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)

The incidence of pancreas divisum (PD) was evaluated in a retrospective series of 1,825 successful consecutive ERCPs. One hundred thirty-seven pancreas divisums (7.5%) were found in 80 males and 57 females at a mean age of 49.2 years. The ventral ducts were visualized in 82.5% and the dorsal ducts in 74.1% of attempted cannulations of the minor papilla. Pancreas divisum was significantly more frequent in patients presenting with acute idiopathic pancreatitis (50.0%) or acute biliary pancreatitis (23.7%) than in controls or in the general population. This difference was not found in acute pancreatitis due to other etiologies. Acute pancreatitis associated with PD is generally recurrent, is not severe, but may be complicated by necrotic pseudocysts. The frequency of PD was also significantly increased in patients with gallbladder stones but not with common bile duct stones. In other pathological groups--chronic pancreatitis and pancreatic cancer--the frequency of pancreas divisum was not statistically different from that observed in controls and/or in the general population. We conclude that on a statistical basis, PD is a probable cause of acute pancreatitis, especially in its idiopathic recurrent variety, and that its frequency is increased in patients with gallbladder stones.
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PMID:Pancreas divisum is a probable cause of acute pancreatitis: a report of 137 cases. 187 6

Pain from pancreatic cancer is, in most cases, both severe and debilitating. Large doses of morphine are sometimes not tolerated or accepted by the patient, and are often ineffective. It has been claimed that "coeliac plexus block is the simplest, most effective and least hazardous" means of palliation (49, 59); we think that this is true, and that coeliac plexus block should be considered more often than it is today, and at an earlier stage. Only in rare cases should pain from pancreatitis be treated with a nerve block.
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PMID:Nerve block in pancreatic pain. 234 47

Immunoreactive phospholipase A2 (EC 3.1.1.4) was measured by a new sensitive time-resolved fluoroimmunoassay in the serum of 58 healthy subjects and 103 patients with acute pancreatitis. Patients with acute pancreatitis were grouped according to the etiology and clinical severity of the disease. The mean phospholipase A2 concentration in the reference (healthy) group was 5.5 (SD 1.9) micrograms/L. In acute pancreatitis the mean phospholipase A2 concentration was increased on the first day after hospital admission in all groups, and returned to normal somewhat more slowly than did serum amylase, especially in the patients with severe alcoholic pancreatitis. In this latter group the mean concentration of serum phospholipase A2 on the first day was 42.6 (SD 29.5) micrograms/L. In patients with pancreatic cancer, serum phospholipase A2 was 29.2 (SD 21.3) micrograms/L. The phospholipase A2 and amylase values were closely associated in all groups. The clinical sensitivities were 90.9% for severe alcoholic pancreatitis and 87.5% for pancreatic cancer. Immunochemical determination of phospholipase A2 in serum provides fast and specific detection of injury to pancreatic acinar cells. In addition to the early diagnosis of acute pancreatitis, follow-up determinations of phospholipase A2 seem to be useful in differentiating between mild and severe forms of pancreatitis.
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PMID:Immunoreactive phospholipase A2 in serum in acute pancreatitis and pancreatic cancer. 240 88

Fifty-one patients, 35 men and 16 women, with acute pancreatitis were studied prospectively with early computed tomography (CT). Etiological factors for acute pancreatitis were alcohol abuse (n = 28), gallstones (n = 14), pancreas cancer (n = 3) and miscellaneous (n = 6). Admission serum amylase levels ranged between 68-5,856 U/L with a mean of 1,090 +/- 1,369 U/L. The mean serum amylase level was significantly different between patients with alcoholic pancreatitis (439 +/- 302 U/L) and gallstone pancreatitis (2,480 +/- 1,575) (p less than 0.001). The initial pancreatic CT findings and corresponding mean serum amylase levels were in CT grade A (pancreas normal) 1,499 +/- 1,569 U/L (n = 11), in CT grade B (pancreatic enlargement with inflammation confined to pancreas) 1,144 +/- 1,542 U/L (n = 18), in CT grade C (inflammatory extension into one peripancreatic space) 722 +/- 962 U/L (n = 13) and in CT grade D (inflammatory extension into two or more peripancreatic spaces) 590 +/- 369 U/L (n = 9). However, on separating the etiology subgroups, there was no increase or decrease in the serum amylase level with increasing pancreatic inflammatory involvement. Pancreatic complications (pseudocyst, abscess, necrosis) requiring surgical intervention developed only in patients with CT grades C and D. We conclude that within the etiologic subgroups there is no correlation between the initial serum amylase level and the extent of pancreatic involvement visualized by CT. These findings provide a pathological basis for the clinical observation that the initial serum amylase level cannot predict the outcome in acute pancreatitis.
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PMID:Correlation of serum amylase levels with pancreatic pathology and pancreatitis etiology. 245 72

Clinical, evolutive and therapeutical aspects were studied, of 66 cases of patients with pancreatic pseudocysts hospitalized in the clinic over a period of 27 years. Particular modalities of onset were, those of patients with duodenal stenosis, mechanical jaundice, ascites and pleurisy, those in whom symptomatology suggested kidney or cholecystic disease. The intraoperative diagnosis raises the problem of differentiating a retroperitoneal tumor, identifying the possible association with a pancreatic cancer, and the condition when the pseudocysts are found at a certain distance from the pancreas itself. The therapeutical methods are codified, but recidives are possible. Cholecystectomy removes the biliary cause of pancreatitis which can determine the development of pseudocysts. The death rate of these cases was 6.3%.
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PMID:[Pancreatic pseudocysts]. 252 81

The expression of a novel tumour associated antigen CA 242, defined by the monoclonal antibody C 242, was studied by immunoperoxidase staining in formalin-fixed, paraffin-embedded tissue sections from normal pancreata, pancreata with pancreatitis and benign and malignant pancreatic neoplasms. The antigenic determinant of the C 242 antibody is a sialylated carbohydrate structure, related but chemically different from tumour marker antigens CA 19-9 and CA 50. Thirty-eight of 41 (93%) well to moderately differentiated ductal adenocarcinomas of the pancreas and all cystadenocarcinomas were positive for CA 242. The staining was most intense in the apical border of the cells, and in the intraluminal mucus. Only two out of seven poorly differentiated adenocarcinomas stained, and the number of positive cells was smaller than in well differentiated carcinomas. Only occasional cells were stained in one out of five anaplastic carcinomas. Part of large ducts were positive in 91% (21/23) specimens of chronic pancreatitis. In acute pancreatitis small terminal ducts, centro-acinar cells and some large ducts stained for CA 242. In normal pancreas only a few small terminal ducts were CA 242 positive. Carcinomas always stained more strongly for CA 242 than normal pancreatic tissue adjacent to the carcinoma. The results of CA 242 are compared with those of tumour marker antigens CA 50 and CA 19-9. Serum CA 242 levels were determined in 23 of the patients with pancreatic cancer using a fluoroimmunoassay. Fifteen (65%) patients had an elevated value. There was no clear-cut correlation between the serum levels and the immunohistochemical expression of the CA 242 antigen. The expression of CA 242 in pancreatic tissue resembles that of CA 50 and is similar to CA 19-9. The antigen is expressed in serum of many patients with pancreatic cancer and, therefore, is a potential candidate for a serum tumour marker.
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PMID:Tissue expression of the tumour associated antigen CA242 in benign and malignant pancreatic lesions. A comparison with CA 50 and CA 19-9. 255 79

The CA 19-9 antigen content was studied in 163 patients with pancreatic diseases by radioimmunologic method with the use of commercial test-kits ("Sorin", France). Pancreatitis was diagnosed in 67 patients, pancreatic cancer--in 23, cancer of the major duodenal papilla (MDP)--in 14, malignant neoplasms of the stomach, colon and rectum, liver--in 58. All the results were verified by morphologic studies. The control group included 22 donors. In patients with pancreatic cancer, the considerable increase in the CA 19-9 level was noted when compared with antigen content in the norm and in the other patients examined. The indices of CA 19-9 in pancreatitis don't differ from the normal ones. In MDP cancer and malignant tumours of other location with tumour invasion into the pancreas, the serum CA 19-9 level was increased.
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PMID:[Diagnostic value of radioimmunological analysis of CA-19-9 in the blood serum in cancer of the pancreas]. 262 47

Cases of pancreas divisum (PD) were reviewed in our patients and 19 Japanese and 14 English series during the past 10 yr to see any significant association of PD with certain diseases. PD was diagnosed in 20 (0.64%) among our 3121 patients with successful endoscopic pancreatograms (ERP). Of 20 PD patients, acute pancreatitis in one, chronic pancreatitis in two, ampullary cancer in one, and cholelithiasis in five were diagnosed. Incidences of PD were 2.6% (1/38) in acute pancreatitis, 0.8% (2/248) in chronic pancreatitis, 0% (0/100) in pancreatic cancer, 20% (1/5) in ampullary cancer, and 0.8% (5/615) in cholelithiasis. The incidences were similar to overall incidences of ours and other Japanese series (0.69% of 36,171 patients). Higher incidences of acute pancreatitis (12.9% of 559) and pancreatic cancer (5.5% in 448) may result from the higher overall incidence (4.6% in 16,257) in English series. The relationship between pancreatitis and PD has been controversial, but our present data suggest that PD is a coincidental finding and not a predisposing factor to pancreatitis in Japan.
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PMID:Pancreas divisum. A predisposing factor to pancreatitis? 269 89

This article reviews the epidemiology of cancer of the pancreas, both descriptive and analytical, at all times cognizant of the problems of misdiagnosis, particularly underdiagnosis, of this lethal disease that continue to hinder epidemiological studies. Pancreas cancer is consistently reported to occur more frequently in men than in women, in blacks than in whites, and in urban rather than rural population groups. In some countries, the mortality rates continue to rise, whereas in others, declining levels of disease can be seen among members of younger birth cohorts. Although some of these patterns can be explained by variation in pancreas cancer risk factors, many cannot. Analytical studies consistently demonstrate that cigarette smoking increases the risk of cancer of the pancreas, and this appears, at the present time, to be the only clearly demonstrated risk factor for pancreatic cancer. Although the association with disease risk and coffee consumption, alcohol consumption, occupational exposures, diabetes, pancreatitis, and other factors requires clarification, it appears likely that the most fruitful research area in the coming years may involve exploration of pancreatic cancer risk and nutritional practices.
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PMID:Epidemiology of pancreas cancer (1988). 269 90

The purpose of this study is to clarify the clinicopathophysiology of splenic vein occlusion due to pancreatic disease from hemodynamic points of view. We reviewed the angiographic findings and medical records of 82 patients who had pancreatitis, pancreatic cyst or pancreatic cancer in the pancreatic body and tail. According to the site of occlusion in 16 patients with complete splenic vein occlusion, this entity may be divided into two categories: Type A, an occlusion close to the spleen in which short-gastric system seems to be major collateral, and Type B, an occlusion distant from splenic hilum in which gastroepiploic system becomes prominent as collateral. As compared to 7 patients with incomplete splenic vein occlusion, gastric varices and splenomegaly were frequently observed with the patients having complete occlusion. Among these 16 patients, splenic arterial occlusion was superimposed in 3 patients with pancreatic cancer in whom gastric varices were not detected. Thus, clinical features of this entity must be carefully assessed according to the nature of the underlying disease. Based on these observations, three consecutive phases: Phase 1 Insiduous or latent phase, Phase 2 Collateral developing phase, Phase 3 Vanishing phase may be distinguished for splenic vein occlusion secondary to pancreatic disease.
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PMID:[Splenic vein occlusion due to pancreatic disease: regional portal hypertension from hemodynamic points of view]. 277 Jun 83


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