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Autoimmune Pancreatitis (AIP) is an increasingly recognized type of chronic pancreatitis that can be difficult to distinguish from pancreatic carcinoma but which ...
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.
Elevations in lipase are generally considered a better indicator for pancreatitis as it has greater specificity and has a longer half life. [30] However, both enzymes can be elevated in other disease states. In chronic pancreatitis, the fecal pancreatic elastase-1 (FPE-1) test is a marker of
Type 1 diabetes (T1D), formerly known as juvenile diabetes, is an autoimmune disease that occurs when pancreatic cells (beta cells) are destroyed by the body's immune system. [5] In healthy persons, beta cells produce insulin. Insulin is a hormone required by the body to store and convert blood sugar into energy. [6]
The association of idiopathic retroperitoneal fibrosis with various immune-related conditions and response to immunosuppression led to a search for an autoimmune cause of idiopathic RPF. [ 5 ] [ 6 ] Many of these previously idiopathic cases can now be attributed to IgG4-related disease , an autoimmune disorder proposed in 2003.
IgG4-related disease (IgG4-RD), formerly known as IgG4-related systemic disease, is a chronic inflammatory condition characterized by tissue infiltration with lymphocytes and IgG4-secreting plasma cells, various degrees of fibrosis (scarring) and a usually prompt response to oral steroids.
In 2021, Venturi reported that pancreas is able to absorb in great quantity radioactive cesium (Cs-134 and Cs-137) causing a severe and permanent pancreatitis with damage of pancreatic islands, and causing (type 3c) diabetes (pancreatogenic). [5]
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 ).