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

Glomerular hyperfiltration, a risk factor for diabetic nephropathy, has been reported in type I insulin-dependent diabetics, but it is not clear if it occurs in other types of diabetes. To ascertain the prevalence of glomerular hyperfiltration in various types of diabetes, we measured glomerular filtration rate (GFR) in 158 diabetics (91 type I, 36 type II without insulin treatment, 20 type II with insulin treatment, and 11 subjects with diabetes secondary to chronic pancreatitis), and classified them as hyper-, normo-, or hypofiltration according to values measured in 36 age-match controls. After elimination of subjects with overt renal disease or hypertension, glomerular hyperfiltration was detected in 35% of the type I diabetics, 32% of the type II diabetics without insulin treatment, one subject with chronic pancreatitis, and one type II diabetics with insulin treatment. Glomerular hyperfiltration was associated with high blood glucose in type I, insulin-dependent diabetics, and with a high apolipoprotein B/A1 ratio in type II, non-insulin-dependent diabetics without insulin treatment. In all subjects with glomerular hyperfiltration, GFR values and urinary albumin excretion were positively related (r = 0.33; n = 34; p = 0.05). Glomerular hyperfiltration is detectable among all types of diabetics.
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PMID:Glomerular hyperfiltration in type I, type II, and secondary diabetes. 156 54

Between January 1985 and September 1989, 75 patients presenting with severe chronic pancreatitis with distal stricture and upstream dilatation underwent stenting of the main pancreatic duct (MPD) through the major papilla (n = 54) or minor papilla (n = 21) in order to drain the predominant duct through a 10F plastic prosthesis. All patients had undergone biliary and pancreatic sphincterotomy with a few cases of complications, and the majority (84%) also ESWL in the period from October 1987 onwards without complications. Relief of pain (94%) occurred parallel to a decrease in the MPD diameter. In a mean follow-up period of 37 months improvement of the nutrition status and relief of pain was seen. Clogging of these large plastic stents was treated by replacement or by another endoscopic or surgical procedure. Complications were treated endoscopically. Further measures necessary due to failure of stenting consisted of laterolateral pancreatico-jejunostomy in 15% of patients and placement of self-expanding 18F metal mesh stents in 29%. There was no mortality due to surgery. It is concluded that stenting of distal strictures in the MPD can lead to rapid resolution of pancreatic pain due to ductal hypertension and is the best means for determining the cause of pain, providing an alternative to surgery. Significant improvement of a stricture by prolonged stenting is however unusual, and such patients treated endoscopically require close follow-up with stent replacement approximately once a year.
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PMID:Stenting in severe chronic pancreatitis: results of medium-term follow-up in seventy-six patients. 160 13

We investigated the etiology of interstitial hypertension in chronic pancreatitis by examining the relationship between pancreatic ductal and interstitial pressures in cats. The main pancreatic duct was cannulated in the tail of the gland and perfused at 1, 2, or 5 ml/hr, to simulate pancreatic secretion. Intraductal and interstitial pressures were measured in four groups of animals: (1) normal cats; (2) normal cats after acutely narrowing the main duct to 25% of its original diameter; (3) normal cats after encasing the body and tail in a rigid latex capsule; and (4) cats with chronic pancreatitis created by narrowing the main duct five weeks earlier. Duct perfusion increased intraductal pressure in all of the cats, but significantly more in groups 2, 3, and 4 compared to group 1. Pancreatic interstitial pressure was unchanged by duct perfusion in groups 1 and 2, but increased in groups 3 and 4. We concluded that the compliant tissue of the normal pancreas expanded to effectively dissipate the increase in duct pressure associated with duct perfusion. In chronic pancreatitis, the inelastic parenchyma and capsule limited the distensibility of the gland, which resulted in elevated interstitial pressures during duct perfusion.
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PMID:Pancreatic ductal and interstitial pressures in cats with chronic pancreatitis. 173 46

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

Between January 1985 and September 1989, 75 patients presenting with severe chronic pancreatitis with distal stricture and upstream dilatation underwent stenting of the main pancreatic duct (MPD) through the major papilla (n = 54) or minor papilla (n = 21) in order to drain the predominant duct through a 10 F plastic prosthesis. All patients had undergone biliary and pancreatic sphincterotomy with a few cases of complications, and the majority (84%) also ESWL in the period from October 1987 onwards without complications. Relief of pain (94%) occurred parallel to a decrease in the MPD diameter. In a mean follow-up period of 37 months improvement of the nutrition status and relief of pain was seen. Clogging of these large plastic stents was treated by replacement or by another endoscopic or surgical procedure. Complications were treated endoscopically. Further measures necessary due to failure of stenting consisted of laterolateral pancreatico-jejunostomy in 15% of patients and placement of self-expanding 18 F metal mesh stents in 29%. There was no mortality due to surgery. It is concluded that stenting of distal strictures in the MPD can lead to rapid resolution of pancreatic pain due to ductal hypertension and is the best means for determining the cause of pain, providing an alternative to surgery. Significant improvement of a stricture by prolonged stenting is however unusual, and such patients treated endoscopically require close follow-up with stent replacement approximately once a year.
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PMID:Stenting in severe chronic pancreatitis: results of medium-term follow-up in seventy-six patients. 186 Apr 48

To assess the contribution of parenchymal hypertension to pain, pancreatic tissue pressures were measured intraoperatively in 17 patients with chronic pancreatitis and in four other patients undergoing pancreatic surgery (reference group). The technique involved direct fine needle cannulation of the pancreas using a flow infusion system, which measured parenchymal resistance to this infusion. Three to six recordings were obtained at each site. In chronic pancreatitis the pressure (mean +/- s.e.m.) was substantially elevated in all regions of the pancreas compared with reference subjects: head (257 +/- 59 versus 19 +/- 5 mmHg, P less than 0.05); body (201 +/- 51 versus 13 +/- 6 mmHg, P less than 0.05) and tail (161 +/- 45 versus 11 +/- 3 mmHg, P less than 0.05). Elevation was greater in areas of calcific disease (281-383 mmHg) than in non-calcific disease (81-120 mmHg, P less than 0.05). Mean pancreatic ductal pressure in 10 patients (seven with calcific disease) was 20 +/- 4 mmHg. Differential pressure measurements within the pancreas helped determine the extent of resection in six patients with diffuse disease. The greatly increased tissue pressures in chronic pancreatitis, especially in the presence of calcification, suggest a possible 'compartment syndrome'.
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PMID:Pancreatic tissue and ductal pressures in chronic pancreatitis. 159 31

The cause of pain in chronic pancreatitis appears to be related to ductal and parenchymal hypertension and possibly to pancreatic ischemia. The management of pain needs a multidisciplinary approach. Medical measures such as abstinence from alcohol and therapy with mild analgesics are useful. Surgery should be considered when the pain begins to interfere with the patient's quality of life. Ductal drainage operations may be indicated when the duct is dilatated. The alternative is pancreatic resection, which, although safe and effective, creates diabetes when much of the pancreas is removed. Newer operations that relieve pain while preserving function are being devised.
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PMID:The cause and management of the pain of chronic pancreatitis. 226 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

The most common complication of chronic pancreatitis is pain, which in many cases seems related to pancreatic ductal obstruction with ductal hypertension. Longitudinal pancreaticojejunostomy is indicated in patients with a dilated (larger than 7 mm) duct and pain that requires narcotic analgesics for relief. Chronic pseudocysts may be corrected surgically without the usual 6-week wait, and asymptomatic pseudocysts less than 4 cm in diameter may not require surgery at all. The relative efficacy and risks of percutaneous drainage of pseudocysts versus the standard surgical approaches need to be studied. Pancreatic fistulas may be external or internal, where pancreatic ascites or hydrothorax can be the clinical manifestation. The pharmacologic suppression of pancreatic secretion (e.g., with somatostatin) may be useful in their management, but surgery may be required. Pancreatic resection or internal drainage is usually effective. Persistent jaundice should be relieved surgically by choledochoduodenostomy to avoid the development of secondary biliary cirrhosis. Obstruction at various levels of the gastrointestinal tract (duodenum, small bowel, colon) may require bypass (gastrojejunostomy) or resection. Hemorrhage from major arteries is an infrequent but often lethal complication of chronic pancreatitis, especially associated with pseudocysts. Angiography is invaluable for diagnosis and occasionally for treatment (embolization). Surgery is preferred in good-risk patients, with suture ligation (resection) of the bleeding source. Chronic pancreatitis is the most common cause of splenic vein thrombosis. The resultant hemorrhage from gastric varices is managed effectively by splenectomy.
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PMID:Complications of chronic pancreatitis. 265 60

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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