Abstract:Acute and chronic alcoholic pancreatitis, but not biliary pancreatitis, may affect CDT levels. Pancreatitis does not invalidate the use of CDT as a marker of alcohol abuse. CDT can be a useful test for distinguishing alcoholic from non-alcoholic pancreatitis. Changes in CDT level indicate disturbances in transferrin glycosylation in the course of alcoholic pancreatic diseases.
“…Additionally, transferrin is a negative acute-phase protein, whose concentration decreases during inflammatory responses [ 4 ]. Previously, we reported the changed profile of carbohydrate-deficient transferrin (a sum of the asialo, monosialo and disialo isoforms of transferrin, CDT for short) in pancreatic diseases, including pancreatitis of different etiologies (alcoholic and biliary) [ 5 ] and in pancreatic cancers [ 6 ]. It has been also shown that transferrin sialylation can be a potential prognostic marker for the severity of acute pancreatitis [ 7 ].…”
Total transferrin concentration changes in acute-phase reactions. Additionally, the alteration of transferrin glycosylation in inflammations can occur. The aim of this study is to evaluate the effect of pancreatitis on the serum profile of transferrin isoforms. The tested groups consisted of 84 patients with acute pancreatitis and 42 patients with chronic hepatitis. Transferrin isoforms were analyzed by capillary electrophoresis on a MINICAP electrophoretic system (Sebia, France). There was a significant decrease in the concentration of pentasialotransferrin in both acute and chronic pancreatitis, and a significant increase in tetrasialotransferrin in the acute pancreatitis group when compared to the control group. There were no significant changes in transferrin isoforms between the acute and chronic pancreatitis groups, and between the edematous and necrotizing forms of the disease. Considering the etiology of acute pancreatitis, we noticed higher values of bile acids and γ-glutamyltransferase in acute pancreatitis of alcoholic etiology than that in pancreatitis of other etiologies. In conclusion, the alterations in transferrin isoform profile in acute and chronic pancreatitis are not organ specific. Because similar changes were observed in hepatitis, we can conclude that the serum profile of transferrin isoforms is involved in the pathogenesis of the disease.
“…Additionally, transferrin is a negative acute-phase protein, whose concentration decreases during inflammatory responses [ 4 ]. Previously, we reported the changed profile of carbohydrate-deficient transferrin (a sum of the asialo, monosialo and disialo isoforms of transferrin, CDT for short) in pancreatic diseases, including pancreatitis of different etiologies (alcoholic and biliary) [ 5 ] and in pancreatic cancers [ 6 ]. It has been also shown that transferrin sialylation can be a potential prognostic marker for the severity of acute pancreatitis [ 7 ].…”
Total transferrin concentration changes in acute-phase reactions. Additionally, the alteration of transferrin glycosylation in inflammations can occur. The aim of this study is to evaluate the effect of pancreatitis on the serum profile of transferrin isoforms. The tested groups consisted of 84 patients with acute pancreatitis and 42 patients with chronic hepatitis. Transferrin isoforms were analyzed by capillary electrophoresis on a MINICAP electrophoretic system (Sebia, France). There was a significant decrease in the concentration of pentasialotransferrin in both acute and chronic pancreatitis, and a significant increase in tetrasialotransferrin in the acute pancreatitis group when compared to the control group. There were no significant changes in transferrin isoforms between the acute and chronic pancreatitis groups, and between the edematous and necrotizing forms of the disease. Considering the etiology of acute pancreatitis, we noticed higher values of bile acids and γ-glutamyltransferase in acute pancreatitis of alcoholic etiology than that in pancreatitis of other etiologies. In conclusion, the alterations in transferrin isoform profile in acute and chronic pancreatitis are not organ specific. Because similar changes were observed in hepatitis, we can conclude that the serum profile of transferrin isoforms is involved in the pathogenesis of the disease.
Acute pancreatitis (AP) is one of the most common gastroenterological indications for emergency admittance and hospitalization. Gallstones, alcohol consumption or the presence of additional initiating factors give rise to a disease with a diverse clinical appearance and a hard-to predict course of progression. One major challenge in the treatment of AP patients is the early identification of patients at risk for the development of systemic complications and organ failure. In addition, 20%–30% of patients with a first episode of AP later experience progress to recurrent or chronic disease. Complex gene–environment interactions have been identified to play a role in the pathogenesis of pancreatitis, but so far no predictive genetic biomarkers could be implemented into the routine clinical care of AP patients. The current review explains common and rare etiologies of acute pancreatitis with emphasis on underlying genetic aberrations and ensuing clinical management.
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