Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A general review of bisalbuminemia is presented. Besides congenital bisalbuminemia there is an acquired form of bisalbuminemia that appears following treatment with high dosis of penicillin and cephalosporin, or in cases of acute pancreatitis after the development of a pancreatic pseudocyst. There is one type of abnormal albumin that migrates faster than normal albumin (rapid variant) and another type that is slower (slow variant). Different subtypes of each one have been recognized. There is no immunological difference between normal albumin and the variants. From a clinical point of view, bisalbuminemia per se does not cause any observable alterations. This is an important finding, however, because of the possibility that some physiologic or pharmacologic substances may not be bound to the abnormal variants as well as to normal albumin. When bisalbuminemia appears following an episode of pancreatitis it may be indicative of a pancreatic pseudocyst.
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PMID:[Bisalbuminemia (author's transl)]. 52 68

The etiological factors in 130 cases of acute pancreatitis occurring in a community with a low alcohol intake were reviewed. Alcohol was an insignificant factor in the etiology of acute pancreatitis. So-called idiopathic pancreatitis, occurring mainly in the older age group, was diagnosed in 19% of the cases. This is in contradistinction to findings in populations with excessive alcohol intake, where idiopathic pancreatitis is seen in all age groups. Similar age and sex distribution, as well as biochemical evidence of cholestasis, were seen in both the group suffering from gallbladder disease and in the idiopathic group. A more aggressive diagnostic work-up, including surgical exploration, is warranted, in view of the clinical overlap of biliary tract disease and idiopathic pancreatitis.
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PMID:Acute pancreatitis in a community with a low alcohol intake. 53 46

The importance of the papillary structure in the control of biliary and pancreatic outflow induced the authors to investigate the effect of papillary damage, chemical and physical, on the pancreatic parenchyma of the rat. The results show that mild papillary lesions produce acute interstitial flogosis of the pancreas; in 16,6% of the investigated animals this inflammation develops with the clear findings of a lethal acute haemorrhagic pancreatitis. This model is like the aspects of the post-operative acute pancreatitis.
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PMID:[Experimental acute pancreatitis caused by papillary lesions in the rat]. 55 69

The role of CT in acute diseases of the pancreas is discussed, in the light of personal experience (25 cases). In acute pancreatitis (22 cases), CT was useful in particular for: differential diagnosis between the necrotic-hemorrhagic type and the edematous type; detection of extra-pancreatic collections and evaluation of their extent; post-operative follow-up of necrotic-hemorrhagic pancreatitis. In the other more rare empergencies (3 cases), CT could recognize respectively the rupture of an infected pseudo-cyst, and intra-cystic hemorrhage, a mediastinitis due to the spread of ascitic fluid containing pancreatic enzymes into the mediastinum. CT always provided diagnostic information which the other radiological techniques did not provide; therefore in acute diseases of the pancreas CT is the method of choice.
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PMID:[The role of computed axial tomography in pancreatic emergencies (author's transl)]. 55 86

The effect of chronic alcohol pretreatment and various pancreatobiliary secretions on the severity of experimental pancreatitis was studied in the rat. 95 rats were pretreated with ethanol (20% w/v, 1.1 ml/100 g body weight) five times weekly for 10 to 12 weeks by gastric intubation. 88 rats served as controls. Pancreatic lesions were produced by retograde injection of different pancreatobiliary secretions into the pancreatic ducts. The secretions were collected from both normal and chronically alcohol-fed rats, and each was used for induction of experimental pancreatitis in the control and alcohol pretreated rats. Bile obtained from normal rats was no more toxic to the pancreas than 0.9% saline solution, while bile obtained from the chronically alcohol-fed rats caused significantly more serious lesions to the pancreas than did normal rat bile. Bile-pancreatic juice (mixture of secretions at papilla of Vater) of normal and chronically alcohol-fed rats was as toxic as the bile of the alcohol-fed rats. Alcohol pretreatment had no significant effect on the severity of pancreatitis when control and alcohol-fed groups separately or the whole material according to pretreatment was examined. These results suggest that the metabolic effects of ethanol on the pancreas as such do not sensitize the pancreas to acute pancreatitis. An exogenous mechanism is required. The reflux of toxic alcoholic bile into the pancreas might act as an induction factor in acute alcohol pancreatitis.
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PMID:Alcohol and acute pancreatitis. An experimental study in the rat. 56 39

Stenosing odditis represents only 4.5 p. cent of all benign lesions of the extrahepatic bile ducts. Their diagnosis is made by peroperative radiomanometry, but clinically they are suggested by a past history and serious clinical signs. The pancreatic involvement is rarely macroscopic (10 p. cent of cases of which 5 p. cent are severe) and acute pancreatitis due to stricture of the sphincter without gall stones is exceptional. Associated biliary lesions are frequent; in 50 p. cent of cases, of lithiasis of the common bile duct or pancreatitis, in 66 p. cent of cases of residual odditis. The treatment is surgical. Sphincterotomy should be reserved for young subjects with a slightly dilated common bile duct, or when necessary to extract a gall stone from the lower end of the bile duct. Biliary by pass operations are all the more indicated when the patient is elderly or the common bile duct more dilated. Local complications are the most frequent and the most serious after sphincterotomy; the local complications of biliary by pass operations are usually very simple. The late results of biliary by-pass operations are better than those of sphincterotomy, which confirms that the pancreatic complications of odditis are rare or well tolerated. The presence of chronic pancreatitis in association is not an aggravating factor.
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PMID:[Stenosing odditis: diagnosis and treatment. Report of 109 cases (author's transl)]. 59 95

The five major diseases of the pancreas together make a significant contribution to morbidity and mortality among the people of the United States. These diseases are diabetes, cystic fibrosis, acute and chronic pancreatitis, and carcinoma of the exocrine pancreas. Four of these diseases can be modeled in laboratory animals by acute or chronic administration of chemical poisons or carcinogens. Human pancreatic diseases attributed to the effect of chemical agents including alcohol and drugs include many cases of chronic pancreatitis and some cases of acute pancreatitis. The cause is not known in many cases of human pancreatitis, including interstitial, acute, and chronic clinical forms. Epidemiologic studies suggest that the increasing incidence of carcinoma of the exocrine pancreas in the United States may reflect chemical carcinogenesis. On the basis of experimental observations, we know that pancreatic islet cells can be damaged directly by toxic chemicals, and that islet cell tumors can be chemically induced. Thus, there is adequate background data to conclude that several pancreatic diseases of obscure etiology may be due in part to hitherto unidentified toxic effects of chemical agents encountered in personal or general environments.
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PMID:Environmental factors and diseases of the pancreas. 59 42

Acute pancreatitis was induced in 245 rats by retrograde instillation of Na-taurocholate into the pancreatic duct. Mortality rate in animals treated 6-hourly with glucagon (1 mg/kg) after induction of pancreatitis was 50% as compared to 30% deaths in the controls treated with 0,9% NaCl (chi2-test: p less than 0,05). Mortality rate in animals treated 6-hourly with the same dose of glucagon before induction of pancreatitis was 36,5% as compared to 28% deaths in the corresponding controls (chi2-test: p greater than 0,05). Glucagon in lower doses (0,1-0,5 mg/kg every 6 hours) did not alter mortality rates as compared to animals treated with 0,9% NaCl. 2. A nonletal form of pancreatitis was induced in 26 rats by ligation of the pancreatic duct. Injection of glucagon (1 mg/kg) seemed to suppress amylase activities in blood for a short period of appr. 1 hour. However, 7 and 9 hours after induction of pancreatitis, amylase activities were significantly higher in animals treated one or two times with glucagon as compared to untreated controls. It is concluded that glucagon in the high dose of 1-4 mg/kg/24 hours does not only not influence the course of acute experimental pancreatitis in rats but can even deteriorate it.
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PMID:A controlled trial of glucagon in acute experimental pancreatitis in rats. 60 26

The amylase/creatinine clearance ratio (Cam/Ccr ratio) was determined in 239 subjects. In 87 hospitalised patients without pancreatic disease (controls) the Cam/Ccr ratio was 3.02 +/- 0.69 (mean +/- ISD). The ratio was above the normal range in all patients with acute pancreatitis but was normal in those with chronic pancreatitis and carcinoma of the pancreas. In 18 patients with choledocholithiasis a raised ratio distinguished those with pancreatitis as assessed independently by the surgeon at laparotomy from those with a macroscopically normal pancreas. Raised Cam/Ccr ratios were also found in diabetics with ketoacidosis and in three patients with fulminant alcoholic liver disease. Though a positive correlation was found between the Cam/Ccr ratio and serum creatinine concentration, abnormally high ratios did not occur in 30 patients with chronic renal failure. A significant increase in Cam/Ccr ratios was produced in six healthy volunteers by intravenous injection of glucagon. However, it is unlikely that hyperglucagonaemia alone accounts for the increased Cam/Ccr ratio seen in acute pancreatitis, as no correlation was found between the clearance ratio and the plasma glucagon concentration in a series of patients. In two other patients in whom excess circulating pancreatic polypeptide was detected the Cam/Ccr ratio was normal. It is concluded that, in view of the sensitivity and relative specificity of finding an increased Cam/Ccr ratio in acute pancreatitis, its determination should be valuable clinically, especially in those cases of hyperamylasaemia where the cause is in doubt. The mechanism whereby the ratio is increased is unknown, and it is unlikely that either glucagon or pancreatic polypeptide is a major factor in its production.
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PMID:Mechanism and specificity of increased amylase/creatinine clearance ratio in pancreatitis. 60 90

The authors' experience with antienzymic treatment of 214 patients having acute pancreatitis is summarized. A method for calculating a dose of antienzymic substances by general activity of trypsin in blood and peritoneal exudate is suggested. By means of radioindication it was found that the maximum accumulation of the inhibitors in the pancreatic gland was dependent on the methods of their injection. It has been shown that the basic therapeutic effect of the inhibitors is to inactivate proteolytic enzymes. The injection of the inhibitors, depending on the form of pancreatitis, intravenously, intraperitoneally and in the celiac artery would eliminate enzymic toxemia in early stages of the disease, prevent the transition of edematous acute pancreatitis into hemorrhagic or necrotic one and avert autolysis of the pancreas.
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PMID:[Modern principles in the inhibitor therapy of acute pancreatitis]. 60 39


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