Σφακιανάκης Αλέξανδρος
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5 Άγιος Νικόλαος
Κρήτη 72100
00302841026182
00306932607174
alsfakia@gmail.com

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! # Ola via Alexandros G.Sfakianakis on Inoreader

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Πέμπτη 7 Φεβρουαρίου 2019

Serum polyamine metabolic profile in autoimmune thyroid disease (AITD) patients

Summary

Objective

Polyamines are indispensable polycations and play important physiological roles in living cells. Some polyamine metabolites have been associated with autoimmune disorders. The aims of this study were to profile polyamine metabolites in autoimmune thyroid disease (AITD) and predict whether polyamine metabolites are associated with thyroid hormone, thyroid autoantibodies or disease progression.

Design, patients and measurements

A total of 136 participants were recruited, including Graves' disease (GD) (n=36), Hashimoto's thyroiditis (HT) (n=33) and thyroid autoantibody‐positive (pTAb) (n=29) patients and 38 age‐ and sex‐matched healthy controls (HCs). Fourteen polyamine metabolites, including polyamine precursors, polyamines and polyamine catabolite, were measured by UFLC‐MS/MS.

Results

Both GD and HT patients had higher L‐arginine, L‐ornithine, lysine and agmatine levels and lower putrescine, 1,3‐diaminopropane, spermine, N‐acetylputrescine levels than HCs. Some polyamine metabolite levels were different only in GD or HT patients compared to HCs: GD patients had significantly higher spermidine, N‐acetylspermidine and γ‐aminobutyric acid and lower cadaverine, whereas HT patients had significantly decreased N‐acetylspermine. Only spermine and N‐acetylspermine were significantly lower in pTAb than HCs. The spermine:spermidine ratio was significantly reduced in all AITD patients. In addition, spermine was negatively correlated with thyroid‐specific antibodies grade. N‐acetylspermidine might be a risk factor for pTAb progression to overt hypothyroidism.

Conclusions

Compared with the HCs, most metabolites of GD and HT showed similar patterns, suggesting the possibility of a common pathophysiological basis or metabolic pathway. Moreover, pTAb progression to overt hypothyroidism may be related to high N‐acetylspermidine. Thyroid autoimmunity was associated with low spermine.

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