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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Duodenal stenosis in chronic relapsing pancreatitis occurs in 20% of our patients. In 21 of our cases, the stenosis was always in the descending portion of the duodenum, and in two-thirds it caused an obstruction. The stenosis is always concentric with destruction of the mucosal pattern, widening of the neighbouring folds, irregular contours, and, possibly, straightening of the medial margin of the duodenum. There may be widening of the duodenal loop and frequently the duodenal loop is dilated. The causes for these appearances vary, but a peri-pancreatitis or duodenitis are most frequent. There is no close relationship with the severity of the pancreatitis. Our findings are compared with the small number of reports to be found in the literature.
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PMID:[Duodenal stenosis in chronic relapsing pancreatitis (author's transl)]. 14 44

Amylase isoenzyme analysis of serum and urine has been performed in 4001 normal persons and 500 patients with various disease using electrophoresis on thin layer polyacrylamide gel. Although elevation of amylase activity in amylase-1 and 2 has been reported to be the specific findings in patients with pancreatitis, 1.69% of normal persons had an elevated Amylase-2(named "Dominant Amylase-2") up to the same levels as major isoenzymes (Amylase-1 and 3), along with Amylase-1. Pedigree study confirmed an autosomal dominant mode of inheritance for Dominant Amylase-2. Knowledge of the genetic polymorphism is of importance in clinical assessment of amylase isoenzymes in patients having an elevated Amylase-2 suggestive of pancreatitis. Predominance of the pancreatic components in serum and urine has been revealed to be a specific index of pancreatic involvement. However, the existecne of an inherited trait of pancreatitis-like isoamylase pattern in healthy individuals must be borne in mind. On the basis of the present study, it may be concluded that a rise in the pancreatic type isoenzymes may not necessarily indicate underlying pancreatitis, especially in the absence of elevated amylase and lipase levels.
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PMID:Clinical evaluation of the pancreatitis-like isoamylase pattern in normal persons. 15 Sep 92

The course of uncomplicated pancreatitis was followed by sonography in 45 patients. The changes during the disease and their temporal relationship to the clinical stage are illustrated by an example. During the initial phase of the disease the sonographic findings may be so slight that they are easily missed, although clinical symptoms are present. It is only during the main phase of the disease that the typical sonographic findings of acute pancreatitis develop. At this time, maximal increase in amylase activity has usually passed. During recovery, with uninterrupted clinical and biochemical improvement, changes in the sonogram can still be seen for between three weeks and four months.
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PMID:[Diagnostic criteria for pancreatic sonography during the course of uncomplicated acute pancreatitis (author's transl)]. 15 73

The computer tomographic appearances of acute pancreatitis have been analysed 33 patients. It is usually a simple matter to distinguish between the acute, oedematous pancreatitis, which can be treated conservatively, and the suppurative pancreatitis with haemorrhagic and necrotising features, which require surgical exploration.
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PMID:[Computer tomography in acute pancreatitis (author's transl)]. 15 16

Rat exocrine pancreatic function was studied structurally and biochemically after the in vivo production of actue interstitial pancreatitis by supramaximal stimulation with caerulein. Two major phases in the reaction of the gland were observed: During the first two days after cessation of the supramaximal stimulation a progressive infiltration of the interstitium and the pancreatic tissue with polymorphonuclear leucocytes, lymphocytes and macrophages occurred which led to further destruction of the gland and to decreased functional response. From two days after the cessation of the treatment, hypertrophy of centro-acinar cells and an increased rate of mitotic activity indicated regeneration of the pancreas. This was combined with an accelerated in vitro discharge of newly synthesized proteins over a period of four days. Between days three and six after the initial treatment mitotic activity was also observed in fully differentiated exocrine cells. Total structural and functional recovery of the pancreas was achieved nine to tweleve days after the cessation of the supramaximal stimulation.
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PMID:Course and spontaneous regression of acute pancreatitis in the rat. 15 97

15 streptozotocin-diabetic wistar rats (an application of a single dose of 64 mg/kg body weight streptozotocin) and a control group of 12 wistar rats with a healthy metabolism have been examined. The majority of B-cells was largely degranulated, insulin was hardly or not to be found with histochemical methods. The A- and B-cells of 11 test animals showed pathological findings: Karyolysis, the dissolution of cell membranes and the decay of cytoplasm which are criteria of necrosis. Besides a round-cell infiltration could be found as a symptom of insulitis. The B-cells showed only single granula under the electron microscope. The endoplasmatic reticulum was only poorly developed and with hardly any ribosomes. There were only very little mitochondria and no GOLGI's apparatus. The cell membrane was smooth and not enlarged by microvilli. Emiocytosis-figures were missing. No changes of nuclei could be noticed. The findings on organelles correlate well with the microscopical results. The exocrine parenchyma contained regions showing the decay of the lobule structure as well as of single acini. The acinus cells were in necrosis. The connective tissue was obviously increased. There were regions in the stroma with a round-cell infiltration as found with a pancreatitis. Both these and the results discussed from our literature show that streptozotocin does not only affect the B-cells of the islets of LANGERHANS, but also the exocrine pancreas and other organs.
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PMID:[Histotopochemical and electronmicroscopical investigations of Wistar-rats with streptozotocin diabetes (author's transl)]. 15 64

Aprotinin, a protease inhibitor, has been used in a wide variety of pathophysiological states thought to be associated with an increase in protease activity. Opinion differ with respect to the success of the therapy. This paper proposes a rationale for the therapeutic action of aprotinin based on biochemical and physiological evidence. In the kallikrein-kinin system, in addition to kallikrein, other serine-esterases such as trypsin, plasmin, etc. can generate kinin production. In certain disease states such as pancreatitis there is not only an increase in serine-protease activity but frequently these enzymes reach parts of the organism where they are not found in health. Thus in such circumstances increased production of kinins can result. The consequences of increased kinin generation are discussed in light of work indicating their role in metabolic and circulatory homeostasis. Aprotinin is specifically a serine-esterase inhibitor. It is suggested that perhaps the most important action of this compound is as an inhibitor of the kallikrein-kinin system. On this basis a therapeutic regime in various disease states for the use of aprotinin, which allows for control of kinin generation, is suggested.
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PMID:A rationale for the therapeutic action of aprotinin. 15 36

Endoscopic retrograde pancreaticocholangiography (ERPC) has been performed in 140 patients, mainly Blacks and Indians. The first 100 patients have been analysed. The greatest diagnostic yield in this series is in (suspected) obstructive jaundice, where 26 diagnoses were made in 35 patients. In 40 patients with pancreatitis, the widest ducts were seen in 12 patients with calcific pancreatitis, but the procedure was of less help than expected. This was because no patients with continual pain after cessation of alcohol intake were found with operable strictures of the main pancreatic duct. The pancreatic function test with secretin and cholecystokinin-pancreozymin correctly diagnosed 4 patients with non-calcific pancreatitis in whom the ERPC was normal. There was a useful diagnostic yield in patients with unexplained upper gastrointestinal symptoms (15 diagnoses were made in 23 patients).
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PMID:Technique and results of endoscopic retrograde pancreaticocholangiography. A preliminary report on 140 patients. 16 2

The authors report 3 cases and report the diagnostic usefulness of two signs of minor cholestasis described by one of them in 1966. A relative increase, in the absence of obvious virus hepatitis or cirrhosis, of the serum bilirubin, cholesterol, lipids and alkaline phosphatase, together with B.S.P. excretion. suggest minor cholestasis. The sign of "metacritical aggravation" when there is some suspicion of minor cholestasis, the supervision of the course of the disease, or a retrospective inquiry, permit, in the presence of minor symptoms, such as, pain, fever, jaundice, or pruritus, one to make the diagnosis of minor cholestasis. The latter is due either to the presence of small gall stones in the common bile duct, or to inflammation of the ampulla of Vater, or sphincter of Oddi, a Vaterian ampulloma, pancreatitis, or following damage to the common bile duct. In practice, liver biopsy confirms the diagnosis, and intravenous cholangiography, by the perfusion method, is usually able to demonstrate obstruction of the common bile duct.
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PMID:[Relative increase and metacritic aggravation in the diagnosis of anicteric cholestasis]. 16 83

Massive ascites is are complication, but not exceptional, in pancreatitis. In a series of ten personal cases and a review of one hundred cases in the world literature, the authors attempt to define the main pathological and clinical characteristics of this disease and the best treatment. Ascites may follow abdominal trauma, involving the pancreas, sometimes it occurs during known chronic pancreatitis, often it is the first sign of pancreatic disease, whether acute or chronic. High levels of pancreatic enzymes in the ascitic fluid are the main factor in diagnosis of pancreatic ascites. The mechanism of formation of the ascites is loss of pancreatic fluid into the peritoneal cavity owing to a breach in the pancreas, the presence of enzyme-rich fluid, causing secondarily "chemical" peritonitis. Paracentesis abdominis or drainage of the fluid during exploratory laparotomy, permits one to obtain in certain cases, a cure of the ascites, but surgical drainage by an anastomosis between the pancreatic cyst and the digestive tract (pancreatico-digestive anastomosis), has the advantage of ensuring treatment of the ascites and of the responsible pancreatic disease.
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PMID:[Massive ascites in pancreatitis. Review apropos of 10 personal cases]. 17 57


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