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Inflammation of the pancreas.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.



acute or chronic inflammation of the pancreas.

Acute pancreatitis may be edematous, hemorrhagic, necrotic, or purulent. It is caused by overeating; by diseases of the stomach, duodenum, biliary tract, or liver; or by stenosis of the gland’s ducts. In acute pancreatitis the pancreas is digested by its own enzymes—trypsin, chymotrypsin, and lipase. When the gland’s tissue decomposes, kinins are released. They decrease arterial pressure and are a factor in blood circulation disorder of both organic and reflex origin in the pancreas. The kinins also cause bile to flow into the gland’s ducts, which damages their walls.

Acute pancreatitis may be marked by very severe abdominal pains, persistent vomiting, and collapse. Complications are peritonitis, abscesses, cysts of the gland, and diabetes mellitus. The disease is treated by narcotics, antibiotics, vasoconstrictors, and such antienzyme preparations as trasilol and contrical and by A. V. Vishnevskii’s paranephric novocain blockade. Serious complications are treated surgically.

In chronic pancreatitis, the gland’s external and internal secretions gradually become insufficient. The disease is treated by diet, antispasmodics, substitutes, cholegogues, antibiotics, and antienzyme preparations. During periods of remission, the patient may receive treatment at a health resort.


Shelagurov, A. A. Bolezni podzheludochnoi zhelezy. Moscow, 1970.


The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.
References in periodicals archive ?
Allergic manifestations in autoimmune pancreatitis. Eur J Gastroenterol Hepatol 2009;21:1136-9.
Autoimmune pancreatitis associated with renal lesions mimicking metastatic tumours.
Arai et al., "Chronic fibroinflammatory responses in autoimmune pancreatitis depend on IFN-a and IL-33 produced by plasmacytoid dendritic cells," The Journal of Immunology, vol.
According to the International Consensus Diagnostic Criteria for Autoimmune Pancreatitis published in 2011 [19], ampullary biopsy showing abundant IgG4-positive plasma cells (>10 cells per high-power field) can be used if pancreatic tissue is not available for diagnosing autoimmune pancreatitis if other criteria are met, which is the case in our patient.
Kiyosawa, "Immunoglobin G4-hepatopathy: association of immunoglobin G4-bearing plasma cells in liver with autoimmune pancreatitis," Hepatology, vol.
At least in Japanese populations, IgG4-related autoimmune pancreatitis has a male to female ratio of 3-4:1, (11) but this ratio decreases nearly to unity in the context of head and neck disease.
Kuriyama et al., "Plasmacytoid dendritic cell activation and IFN-a production are prominent features of murine autoimmune pancreatitis and human IgG4related autoimmune pancreatitis," Journal of Immunology, vol.
Fukushima et al., "Membranoproliferative glomerulonephritis-like glomerular disease and concurrent tubulointerstitial nephritis complicating IgG4-related autoimmune pancreatitis," Internal Medicine, vol.
Autoimmune pancreatitis associated with primary sclerosing cholangitis: MR imaging findings.
This constellation of autoimmune diseases was initially recognized as autoimmune pancreatitis in 2001 and by 2003, extra pancreatic tissue and virtually any organ or system of the body involvement was documented.3
Recent concepts of autoimmune pancreatitis and IgG4-related disease.

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