More research is now focused on pancreatic steatosis. Multiple definitions, clinical associations and synonyms for pancreatic steatosis are described in the literature and can be confusing. The integration and comparison of several studies concerning this topic is therefore challenging. In the past, pancreatic steatosis was considered an innocuous condition, a bystander of many underlying diseases (such as congenital syndromes, hemochromatosis and viral infection). However, evidence that pancreatic steatosis (strongly associated with obesity and the metabolic syndrome) has a role in type 2 diabetes mellitus, pancreatic exocrine dysfunction, acute pancreatitis, pancreatic cancer and the formation of pancreatic fistula after pancreatic surgery is emerging. This Review focuses on the different etiological factors and the clinical consequences of pancreatic steatosis.
Establishing a biliary etiology in acute pancreatitis is clinically important because of the potential need for invasive treatment, such as endoscopic retrograde cholangiopancreatography. The etiology of acute biliary pancreatitis (ABP) is multifactorial and complex. Passage of small gallbladder stones or biliary sludge through the ampulla of Vater seems to be important in the pathogenesis of ABP. Other factors, such as anatomical variations associated with an increased biliopancreatic reflux, bile and pancreatic juice exclusion from the duodenum, and genetic factors might contribute to the development of ABP. A diagnosis of a biliary etiology in acute pancreatitis is supported by both laboratory and imaging investigations. An increased serum level of alanine aminotransferase (>1.0 microkat/l) is associated with a high probability of gallstone pancreatitis (positive predictive value 80-90%). Confirmation of choledocholithiasis is most accurately obtained using endoscopic ultrasonography or magnetic resonance cholangiopancreatography. This Review discusses the pathogenesis of ABP and the clinical techniques used to predict and establish a biliary origin in patients with suspected ABP.
To our knowledge, no study in humans had studied the effect of tobacco smoking on pancreatic tissue. We have demonstrated for the first time that current cigarette smoking is associated with total PF-specifically, intralobular PF-as compared with nonsmokers.
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