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)

We used a vascular access system (VAS) for continuous arterial infusion (CAI) of a protease inhibitor in two patients with acute necrotizing pancreatitis. The infusion catheter was placed into the dorsal pancreatic artery in the first patient and into the gastroduodenal artery in the second, via a femoral artery approach. An implantable port was then connected to the catheter and was secured in a subcutaneous pocket prepared in the right lower abdomen. No complications related to the VAS were encountered. This system provided safe and uncontaminated vascular access for successful CAI for acute pancreatitis.
Cardiovasc Intervent Radiol
PMID:Vascular access system for continuous arterial infusion of a protease inhibitor in acute necrotizing pancreatitis. 1050 1

A case is presented of a 70-year-old man treated for 3 months for necrotizing pancreatitis with multiorgan failure. The autopsy revealed enterococcal endocarditis affecting all eleven valvular cusps of the four heart valves.
Cardiovasc Pathol
PMID:Active infective endocarditis involving all four cardiac valves. 1106 77

We report the case of a 37-year-old man with necrotizing pancreatitis associated with inflammatory extrahepatic portal vein stenosis and progressive ascites. Four months after the acute onset, when no signs of infection were present, portal decompression was performed to treat refractory ascites. Transjugular transhepatic venoplasty failed to dilate the stenosis in the extrahepatic portion of the portal vein sufficiently. Therefore a Wallstent was implanted, resulting in almost normal diameter of the vessel. In follow-up imaging studies the stent and the portal vein were still patent 12 months after the intervention and total resolution of the ascites was observed.
Cardiovasc Intervent Radiol
PMID:Transjugular portal venous stenting in inflammatory extrahepatic portal vein stenosis. 1235 15

Pancreatic pseudoaneurysm is a relatively uncommon complication of chronic pancreatitis, with an associated high mortality if rupture or hemorrhage occurs. We present a case of pancreatic pseudoaneurysm complicating pancreatitis which was successfully treated by direct percutaneous injection of thrombin into the aneurysmal sac. Follow-up at 8 weeks did not demonstrate recurrence. This case indicates that percutaneous thrombin injection offers effective treatment of visceral arterial pseudoaneurysms.
Cardiovasc Intervent Radiol
PMID:Ultrasonic-guided percutaneous injection of pancreatic pseudoaneurysm with thrombin. 1456 87

One month after onset of an acute biliary pancreatitis, a 75-year-old man developed refractory ascites. Duplex ultrasound and CT scan revealed a focal stenosis of the extrahepatic portal vein as confirmed by transhepatic direct portography. In the same session, this stenosis, responsible for symptomatic prehepatic portal hypertension, was successfully dilated and stented and afterwards a residual pressure gradient of 1 mmHg over the stented segment was measured. One week after the stenting procedure the patient was free of ascites and control physical and biochemical examination one year later is completely normal.
Cardiovasc Intervent Radiol
PMID:Pancreatitis-induced extrahepatic portal vein stenosis treated by percutaneous transhepatic stent placement. 1466 23

Dyslipidemia, characterized by elevated serum levels of triglycerides and reduced levels of total cholesterol, low-density lipoprotein-cholesterol (LDL-C) and high-density lipoprotein-cholesterol, has been recognized in patients with human immunodeficiency virus (HIV) infection. It is thought that elevated levels of circulating cytokines, such as tumor necrosis factor-alpha and interferon-alpha, may alter lipid metabolism in patients with HIV infection. Protease inhibitors, such as saquinavir, indinavir and ritonavir, have been found to decrease mortality and improve quality of life in patients with HIV infection. However, these drugs have been associated with a syndrome of fat redistribution, insulin resistance, and hyperlipidemia. Elevations in serum total cholesterol and triglyceride levels, along with dyslipidemia that typically occurs in patients with HIV infection, may predispose patients to complications such as premature atherosclerosis and pancreatitis. It has been estimated that hypercholesterolemia and hypertriglyceridemia occur in greater than 50% of protease inhibitor recipients after 2 years of therapy, and that the risk of developing hyperlipidemia increases with the duration of treatment with protease inhibitors. In general, treatment of hyperlipidemia should follow National Cholesterol Education Program guidelines; efforts should be made to modify/control coronary heart disease risk factors (i.e. smoking; hypertension; diabetes mellitus) and maximize lifestyle modifications, primarily dietary intervention and exercise, in these patients. Where indicated, treatment usually consists of either pravastatin or atorvastatin for patients with elevated serum levels of LDL-C and/or total cholesterol. Atorvastatin is more potent in lowering serum total cholesterol and triglycerides compared with other hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, but it is also associated with more drug interactions compared with pravastatin. Simvastatin and lovastatin are significantly metabolized by cytochrome P450 enzymes (CYP3A4) and are therefore not recommended for coadministration with protease inhibitors. A fibric acid derivative (gemfibrozil or fenofibrate) should be used in patients with primary hypertriglyceridemia. However, it must be kept in mind that protease inhibitors, such as nelfinavir and ritonavir, induce enzymes involved in the metabolism of the fibric acid derivatives and may, therefore, reduce the lipid-lowering activity of coadministered gemfibrozil or fenofibrate. In certain patients HMG-CoA reductase inhibitors may be used in combination with fibric acid derivatives but patients should be carefully monitored for liver and skeletal muscle toxicity. Select patients may experience improvements in serum lipid levels when their offending protease inhibitor(s) is/are exchanged for efavirenz, nevirapine, or abacavir; however each patient's virologic and immunologic status must be taken closely into consideration.
Am J Cardiovasc Drugs 2002
PMID:Management of protease inhibitor-associated hyperlipidemia. 1472 85

Combined hyperlipidemia is increasing in frequency and is the most common lipid disorder associated with obesity, insulin resistance and diabetes mellitus. It is associated with other features of the metabolic syndrome including hypertension, hyperuricemia, hyperinsulinemia and highly atherogenic subfractions of lipoprotein remnant particles including small dense low density lipoprotein-cholesterol. This review examines the mechanisms by which combined hyperlipidemia arises and the various drugs including fibric acid derivatives, hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, and nicotinic acid which can be used either as monotherapy or in combination to manage it and to improve prognosis from atherosclerotic disease in diabetes mellitus, insulin resistant states and primary combined hyperlipidemia. The therapeutic approach to combined hyperlipidemia involves determination of whether the cause is hepatocyte damage or metabolic derangements. Combined hyperlipidemia due to hepatocyte damage should be treated by attention to the primary cause. In the case of metabolic dysfunction because of imbalance in glucose and fat metabolism, therapy of diabetes mellitus and obesity should be optimised prior to commencement of lipid lowering drugs. Both fibric acid derivatives and HMG-CoA reductase inhibitors can be used in the treatment of combined hyperlipidemia with fibric acid derivatives having greater effects on triglycerides and HMG-CoA reductase inhibitors on LDL-C though both have effects on the other cardiovascular risk factors. There is some evidence of benefit with both interventions in mild combined hyperlipidemias and large scale trials are underway. Fibric acid derivatives and HMG-CoA reductase inhibitor therapy can be combined with care, provided that gemfibrozil is avoided, fibric acid derivatives are given in the mornings and shorter half -life HMG-CoA reductase inhibitors are used at night. Combined hyperlipidemia emergencies occur with predominant hypertriglyceridemia in pregnancy or as a cause of pancreatitis. Therapy in the former should aim to reduce chylomicron production by a low fat diet and intervention to suppress VLDL-C secretion using omega-3 fatty acids. In the latter case, fluid therapy alone and medium chain plasma triglyceride infusions usually reduce levels satisfactorily though apheresis may be required. Blood glucose levels also need aggressive management in these conditions. Combined hyperlipidemia is likely to become an increasing problem with the increase in the prevalence of obesity and diabetes mellitus and needs aggressive management to reduce cardiovascular risk.
Am J Cardiovasc Drugs 2001
PMID:Drug treatment of combined hyperlipidemia. 1472 15

Pseudoaneurysm is a relatively rare but serious complication of pancreatitis which is often fatal. We report successful stent-graft placement in the superior mesenteric artery in a 45-year-old man with a pancreatic pseudocyst that grew during therapy for chronic pancreatitis and developed into a pseudoaneurysm. After a stent graft was inserted in the superior mesenteric artery, the pseudoaneurysm disappeared and no further complications developed. Stentgraft placement was considered to be a useful therapy for pseudoaneurysms in the superior mesenteric arterial region.
Cardiovasc Intervent Radiol
PMID:Superior mesenteric artery stent-graft placement in a patient with pseudoaneurysm developing from a pancreatic pseudocyst. 1510 33

Endothelin (ET) is among the strongest endogenous vasoconstrictors known and a potent mitogen. A rich body of experimental evidence suggests that ET contributes to vascular remodeling and end-organ damage in several cardiovascular conditions. Therefore, blockade of ET receptors has been suggested as an attractive target in a number of acute and chronic cardiovascular indications, including pulmonary arterial hypertension (PAH), systemic hypertension, and heart failure. To date, clinical studies have confirmed expectations in PAH and yielded promising initial results in systemic hypertension, which are currently awaiting confirmation in large-scale trials. In contrast, no added benefit could be demonstrated in large clinical trials on top of current standard treatment in both acute and chronic heart failure. Further clinical development in heart failure has therefore been suspended. Other indications that are currently being studied clinically or would possibly merit clinical trials include acute myocardial ischemia and reperfusion, cerebral vasospasm after intracranial bleeding, glaucoma, acute severe pancreatitis, systemic sclerosis, (diabetic) renal failure, restenosis after angioplasty/stent implantation, and late transplant rejection. This article critically reviews the available clinical data on ET receptor antagonism in cardiovascular indications against the background of the underlying preclinical research.
J Cardiovasc Pharmacol 2005 Feb
PMID:Endothelin receptor antagonists: clinical realities and future directions. 1565 68

A 26-year-old man presented with high output heart failure and severe systolic left ventricular dysfunction. The underlying cause was determined to be thyrotoxicosis. With aggressive treatment of the hyperthyroid state, near-normalization of the patient's left ventricular systolic function was achieved. Unfortunately, he succumbed to pancreatitis, followed by multiple ICU complications. A brief review of the literature is provided.
Cardiovasc Pathol
PMID:Thyrotoxicosis-an uncommon cause of heart failure. 1571 Feb 88


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