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 45-year-old man presented with what was thought to be a mass in the left upper lung and a pericardial friction rub. He was subsequently discovered to have a loculated pleural effusion and pericardial effusion associated with chronic pancreatitis. This is the first instance we were able to find of pancreatitis mimicking bronchogenic carcinoma with pericardial metastasis.
South Med J 1977 Dec
PMID:Pancreatic pleuropericardial effusions presenting as tumor of the lung. 59 5

Acute hemorrhagic pancreatitis was created in dogs using the closed duodenal loop technique. After 18 hours, a a constant rate of pancreatic exocrine secretion was stimulated with secretin. A direct relationship was observed between the percentage inhibition of secretin-stimulated pancreatic exocrine flow and the dose of antidiuretic hormone administered to dogs with acute hemorrhagic pancreatitis. The acute hemorrhagic pancreatitis reduced the sensitivity of the exocrine pancreas to secretin and antidiuretic hormone.
Am Surg 1977 Dec
PMID:Acute hemorrhagic pancreatitis in the dog. 5. The effect of antidiuretic hormone on pancreatic exocrine secretion. 59 24

In acute experimental pancreatitis in the rat neither intravenous nor intramuscular therapy with the antifibrinolytic drug PAMBA (p-aminomethylbenzoic-acid) had any influence on the lethality, enzyme content in either serum, ascites and pancreas or on the amount of destruction of the organ.
Z Gastroenterol 1977 Dec
PMID:[Therapy of acute experimental pancreatitis with the antifibrinolytic drug PAMBA (author's transl)]. 60 25

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.
Z Gastroenterol 1977 Dec
PMID:A controlled trial of glucagon in acute experimental pancreatitis in rats. 60 26

149 cases of chronic cholecystitis (65), cholecysto-pancreatitis (40), and pancreatitis (44) were examined by means of biochemical and radiioisotope methods. The acute stage of the disease was observed in 76 patients, 73 patients were in the intermission period. It was found that in chronic cholecystitis and pancreatitis renal and hepatic functional disorders do occur but their latent clinical course is detectable only by means of renography and hepatography, which should be taken into account at the establishment of the diagnosis, treatment and prognosis of the given diseases.
Vestn Khir Im I I Grek 1977 Dec
PMID:[Detection of latent forms of hepatic and renal functional disorders in chronic cholecystitis and pancreatitis]. 60 27

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.
Vestn Khir Im I I Grek 1977 Dec
PMID:[Modern principles in the inhibitor therapy of acute pancreatitis]. 60 39

Studies have been performed on pure pancreatic juice obtained by direct cannulation of the pancreatic duct in 2 patients with acute pancreatitis. The striking abnormalities observed, which were in marked contrast to our observations in 15 normal subjects, were high concentrations of protein throughout the period of secretin stimulation and the sporadic appearance of free proteolytic activity in many 1-min specimens throughout the collection period. In 1 subject repeat studies were performed after resolution of the pancreatitis when the profile observed was normal. Our findings are consistent with the hypothesis that obstruction of ductules and intraductal activation of zymogens may be important in the pathogenesis of acute pancreatitis.
Gastroenterology 1978 Dec
PMID:Profiles of pure pancreatic secretions in patients with acute pancreatitis: the possible role of proteolytic enzymes in pathogenesis. 71 Aug 62

The previously estimated incidence of pseudocyst formation in hereditary pancreatitis is approximately 10%. Our experience in nine patients with hereditary pancreatitis yielded five surgically documented pseudocysts and three additional patients with radiographically documented mass effects. Recent studies have shown a 20% spontaneous regression rate for pancreatic pseudocysts (of all etiologies), when evaluated by B-mode ultrasonography; our experience suggests that the incidence of pseudocyst formation in hereditary pancreatitis is considerably higher than previously suspected. Ultrasonography is thought to be an excellent method for diagnosing this entity, of evaluating mass effects identified on radiographic studies, and of providing sequential evaluation of pseudocysts treated surgically or conservatively.
J Pediatr 1978 Dec
PMID:Pseudocyst formation in hereditary pancreatitis. 72 38

The role of the complement system was studied in Na-taurocholate pancreatitis in rats. Complement activity (CH 50) was determined at various times in the course of pancreatitis. Immediately after induction of acute pancreatitis, serum complement activity declined and massive C 3 deposits could be detected in the vicinity of acinar necroses and necrobioses. After a phase of recovery three to six hours postoperatively a second complement consumption occurred. Lethality rate increased as serum complement activity fell below 50% of preoperative values. The degree of C 3 deposition increased up to six hours. Decline of serum complement activity and deposition within the pancreas seemed to be correlated with histologically demonstrable tissue lesion. The first decline of complement activity in serum is thought to be caused by liberation of complement activating substances within the pancreas due to the detergent action of Na-taurocholate itself. The second decline, however, may be due to the liberation of complement activating and/or destroying enzymes into the blood stream.
Res Exp Med (Berl) 1978 Dec 27
PMID:Complement system in sodium taurocholate pancreatitis in the rat. 73 45

Twenty patients with longstanding alcoholism and biopsy-proven alcoholic liver disease presented with marked elevation of serum alkaline phosphatase (in excess of four times the upper limit of normal). None had a past or present history to suggest pancreatitis or biliary tract disease, nor had any of these patients recently taken medication which could be implicated in cholestatic jaundice. Thirteen (65%) of this group either had radiologic or post mortem confirmation of nonobstructed biliary systems. The histologic findings in this group of patients were compared with those of a group of patients with alcoholic liver disease and normal or only mild elevation of serum alkaline phosphatase. Significantly more hepatocellular necrosis (P less than 0.05), alcoholic hyaline (P less than 0.02), and cholestasis (P less than 0.002) were noted in the severely hyperphosphatasemic group. Minimal degrees of steatosis were found in both groups. These data indicate that intrahepatic cholestasis occurs in patients with alcoholic liver disease, and this may often be secondary to alcoholic hepatitis. Overemphasis has previously been given to alcoholic fatty liver as a cause of this syndrome.
Am J Dig Dis 1978 Dec
PMID:Alcoholic liver disease presenting with marked elevation of serum alkaline phosphatase. A combined clinical and pathological study. 73 13


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