Endocrine Abstracts

The aim of this study was to assess thyroid homeostasis in patients with liver cirrhosis (LC) of non-viral etiology and analyze the association between serum thyroid parameters and A/C polymorphism in the deiodinase type 1 (DIO1) gene in these patients.

Material and Methods: The study was conducted on 70 subjects: 50 patients with (LC) and 20 healthy controls. The thyroid homeostasis was evaluated by using «thyroid function tests», measurement of serum free thyroxine (fT₄), free triiodothyronine (fT₃) and thyroid stimulating hormone (TSH). A/C polymorphysm in the DIO1 gene was studied using a polymerase chain reaction.

Results: The level of fT₃ was reduced by 12.1% (P <0.01) in patients with (LC), fT₄ level was increased by 15.1% (P < 0.01) in group of patients with (LC) compared to healthy controls. These changes, obviously, are the result of a decrease in the activity of DIO1 and inhibition of T₄ to T3 transformation. The theory might be confirmed by significantly reduced fT₃/fT₄ ratio (by 21.6%, P < 0.001), that decreased below the reference range in 78% patients with (LC). At the same time, fT₄/fT₃ ratio increased by 24.1% (P < 0.001) compared to healthy controls, that can be attributed to the non-thyroidal illness syndrome in these patients. Elevation of TSH level by 28.7% and TSH/fT₃ ratio by 45.7% were determined in patients with (LC) compared to healthy controls (P < 0.05). The study did not reveal an association between the genotypes of DIO1 gene and the level of TSH in serum. However, it has been established that the presence of the C-allele was associated with elevation of fT₃ level and fT₃/fT₄ ratio, decreasing of fT₄/fT₃ ratio and fT₄ level, while the presence of A-allele resulted in a decrease in fT₃/fT₄ ratio and serum fT₃ with the increase in T₄ level in patients with chronic hepatitis.

Conclusions: Liver cirrhosis is accompanied by the development of non-thyroidal illness syndrome with a reduction in free triiodothyronine level (by 12.1%, P < 0.01), an increase in free thyroxine and thyroid stimulating hormone levels (by 15.1%, P < 0.01 and 28.7%, P < 0.05 respectively), a decrease in fT₃/fT₄ peripheral conversion rate (by 21.6%, P < 0.001). Pathological changes in thyroid metabolism are associated with A/C polymorphism in the DIO1 gene.