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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An electrophoretic technique for demonstrating amylase isoenzymes is described. After separation in an agarose gel containing a linear polyacrylamide polymer to reduce electroendosmotic flow, the amylase fractions are visualized by incubation with a commercially available dye-starch polymer (Phadebas Amylase Test). The technique detects amylase fractions with activities below 10 U/l. Some characteristic changes in such diseases as acute and chronic pancreatitis, cystic fibrosis of the pancreas, macroamylasemia and inherited variants as well as after maxillofacial surgery are mentioned.
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PMID:Electrophoretic separation, detection, and variation of amylase isoenzymes. 4 75

Samples of plasma or serum from 53 cystic fibrosis (CF) patients, 90 relatives of CF patients , and 159 controls have been incubated with porcine or bovine 125I-trypsin, electrophoresed on polyacrylamide gel, and autoradiographed. In these individuals, the main binding protein for 125I-trypsin has been shown to be alpha 2-macroglobulin (alpha 2M). Using this method of analysis, no difference in electrophoretic migration of 125I-trypsin-alpha 2M complexes has been observed between CF and control individuals. However, trypsin binding to IgG has been observed in 80% of CF patients, 30% of their mothers, 3% of controls, and in two patients affected with pancreatitis. These trypsin binding immunoglobulins are called TbIg, and specifically, Tb1gG when referring to the G class. Experimental evidence indicates that binding of trypsin to IgG occurs through the Fab portion of the molecule. Tb1gG must be antibodies most probably induced by the exogenous trypsin ingested daily by most CF patients (and by patients affected with chronic pancreatitis). Antibodies against porcine pancreatic elastase have been observed using the same analysis, but not as frequently as Tb1g.
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PMID:Binding of 125I-labeled proteinases to plasma proteins in cystic fibrosis. 9 5

This review describes the development and application of a novel test to determine levels of human immunoreactive trypsin, an enzyme produced solely by the pancreas, in biological fluids. Being organ-specific, the assay of immunoreactive trypsin should be an ideal marker of pancreatic function, and this is supported by the results of a number of clinical and research investigations. Use of this assay in studies of chronic pancreatitis, juvenile-onset diabetes, and cystic fibrosis has yielded much valuable data, and it is expected that further research will lead to an improved understanding of these and other conditions associated with the pancreas in health and disease.
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PMID:Radioimmunoassay of trypsin. A new aid in the assessment of pancreatic function. 51 80

Immunoreactive serum trypsin was measured with a double antibody radioimmunoassay in normal subjects and patients with various diseases of the pancreas. The normal range is 115-350 ng/ml with a geometric mean of 212 ng/ml. No trypsin was found in serum after total duodenopancreatectomy, in about 75% of patients with cystic fibrosis and in a few patients with pancreas carcinoma or chronic pancreatitis. Reduced serum trypsin levels between 10 and 100 ng/ml were measured in the remaining 25% of cystic fibrosis and in one third of the patients with chronic pancreatitis. Serum trypsin was increased to 700-17,000 ng/ml in all patients with acute pancreatitis or during the acute phase of chronic pancreatitis. Absent or reduced serum trypsin is a reliable indicator of total or partial exocrine pancreatic insufficiency whereas considerably increased serum trypsin concentration do indicate acute pancreatitis.
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PMID:Immunoreactive serum trypsin in diseases of the pancreas. 52 26

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

In order to study the disposition which is thought to be latent in chronic pancreatitis, we investigated the sweat chloride concentration of 95 normal subjects, 43 cases of chronic pancreatitis, 12 cases of cholelithiasis, 15 cases of peptic ulcers, 16 cases of hepatic diseases and 23 cases of diabetes mellitus with the sweat test, using the method of pilocarpine iontophoresis. We obtained the following results. (1) In normal subjects, the sweat chloride concentration was inclined to rise gradually with age from childhood to adulthood; the mean value of sweat chloride concentration was 30.0 mEq/liter in adults from 20 years old, and the upper limit was about 60 mEq/liter. (2) The mean value of sweat chloride concentration was 60.0 mEq/liter in chronic calcifying pancreatitis; this value was markedly higher than that of control subjects of the same age (p is less than 0.001). (3) The mean value of sweat chloride concentration in cholelithiasis, peptic ulcer and hepatic diseases did not differ significantly from control subjects. The mean value of sweat chloride concentration in diabetes mellitus was significantly higher than that of control subjects (p is less than 0.01), but was significantly lower than that in chronic pancreatitis (p is less than 0.01). (4) It was supposed that some cases of chronic pancreatitis have a congenital disposition toward abnormal secretion of sweat glands and epithelium in the pancreatic duct, resembling cystic fibrosis, and this disposition leads easily to pancreatic disorders when the individual is exposed to various external factors.
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PMID:The significance of the sweat test in chronic pancreatitis. 67 78

The exocrine pancreas is a gland which secretes water, enzymes and electrolytes into the intestinal lunar. These enzymes for the normal digestion of food and a deficit, whether due to a seduced secretion (chronic pancreatitis, cystic fibrosis), or dysfunction in the chronology of their secretion (following truncal vagotomy) will cause malabsorption which often develops, in clinical terms, into malnutrition sometimes this functional deficit is secondary to other pathologies or surgical operations which alter the digestive tract physiology, preventing the correct combination of nutrients and pancreatic enzymes together with the biliary salts. The outcome is malabsorption, mainly of fast and fat soluble vitamins. As the onset is slow and forms part of a chronic, pathology, diagnosis is difficult, for which reason it is included in the general group of malabsorption due to pancreatic insufficiency or surgical sequelae, finally resulting in pancreatic failure or problems following surgery. The purpose of this publication is to review one by one all the situations in which there is an alteration in the function of the pancreatic enzymes, with emphasis on cases in which a defined malabsorption syndrome will result, and in which the prescription of exogenous pancreatic enzymes will imposiue the picture.
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PMID:[Exocrine pancreatic insufficiency. Organic and functional deficiencies]. 157 5

Two patients with specific pancreatic amylase deficiency are described. The greatly reduced pancreatic amylase activity was not due to an enzymatically inactive amylase molecule but to an almost complete absence of the molecule itself. The findings are of diagnostic importance as they show that low pancreatic amylase activity in serum or duodenal aspirates, or both, does not necessarily represent chronic exocrine pancreatic disease such as chronic pancreatitis, carcinoma of the pancreas, or cystic fibrosis but may be an isolated finding. In one of our patients a familial occurrence was shown, indicating a congenital deficiency.
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PMID:Selective deficiency of pancreatic amylase. 171 Feb

The overlapping features of the acquired diseases acute pancreatitis and chronic pancreatitis on the one hand, and of chronic pancreatitis and pancreatic involvement in the congenital condition cystic fibrosis on the other, suggest that the basic mechanism of pancreatic injury may be the same in each illness. We propose that pancreatic oxidant stress is the common denominator and, furthermore, that this is facilitated by a shortfall of micronutrient antioxidants in the face of heightened free radical activity through different sources. If so antioxidant supplements should alleviate symptoms. This deduction was supported by an exploratory dose-seeking study that spanned five years in 20 patients with recurrent (non-gall stone) acute or chronic pancreatitis and confirmed by a 20-week double-blind placebo-controlled crossover trial of the successful combination (daily doses of 600 micrograms organic selenium, 0.54 g vitamin C, 9000 IU B-carotene, 270 IU vitamin E and 2 g methionine) in a further 20 cases. A randomised trial of glutathione precursors, given intravenously for 24 hours after admission in patients with a first attack of acute pancreatitis, is in progress. Long-term trials of oral antioxidant formulas are planned in patients with cystic fibrosis.
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PMID:Rationale for antioxidant therapy in pancreatitis and cystic fibrosis. 224 39

The ductular accumulation of "abnormal mucus" is the key histologic feature in cystic fibrosis. This material is periodic acid-Schiff positive and diastase resistant, suggesting that it is glycoprotein in nature. We used the avidin-biotin-peroxidase method to identify this material using antibodies to the serum glycoproteins carcinoembryonic antigen, alpha 1-antitrypsin, and alpha-fetoprotein on paraffin sections of pancreas obtained from a total of 21 patients: 9 with cystic fibrosis, 5 with chronic pancreatitis, and 7 controls. The control patients had normal pancreatic histologic findings, no alpha 1-antitrypsin or alpha-fetoprotein was demonstrated, and only the ductular epithelium reacted weakly for carcinoembryonic antigen. The pancreas in pancreatitis showed fibrosis, acinar atrophy, and ectasia of the ducts that contained only a small amount of periodic acid-Schiff-positive material. This material reacted weakly for carcinoembryonic antigen and alpha 1-antitrypsin. The appearance of the pancreas in cystic fibrosis was similar to that in chronic pancreatitis. However, the ducts contained a greater amount of periodic acid-Schiff-positive material, mostly in the form of globules that reacted strongly for carcinoembryonic antigen and alpha 1-antitrypsin and weakly for alpha-fetoprotein, as did the ductular epithelium. This study shows that the periodic acid-Schiff-positive material in cystic fibrosis contains at least the three serum glycoproteins and that the accumulation may represent a possible defect in cellular synthesis, assembly, or transport of glycoproteins in the ducts.
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PMID:Carcinoembryonic antigen, alpha 1-antitrypsin, and alpha-fetoprotein in the pancreas of patients with cystic fibrosis. 247 7


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