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-alpha, 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.
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-alpha, 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 illpatients. Further exploration of resistin as a therapeutic target and marker of disease is merited.
Authors: Tonguç U Yilmaz; Mustafa Kerem; Canan Y Demirtaş; Ozge Pasaoǧlu; Oge Taşcilar; Omer Sakrak; Kürşat Dikmen; Tarkan Karahan Journal: Sultan Qaboos Univ Med J Date: 2014-10-14
Authors: Shali Mazaki-Tovi; Edi Vaisbuch; Roberto Romero; Juan Pedro Kusanovic; Tinnakorn Chaiworapongsa; Sun Kwon Kim; Giovanna Ogge; Bo Hyun Yoon; Zhong Dong; Juan M Gonzalez; Maria Teresa Gervasi; Sonia S Hassan Journal: Am J Reprod Immunol Date: 2010-02-18 Impact factor: 3.886
Authors: Andreas Hillenbrand; Uwe Knippschild; Manfred Weiss; Hubert Schrezenmeier; Doris Henne-Bruns; Markus Huber-Lang; Anna M Wolf Journal: BMC Surg Date: 2010-09-09 Impact factor: 2.102