الفهرس 
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Abstract
Sepsis and septic shock are life threatening medical emergencies and they were redefined many times according to medical updates. The latest definition stated that sepsis is due to a dysregulated host response to infection resulting in organ dysfunction, while septic shock was defined as sepsis accompanied by cellular and metabolic dysfunction. Inflammatory and coagulation processes occur in sepsis and the innate immune system of the host and the infectious pathogen interact to produce the underlying pathology. Both host and pathogen features influence how strong the response will be. An excessively proinflammatory state occurs first as a systemic inflammatory response syndrome (SIRS), followed by a compensatory anti-inflammatory response syndrome (CARS) as the excessively anti-inflammatory condition. SIRS can be detected by measuring white blood cells count and vital signs like temperature, heart rate and respiratory rate. SIRS results in death from organ dysfunction, whereas CARS’s immunosuppression results in death from secondary infections so the excessive uncontrolled immunological reaction causes this harm and multiple organ dysfunctions may occur. Treatment requires immediate diagnosis and aggressive management, so it is important to be quickly identified to prevent complications. According to Sepsis 3 task force, organ dysfunction is diagnosed by having a change in the sequential organ failure assessment score (SOFA) of ≥2 points and it is obvious that microbiological culture is needed for detecting the infection and for proper treatment. The task force also stated that lactate level must exceed 18 mg/dl for septic shock diagnosis despite adequate fluid resuscitation. The most commonly used markers for sepsis detection are C reactive protein (CRP), procalcitonin (PCT) and lactate, reflecting inflammation and hypoperfusion. Hence, there is not one single specific marker for sepsis & septic shock diagnosis. However, these markers are expensive and they may not be accurate as predictors for severity or mortality rate. In addition to the markers and the culture, severity scores and organ dysfunction scores like the acute physiology and chronic health evaluation II (APACHE II) and Sequential organ failure assessment (SOFA) scores, respectively, are assistant guides for detecting patient severity degree and prognosis. There is a crucial need for alternatives to PCT and CRP aiming to be cost effective and more reliable in predicting sepsis severity and mortality rates. This led researchers to investigate many markers for their role in sepsis including the soluble receptors of surface markers like the soluble urokinase type plasminogen activator receptor (suPAR) & the soluble triggering receptor expressed on myeloid cells 1 (sTREM 1) and this was the concern of the present study in order to detect if suPAR and sTREM 1 could aid in the early detection of sepsis or in prognosis.
suPAR is the soluble form of uPAR which is expressed by the immune cells like neutrophils and macrophages. Its expression increases in response to inflammatory insults, reflecting its increase in sepsis and septic shock in a way referring to immune system activation. This induction may have its impact on the prognosis of the cases; thus, it could be used for sepsis diagnosis and prognosis.
sTREM 1 is known as the soluble form of TREM 1 which is expressed on myeloid cells. It can be found in many inflammatory conditions such as COPD, rheumatoid arthritis, sepsis and septic shock so it is not a specific marker for sepsis. It acts as a decoy receptor to weaken the inflammatory reaction. Hence, sTREM 1 increase may reflect sepsis detection and mortality rate.
This study included three main groups as the SIRS, sepsis and control groups, the sepsis group included sepsis and septic shock cases. Each of which was tested equally for vital signs, CBC, coagulation parameters, lactate, CRP, suPAR, sTREM 1 and other routine markers. Sepsis and septic shock patients were also sorted as survivors or non survivors.
suPAR and sTREM 1 were assayed using ELISA kits. Statistical analysis was done for all markers included in the study for each group to detect their significance. In addition, ROC curves were made to investigate the diagnostic performance of the markers.
CRP, PCT and suPAR were significantly higher in the sepsis and septic shock groups than the control group while lactate was significantly higher in the septic shock group than the control group. PCT and suPAR were significantly higher in the sepsis group than the SIRS group. Lactate was the only significant marker among sepsis and septic shock groups in this study. sTREM 1 was not significant between any of the control, SIRS, sepsis and septic shock groups.
Regarding mortality prediction, only severity scores; APACHE II and SOFA were able to distinguish between survivors and non survivors.
ROC curves for distinguishing between sepsis and control groups showed significant diagnostic performance for CRP, PCT, lactate and suPAR, while those for discriminating sepsis from SIRS revealed that SOFA score, PCT, APACHE II score and suPAR were significant.
As regards the discrimination between sepsis and septic shock groups, the only significant diagnostic variables were lactate and SOFA score.
ROC curves for mortality prediction revealed that only APACHE II score followed by SOFA score had significant diagnostic performance.