Soluble Triggering Receptor Expressed on Myeloid Cells in Severe Acute Pancreatitis (STREM-1)

The major cause of death, next to early organ failure, is secondary infection of pancreatic or peripancreatic necrotic tissue, leading to sepsis and multiple organ failure. The diagnosis and treatment of infected necrosis in SAP remain a major challenge for clinicians. The necrotic infection is defined when microorganisms are isolated from the samples of ultrasound or computed tomography (CT) guided fine needle aspiration (FNA). Unfortunately, a negative biopsy result can not completely rule out infection and the repeated aspirations may lead to bleeding or iatrogenic infection. Moreover, whatever the microbiologic diagnostic procedure chosen, further laboratory processing and delays of 24 to 48 hours are required for definitive quantitative microbial culture results. Meanwhile, clinicians often feel uncomfortable about the diagnosis and may administer unneeded antibiotics while awaiting laboratory results.

Secondary infection of necrotic tissue in SAP patients is virtually always an indication for intervention. The traditional approach is open necrosectomy to completely remove the infected necrotic tissue. This invasive approach is associated with high rates of complications (34 to 95%) and death (11 to 39%).As an alternative to open necrosectomy, less invasive techniques, including percutaneous drainage and endoscopic (transgastric) drainage, are increasingly being used.These steps may postpone or even obviate surgical necrosectomy with reducing complications and death.It remains uncertain which intervention is optimal in terms of clinical conditions of these patients and the severity of local infection.

Therefore, many biologic markers have been studied in an effort to improve the diagnostic rate and determine the the severity of necrosis infection but with disappointing results. The triggering receptor expressed on myeloid cells (TREM-1) is a member of the immunoglobulin superfamily whose expression on phagocytes is up-regulated by exposure to bacteria and fungi. TREM-1 mediates the acute inflammatory response to microbial products.[27] TREM-1 is also shed by the membrane of activated phagocytes and can be found in a soluble form in body fluids. We evaluated whether the lever of soluble TREM-1 (sTREM-1) in FNA fluid from patients who suspected infection is a good marker of secondary infection of necrotic tissue and an indicator of the proper treatment between drainage and necrosectomy.