Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HELLP syndrome continues to be a clinical entity of difficult diagnosis. Weinstein first defined it in 1982 giving the practicing obstetrician a sequence of useful initials (H = hemolysis; EL = elevated liver enzymes; LP = low platelets). Since then a lot has been written and it has become clear that the syndrome is a form of severe preeclampsia. The American College of Obstetrics and Gynecology does not include HELLP in the description of severe pre-eclampsia as such but does accept each of its components as being part of severe pre-eclampsia. The case presented deals with a 33 year old white female, admitted at 27 weeks gestation with nausea, epigastric pain resembling acute abdomen, nose bleeding and mild hypertension. The analysis revealed an abnormal liver profile with elevated GOT, GPT and LDH, heavy proteinuria (14.4 g/day), decreased platelet count (92000/mm3) and elevated total bilirubin. Pregnancy was terminated by cesarean section 24 hours after admission because the patient's condition was deteriorating. Obviously in pre-eclampsia/eclampsia there is a systematic injury to all tissues. Proof of this is the hypertension as a consequence of vascular spasm and proteinuria due to glomerular injury. In HELLP the sequence of events is probably altered; hepatic injury precedes vascular and renal injury of conventional preeclampsia. The syndrome results from many clinical and pathological symptoms derived from endothelial microvascular injury which determine a rapid platelet activation causing vascular spasm, platelet aggregation and further endothelial injury through a feedback mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Massive proteinuria and HELLP syndrome]. 130 8

This study was undertaken to assess our experience with the first 50 patients who underwent CABG without cardiopulmonary bypass. In seven patients left internal mammary artery to left anterior descending artery (LIMA-LAD) grafting was performed through a short left anterior thoracotomy. In 43 other patients median sternotomy was used. Primary CABG was performed in 48 patients; there were two reoperations. Eleven patients had unstable angina. Three patients had left ventricular ejection fraction (LVEF) equal to or lower than 25%. One patient had carcinoma of the right lung coexisting with unstable angina and underwent also right lower lobectomy. In each patient the clinical course, 12-lead ECG, transthoracic echocardiography and the serum levels of creatine kinase (CPK), alanine aminotransferase (ALAT), aspartate aminotransferase (AspAT) were assessed. The need for inotropic or intraaortic balloon counterpulsation (IABP) support and blood transfusion was also recorded. There were three deaths, all in the sternotomy group (6%). A patient with systemic lupus erythemetodes (SLE) died of postoperative MI due to graft thrombosis. Another patient who was found to have porcelain aorta and had LIMA-LAD grafting as a rescue procedure died of MI with low cardiac output. The third patient with unstable angina and ejection fraction of 30% developed postoperative MI with ventricular arrhythmia. One patient with LIMA-LAD graft in whom percutaneous translaminal coronary angioplasty (PTCA) had been abandoned because of coronary spasm developed acute myocardial ischaemia 5 h postoperatively. He had a vein graft placed to LAD in cardiopulmonary bypass, his further course was uneventful. Six patients had IABP support. Nine patients needed inotropic support. Ten patients received blood transfusion. Twelve-lead ECG did not show acute ischaemia or MI, apart from the above described cases. Echocardiographic check showed improved IVS contractility in three patients and better apex motion in one case. In the other survivors the echocardiographic findings were the same as before the procedure. ALAT and AspAT serum levels were normal in all the survivors, and the CPK levels did not exceed 200 IU/ml. One patient from the mini-thoracotomy group had recurrent angina 2 months after the procedure. His left internal mammary artery (LIMA) graft was occluded; we replaced it with a vein graft. All 47 survivors remain asymptomatic, with the mean follow-up time of 6 months. Coronary surgery without cardiopulmonary bypass seems a valuable alternative for high-risk patients.
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PMID:Coronary artery bypass grafting without cardiopulmonary bypass--initial experience of 50 cases. 981 90

Pancreatitis is a rare adverse effect of codeine. We report the case of a 42-year-old man who suffered from epigastric pain 1 hour after taking a tablet containing amoxicillin plus clavulanic acid (500/125 mg) and another tablet containing acetaminophen plus codeine (500/30 mg) for a respiratory infection. He was admitted to the emergency room and was treated with metamizol and pantoprazole. A few minutes after receiving intravenous doses of both drugs he developed a maculopapular and itching eruption with facial angioedema. Laboratory tests showed high levels of serum amylase, GOT, GPT and total bilirubin. Serological tests for several viruses showed no evidence of recent infection. Ultrasonography was negative for biliary lithiasis and showed only cholecystectomy performed in 2000. The patient was sent to our department where skin prick and oral challenge tests were performed with negative results. For ethical reasons, oral challenge with codeine was not carried out. We believe that our patient had codeine-induced pancreatitis. The most likely underlying pathophysiological mechanism was probably codeine-induced spasm of the sphincter of Oddi combined with sphincter of Oddi dysfunction related to a previous cholecystectomy. Allergy departments should be aware of possible non-immunological adverse.
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PMID:Pancreatitis due to codeine. 1594 33

A 63-year-old man with chronic hepatitis C and persistently normal alanine aminotransferase levels was treated with peginterferon alpha-2a (180 microg weekly) and ribavirin (800 mg daily). Hepatitis C virus-ribonucleic acid was negative at week 4. After 12 weeks of therapy, haemoglobin levels had decreased by 3.5mg/dL, and he developed a syncope episode with electrocardiographic signs of myocardial ischaemia. Antiviral treatment was stopped and the ischaemia-like electrocardiographic changes resolved completely within 2 months. Eight months later, because of the previous rapid virological response and patient motivation, he was treated again with peginterferon and ribavirin. Baseline and weekly electrocardiographic recordings were obtained during treatment. At week 4 hepatitis C virus-ribonucleic acid was negative. At week 8, when the haemoglobin levels had decreased by 3.4 mg/dL, the patient developed the same ischaemia-like changes that occurred during the previous treatment. Antiviral therapy was stopped and the electrocardiographic ischaemia-like changes disappeared after 1 month. The patient neither had a history of previous cardiovascular diseases, nor evidence of current disease at myocardial scintigraphy. However, a coronary microvessel spasm, possibly related to drug-toxicity and/or anaemia could not be excluded. This case indicates the need of strict electrocardiographic monitoring in elderly patients undergoing treatment with peginterferon and ribavirin.
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PMID:Recurrent myocardial ischaemia during combination antiviral therapy in a patient with chronic hepatitis C and normal aminotransferase levels. 1791 10

There are currently 2 major therapeutic options for the treatment of hepatic artery complications: endovascular intervention and open surgery. We herein report a retrospective analysis of 14 pediatric patients with hepatic artery complications after pediatric living donor liver transplantation (LDLT) at our institution. We divided them into an open surgery group and an endovascular intervention group based on their primary treatment, and compared the results and outcomes. We then evaluated which procedure is more effective and less invasive. In the open surgery group, recurrent stenosis or spasm of the hepatic artery occurred in 3 of the 8 patients (37.5%). In the endovascular intervention group, 5 of the 6 patients were technically successfully treated by only endovascular treatment. Of the 5 successfully treated patients, 3 developed recurrent stenosis (60%). There were significant differences in the mean length of the operation for the first treatment of hepatic artery complications (open surgery, 428 minutes vs endovascular intervention, 160 minutes; P = .01) and in the mean value of the posttreatment aspartate aminotransferase (AST)/alanine aminotransferase (ALT) (open surgery > endovascular intervention; P = .04/.05). Although endovascular intervention needs to be examined in further studies to reduce the rate of relapse, it is a less invasive method for the patient and graft than open surgery.
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PMID:A comparison of open surgery and endovascular intervention for hepatic artery complications after pediatric liver transplantation. 2337 20