CP is determined by a continuing (aseptic) inflammation of the gland, characterized by irreversible morphological and functional damage. The most common reasons are chronic alcohol abuse (70%) and cholelithiasis (20%), rare cases are caused by cystic fibrosis or are idiopathic, without any apparent cause. Typically, patients 30-40 years of age present with a history of epigastric pain (95%), weight loss (95%) and signs of endo-/exocrine deficiency (diabetes mellitus 58%, malabsorption syndrome and steatorrhea 80%). Acute exacerbations of CP are accompanied by episodes of pain that may mimic an acute abdomen. With progressive destruction of the gland, CP can become painless after several years. In about 1.5-12% of cases, CP can be complicated by pancreatic cancer.
Tumor markers such as CA 19-9 and CA-50 may also be elevated transiently and are unspecific. Laboratory tests for secretin-creozyme and secretin-cerulein have a high diagnostic accuracy, except in the early stages, but are invasive and cumbersome for the patient. These tests are of particular importance for the diagnostically challenging, newly defined small duct CP, where chronic inflammation occurs without duct abnormalities.
In CP, the most characteristic findings are dilatations of the pancreatic main duct and of ductal side branches (70-90%) together with small cystic changes, scattered glandular and ductal calcifications (40-50%), and ductal protein plugs. The grade and shape of ductal dilatation may help to differentiate chronic (benign) obstructions from malignant occlusions. In CP the contour of the pancreatic duct and its side branches is commonly irregular (73%), while this is true only in 15% of the cases in pancreatic malignancies. Additionally, the duct commonly forms less than 50% of the pancreatic anterior-posterior diameter in CP, while the opposite is true in pancreatic cancers (due to obstructive atrophy) (Fig. 5).
In CP, the gland may present a normal appearance in 15-20% of cases, however, a diffuse (50%) or focal (25%) enlargement is more common, and may raise the suspicion of a neoplasm. With time, atrophy of the organ will occur in 10-50%. The varying appearance of CP explains the shortcomings in establishing diagnosis: without gross morphologic changes it is very difficult to diagnose incipient forms of CP. Moreover, morphologic changes correlate very poorly with the functional exocrine and endocrine deficit, therefore endoscopically-guided (endo-scopical US) or percutaneous biopsy may be necessary for differentiation.
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