Idiopathic (i.e microlithiasis) ·
Endoscopic retrograde cholangiopancreatography (ERCP)
Trauma (especially blunt abdominal trauma)·
Scorpion bites (Tityus trinitatis, Trinidad)
Mumps. But also: CMV, EBV, HIV, Varicella, Rubella
Autoimmune (IBD, PAN, SLE) or Genetics (CFTR or Trypsin inhibitor)
Surgery (abdominal and non abdominal operations)·
Hyperlipidemia (TG >10mmol/L or >1000mg/dL). Hypothermia, Hypercalcemia
Ethanol alcohol (acute and chronic alcoholism)
Drugs (azathioprine, 6-mercaptopurine, diuretics (e.g., thiazides, furosemide), estrogens/steroids, tetracycline, valproic acid, anti-HIV medications)
EACH MECHANISM IS NOT CLEARLY UNDERSTOOD!
Theory: AUTO-DIGESTION: proteolytic enzymes (e.g., trypsinogen, chymotrypsinogen, pro elastase, and lipolytic enzymes such as phospholipase A2) are activated in the pancreas rather than in the intestinal lumen. A number of factors (e.g., endotoxins, exotoxins, viral infections, ischemia, anoxia, lysosomal calcium, and direct trauma) are believed to facilitate activation of trypsin.
A common finding described on computed tomography (CT) imaging. A disease with a peribronchovascular distribution…