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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increasing surgical experience with the immediate consequences of pancreatic injuries has resulted from parallel growth in the volume of motor vehicle accidents and societal violence. However, few surgeons are aware that complications may be considerably delayed following pancreatic trauma, occurring in some cases months to years after apparent recovery from the original injury. In four patients with blunt pancreatic trauma initially treated by non-operative means, stricture of the main pancreatic duct developed over a period of months as a result of progressive fibrosis at the site of ductal injury. Pancreatic duct hypertension was demonstrated to be present in the obstructed duct, and secondary changes of chronic pancreatitis developed in the obstructed segment of the gland ("upstream" chronic pancreatitis). Seven similar patients with delayed onset of chronic obstructive pancreatitis after pancreatic trauma were found in the literature. Symptoms related to these acquired ductal strictures are most commonly those of abdominal pain and recurrent episodes of acute pancreatitis. Recognition of post-traumatic chronic obstructive pancreatitis principally involves awareness that injuries to the pancreatic duct can produce remote complications. Pancreatoenteric drainage, or resection of the obstructed segment of pancreas, provides prompt and effective relief.
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PMID:Chronic obstructive pancreatitis as a delayed complication of pancreatic trauma. 177 10

The aim of this study was to investigate the usefulness of serum bilirubin, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (APh) and real time ultrasonography (US) in distinguishing between gallstone and non gallstone related acute pancreatitis (A.P.). The second aim was to evaluate whether or nor there was biliary tract hypertension. Both aims were designed in order to evaluate them in the early stage of A.P. Two Groups of patients were studied. Group 1--gallstone related A.P., 63 pts. Group 2--Non gallstone related A.P. 21 pts. Fifty nine (93.6%) of Group 1 and 11 (52.3%) of Group 2 had surgical confirmation. In the other, the diagnosis was based on US and C.T. Blood samples were taken during the three days after admission for biochemical test and US was performed within the same period. Statistical evaluation and Student's t test were used. Biochemical test: when the cut off level was expressed by the upper limit of normal (ULN), the highest diagnostic sensibility was (table 1): ALT 85.7%, APH 80.9%. AST 71%, bilirubin 65%. When the cut off level was chosen at twice the ULN (Table 1), the sensibility was: ALT 61.9%, bilirubin and AST 47%, APh 30%, Group 2 (Table 2) values higher than the ULN were: AST 42.8%, bilirubin 33%, ALT 19%, APh 14.2%. The differences between the two Groups were statistically significant: APh and bilirubin P less than 0.001, ALT less than 0.05 m AST, NS. Ultrasonography: Group 1: gallstones were detected in 96.6% (58/60). Biliary tree was not visualized in 10 (15.8%), diagnosed as normal in 38 (60.3%) and pathologic (dilatation and/or lithiasis) in 15 (23.8%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Value of laboratory tests and echography in the diagnosis of biliary disease in the initial phase of acute pancreatitis]. 209 97

Secondary hyperlipidaemia is common and occurs frequently in disorders such as obesity, alcoholism, diabetes mellitus, hypothyroidism, liver and renal diseases and as a side-effect of drug therapy, particularly for hypertension. Its management may be important to prevent complications such as coronary heart disease and acute pancreatitis. Its study provides many fascinating insights into lipoprotein pathophysiology.
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PMID:Secondary hyperlipidaemia. 210 Jun 85

We report on a patient with acute pancreatitis whose pain was resistant to simultaneous administration of morphine, procaine and Buscopan. This episode was complicated by development of hypertension, tachycardia, angina pectoris, ventricular arrhythmias and electrocardiographic modifications. Analgesia was provided by epidural administration of fentanyl and bupivacaine and brought about rapid resolution of all symptoms. The usefulness of epidural analgesia in acute pancreatitis is discussed.
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PMID:[The value of epidural analgesia in acute pancreatitis]. 230 24

11 cases of primary hyperparathyroidism were seen during 1975-1988. Follow up has varied from 1-10 years. Renal disease in the form of renal calculi and nephro-calcinosis was observed in nine cases (81.8%). Two presented in chronic renal failure and required dialysis. Bone disease was found radiologically in six patients (54.5%); two had bone cysts in multiple bones while all six had subperiosteal bone erosion. Hypertension was found in three patients (27.3%). Proximal myopathy was observed in two cases (18.1%). One patient each presented with hypercalcaemic crisis, chondrocalcinosis and acute pancreatitis. The calcification of blood vessels and cornea was seen in two cases.
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PMID:Primary hyperparathyroidism. 238 Jan 35

The relationship between pancreatic duct pressure, duct permeability to macromolecules and the development of acute pancreatitis was studied in a cat model. Perfusion of the pancreatic duct with 15 mM glycodeoxycholic acid, ethanol administration, or secretagogue-stimulated pancreatic secretion against greater than 50 per cent duct obstruction resulted in an increase in peak pancreatic duct pressure in all animals. Duct permeability to 20,000 molecular weight dextran molecules was increased in 22 of 29 experimental animals compared with two of 22 control animals (P less than 0.01). Perfusion of the pancreatic duct with activated pancreatic enzymes resulted in acute pancreatitis in 24 of 29 experimental animals compared with three of 22 control animals (P less than 0.01). These results suggest that pancreatic ductal hypertension, resulting in increased ductal permeability to large molecules, may be a common early event in gallstone and alcoholic pancreatitis.
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PMID:Pancreatic duct pressure, duct permeability and acute pancreatitis. 247

In this study, the Authors have provoked experimentally acute pancreatitis in the rat by different methods, in order to find out morphological modifications of the pancreas in the initial stage of the disease. In case of biliary and pancreatic duct obstruction with pure pancreatic reflux, both oedema and inflammatory infiltrations were evident, whereas, in the presence of biliary reflux too, more serious histological features were detected. In conclusion, the first sign of alteration in acute pancreatitis could be represented by the association of intraductal hypertension and pure pancreatic reflux.
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PMID:[Etiopathogenetic and histopathologic aspects of acute necrotico-hemorrhagic pancreatitis in experimental animals]. 251 69

We report a patient who was admitted to hospital with acute pancreatitis but who also had malignant phase hypertension. Whilst his alcohol intake was high, there was no objective evidence of alcoholic liver disease and no other underlying cause for pancreatitis was found. The pancreatitis may therefore have been due to pancreatic infarctions associated with fibrinoid necrosis. In all patients with acute pancreatitis, the diagnosis of malignant hypertension should be considered.
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PMID:Malignant hypertension presenting as acute pancreatitis. 260 24

Full functional and morphologic restitution of the pancreas is possible after an attack of acute pancreatitis if the initiating agent or process is removed, whereas chronic pancreatitis is associated with irreversible changes. Most attacks of acute pancreatitis are related to biliary tract stone disease, and it is likely that the offending stone causes obstruction of the pancreatic duct with ductal hypertension. Some recent experimental observations suggest that acute pancreatitis may involve intra-acinar cell activation of digestive enzymes by lysosomal hydrolases. Most patients with chronic pancreatitis develop their disease after many years of ethanol abuse, but the events underlying the pathogenesis of chronic pancreatitis are not known.
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PMID:Classification and pathogenesis of pancreatitis. 265 59

We tested the new radioimmunoassay method of serum phospholipase A2 (PLA2). In healthy individuals, serum PLA2 concentrations were 301 +/- 65.6 ng/dl (mean +/- SD), and in patients with acute pancreatitis, significant elevations of serum PLA2 concentrations were observed. In clinical course of acute pancreatitis, serum PLA2 was maintained high level more longer than serum amylase and elastase 1. In patients with chronic pancreatitis, serum PLA2 concentration were low at a stage of severe exocrine dysfunction, and high at a stage of acute exacerbation. In patients with pancreatic cancer, serum PLA2 concentration were changed in accord with severity of disease states. After endoscopic retrograde pancreatography, serum PLA2 levels immediately elevated significantly, and returned to basal levels 24 hours later. Serum PLA2 concentrations were within normal range in patients with other malignant tumors, diabetes mellitus, chronic liver diseases, and hypertension, whereas in patients with chronic renal failure serum PLA2 concentrations were elevated. These results suggest that measurement of serum PLA2 can be clinically useful for diagnosis of pancreatitis and monitoring of mild and severe stage of pancreatitis.
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PMID:[Clinical studies of serum phospholipase A2 immunoreactivity]. 279 50


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