Résumé
The whole mark of the pathogenesis of the nonthyroidal illness [NTI] syndrome is a decreased activity of hepatic type I 5'-deiodinase resulting in decreased transformation of T4 to T3 and increased rT3 and T4/T3 ratio. Much interest is centered on the role of cytokines in the etiology of the NTI syndrome. In this work we assessed the relation between serum thyroid hormone changes in the NTI and activation of the cytokine network as reflected by the serum levels of IL-6 and soluble TNF alpha R proteins [sTNF alpha Rp[55] and sTNF alpha Rp[75]]. Forty patients of NTI with low serum T3 [<1.3 nmol/l] and high T4/T3 ratio [>56/1] and 18 normal controls were included in this study. The patients were divided into two groups according to the serum levels of T4 as follows: Group I: Included 24 patients with subnormal T3 [<1.3 nmol/l] and normal T4 [>75 nmoI/I] levels. Group U: Included 16 patients with subnormal T3 [<1.3 nmoI/I] and T4 [<75 nmol/l] serum levels. Serum T3, T4 and TSH were determined by radioimmunoassay, and FT3 was estimated by ultrafiltration. IL-6, sTNF alpha Rp[55] and sTNF alpha Rp[75] were determined by enzyme linked immunoassays. Significant decrease in T3, FT3, T4 and TSH serum levels and increase in T4/T3 ratio, IL-6, sTNF alpha Rp[55] and sTNF alpha Rp[75] in each of the 2 patient groups as compared to controls and in Group U as compared to Group I were obtained. Taking all patients together, T3 and FT3 were highly correlated with each other and were negatively correlated with IL-6 and sTNF alpha R proteins. A strong relation was observed between serum IL-6, sTNF alpha Rp[55] and sTNF alpha Rp[75]. IL-6 and sTNF alpha R proteins, the anti-inflammatory cytokines might be determinants of the horrn that occur in SES as a useful mechanism to counteract excessive catabolism, minimize protein wasting and save energy expenditure during illness, however, in patients who manifest low T4, a maladaptation that aggravates the underlying illness might warrant T3 supplementation, glucose-insulin potassium/T3, and other recently administered modalities of therapy