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

Previous studies on pancreatic calculi (PC) from alcoholic pancreatitis and our recent studies on calculi from tropical pancreatitis have shown them to consist mainly of CaCO3 with minute quantities of Mg. However, no attempt was made to look for other elements in PC. This is because of the difficulty in obtaining adequate samples of PC, coupled with the technical limitations in analyzing multi-elements from small samples. In this study, our aim was to analyze the major, minor and trace elements of PC from different parts of the world. DC plasma emission spectroscopy, a modern method that permits determination of multiple elements from small samples, was used in elemental analysis. We identified 17 elements in addition to calcium. Selenium was looked for but was absent. It was interesting that the elemental composition of PC in four patients from different geographical areas with divergent etiological factors remained the same. Absence of Se is of interest, as Se deficiency is associated with pancreatic fibrosis in experimental animals and it is often noted in chronic alcoholics and the malnourished. This preliminary study emphasizes the need for analysis of the elemental composition of pancreatic juice in normals and in conditions predisposing to chronic pancreatitis, to understand lithogenesis and possibly also the etiology of, at least, some types of pancreatitis.
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PMID:DC plasma emission spectroscopic analysis of pancreatic calculi. 368 Oct 37

This study was designed to search for a way to inhibit pancreatic fibrosis following acute pancreatitis. Experimental necrotizing pancreatitis was induced by a freezing procedure in the pancreas of male Wistar rats. After the freezing procedure, the rats were divided into 3 groups: nothing addition was done to the control group, while the other 2 groups received daily intraperitoneal administration of antifibrotic substances (colchicine or L-azetidine-2-carboxylic acid (AZC)) for 6 weeks. Pancreatic enzymes in the serum were not markedly influenced by administration of antifibrotic substances, and there were no differences in the ratios of dry to wet weights of the pancreas between groups with and without these drugs. After freezing, the hydroxyproline levels in the pancreas of the control group increased from 1 to 4 weeks and then decreased during the 5th and 6th weeks. All groups receiving colchicine or AZC exhibited a significant decrease in the hydroxyproline levels at 2 to 4 weeks compared with the control group (P less than 0.01). Histological examination also showed the inhibition of pancreatic fibrosis, agreeing with changes in the hydroxyproline levels in groups receiving colchicine or AZC. These results suggest that administration of antifibrotic substances, colchicine and AZC, have the possibility of inhibiting pancreatic fibrosis following acute pancreatitis.
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PMID:Effects of antifibrotic substances on pancreatic fibrosis following acute necrotizing pancreatitis. 378 Nov 73

We studied 10 patients with pancreatitis who had persistent cholestasis secondary to compression of the common bile duct by a pancreatic pseudocyst. Elevation of the serum bilirubin or alkaline phosphatase levels, or both, (sensitive indicators of cholestasis) was present in each of our patients. The diagnosis of a pancreatic pseudocyst is best made by CAT scan and ultrasonography. These techniques will delineate the small intrapancreatic pseudocyst that otherwise may be difficult to recognize on inspection at operation. Endoscopic retrograde cholangiography and pancreatography are desirable because they delineate the anatomic alterations of the pancreatic and common bile ducts and may contribute information pertaining to the possibility of common duct obstruction by pancreatic fibrosis. In our opinion, cholestasis secondary to bile duct compression by a pseudocyst is an indication for operation. Each of our 10 patients had drainage of their pseudocysts. Cystoduodenostomy, performed in seven patients, was the method most commonly used. If there is concern regarding the patency of the common duct after drainage of the cyst, intraoperative cholangiography should be performed. This was carried out in three patients. In each patient, the preoperative elevations of serum alkaline phosphatase and serum bilirubin levels returned to normal limits after operative decompression of a pancreatic pseudocyst alone without an accompanying or subsequent bilioenteric bypass being required.
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PMID:Cholestasis due to compression of the common bile duct by pancreatic pseudocysts. 683 58

Suppurative cholangitis in 5 aged cats was characterized clinically by weight loss, depression, dehydration, icterus, and fever. The major abnormal laboratory findings were a severe left shift of WBC and a high, conjugated bilirubin concentration consistent with an inflammatory process and cholestasis. Gross pathologic findings included periductal biliary fibrosis (4 cats), periductal pancreatic fibrosis (2 cats), cholelithiasis (2 cats), deformation of the gallbladder (2 cats), and chronic interstitial pancreatitis (2 cats). Histopathologic findings in all cases were portal hepatic fibrosis, biliary hyperplasia, and suppurative exudate within dilated intrahepatic biliary ducts. Weight loss and portal fibrosis were suggestive of chronic, intermittent illness. The pathogenesis appeared to involve invasion of the bile duct by enteric bacteria. Cholangitis was observed to occur in association with pancreatitis, cholelithiasis, or anatomic abnormalities of the biliary tract.
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PMID:Suppurative cholangitis in cats. 686 38

Sodium taurocholate injected into the pancreatic duct system of the rat caused acute haemorrhagic pancreatitis. The pancreatic lesions were immediate and characterized by interstitial oedema, extensive necrotic changes of the acinar cells, and haemorrhages during the first 24 h after the injection. In animals surviving 72 h there were marked acinar atrophy and pancreatic fibrosis. The mortality increased according to the amount of sodium taurocholate injected. Except for necrosis of occasional liver cells, other organs examined were histologically normal. This investigation created an experimental model for studying the pathogenesis of acute pancreatitis. The results support the hypothesis that bile can initiate acute haemorrhagic pancreatitis.
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PMID:Experimental pancreatitis in the rat. Sodium taurocholate-induced acute haemorrhagic pancreatitis. 743 3

Chronic renal failure affects the physiological function of many organ systems. One of them is the exocrine pancreas. Although varying degrees of pancreatic insufficiency are the dominating clinical characteristic of uraemic pancreatic disease, it remains unclear whether this disease should be regarded as a manifestation of chronic pancreatitis, arising from recurring attacks of acute pancreatitis, or represents a distinct entity. The exocrine pancreas was studied in a model of experimental renal failure. The pancreas was removed from each rat at selected time points over eight weeks after subtotal nephrectomy and from a standard rat model of pancreatitis for comparison. The data show that the in vitro secretory response is considerably changed in renal failure (increased during early acute and decreased during chronic renal failure). While the pancreatic content of digestive enzymes progressively declines, DNA and protein synthesis increase over time. Acinar cell deletion is increased and accompanied by an increased rate of mitosis. This increased cellular turnover is not associated with tissue oedema, pancreatic fibrosis, inflammatory changes, autophagocytosis or subcellular redistribution of lysosomal hydrolases, all of which are characteristic for pancreatitis. The ultrastructural changes of uraemic pancreatic disease bear no resemblance to the changes seen in pancreatitis. It is concluded that the morphological and biochemical changes in early uraemic pancreatic disease are quite distinct, correspond with toxic damage of the pancreas, and are dominated by functional impairment and an increased cellular turnover.
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PMID:Origin and development of exocrine pancreatic insufficiency in experimental renal failure. 782 20

Pancreatic fibrosis in patients with alcoholic dependence syndrome was studied histopathologically. In 30 of 41 autopsied patients with alcoholic dependence syndrome, fibrosis was observed despite the absence of clinical pancreatitis. The fibrosis was categorized into three types, according to Martin's classification: intralobular sclerosis in 15 cases, perilobular sclerosis in seven cases, and a mixed intralobular and perilobular sclerosis in the remaining eight cases. The type of the fibrosis was not related to the duration of alcohol abuse. Alcoholic liver cirrhosis was coexistent in 23 of the 30 cases of pancreatic fibrosis. These cases were also divided into categories according to the three types, as follows: intralobular sclerosis in 12 (80%) of 15 cases, perilobular sclerosis in four (57%) of seven cases, and mixed sclerosis in seven (88%) of eight cases. That is, intralobular and mixed sclerosis were frequently coexistent with alcoholic liver cirrhosis. When the pancreases from the 19 subjects with intralobular sclerosis and mixed sclerosis coexistent with liver cirrhosis in alcoholic dependence syndrome were compared with 20 pancreases from patients with nonalcoholic liver cirrhosis, periacinar (or intralobular) fibrosis was found in all cases of the former, but in none of the latter. Hence, it was concluded that periacinar fibrosis occurred as a result of alcohol abuse. Pancreatic fibrosis in patients with alcoholic dependence syndrome was distributed mainly in the intralobular areas and was frequently coexistent with alcoholic liver cirrhosis.
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PMID:Pancreatic fibrosis in patients with alcoholic dependence syndrome. 821 22

Genetic predisposition to alcoholism and alcoholic liver disease has been reported. However, genetic susceptibility to alcoholic pancreatitis is still a matter of debate. To determine it, we examined genotype patterns of aldehyde dehydrogenase (ALDH2), alcohol dehydrogenase (ADH2 and ADH3), and cytochrome P-4502E1 (CYP2E1) in alcoholic pancreatitis patients. In 296 alcoholic patients, 52 cases showed findings of chronic pancreatitis by ultrasonography and x-ray computed tomography and/or had a history of pancreatitis (P+). The remaining 244 patients had neither abnormal findings of the image examinations nor a history of pancreatitis (P-). As for the ADH2 genotype, distribution of 2(1)/2(1), 2(1)/2(2), and 2(2)/2(2) was 22, 37, and 42% in P+ patients, whereas 34, 35, and 30% in P- patients, respectively. The frequency of ADH2(2)/2(2) genotype was significantly higher in P+ patients, compared with that in P- patients. There were no significant differences in the distribution of ADH3, ALDH2, and CYP2E1 genotypes between P+ and P- patients. In 14 alcoholic patients who showed low contents of fecal chymotrypsin, which suggests dysfunction of pancreatic exocrine, the rate of ADH2(2)/2(2) genotype also tended to be higher (50%) than in 74 controls who showed normal contents of the fecal chymotrypsin (28%). No differences were observed in genotypes of ADH3, ALDH2, and CYP2E1. Moreover, the frequency of ADH2(2)/2(2) genotype was significantly higher in autopsy cases with interlobular fibrosis in the pancreas, which suggests alcoholic pancreatic damage, than in cases with only intralobular pancreatic fibrosis. These data suggest that the risk of alcoholic pancreatitis seems to be associated with the presence of ADH2(2)/2(2) genotype.
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PMID:Genotypes of alcohol-metabolizing enzymes and the risk for alcoholic chronic pancreatitis in Japanese alcoholics. 898 24

We report a new case of idiopathic hypereosinophilic syndrome with multivisceral digestive failure. After an erroneous diagnosis of pancreatic cancer, the pathological examination of pancreaticoduodenectomy specimen demonstrated pancreatic fibrosis with eosinophilic infiltration without gastritis or duodenitis. The diagnosis of idiopathic hypereosinophilic syndrome was made three months later upon the classical criteria: a) blood eosinophilia of 1.5 G/L or more, persisting for more than 6 months; b) lack of evidence for any other recognised cause of eosinophilia: c) multiple organ systemic involvement: rheumatologic, cutaneous and digestive (pancreatitis, ascites and diarrhoea): d) previous history of allergic disease and increased plasmatic IgE levels; e) absence of leukemic markers. This case emphasises the difficulty in classifying eosinophilic infiltration of the gut and the possibility of transitional forms between eosinophilic gastro-enteritis and idiopathic hypereosinophilic syndrome. We argue that in case of eosinophilic infiltration of the gut, systematic research of multiple organ systemic involvement is mandatory.
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PMID:[Pancreatic involvement, ascites and diarrhea in idiopathic hypereosinophilic syndrome]. 929 82

The present study was done to determine the additional influence of daily ethanol intake (15% in drinking water ad libitum) on long-term toxic effects of a single administration of dibutyltin dichloride (DBTC, 8 mg/kg b.w. i.v.) in pancreas and liver of rats. Pathohistological changes in pancreas, bile duct and liver as well as pathobiochemical parameters of pancreatitis (amylase and lipase activity), liver lesions (alkaline phosphatase activity and bilirubin) and fibrosis (hydroxyproline and hyaluronic acid) were measured 1 day and 1 to 24 weeks after DBTC- and DBTC/ethanol administration. DBTC alone induced in rats an acute interstitial pancreatitis as well as acute bile duct and liver lesions in the early experimental phase. Later on, the acute inflammatory processes in pancreas and liver took a chronic course resulting in pancreatic fibrosis and liver cirrhosis. Ethanol increased the toxic effects of DBTC on pancreas and liver during the acute and chronic course. In the acute phase lasting 1 day to 2 weeks, ethanol enhanced the DBTC toxicity on acinar cell and bilio-pancreatic duct epithelium as well as the formation of obstructive ductal plugs by necrotic cell debris. The obstruction and cholestasis in the DBTC/ethanol-group were significantly stronger as in the DBTC-group. The significant increase of hydroxyproline in urine and hyaluronic acid in serum of the DBTC/ethanol treated rats after 12 to 24 weeks was connected with a more severe chronic inflammatory fibrosis in pancreas and liver in comparison to the DBTC-treated group.
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PMID:The influence of ethanol on long-term effects of dibutyltin dichloride (DBTC) in pancreas and liver of rats. 958 82


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