Euthyroid sick syndrome (ESS) is commonly observed in various acute and chronic illness as risk factor for mortality in patients with severe diseases, with lower triiodothyronine (T3) and free triiodothyronine (fT3).To explore the relationship between disease severity and thyroid function in critically ill Chinese patients with ESS.A total of 51 patients admitted to intensive care unit were examined to determine acute physiology and chronic health assessment II (APACHE II) scores within 24 hours of admission; thyroid function tests (TSH, fT3, fT4, tT3, tT4) and rT3 levels were determined on the second day. Based on the test results, patients were divided into euthyroid (n = 13), decreased fT3 or fT4 (n = 17), and decreased TSH (n = 21) groups. APACHE II scores and thyroid function were compared between the 3 groups. Furthermore, the relationship between the severity of disease and euthyroid sick syndrome was assessed.Out of 51 patients, 38 were men and 13 were women [mean age (± SD): 60.39 (± 19.32) years; range, 15–88 years]. APACHE II scores and rT3 levels were increased in all the 3 groups (P > .05). APACHE II scores showed a positive correlation with rT3 (P = .004, r = 0.379).Critically ill Chinese patients with ESS have a poor health state. Higher rT3 values are associated with severe disease.

Background Sepsis is an organ dysfunction characterized by systemic inflammatory response. Micro(mi)ribonucleic acids take part in the regulation of the inflammatory response in many conditions. However, the role and mechanism of miR-106a and anoctamin 1 (ANO1) in the inflammatory response in sepsis remain largely unknown. Material/Methods The serum samples were collected from 31 sepsis patients and healthy volunteers. Lipopolysaccharide (LPS)-treated RAW264.7 cells were used for the study in vitro . The inflammatory response was investigated via interleukin-6 and tumor necrosis factor-alpha levels using quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay. The expression abundances of miR-106a and ANO1 were detected via qRT-PCR or western blot. The target association between miR-106a and ANO1 was explored using dual-luciferase reporter analysis. Results The inflammatory response was trigged in sepsis and LPS-treated RAW264.7 cells. miR-106a expression was enhanced and ANO1 declined in sepsis and LPS-treated RAW264.7 cells. Overexpression of ANO1 suppressed the inflammatory response and knockdown of ANO1 promoted the inflammatory response in RAW264.7 cells. ANO1 was directly targeted via miR-106a, and miR-106a reversed ANO1-mediated inflammatory inhibition in LPS-treated RAW264.7 cells. Conclusions MiR-106a regulated LPS-induced inflammatory response by targeting ANO1 in RAW264.7 cells, indicating the potential value of miR-106a for treatment of inflammatory diseases, including sepsis.