Didem Aliefendioglu1, Tuğba Gürsoy2, Osman Çağlayan3, Alev Aktaş2, Fahri Ovalı2. 1. Pediatrics and Biochemistry Department, Kırıkkale University Medical Faculty, Kırıkkale, Turkey. Electronic address: didem.aliefendioglu@gmail.com. 2. Zeynep Kamil Maternity and Children's Education and Training Hospital, NICU, Istanbul, Turkey. 3. Pediatrics and Biochemistry Department, Kırıkkale University Medical Faculty, Kırıkkale, Turkey.
Abstract
BACKGROUND: Sepsis is an important cause of neonatal death and perinatal brain damage, particularly in preterm infants. It is thought that activation of the inflammatory cascade triggered by cytokine might play a role in the pathogenesis of sepsis. Recent evidence supports a role for resistin in inflammation. There are no data in the literature on resistin levels of premature newborns with sepsis, which can also cause inflammatory response. The objective of this study was to evaluate whether resistin can be used as an indicator in neonatal sepsis of preterm babies. MATERIALS AND METHODS: Forty-three premature newborns considered to have sepsis were included in the study. Forty-three gestational and postnatal age- and sex-matched premature newborns without premature prolonged rupture of membrane or sepsis served as controls. RESULTS: The median resistin and interleukin-6 (IL-6) levels of the premature babies with sepsis were 85.9 ng/mL and 342.7 pg/mL, respectively, and were higher than those of the control group (29.9 ng/mL and 17.7 pg/mL, respectively). The sensitivity, specificity, positive, and negative predictive values for resistin were 73.7%, 45.8%, 68.3%, and 52.4%, respectively. CONCLUSION: Resistin levels were higher in premature newborns with sepsis and correlated with IL-6 levels, which is an indicator of neonatal sepsis. This suggests that resistin may also be used in the diagnosis of neonatal sepsis. However, it has limited value when compared with the other inflammatory markers including C-reactive protein, procalcitonin, and IL-6.
BACKGROUND:Sepsis is an important cause of neonatal death and perinatal brain damage, particularly in preterm infants. It is thought that activation of the inflammatory cascade triggered by cytokine might play a role in the pathogenesis of sepsis. Recent evidence supports a role for resistin in inflammation. There are no data in the literature on resistin levels of premature newborns with sepsis, which can also cause inflammatory response. The objective of this study was to evaluate whether resistin can be used as an indicator in neonatal sepsis of preterm babies. MATERIALS AND METHODS: Forty-three premature newborns considered to have sepsis were included in the study. Forty-three gestational and postnatal age- and sex-matched premature newborns without premature prolonged rupture of membrane or sepsis served as controls. RESULTS: The median resistin and interleukin-6 (IL-6) levels of the premature babies with sepsis were 85.9 ng/mL and 342.7 pg/mL, respectively, and were higher than those of the control group (29.9 ng/mL and 17.7 pg/mL, respectively). The sensitivity, specificity, positive, and negative predictive values for resistin were 73.7%, 45.8%, 68.3%, and 52.4%, respectively. CONCLUSION: Resistin levels were higher in premature newborns with sepsis and correlated with IL-6 levels, which is an indicator of neonatal sepsis. This suggests that resistin may also be used in the diagnosis of neonatal sepsis. However, it has limited value when compared with the other inflammatory markers including C-reactive protein, procalcitonin, and IL-6.
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