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

Purulent pericarditis is an infrequent complication of infections originating in another body location. Symptoms and signs are often absent; a high index of awareness is required for its diagnosis. A patient recovering from extensive necrotic-hemorrhagic pancreatitis presented with tamponade due to methicillin-resistant Staphylococcus aureus (MRSA) purulent pericarditis, further complicated by MRSA endocarditis. Treatment included pericardectomy, IV vancomycin and teicoplanin.
Acta Cardiol 1991
PMID:Purulent pericarditis due to methicillin-resistant Staphylococcus aureus. A case report. 183 57

The control of coronary artery disease depends primarily on its prevention at an early stage. Researchers generally agree that early prevention depends on the elimination or treatment of known risk factors, among which hyperlipidemia occupies a central position. Two European Consensus Conferences have concluded that therapy of hyperlipidemia should always start with dietary counseling. First, subjects with body mass indexes (weight/height) greater than 27 should lose weight. Second, the lipid-lowering diet should provide 55% of calories from carbohydrates; 10 to 15% from protein; and up to 30% from fat comprising 10% each of saturated, monounsaturated and polyunsaturated fatty acids; less than 300 mg/day cholesterol; 35 g/day of fiber derived largely from legumes and other vegetables; and fruit. Further reduction of fat consumption (to 20 to 25% of total energy) and of cholesterol (to less than 150 mg/day) may be attempted when patients respond inadequately to the standard diet. The goal of treatment is to minimize the risk of coronary artery disease and of pancreatitis. Where possible, a low-density lipoprotein cholesterol level of 135 mg/dl (3.5 mmol/liter) should be the goal in hypercholesterolemic patients with multiple or severe risk factors and a level of 155 mg/dl (4 mmol/liter) in the absence of other risk factors. Also, high-density lipoprotein cholesterol greater than 35 mg/dl and triglycerides less than 200 mg/dl are considered important goals of treatment. Some patients with hyperlipidemia do not respond adequately to diet and correction of underlying causes; drug treatment should then be instituted, but careful attention to diet should be continued.
Am J Cardiol 1990 Mar 20
PMID:At what levels of total low- or high-density lipoprotein cholesterol should diet/drug therapy be initiated? European guidelines. 218 Feb 66

Serum amylase was studied in twenty seven patients submitted to cardiac operation. The ages ranged between 16 and 74 (mean 55) years; twenty one (78) were male and six (22%) female. Myocardial revascularization was carried on in 17 patients, mitral valve replacement in four patients, aortic valve replacement in two patients, plastic surgery of the aortic valve in two patients, plastic surgery of the mitral valve in one patient. Blalock Taussig anastomosis was carried on in one patient. The serum amylase was determined in samples obtained before operations, 24 hours and 48 hours postoperatively. Seven (26%) patients showed postoperative elevation of seric amylase in the absence of clinical signs of pancreatitis. Thus, postoperative elevation of seric amylase after cardiac surgery may occur in the absence of pancreatitis and may be due to other factors associated with the patient, with the operative procedure, with drugs used and with surgical complications.
Arq Bras Cardiol 1989 Mar
PMID:[Postoperative serum amylases of patients undergoing cardiac surgery]. 248 Jul 67

Of 400 patients with acute, chronic or chronic relapsing pancreatitis surveyed in the present study, only 54 had had ECG in their files. Among these, 80% showed ECG alterations, mostly sinus tachycardia and diffuse disturbances of ventricular repolarization. The causes of these alterations are, as yet controversial. Some explanations for these alterations are hypovolemia, sepsis and acute inflammatory state. Other important findings in the patients were bundle branch block, not encountered either before the pancreatic crisis or after its resolution, nor was dielectric effect and lesion current observed in either the acute and chronic forms. The possibility of the presence of previous cardiopathy in patients with high alcoholic intake, Chagas' disease, high blood pressure or diabetes, which are quite likely in these patients, should be recalled as important factors: marked electrolytes disorders were not frequent and did not correlate with ECG findings. The aim of this study is to highlight the importance of ECG during systematic search in the follow-up of patients with pancreatitis, in order to better understand associated cardiac disorders and to improve diagnosis, prevention and treatment.
Arq Bras Cardiol 1989 May
PMID:[Electrocardiographic changes in pancreatitis]. 260 72

Information on the prevalence of ECG abnormalities in patients with acute pancreatitis together with pertinent simultaneous laboratory data have been missing. This prospective study was undertaken in order to clarify these points. 54 patients with 72 acute attacks of pancreatitis were examined. 31 patients (57%) had transient ECG abnormalities. The ECG changes consisted mainly of unspecific T-wave changes (25 cases) and accelerated atrial or nodal rhythms (8 cases). The ECG changes were more common in patients with biliary etiology (80%) than in patients with alcoholic etiology (49%), probably partly due to the higher age of the patients with biliary disease. The laboratory data did not give any clue to the cause of the ECG changes. The authors believe that the ECG changes may be due to underlying ischemic heart disease unmasked by the stress of acute pancreatitis, and/or imbalance of the autonomous nervous system.
Acta Cardiol 1980
PMID:Transient ECG changes during acute attacks of pancreatitis. 616 2

Transient electrocardiographic changes in patients with acute cholecystitis, pancreatitis, and pneumonia have been reported in the past. These changes usually are in the form of T-wave inversion, ST-segment depression, and rarely ST-segment elevation in the absence of coronary artery disease. To the authors' knowledge, this is the first report documenting both left ventricular segmental wall motion abnormality and electrocardiographic changes of myocardial injury in the presence of acute pancreatitis.
Clin Cardiol 1994 Sep
PMID:Electrocardiographic and segmental wall motion abnormalities in pancreatitis mimicking myocardial infarction. 772 Feb 88

The authors report two cases of cholesterol embolism and review the literature on this subject. Cholesterol crystal emboli are very serious complication of atheroma, generally situated in the aorta and usually in patients in their sixties. The frequency of cholesterol embolism is 20% in autopsy studies in this population. The embolic process accounts for the polymorphic clinical feature. Clinical signs are always delayed in relation to triggering factors. The symptoms can sometimes simulate a systemic disease. Cutaneous signs are present in 40 to 75% of cases. Acute renal failure is present in 30% of cases. Other signs may also be observed: alteration of the general state, fever, neurological disorders, pain of the lower limbs, myalgia, gastrointestinal haemorrhage or perforation, ischaemic colitis, pancreatitis, mesenteric or coronary angina. A triggering factor is revealed in 80% of cases: aortic surgery, retrograde aortic catheterization, fibrinolysis or oral anticoagulant treatment. The prognosis is poor due to the clinical context, the patient's age and the absence of any specific treatment. The short-term mortality is 60 to 80% according to various series. The best treatment is prevention: carefully assess the indication for an endovascular procedure in an atheromatous patient; if necessary, perform transoesophageal ultrasonography to evaluate the risk; whenever possible change the incision in vascular investigations or operative procedures in high-risk patients.
Ann Cardiol Angeiol (Paris) 1995 Oct
PMID:[Systemic cholesterol embolism]. 866 92

Hyperlipidemia is recognized as one of the major risk factors for the development of coronary artery disease and progression of atherosclerotic lesions. Dietary therapy together with hypolipidemic drugs are central to the management of hyperlipidemia, which aims to prevent atherosclerotic plaque progression, induce regression, and so decrease the risk of acute coronary events in patients with pre-existing coronary or peripheral vascular disease. In patients at high risk of coronary artery disease but without evidence of atherosclerosis, treatment is designed to prevent the premature development of coronary artery disease, whereas in those with hypertriglyceridemia, treatment aims to prevent the development of hepatomegaly, splenomegaly, and pancreatitis. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, are the most potent lipid-lowering agents currently available, and their use in the treatment of hyperlipidemia provides the focus for this review. Particular emphasis is given to cerivastatin, a new HMG-CoA reductase inhibitor that combines potent cholesterol-lowering properties with significant triglyceride-reducing effects. Recently completed primary and secondary intervention trials have shown that the significant reductions in low-density lipoprotein (LDL) cholesterol achieved with statins result in significant reductions in morbidity and mortality associated with coronary artery disease as well as reductions in the incidence of stroke and total mortality. Such benefits occur early in the course of statin therapy and have led to suggestions that these drugs may possess antiatherogenic effects over and above their capacity to lower atherogenic lipids and lipoproteins. Experimental studies have also shown statin-induced improvements in endothelial function, decreased platelet thrombus formation, improvements in fibrinolytic activity, and reductions in the frequency of transient myocardial ischemia.
Am J Cardiol 1998 Aug 27
PMID:Current and future treatment of hyperlipidemia: the role of statins. 973 40

A 72-year-old woman presented to hospital with rapidly progressive dyspnea and chest pain on exertion. Physical findings included a grade 3/6 systolic murmur increased by the Valsalva manoeuvre. Transthoracic echocardiography revealed concentric left ventricular hypertrophy, systolic anterior motion of the mitral valve and critical dynamic outflow tract obstruction. The myocardium was strikingly heterogeneous with hyperdynamic left ventricular systolic function. Laboratory findings included severe hypercalcemia secondary to primary hyperparathyroidism. The patient's outcome was unfavourable with nephrogenic diabetes insipidus, pancreatitis, shock, severe acidosis and death. Postmortem examination confirmed the presence of severe concentric left ventricular hypertrophy, a narrowed left ventricular outflow tract and localized endocardial fibrosis of the left interventricular septum. Microscopic findings showed diffuse calcium deposits of the myocardium, coronary arteries, kidneys and lungs. This appears to be the first report of two-dimensional and Doppler echocardiographic findings in hypercalcemic cardiomyopathy mimicking obstructive hypertrophic cardiomyopathy.
Can J Cardiol 1998 Nov
PMID:Hypercalcemic cardiomyopathy associated with primary hyperparathyroidism mimicking primary obstructive hypertrophic cardiomyopathy. 985 22

Approximately 2% of pancreatitis in adults is drug induced. Although some angiotensin-converting enzyme (ACE) inhibitors have been associated with pancreatitis, to the knowledge of the authors this is the first reported case involving benazepril. This case report presents laboratory- and image-proven pancreatitis in a noninsulin dependent 70-year-old man. The patient took benazepril at three different times and experienced the same epigastric symptoms 30 min after each dose. Possible mechanisms are reviewed. Clinicians should strongly consider discontinuing ACE inhibitors, including benazepril, in patients with pancreatitis of no identifiable source.
Clin Cardiol 1999 Jan
PMID:Angiotensin-converting enzyme inhibitor-induced pancreatitis. 992 57


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