Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of gene transfer systems to study cell function makes it apparent that overexpression of a transgene can restore or improve the function of a protein and positively influence cell function in a predetermined manner for purposes of counterbalancing cellular pathophysiology. The ability of some gene transfer vehicles to produce transgene product within hours of delivery positions gene transfer as a unique pharmaceutical administration system that can quickly affect production of biologic response modifiers in a highly compartmentalized fashion. This approach can be expected to overcome many of the adverse effects and high costs of systemic delivery of recombinant pharmaceuticals. This review highlights recent advances toward development of gene therapies for acute illnesses with particular emphasis on preclinical models of disease. In this context, a growing body of data suggests that gene therapies for polygenic and non-genetic diseases such as asthma, cardiogenic and non-cardiogenic pulmonary edema, stroke, subarachnoid hemorrhage, seizures, acute myocardial infarction, endovascular thrombosis, and infections may someday be options for the treatment of patients.
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PMID:Gene therapy for acute diseases. 1173 35

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

Rheumatological conditions can sometimes present as emergencies. These can occur due to the disease process or may be iatrogenic. Some of the important articular emergencies are septic arthritis, acute polyarthritis and atlanto-axial dislocation. Classical polyarteritis nodosa may present with massive gastro-intestinal bleeding, intestinal perforation or acute pancreatitis. Adult respiratory distress syndrome, bilateral pneumonitis and diffuse alveolar haemorrhage due to systemic lupus erythematosus or systemic necrotising vasculitis and ventilatory failure due to polymyositis are some of the respiratory emergencies. Scleroderma is well known to cause renal crisis which can be fatal if not diagnosed and managed promptly. Microscopic polyangiitis and Wegener's granulomatosis may cause rapidly progressive renal failure. Cerebrovascular accident, cortical vein thrombosis, seizures and acute psychosis are important neurological complications of rheumatic disease. Cardiac emergencies include tamponade, acute myocarditis and acute myocardial infarction. Vision can be threatened in Behcet's disease, temporal arteritis and seronegative spondylarthritis. Catastrophic antiphospholipid syndrome is a devastating emergency. The management of above emergencies includes critical care, immunosuppression when indicated and withdrawal of the offending drug. Anticoagulants have to be used in the management of antiphospholipid syndrome. A good understanding of these conditions is of paramount importance for proper management.
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PMID:Emergencies in rheumatology. 1516 86

The World Health Organization recognizes biochemical markers of myocardial injury as one of the three criteria for the diagnosis of acute myocardial infarction. We report the first case of elevated troponin I in a patient after a grand mal seizure in the hospital, with no evidence of myocardial infarction and no rhabdomyolysis. Cardiac catheterization and two-dimensional echocardiographic findings were normal. Four months later, the patient was readmitted, again having experienced a grand mal seizure. She was asymptomatic for cardiac disease in both instances. There was a temporal correlation between troponin I levels and seizures. Studies have shown that a troponin level above 3.5 ng/mL implies significant myocardial injury. Our patient had troponin I values as high as 5.5 ng/mL and 6.3 ng/mL. This case implies that troponin I can be significantly increased after a grand mal seizure, and with low clinical suspicion for myocardial injury this abnormality should be disregarded.
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PMID:Elevated serum cardiac troponin I level in a patient after a grand mal seizure and with no evidence of cardiac disease. 1536 81

We report a case with epileptic seizures, cognitive dysfunction, livedo reticularis, renal microangiopathy, acute myocardial infarction and high titres of anticentromere antibodies (ACA) and IgG/IgM anticardiolipin antibodies. This is a rare association between primary antiphospholipid syndrome and ACA positivity that has not been reported so far in the literature.
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PMID:A case with epilepsy, cognitive impairment, renal microangiopathy and high titres of anticentromere and anticardiolipin antibodies. 1617 35

A novel delta-receptor selective compound, ARD-353 [4-((2R,5S)-4-(R)-(4-diethylcarbamoylphenyl)(3-hydroxyphenyl)methyl)-2, 5-dimethylpiperazin-1-ylmethyl)benzoic acid], was evaluated for activity on infarct size in a rat model of acute myocardial infarction. ARD-353 was characterized as having delta receptor selectivity using radioligand binding and had no apparent selectivity between delta receptor subtypes as determined by [(3)H] cyclic [D-Pen(2),D-Pen(5)]enkephalin (delta(1)) and [(3)H]Deltorphin II (delta(2)) competition binding. ARD-353 also showed selective delta receptor agonist activity in mouse-isolated vas deferens. There was no evidence of any seizure-like convulsions when ARD-353 was administered to mice either i.v. or p.o., implying minimal penetration of the blood-brain barrier. ARD-353 decreased infarct size in a left anterior descending coronary artery (LAD) occlusion model of myocardial infarction. In animals pretreated with ARD-353 (i.v.) and then subjected to 30 min of LAD occlusion followed by 90 min of reperfusion, infarct size was reduced in a dose-dependent manner compared with vehicle-treated controls. The effects of ARD-353 on infarct size were blocked by the delta(1)-opioid selective antagonist 7-benzylidenenaltrexone, indicating a significant role for the delta(1)-opioid receptor in the cardioprotective mechanism of ARD-353. ARD-353 (0.3 mg/kg i.v.) produced significant protection when administered 5 min and 12 and 48 h before ischemic insult or when given immediately after the ischemic insult (at the start of reperfusion). Given the lack of central nervous system effects and beneficial efficacy in the rat model of myocardial ischemia, it is felt that ARD-353 is the first nonpeptide delta-receptor agonist with true potential for clinical use before surgically induced ischemia or in an emergency setting.
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PMID:ARD-353 [4-((2R,5S)-4-(R)-(4-diethylcarbamoylphenyl)(3-hydroxyphenyl)methyl)-2,5-dimethylpiperazin-1-ylmethyl)benzoic acid], a novel nonpeptide delta receptor agonist, reduces myocardial infarct size without central effects. 1618 52

A 50-year-old patient had status epilepticus and no adequate reactions nine days after prolonged out-of-hospital cardiac arrest. The cause of the arrest was acute myocardial infarction which was treated successfully with percutaneous cardiac intervention (PCI) and a stent placement. He was treated with therapeutic hypothermia (33 degrees C) for 24h and in intensive care with respiratory support for 42 days. One year later he has fully recovered and is back to normal life and academic work. The previously reported 100% prognosis of a poor neurological outcome in the presence of seizures 72 h post arrest may need to be re-examined after introduction of therapeutic hypothermia.
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PMID:Determination of prognosis after cardiac arrest may be more difficult after introduction of therapeutic hypothermia. 1651 42

We report the first case in the literature of acute myocardial infarction due to very late (5 years) drug-eluting stent (DES) thrombosis presenting with inferior ST-elevation myocardial infarction immediately after epileptic convulsive seizures in a patient with known coronary artery disease. A bare-metal stent had been implanted in the left anterior descending coronary artery in 2002, and a drug-eluting stent implanted in the right coronary artery in 2003. We discuss the possible pathogenetic mechanisms implied in convulsive epileptic crisis resulting in development of very late DES thrombosis.
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PMID:Myocardial infarction due to late stent thrombosis following epileptic convulsive seizures. 1965 91

The majority of cardiac related deaths are due to ischemic heart disease, with the most common clinical scenario being severe coronary artery atherosclerosis resulting in left ventricular myocardial infarction. However, infarction of other cardiac chambers does occur, and often has specific clinical associations. We report a case of a 70-year-old man who suffered from left atrial infarction that resulted in a transmural rupture of his left atrium. The patient had a history of rheumatic heart disease, mitral valve stenosis, and severe atherosclerotic coronary artery disease. Four days before death, he underwent mitral valve replacement and left circumflex coronary artery bypass. Two days later, he developed atrial fibrillation. On the day of death, he had decreased mental status, questionable seizure activity, hematemesis, ventricular tachycardia, and eventually asystole. At autopsy, he had significant hemopericardium with a fibrinous pericarditis and bilateral hemothoraces (total blood volume: 1250 mL). A 0.1 to 0.2 cm left atrial transmural defect was identified. The prosthetic mitral valve was free of vegetations, and completely intact. Similarly, the left circumflex artery bypass graft was completely patent and unremarkable. Severe calcific atherosclerosis was of his native left circumflex and left main coronary arteries. Microscopic examination revealed acute myocardial infarction of the left atrium at the rupture site. The anatomy of atrial circulation as well as the pathology and consequences of atrial infarction are discussed.
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PMID:Left atrial infarction: a case report and review of the literature. 1994 18

To report a case of delayed myocardial infraction after rituximab infusion. A 52-year-old woman with history of refractory idiopathic thrombocytopenic purpura had hypertension, seizure, and mild coronary artery disease and received rituximab; after 24 hours, she returned back with chest pain, nausea, and vomiting. Her electrocardiogram showed a ST-elevation in the II, III, aVF, and aVR lead and ST depression in I and aVL lead; after another complementary test, the myocardial infraction was confirmed. The patient was sent to the intensive care unit, and after 8-day hospitalization, she was discharged. Based on the Naranjo Probability Scale, the likelihood of rituximab-induced acute myocardial infarction in this case was probable. Rituximab is generally well tolerated; however, cardiovascular effects of this drug can be fatal. The side effects usually occur during or a short time after infusion; this case demonstrated that rituximab side effects may occur with delay. This case demonstrates, although a rare phenomenon, myocardial infraction may occur after 24 hours and clinicians should be aware of this fatal effect even after a period of time in patients receiving rituximab, especially in patients with history of coronary artery disease.
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PMID:Delayed Myocardial Infarction Associated With Rituximab Infusion: A Case Report and Literature Review. 2619 24


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