyroidism in any patients. No other potential causes of TSH suppression, including medication changes or interference in the TSH assay, could be identified. Thus, metformin administration is associated with a significant fall in TSH useful to avoid iatrogenic subclinical hyperthyroidism.

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