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Pronounced elevation of resistin correlates with severity of disease in severe sepsis and septic shock

2007; Lippincott Williams & Wilkins; Volume: 35; Issue: 6 Linguagem: Inglês

10.1097/01.ccm.0000266536.14736.03

1530-0293

Jonas Sundén‐Cullberg, Thomas Nyström, Martin L. Lee, G. E. Mullins, L. Tokics, Jan Andersson, Anna Norrby‐Teglund, Carl Johan Treutiger,

Inflammation biomarkers and pathways

Objective: Resistin induces insulin resistance in mice. In humans, recent data suggest that resistin functions as a proinflammatory cytokine. Here, we studied resistin up to 2 wks after admission in patients with septic shock and/or severe sepsis. Design: Two prospective studies of patients with sepsis and in vitro studies of resistin interaction with monocytes. Setting: Intensive care unit at Karolinska University Hospital and Center for Infectious Medicine, Karolinska Institute, Huddinge, Sweden. Patients: Twenty-nine patients with severe sepsis and 66 with septic shock. Interventions: None. Measurements and Main Results: Ninety-five patients were studied, 25 of whom died within 28 days. Resistin and cytokine levels and routine biochemistry were measured at three to six defined time points during the first 2 wks after admission and were correlated to other cytokines, glucose levels, body mass index, Acute Physiology and Chronic Health Evaluation II, and Sepsis-related Organ Failure Assessment scores. Serum resistin was significantly elevated compared with healthy controls (p < .000001) and correlated with severity of disease as measured by Acute Physiology and Chronic Health Evaluation II and Sepsis-related Organ Failure Assessment scores, with an increasingly strong degree of correlation over time. Median levels were four- to eight-fold higher than controls and remained high up to 2 wks after admission to the intensive care unit. Levels correlated with interleukin-6, interleukin-8, interleukin-10, tumor necrosis factor-α, creatinine, D-dimer, and lactate, but not with p-glucose or body mass index. In vitro, resistin was released from monocytes after stimulation with either lipopolysaccharide or high mobility group box 1 protein. Recombinant resistin itself up-regulated intercellular adhesion molecule-1 on monocytes. Conclusions: This is the first study assessing systemic levels of resistin in patients with septic shock/severe sepsis. We show that resistin is a marker of severity of disease and possibly a mediator of the prolonged inflammatory state seen in infected critically ill patients. Further exploration of resistin as a therapeutic target and marker of disease is merited.