In the fact of high prevalence of Euthyroid Sick Syndrome (ESS), there was detected in Non-Thyroidal Illness (NTI) 
including Chronic Renal Insufficiency (CRI) may be linked to IL-6 and IL-10 alterations. This alterations might be involved in ESS pathogenesis even it is not the only key player, according to an article in the January 2008 issue of the BioMed Central journal.
According to the article, the aim of the research was because of the possible role of cytokines including interleukins (IL) in systemic non-thyroidal illnesses’ (NTI) pathogenesis and consequently the frequently associated alterations in thyroid hormone (TH) concentrations constituting the euthyroid sick syndrome (ESS), the researcher want to elucidate the possible relation between IL-6 & IL-10 and any documented ESS in a cohort of patients with NTI.
The researchers recruited sixty patients and twenty healthy volunteers that subdivided into three subgroups depending on their underlying NTI then included 20 patients with CRI, Congestive Heart Failure (CHF), and ICU patients with myocardial infarction (MI). Total T4 and T3 was carried out as well as the circulating serum levels of IL-6 and IL-10, thyroid stimulating hormone (TSH).
Hamdy A Abo-Zenah and colleagues from Departments Of Internal Medicine, Faculty Of Medicine, Menufiya University, Egypt; Molecular Diagnostic Department, Genetic Engineering and Biotechnology Research Institute, Menufiya University, Egypt; Mansura Urology and Nephrology Institute, Mansura University, Egypt have carried out this cross-sectional observational study to link thyroid function and the cytokines; IL-6 as well as IL-10 in a group of patients with ESS associated with variable NTI including chronic renal insufficiency (CRI).
After result, they discussed that an acute disturbance of IL-6 and or IL-10 may be involved in development of ESS which were supported by few retrospective study. Then concluded :
euthyroid sick syndrome occurs in many patients with a wide range of non-thyroidal illnesses in association with an appreciable perturbation in IL-6 as well as IL-10 and that its pathogenesis might be regulated by IL-6 with possible involvement of some other, yet unrecognized, key players in some specific forms of NTI as chronic renal insufficiency.
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