scholarly journals Polymorphonuclear leukocyte dysregulation during the systemic inflammatory response syndrome

Blood ◽  
1994 ◽  
Vol 83 (5) ◽  
pp. 1398-1407 ◽  
Author(s):  
HH Simms ◽  
R D'Amico

Altered polymorphonuclear leukocyte (PMN) function is thought to contribute to organ dysfunction during the systemic inflammatory response syndrome (SIRS). To test this hypothesis, we evaluated whole blood PMN function adherent to fibronectin or laminin in patients with mild or severe acute pancreatitis as a paradigm for sirs. Whole-blood PMN intracellular H2O2 production, expression of CD32w (Fc gamma R II), CD16 (Fc gamma R III), and phagocytosis were performed using dichlorofluorescein diacetate, fluorescein isothiocyanate-labeled anti- CD32w, CD16, and serum-opsonized fluorescent microspheres. Group I (n x 7) represents normal control individuals; group II (n x 11) represents patients with mild acute pancreatitis. Group III (n x 15) represents critically ill patients with severe acute pancreatitis. Adherence of PMN from groups I and II to matrix proteins resulted in a 5% to 20% increase in each PMN function assayed whereas adherence of PMN from group III to matrix proteins resulted in 50% to 75% increases in each PMN function assayed. Pertussis toxin, pentoxifylline, and dibutyryl cyclic adenosine monophosphate (cAMP) each reduced group I-II H2O2 production and phagocytosis. Pentoxifylline and dibutyryl cAMP but not pertussis toxin reduced group III H2O2 production. Both intracellular H2O2 and phagocytosis assays from group III but not groups I-II showed exaggerated upregulation when exposed to NaF (4 mmol/L). Anti- interleukin-6 reduced the increase in intracellular H2O2 production in group III patients and significantly altered the exaggerated oxidative response to NaF. Longitudinal studies of group III whole-blood PMN showed persistent upregulation of intracellular H2O2 production in those patients whose hospital courses were complicated by multiple system organ failure. These results demonstrate abnormal whole blood PMN function during the systemic inflammatory response syndrome in the presence of fibronectin, or laminin and that this is mediated in part via a pertussis toxin insensitive altered guanosine triphosphate- binding protein.

Blood ◽  
1994 ◽  
Vol 83 (5) ◽  
pp. 1398-1407 ◽  
Author(s):  
HH Simms ◽  
R D'Amico

Abstract Altered polymorphonuclear leukocyte (PMN) function is thought to contribute to organ dysfunction during the systemic inflammatory response syndrome (SIRS). To test this hypothesis, we evaluated whole blood PMN function adherent to fibronectin or laminin in patients with mild or severe acute pancreatitis as a paradigm for sirs. Whole-blood PMN intracellular H2O2 production, expression of CD32w (Fc gamma R II), CD16 (Fc gamma R III), and phagocytosis were performed using dichlorofluorescein diacetate, fluorescein isothiocyanate-labeled anti- CD32w, CD16, and serum-opsonized fluorescent microspheres. Group I (n x 7) represents normal control individuals; group II (n x 11) represents patients with mild acute pancreatitis. Group III (n x 15) represents critically ill patients with severe acute pancreatitis. Adherence of PMN from groups I and II to matrix proteins resulted in a 5% to 20% increase in each PMN function assayed whereas adherence of PMN from group III to matrix proteins resulted in 50% to 75% increases in each PMN function assayed. Pertussis toxin, pentoxifylline, and dibutyryl cyclic adenosine monophosphate (cAMP) each reduced group I-II H2O2 production and phagocytosis. Pentoxifylline and dibutyryl cAMP but not pertussis toxin reduced group III H2O2 production. Both intracellular H2O2 and phagocytosis assays from group III but not groups I-II showed exaggerated upregulation when exposed to NaF (4 mmol/L). Anti- interleukin-6 reduced the increase in intracellular H2O2 production in group III patients and significantly altered the exaggerated oxidative response to NaF. Longitudinal studies of group III whole-blood PMN showed persistent upregulation of intracellular H2O2 production in those patients whose hospital courses were complicated by multiple system organ failure. These results demonstrate abnormal whole blood PMN function during the systemic inflammatory response syndrome in the presence of fibronectin, or laminin and that this is mediated in part via a pertussis toxin insensitive altered guanosine triphosphate- binding protein.


2018 ◽  
Vol 25 (2) ◽  
Author(s):  
Natalya Maksymchuk ◽  
Viktor Konovchuk

The preparations of polyhydric alcohols, namely sorbitol-based ones, and their combination with adjuvant therapy, namely L-arginine are sufficiently promising for treatment of purulent-septic complications. The systemic nature of their action makes it appropriate to carry out studies of specific effect on the circulatory system, since their wide homeostatic and pharmacodynamic spectrum is beyond doubt for other systems and organs within the “efficiency-safety” algorithm.The objective of the research was to study the effect of combined use of sorbilact and L-arginine on the cardiovascular system of patients with endogenous intoxication syndrome during the period of developing early secondary autoaggression.Materials and methods. The study included 117 patients who were divided into the following groups: Group I consisted of 31 patients with systemic inflammatory response syndrome; Group II included 27 patients with endogenous intoxication syndrome treated according to 2016 Surviving Sepsis Campaign; Group ІІI comprised 29 patients with endogenous intoxication syndrome who received sorbilact in addition to standard therapy; Group IV included 30 patients with systemic inflammatory response syndrome who received standard therapy as well as sorbilact and L-arginine.Results. Co-administration of sorbilact and L-arginine was accompanied by an increase in stroke volume and cardiac output, activation of left ventricular minute work alongside with a moderate decrease in mean arterial pressure and systemic vascular resistance.Conclusions. The application of sorbilact and L-arginine in patients with endogenous intoxication syndrome provides hemodynamic stability.


2019 ◽  
Vol 8 (2) ◽  
pp. 92-95
Author(s):  
Uttam Laudari ◽  
Abishek Thapa ◽  
Tanka Prasad Bohara ◽  
Shail Rupakheti ◽  
Mukund Raj Joshi

Background: Clinically, the Systemic Inflammatory Response Syndrome (SIRS) is identified by two or more symptoms including fever or hypothermia, tachycardia, tachypnea and change in blood leukocyte count. The relationship between SIRS symptoms at the time of presentation and severity of pancreatitis is yet to be determined though progression of SIRS in subsequent days has already been correlated.Objectives: To determine the severity of pancreatitis with SIRS score at the time of admission.Methodology: A retrospective cohort study of patients admitted to Department of Surgery, Kathmandu Medical College Teaching Hospital (KMCTH) with diagnosis of Acute Pancreatitis (AP) from December 2014 to January 2016 was conducted. Clinical, biochemical and imaging data were collected from the medical record section. Patients with diagnosis of acute pancreatitis as per Revised Atlanta Classification 2012 were included in the study. SIRS score at time of admission was correlated with Modified Marshall scoring system for organ dysfunction. Patients were grouped into severe and nonsevere group. Sensitivity, specificity and predictive values of SIRS score at admission for organ failure were calculated.Results: Among the 41 patients admitted with diagnosis of acute pancreatitis irrespective of cause, the sensitivity of SIRS score ≥2 at admission in predicting severe pancreatitis was 60 %, specificity was 20%, positive predictive value was 28% and negative predictive value was 20 %, with p-value of 0.52 and odds ratio of 1.6 (CI: 0.376-6.808).Conclusion: SIRS score at admission cannot be solely used in predicting acute severe pancreatitis. Patients can be stratified in resource deficit setting for timely referral to tertiary centre.


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