Endocrine Abstracts

Background: Overt and subclinical hypothyroidisms are associated with altered cerebral blood flow (CBF) which may be reversed with levothyroxine treatment (T4T). Subclinical hypothyroidism (SCH) is associated with fatigue but it is unclear whether fatigue is related to abnormal CBF and whether T4T has a beneficial impact. We therefore studied fatigued SCH patients before and after T4T and euthyroid non-fatigued healthy controls (HC).

Methods: CBF was measured by arterial spin labelling magnetic resonance imaging on a 3T scanner in 20 SCH subjects (age 40.2±12.1, serum thyroid stimulating hormone (TSH) between 4-10 mIU/l and normal serum free thyroxine) at baseline and after 6 months of T4T 1.6 μg/kg per day (n=17 due to dropouts), as well as in 20 age and gender matched HCs. Fatigue was measured by fatigue index score (FIS).

Results: In HC, SCH at baseline and post treatment, the TSH (mean±S.D.) was 2.1±0.9, 6.7±1.8 and 1.9±1.0 mIU/l respectively; FIS was 4.3±5.0, 76.6±23.7 and 34.2±35.7 respectively; and the whole grey matter CBF was 46.9±5.8, 48.8±6.9 and 46.7±8.5 ml/100 g per min respectively. CBF in SCH was non-significantly higher than in HC (P=0.3), and showed a significant decrease after T4T (P=0.013). FIS in SCH was significantly higher than in HC (P<0.001), and showed a significant decrease after T4T (P<0.001). At baseline FIS were not correlated with CBF in SCH.

Conclusions: We found in SCH a non-significant increase in CBF, which was significantly reduced by T4T to the level seen in HC. This suggests that increased CBF was secondary to SCH state. We postulate that slight increase in CBF in SCH may be an over-compensatory response to tissue hypothyroidism. Normalisation of increased blood flow velocities in overt hypothyroidism was found by one group before. The observed fatigue was not associated with CBF in SCH, suggesting that CBF is not a marker of fatigue in SCH.

Declaration of funding: Charity foundation ref no. 22094167.