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 presence of a macro enzyme, i.e. an enzyme with an abnormally high molecular weight, frequently leads to a genuinely increased serum activity or an interference in laboratory assays. This may thereby result in false positive diagnoses, such as acute myocardial infarction or pancreatitis. The various forms of macro enzymes are reviewed. In the case of immune complexes the immunoglobulins and (iso)-enzymes involved are discussed, as well as the specificity of the interaction, the prevalence and clinical relevance, associations with autoimmune or other diseases, and their behaviour in laboratory assays.
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PMID:Macro enzymes: prevalence, composition, detection and clinical relevance. 218 94

alpha-Amylase isozymes were separated by electrophoresis in cellulose acetate to detect the isoforms of the chromogenic substrate manufactured by Lachema, Czechoslovakia. In a group of 20 normal subjects aged 25 to 45, alpha-amylase pancreatic isozyme activity prevailed. Patients with acute myocardial infarction developed, during 36 hours after the onset of the anginal attack, a reduction in the ratio of pancreatic amylase/salivary amylase activities in both increased and normal total alpha-amylase activities. The suggested modified technique of electrophoretic separation of alpha-amylase isozymes may become an effective method for differential diagnosis. Use of this method will help locate the source of hyperamylasemia in various diseases and will thus specify the diagnosis, ruling out the useless therapy for pancreatitis.
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PMID:[Separation of alpha-amylase isoenzymes using cellulose acetate electrophoresis]. 248 11

Mortality and morbidity from ischaemic heart disease (IHD) was studied in 5404 Finnish males aged 35-64 years who had been hospitalised for alcohol-related disease in 1972 without any admissions for IHD during that same period. By record-linkage, morbidity and mortality were followed up to the end of 1975. The mortality of patients with alcohol-related diseases was compared to 1120 patients with acute appendicitis by calculating indirectly age-standardised mortality ratios (SMR). The mortality and morbidity of 5963 patients with acute myocardial infarction or angina pectoris was also studied. The following SMRs for IHD mortality, non-fatal-IHD-hospitalisation and for mortality from all causes respectively, were found: acute myocardial infarction 11.6, 7.2 and 7.2; alcohol intoxication 6.0, 4.5 and 4.5; angina pectoris 5.2, 10.5 and 3.4; liver cirrhosis 2.2, 2.5 and 11.8; alcoholism 1.9, 1.9 and 3.6; pancreatitis 1.8, 1.2 and 4.4; alcohol psychosis 1.7, 2.5 and 4.2. IHD mortality and morbidity appeared to be more prevalent in patients hospitalised with alcohol intoxication than in patients with other alcohol-related diseases. This suggests that rapid drinking predisposes both to serious intoxication and to fatal disturbances of cardiac rhythm.
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PMID:Alcohol-related diseases associated with ischaemic heart disease: a three-year follow-up of middle-aged male hospital patients. 376 98

Hyperlactatemia is frequently observed in critically ill patients. A correlation of blood lactate concentrations and outcome of patients has been proven in circulatory shock, circulatory arrest, acute myocardial infarction, acute hypnotic drug poisoning and severe pancreatitis. However, the prognostic relevance of hyperlactatemia yields from statistical examinations in larger groups of patients. It should not be misused as a reliable prognostic sign in the individual patient, but is of high value in comparing groups of patients. In individual patients, hyperlactatemia is a useful indicator pointing to the severity of illness and to superimposed complications. Blood lactate is of considerable value for the metabolic monitoring of critically ill patients.
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PMID:Prognostic value of blood lactate in critically ill patients. 632 18

In the general population, endoscopic retrograde cholangiopancreatography (ERCP) with endoscopic sphincterotomy is preferable to surgery as therapy for gallstone pancreatitis and acute cholangitis. It is particularly attractive to perform therapeutic. ERCP for symptomatic choledocholithiasis after recent myocardial infarction because of the increased risk of the alternative therapy of cholecystectomy and choledochal exploration. However, after myocardial infarction, patients might theoretically be particularly susceptible to the cardiopulmonary risks of ERCP. The safety of therapeutic ERCP after myocardial infarction is unknown, with only one previously reported case. In a review of 11,367 patients with acute myocardial infarction at four hospitals, four patients (0.04%) underwent therapeutic ERCP after recent myocardial infarction, for indications of recent biliary pancreatitis in three of the patients and recent cholangitis in all four. Cholangitis occurred before, simultaneous with, or after myocardial infarction in the four cases. Initially, the cholangitis was managed medically in three patients. The fourth patient underwent cholecystostomy with local anesthesia. ERCP was performed at 15, 25, 30, or 56 days after myocardial infarction. Endoscopic cholangiography revealed multiple choledocholithiasis in all cases. The calculi were successfully extracted by endoscopic papillotomy and by sweeping the choledochus with a balloon-tipped catheter or basket in all cases. During ERCP, the vital signs remained stable; no cardiac arrhythmias or cardiovascular complications occurred. However, one patient developed mild pancreatitis after ERCP, which rapidly resolved with medical therapy. The four patients rapidly improved after ERCP, with normalization of serum levels of routine biochemical parameters of liver function. These four cases and the one prior case report demonstrate that therapeutic ERCP is not absolutely contraindicated after myocardial infarction and suggest that therapeutic ERCP is preferable to surgery for symptomatic choledocholithiasis after myocardial infarction because of the increased mortality of surgery after myocardial infarction.
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PMID:Endoscopic retrograde cholangiopancreatography with endoscopic sphincterotomy for symptomatic choledocholithiasis after recent myocardial infarction. 879 7

Ischaemia is a rare but often lethal aetiology of pancreatitis. A 67-year-old man underwent aortocoronary by-pass. Postoperatively, he developed atrial fibrillation and possibly acute myocardial infarction. Later, he had acute pancreatitis and underwent laparotomy for purulent peritonitis due to a ruptured pancreatic abscess. Cholesterolosis was found but no gallstones. The postoperative period was heavily complicated and the patient eventually died due to multiorgan failure. The occurrence of ischaemic pancreatitis should be more readily suspected in patients with abdominal symptoms following surgery that induces ischaemia of the pancreas. It is possible that delay in diagnosis accounts for the high death rate of such postoperative complication.
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PMID:Ischaemic necrotizing pancreatitis after cardiac surgery. A case report and review of the literature. 1066 96

We describe the case of a young HIV-positive patient undergoing three-drug antiretroviral therapy that included a protease inhibitor for 9 months, who was admitted to the hospital with an acute myocardial infarction. A coronary angiogram revealed occlusion caused by a thrombus in the proximal third of the anterior descending artery. Complete recanalization was obtained after an angioplasty was performed. At the time of the infarction, only the triglyceride levels were found to be high. Metabolic alterations associated with the prolonged use of protease inhibitors have been described such as an increase in the triglyceride and cholesterol serum levels, diabetes, resistance to insulin, lipodystrophy, and pancreatitis. The consequences of chronic hyperlipidemia are well known in the medical literature, especially premature coronary artery disease. No family history of coronary artery disease was identified in this patient. Whether the genesis of this localized coronary thrombosis was due to a change in the metabolism of the vascular endothelium caused by the protease inhibitors, or by related dyslipidemia, is still to be determined. In this case, the data suggest a strong link between coronary insufficiency and prolonged use of the protease inhibitor.
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PMID:Acute Myocardial Infarction in a 34-Year-Old HIV-Positive Female Patient While Undergoing Active Antiretroviral Therapy Containing a Protease Inhibitor. 1108 68

Transient electrocardiographic changes in patients with acute pancreatitis are well known in the literature. Mostly these changes are in the form of T-wave inversion, ST-segment depression, and rarely ST-segment elevation without the presence of coronary artery disease. We report a patient, in whom electrocardiographic changes mimicked acute inferior myocardial infarction with subsequent evolution of Q-waves in the inferior leads and ischaemia in the anterior wall. To the authors' knowledge, this is the first report documenting the evolution of Q-waves on surface ECG in the absence of myocardial necrosis verified by postmortem examination in the patient, who died of cardiorespiratory failure and massive haemoperitoneum as a complication of ongoing acute necrotizing haemorrhagic pancreatitis. The authors also discuss diagnostic and therapeutic options in patients with acute pancreatitis and ECG pattern of acute myocardial infarction. Acute pancreatitis may mimic acute myocardial ischaemia (or infarction) or these two diseases may be present at the same time. In differential diagnosis, selective coronarography might be helpful and it allows also immediate revascularisation. Administration of thrombolytic therapy in such patients is not safe and might end up with fatal consequences.
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PMID:[Electrocardiographic changes in patients with acute pancreatitis. Case report and review of the literature]. 1149 89

The electrocardiogram (ECG) is of critical importance in the diagnosis of acute myocardial infarction. Clinical conditions such as acute pericarditis, esophageal rupture, pancreatitis, subarachnoid hemorrhage, perforated duodenal ulcer, pneumothorax and status following elective DC cardioversion result in ECG changes that include ST elevation and T wave inversion. This report aims to increase the awareness of non-cardiac syndromes, with ECG abnormalities mimicking acute myocardial infarction, and thus to avoid unjustified thrombolytic therapy. We describe the case of a patient after epileptic seizures and pathological EEG pattern. The ECG showed repolarization abnormalities suggestive of evolving acute myocardial infarction. The cardiac enzymes (except normal Troponin I) were severely elevated and coronary angiography was normal.
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PMID:[The clinical significance of postictal electrocardiographic changes mimicking acute myocardial infarction]. 1264 80

A 71-year-old man presented with left upper quadrant abdominal pain. Serial electrocardiograms (ECGs) demonstrated an evolving left bundle branch block, a sign of acute myocardial infarction (AMI). However, a coronary angiogram demonstrated minimal coronary artery disease, and serum troponin T was undetectable in serial serum measurements. Later, serum pancreatic enzyme levels were elevated and a computed tomography scan of the abdomen was consistent with pancreatitis. In patients presenting with acute pancreatitis and ECG changes suggesting AMI, measurement of serum troponin T concentrations can aid in differentiating ECG changes driven by acute pancreatitis from those of true myocardial ischemia or infarction.
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PMID:A case of acute pancreatitis presenting with electrocardiographic signs of acute myocardial infarction. 1473 Jan 76


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