Abstract
Acute pancreatitis (AP) manifests itself either as a mild, self-limiting inflammation or a severe, systemic inflammatory process that is associated with various complications and a high mortality rate. It is unknown whether these two forms of the disease can differ in the profile of circulating glycosaminoglycans, which are molecules with huge biological reactivity due to a high density of negative electric charge. Plasma glycosaminoglycans were characterized/quantified in 23 healthy controls, 32 patients with mild AP, and 15 individuals with severe disease using electrophoresis with enzymatic identification (chondroitin sulfate and heparan sulfate) or an ELISA-based test (hyaluronan). Moreover, the correlations between the glycosaminoglycan levels and clinical parameters were evaluated. Both forms of AP showed similar remodeling of the plasma profile of the sulfated glycosaminoglycans. In contrast, only in the patients with mild AP was the level of circulating hyaluronan significantly decreased as compared to the healthy controls. Both forms of AP are associated with systemic changes in the metabolism of glycosaminoglycans. However, the alterations in hyaluronan metabolism may contribute to the disease evolution. The circulating hyaluronan may have some clinical value to predict the severity of AP and to evaluate the clinical status of patients with severe AP.
Highlights
Acute pancreatitis (AP) is the most common inflammatory disease that affects the exocrine part of the pancreas
The detailed mechanisms that are responsible for the distinct clinical manifestation of AP remain unknown, it is believed that a key event in the pathogenesis of severe AP is the occurrence of a persistent systemic inflammatory response syndrome (SIRS), which is subsequently followed by a compensatory anti-inflammatory response syndrome [8]
The analysis revealed that the total plasma concentrations of the hexuronate-containing GAGs in both the patients with mild and severe AP were more than doubled compared to the levels of these macromolecules in the healthy controls (Figure 2)
Summary
Acute pancreatitis (AP) is the most common inflammatory disease that affects the exocrine part of the pancreas. AP is a self-limiting mild inflammatory disease in the majority of patients. Some patients develop a severe form of the disease, which is characterized by the occurrence of a variety of both early and late complications such as (multi)organ failure, pancreatic necrosis, pancreatic fluid collections, and/or sepsis [6,7]. Because of these complications, especially infected pancreatic necrosis and sepsis, severe AP is associated with a high mortality rate [7]. The detailed mechanisms that are responsible for the distinct clinical manifestation of AP remain unknown, it is believed that a key event in the pathogenesis of severe AP is the occurrence of a persistent systemic inflammatory response syndrome (SIRS), which is subsequently followed by a compensatory anti-inflammatory response syndrome [8]
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