Using of TLR2 and TLR4 as Biomarker of Sepsis Severity Detection

Our study has been aimed to find the relation between the expression of toll-like receptors 2, 4, level of TNF-α, IL-10 and soluble HLA-DR with the severity bacterial septic syndrome in Iraqi patients. The quantitative real-time PCR technique has been used for measure TLR2 and TLR4 gene expression in whole blood, and ELISA technique has been used for detection of cytokines TNF-α, IL-10 and soluble HLA-DR from 75 septic syndrome cases (nineteen of patients showed symptoms of systemic inflammatory response syndrome (SIRS); twenty-eight patients have sepsis, seventeen patients suffered from severe sepsis and eleven patients have septic shock) and 55 healthy controls (HC). TLR2 and TLR4 mRNA expression were higher significantly in the all patients (P< 0.05), TNF-α, IL-10 and sHLA-DR serum levels were significantly elevated in the serum of patients with septic syndrome compared with controls (P

Septic syndrome within internal medicine units: finally we have our records!

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Acute Hemolysis in the Emergency Department: Think aboutClostridium perfringens!

Clostridium perfringens(CP) gives several clinical settings, from an asymptomatic to a massive intravascular hemolysis. We report a case of fatal intravascular hemolysis due to CP septicemia having a hepatic supposed starting point in the emergency department. Like in many cases, the diagnosis was made when patient had already gone into shock and died. The CP septicemia often complicated the course of the digestive or genital pathologies. The alpha toxin can damage the structural integrity of the red cell membrane by means of a phospholipase activity. Nevertheless, a massive intravascular hemolysis arises only rarely in this septicemia, only from 7 to 15% of the cases. The emergency physician has to think about this complication in case of hemoglobinuria and/or signs of hemolysis associated with a septic syndrome. An immediate antibiotic treatment adapted as well as the symptomatic treatment of the spread intravascular coagulation could improve the survival of these patients.

Sepsis begins at the interface of pathogen and host

To the modern mind, the term ‘sepsis’ conjures up images of microbes. It is easy to forget that the word predates any understanding of the microbial origins of infectious disease. Derived from the Greek ‘sepsios’ (rotten), sepsis denotes decay: a phenomenon that humans once regarded as a mysterious though inevitable natural process. A living organism does not accept decay passively. Virtually all multicellular life forms are capable of resisting infection through the generation of a vigorous immune response. In mammals, the response is so stereotypic that it has come to define sepsis itself: it is often called the ‘septic syndrome’. Our current understanding of the innate immune system is deeply rooted in the study of sepsis. The chain of events linking infection to tissue injury and cardiovascular collapse is not obvious, and affirmation of the concept required three major discoveries. First, the septic syndrome was found to be caused by toxic products of microbes. Secondly, these toxic substances were found to be toxic because of their propensity to activate cells of the innate immune system, prompting cytokine production. Thirdly, the activating events initiated by microbial toxins were traced to members of an ancient family of defensive molecules, versions of which operate in virtually all multicellular life forms. In mammals, proteins of this family are now known as Toll-like receptors. They represent a point of direct contact, and first contact, between a pathogen and the host immune system.