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Acute pancreatitis (AP) is a sudden inflammation of the pancreas.Causes include a gallstone impacted in the common bile duct or the pancreatic duct, heavy alcohol use, systemic disease, trauma, elevated calcium levels, hypertriglyceridemia (with triglycerides usually being very elevated, over 1000 mg/dL), certain medications, hereditary causes and, in children, mumps.
The Ranson criteria form a clinical prediction rule for predicting the prognosis and mortality risk of acute pancreatitis. They were introduced in 1974 by the English - American pancreatic expert and surgeon Dr. John Ranson (1938–1995).
In patients with PBM, regardless of the presence of biliary dilatation, acute pancreatitis is more common in children (30% of patients) than in adults (9%). [7] Although pancreatitis is often mild with subtle imaging findings, it can also be recurrent. [8] One possible cause of acute pancreatitis linked to PBM is protein plugs. [9]
Pancreatitis is inflammation of the pancreas. There are two forms of pancreatitis, which are different in causes and symptoms, and require different treatment: Acute pancreatitis is a rapid-onset inflammation of the pancreas, most frequently caused by alcoholism or gallstones. Less frequent but important causes are hypertriglyceridemia, drugs ...
Chronic pancreatitis is a long-standing inflammation of the pancreas that alters the organ's normal structure and functions. [1] It can present as episodes of acute inflammation in a previously injured pancreas , or as chronic damage with persistent pain or malabsorption .
Autoimmune pancreatitis may cause a variety of symptoms and signs, which include pancreatic and biliary (bile duct) manifestations, as well as systemic effects of the disease. Two-thirds of patients present with either painless jaundice due to bile duct obstruction or a "mass" in the head of the pancreas, mimicking carcinoma.
Hereditary pancreatitis (HP) is an inflammation of the pancreas due to genetic causes. It was first described in 1952 by Comfort and Steinberg [ 1 ] but it was not until 1996 that Whitcomb et al [ 2 ] isolated the first responsible mutation in the trypsinogen gene ( PRSS1 ) on the long arm of chromosome seven ( 7q35 ).
In septic patients, these clinical signs can also be seen in other proinflammatory conditions, such as trauma, burns, pancreatitis, etc. A follow-up conference, therefore, decided to define the patients with a documented or highly suspicious infection that results in a systemic inflammatory response as having sepsis. [ 18 ]