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

The main pancreatic duct in cats possesses a relatively strong barrier to the diffusion of bicarbonate ions (HCO3-). We studied some of the characteristics of this barrier by perfusing the duct with a solution similar in composition to pancreatic juice before and after exposing the duct mucosa to various test agents. The difference in net flux of HCO3- across the duct before and after exposure to the test agent reflected damage to the barrier. The barrier was damaged by infected bile, aspirin (pH 2.3), hydrochloric acid (pH 2.3), ethanol (5 to 10 per cent), and secondary bile acids. It was not damged by sterile bile, aspirin (pH 6.5), and primary bile acids. These data indicate that the barrier to back diffusion in the pancreatic duct has unique properties, different in some respects from the properties of the gastric mucosal barrier. Furthermore, the barrier is vulnerable to some agents thought possibly to have a role in the pathogenesis of pancreatitis and pancreatic cancer.
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PMID:The pancreatic duct mucosal barrier. 3 7

Pancreatitis occurring in late pregnancy and in the puerperium has been documented as an entity unrelated to cholelithiasis or hyperlipidemia. Canine pancreatic exocrine function has been studied during pregnancy and the puerperium. Pancreatic secretion was evaluated in eight pregnant female mongrel dogs prepared with Thomas duodenal and gastric fistulae, during pregnancy (corresponding to the third trimester in humans), during the puerperium, and several months after whelping. Basal secretion (volume and HCO3) was increased during pregnancy and the puerperium. The response to exogenous secretin (submaximal and maximal) was unchanged during pregnancy but decreased in the puerperium. Resting enzyme output was increased during pregnancy and the puerperium; the responses to cholecystokinin-pancreozymin during pregnancy were even more profoundly increased. Although the mechanism is speculative, these alterations in pancreatic function might contribute to the development of pancreatitis in pregnancy and the puerperium.
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PMID:Pancreatic exocrine secretion during and after pregnancy. 111 67

Fourteen pancreatic calculi from the corresponding number of pancreatic lithiasis patients were examined mineralogically and histochemically. The following results were obtained. The main components of calculi were calcium carbonate in 13 of the 14 cases, and calcium phosphate in the remaining one. Calcium carbonate calculi were all so-called intraductal calculi, with acidic glycoprotein apparently enwrapping the component particles. Acidic glycoproteins acted to bridge calcium carbonate particles, as in the cases of gallstone and urinary stone. The calcium phosphate calculus had a histochemical feature of pathologic calcification with degenerated collagen fibrils as the matrix, suggesting the calcification of the fibrotic pancreatic parenchyma after pancreatitis.
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PMID:Histochemical studies of pancreatic calculi. 115 70

Black and brown pigment gallstones are morphologically, compositionally, and clinically distinct. Black stones form primarily in the gallbladder in sterile bile and are associated with advanced age, chronic hemolysis, alcoholism, cirrhosis, pancreatitis, and total parenteral nutrition. Brown stones form not only within the gallbladder but also within the intrahepatic and extrahepatic ducts; they are uniformly infected with enteric bacteria and are usually associated with ascending cholangitis. Brown stones are related to juxtapapillary duodenal diverticula and are the predominant type of de novo common bile duct stones. Cholecystectomy is usually curative in black pigment stone disease, whereas stones often recur after cholecystectomy for brown stone disease. The pathogenesis of black stones is probably related to nonbacterial, nonenzymatic hydrolysis of bilirubin conjugates. At the pH of bile, this results in two monohydrogenated bilirubin anions that precipitate with calcium ions. Bilirubin monoconjugates that are increased in several conditions, such as Gilbert's syndrome and chronic hemolysis, may play a pivotal role in black stone formation as a source of unconjugated monohydrogenated bilirubin and as a possible co-precipitant with calcium. The precipitation of calcium carbonate and phosphate is influenced by local gallbladder factors. Brown pigment stones are formed in bile infected with enteric bacteria that elaborate hydrolytic enzymes: beta-glucuronidase, phospholipase A, and conjugated bile acid hydrolase. The resulting anions of bilirubin and fatty acids form insoluble calcium salts. We used nb/nb mice with a chronic hemolytic anemia as a model of hemolysis-induced black stone disease. The presence of 40% bilirubin monoconjugates in mouse gallstones indicated the importance of this moiety in the pathogenesis of black stones. Other data obtained by marrow transplantation experiments in mice revealed the relative importance of genotype versus the hemolytic anemia on determinants such as biliary bile acid composition and mucin secretory glands in the mouse gallbladder neck. Additional physical chemical studies of the interaction of unconjugated bilirubin in model bile solutions will be helpful in further delineating the pathogenesis of both black and brown pigment gallstones.
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PMID:Pigment gallstone disease. 202 17

Motilin basal level and that after carbohydrate load were radioimmunoassayed in 26 patients with ulcerative colitis. The results were correlated with the data on motor evacuatory activity of the gastrointestinal tract and clinical manifestations of diarrhea. Basal motilin level was found elevated as against the control (99 rg/ml) in all the patients and surpassed the norm (356-1001 rg/ml) in 6. A significant elevation of motilin content was associated with reduction of the amplitude and number of rhythmic type I contractions, as well as by increased number of type III (propulsive) waves and accelerated transport of the contents via the small intestine. No compensatory rarefying of acid discharge from the stomach, that was observed in reference subjects if transport of contents was accelerated, was detectable in the patients with ulcerative colitis. This resulted in acidification of the enteral medium (pH 5.6 +/- 0.6). Concomitant pancreatitis in 22 patients with reduced production of HCO3- and impaired cavitary hydrolysis of polymer substrate enhanced enteral medium acidification and changed its osmotic pressure. Specific features of enteral medium homeostasis disorders and of impairments of the gastrointestinal tract motor evacuatory function should be borne in mind when planning treatment strategy for diarrhea patients.
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PMID:[Plasma motilin and diarrhea in ulcerative colitis]. 229 81

There are two different forms of chronic pancreatitis: one is obstructive pancreatitis which results from a pre-existing obstacle (usually a tumour or a scar) and the other, much more frequent, is chronic calcifying pancreatitis which seems to begin with the formation of precipitates in acini and ducts, later transformed into stones and calcifications made up of calcium carbonate, and therefore is a pancreatic lithiasis. Since the pancreatic juice is supersaturated in calcium carbonate, the presence of an inhibitor of crystallization must be postulated. This has now been identified as a 13500 daltons molecular weight protein: the pancreatic stone protein secreted by the acinar cells. This protein is decreased in chronic calcifying pancreatitis irrespective of its origin (alcoholic, hereditary, hypercalcaemic, tropical, idiopathic), although its reduction is unrelated to any of these aetiological factors. Chronic alcohol consumption may encourage calcium stone formation possibly by disturbing the cholinergic regulation of pancreatic secretion, with decrease in citrate secretion (citrate is a chelator of calcium) and increase in enzyme secretion. The diagnostic and therapeutic implications of these findings are already obvious.
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PMID:[Chronic calcifying pancreatitis, pancreatic calculi. New data]. 293 79

We present a case of the milk-alkali syndrome occurring in pregnancy, an association not described in the medical literature. Ingestion of calcium carbonate and calcium-containing food was precipitated by the hyperemesis of pregnancy. Complications--hypercalcemia, dehydration, renal insufficiency, and pancreatitis--resolved within days. Here, the milk-alkali syndrome was the cause of the hypercalcemia of pregnancy. This case illustrates a rare cause of and complications from the milk-alkali syndrome.
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PMID:The milk-alkali syndrome in pregnancy. Case report. 321 Oct 90

The most current form of chronic pancreatitis, i.e. chronic calcifying pancreatitis, is often related to nutritional causes. This disease is characterized by formation within the pancreatic ducts and the lumina of accini of precipitates and calculi composed of calcium carbonate and of a newly discovered protein, the pancreatic stone protein (PSP). The formation of precipitates depends on two mechanisms: (1) a non etiological disorder reducing the secretion of PSP. This small phosphoglycoprotein is a calcium stabilizer which prevents the crystallization of calcium carbonate in a super saturated solution such as pancreatic juice, (2) modifications of the pancreatic juice related to the cause of the disease. In Occidental countries the main etiological factor is alcohol consumption associated with protein-and-fat-rich or fat-poor diets. Like hypercalcaemia, another cause of the disease, a chronic consumption of alcohol increases the pancreatic secretion of secretory proteins (enzymes) via its action on the cholinergic nerves. In some tropical countries, chronic pancreatitis is observed in children and associated to malnutrition. However, according to recent studies neither kwashiorkor nor manioc consumption seem to be responsible for the occurrence of this disease.
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PMID:[Etiopathogenesis of chronic nutritional pancreatitis]. 330 3

Pancreatic stones that were removed from the pancreatic ducts of patients with chronic calcifying pancreatitis were decalcified so the organic matrix could be studied by scanning and transmission electron microscopy. The observations made by scanning electron microscopy were compared with those made on undecalcified stones, and the findings were correlated with light microscopic observations. After the calcium carbonate was removed, the stones consisted of multiple partitions arranged like a sponge. They were embedded in a gel-like matrix. The organic partitions frequently were composed of dense surface layers and sparse central reticular accumulations, which had surrounded and bound calcium carbonate crystals. The organic matrix was heterogeneous in texture. Some areas had dense, regular, proteinaceous fibrous material. Deposits resembling fibrin were observed. Altered cellular constituents appeared to make up minor portions of the matrix. Calcium carbonate, which was precipitated in vitro in pancreatic juice, resembled the morphology of pancreatic stones more than that of pure calcium carbonate crystals. These results are consistent with the coformation of pancreatic stones from constituents in the pancreatic juice [including pancreatic stone protein (PSP), glycosaminoglycans, and occasional cells] and precipitated calcium carbonate.
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PMID:Fine structure of the organic matrix of human pancreatic stones. 357 6

Case records from 21 dogs with hypercalcemia and hyperparathyroidism were evaluated. The dogs were greater than or equal to 7 years old, and 6 were Keeshonds. The most common clinical signs were polydipsia/polyuria, listlessness, and muscle weakness. The serum calcium concentrations were 12.1 to 19.6 mg/dl. Serum phosphorus concentrations were low in 5 dogs, within the reference range in 13 dogs, and high in 3 dogs that also had high concentrations of BUN. Twenty dogs had a parathyroid adenoma, and 1 had a parathyroid carcinoma. Nineteen dogs had their parathyroid tumor surgically removed. Within 5 days of tumor removal, 11 of the 19 dogs became hypocalcemic and the remaining 8, normocalcemic. Nine of the 11 hypocalcemic dogs developed clinical signs. Iatrogenic hypercalcemia was induced in 7 of 16 dogs treated orally with calcium carbonate plus vitamin D. Only 1 of 19 dogs that had their parathyroid tumor excised died in hypocalcemic tetany. Two additional dogs died within 2 weeks of surgery, one because of pancreatitis, the other due to renal failure. Eight dogs died 9 to 37 months after surgery of unrelated problems. Eight dogs were alive for at least 7 to 28 months after surgery.
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PMID:Primary hyperparathyroidism in dogs: 21 cases (1976-1986). 365 3


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