Trial Information

Soluble Triggering Receptor Expressed on Myeloid Cells in Severe Acute Pancreatitis: a Marker of Infected Necrosis and Indicator of Treatment

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.