Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The patient was a 53 year-old male who had 3 syncopal episodes over a 6-month period. In the electrophysiological study, ventricular fibrillation (VF) was repeatedly induced by the ventricular extrastimulus method. Intravenous pilsicainide was administered, and the J-point and ST-segment in the right precordial leads became slightly elevated just following drug administration. Five min later, the patient experienced severe nausea and then vomited twice, at which point the electrocardiogram (ECG) showed increased elevation of the J-point and ST-segment. These ECG changes recovered to normal 30 min later. The cause of his syncope was strongly suspected to be related to the VF associated with Brugada syndrome. An interesting aspect of this case was the particular type of J-point and ST-segment elevation that was induced when the patient experienced nausea and vomiting. It is proposed that this phenomenon originated from the vagal stimulation associated with the nausea and vomiting.
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PMID:Brugada syndrome-like ST-segment elevation increase exacerbated by vomiting. 1522 39

A number of newer antianginal agents, including nicorandil, trimetazidine, and ivabradine, have been synthesized in recent years, but ranolazine, a piperazine derivative that partially inhibits fatty acid oxidation and the late INa current in animal models, is of particular interest mechanistically. Earlier clinical trials with immediate-release ranolazine led to the current sustained-release version tested in the Monotherapy Assessment of Ranolazine In Stable Angina (MARISA) (n = 193) and Combination Assessment of Ranolazine In Stable Angina (CARISA) trials (n = 823) of patients with chronic angina and severe limitation of exercise capacity (ie, < 5 metabolic equivalents). MARISA was a placebo-controlled, randomized trial that compared ranolazine monotherapy (500 mg, 1000 mg, and 1500 mg, twice daily) to placebo. CARISA was a placebo-controlled trial that randomized patients on background beta-blocker or calcium antagonist therapy to placebo or ranolazine (750 mg or 1000 mg, twice daily). Both studies showed a significant increase in total exercise duration, time to angina onset, and time to 1 mm ST segment depression. The average magnitude of increase in exercise duration over placebo was 29 to 56 seconds at peak and 24 to 46 seconds at trough with the 3 doses tested in MARISA, and 24 to 34 seconds greater than placebo with the 2 doses used in CARISA. The beneficial effect was achieved without clinically important changes in rest or exercise heart rate or blood pressure. Weekly angina attack frequency and nitroglycerin usage were significantly reduced in a dose-dependent manner in the 12-week CARISA trial. Reported adverse effects were similar in MARISA and CARISA and consisted of asthenia, nausea, constipation, and dizziness. Syncope, reported in 8 patients at doses of 1000 mg twice daily or more may be related to attenuation of alpha-1 receptor activity. The mean QTc interval increased with dose and was less than 10 msec on ranolazine at 1000 mg twice daily. The mortality rates at 1 and 2 years in MARISA and CARISA open-label run-on studies were 2% and less than 5%, acceptable for this high-risk population with limited exercise capacity. In conclusion, clinical trial evidence with ranolazine to date is consistent with its proposed mechanism of action and demonstrates an effective antianginal profile that may benefit patients with severe chronic angina.
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PMID:Efficacy and safety of a metabolic modulator drug in chronic stable angina: review of evidence from clinical trials. 1537 31

A 67-year-old man with neurally mediated syncope (NMS) complicated by prostatic hypertrophy responded well to combined therapy with pirmenol and midodrine. In 2003, syncope occurred while the patient was driving a car. Results of head-up tilt-table testing (HUT) suggested a mixed type of NMS. Oral administration of disopyramide provided severe urinary obstruction. Pirmenol treatment was not associated with syncope during ordinary HUT, but nausea, sweating, and syncope occurred during HUT with provocative administration of isosorbide dinitrate. Combined therapy with pirmenol and midodrine avoided syncope during HUT, and has prevented attacks since discharge from the hospital.
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PMID:A patient responding to combined therapy with pirmenol and midodrine for refractory neurally mediated syncope complicated by prostatic hypertrophy. 1571 44

A 27-year old female had one episode of transient loss of consciousness and several of near-unconsciousness during strenuous exercise and sexual activity. Episodes started with abdominal discomfort or nausea and light headedness. Unconsciousness never exceeded one minute. When trying to stand up, she felt she would lose consciousness again. We performed a bicycle ergometer exercise test, continuously monitoring blood pressure via non-invasive finger photoplethysmography (Finometer, FMS, The Netherlands). Beat-to-beat changes in stroke volume, cardiac output and total peripheral resistance were calculated using Modelflow (FMS, The Netherlands). At a power of 140 W, the patient reported being near exhaustion; shortly after this she reported nausea. She stopped cycling 30 s later, then saw "black spots" and felt an oncoming loss of consciousness. Dismounting the ergometer and squatting provided immediate relief from symptoms. Symptoms during the test were similar to those during previous episodes. The diagnosis was exercise-induced vasovagal reactions. This is the first report that documents the beat-to-beat changes in blood pressure, stroke volume and total peripheral resistance during exercise-induced vasovagal syncope. It illustrates the usefulness of combining exercise testing with continuous non-invasive blood pressure monitoring in the diagnostic work-up of exercise-induced syncope, and shows the therapeutic value of squatting to prevent loss of consciousness in exercise-related vasovagal syncope.
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PMID:Syncope during exercise, documented with continuous blood pressure monitoring during ergometer testing. 1576 6

Hydatid disease is a parasitic infestation caused by a tapeworm of the genus Echinococcus, and it is common in Mediterranean regions. Cystic lesions cause symptoms via compressing adjacent organs or may be totally silent. Morbidity is usually secondary to free rupture of the echinococcal cyst with or without anaphylaxis, infection of the cyst or dysfunction of affected organs. The cyst of Echinococcus granulosus is commonly located in the liver and frequently causes no symptoms. Anaphylactic reactions as a result of cyst perforation generally occur during interventions such as needle aspiration or open surgery; however, the spillage of cyst fluid with intravascular spread resulting from trauma may also trigger anaphylaxis, and rare case reports of this kind are present in the literature. We report the case of a 17-year-old man who was admitted to the public hospital with a sudden onset of nausea, vomiting and fainting. After a short period of intervention in the emergency department he died. As the cause of his sudden death was unknown, a forensic autopsy was carried out by the Forensic Council of Turkey. The autopsy revealed a macroscopically non-ruptured hydatid cyst in the liver and laryngeal oedema. In histopathological examination, two scolices in the pulmonary artery and inflammatory infiltration mainly composed of mast cells in the larynx were detected. Sudden death in this case was attributed to anaphylactic shock caused by intravascular spread of the cyst contents.
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PMID:Non-ruptured hydatid cyst can lead to death by spread of cyst content into bloodstream: an autopsy case. 1587 31

We report a case of idiopathic omental bleeding in a 27-year-old man who was brought to our hospital after the sudden development of intermittent abdominal pain, nausea, and fainting. Computed tomography showed intra-abdominal fluid and emergency laparotomy revealed a hemorrhagic mass in the omental bursa, which was excised. The patient was successfully treated and a diagnosis of idiopathic omental bleeding was made.
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PMID:Idiopathic omental bleeding: report of a case. 1591 99

A community-based study of 425 older African Americans assessed whether their knowledge and behaviors were consistent with current recommendations regarding out-of-hospital sudden heart attack. More than 90% of the study participants were able to recognize major symptoms of sudden heart attack such as chest pain, shortness of breath, weakness, fatigue, fainting, and sweating, and, to a lesser extent, atypical pain, nausea, lightheadedness, and unexplained anxiety. When asked what they would do first in case they witness sudden heart attack, 97% responded that they would call emergency medical services. In contrast, of the participants who actually witnessed sudden heart attack, 80% called emergency medical services, whereas 20% waited to see if the symptoms would go away; called a neighbor, relative, or a friend before contacting emergency medical services; or took the victim to the hospital. These findings show that reported behavioral intentions were satisfactory, but actual bystanders' actions were not always consistent with current recommendations regarding sudden heart attack.
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PMID:Bystanders of out-of-hospital sudden heart attack: knowledge and behaviors among older African Americans. 1601 57

The effects on blood-injury fear and fainting of scripts concerning pain, nausea, and anger and individual differences in trait anxiety and disgust sensitivity were investigated. Eighteen participants were high in disgust sensitivity and trait anxiety, 11 were low in disgust sensitivity but high in trait anxiety, 10 were high in disgust sensitivity but low in trait anxiety, and 16 were low in disgust sensitivity and trait anxiety. Participants were exposed to pain, nausea, and anger scripts during presentation of blood-injury slides. The ability of the scripts to increase symptoms of fear and faintness, on a state version of the Blood-Injection Symptom Scale (BISS; Page, A. C., Bennett, K. S., Carter, O., Smith, J., & Woodmore, K. (1997). Blood-Injection Symptom Scale (BISS): Assessing the structure of phobic symptomatology elicited by blood and injections. Behaviour Research and Therapy, 35, 457-464) were examined. Analyses indicated that individual differences in trait anxiety and disgust sensitivity interact to generate symptoms of faintness when the pain script was read. That is, disgust sensitive and trait anxious participants reported greater faintness relative to other conditions. The implications for theory and treatment of blood-injury-injection phobia are discussed.
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PMID:The role of cognitions, trait anxiety and disgust sensitivity in generating faintness around blood-injury phobic stimuli. 1622 19

Patients with an untreated myocardial infarction may present with serious late complications. 3 patients are described. A 63-year-old woman became progressively more short of breath 4 days after an acute episode of chest pain accompanied by nausea and sweating. It proved to be a cardiogenic shock following a rupture of a papillary muscle. A man aged 65 collapsed 5 days after an episode of back pain and nausea. This was a cardiac tamponade due to rupture of the left ventricle. A woman aged 74 had transient aphasia and during investigations for this was seen to have anomalies on ECG. She had cerebral emboli and a cardiac aneurysm with associated thrombus. All 3 patients recovered following mitral-valve replacement, repair of the rupture and medicinal treatment for the clot, respectively. Around one-third of patients who have a myocardial infarction do not have chest pain but experience shortness of breath, autonomic nervous symptoms (sweating, nausea, vomiting), extreme and inexplicable tiredness and fainting. These atypical symptoms should suggest myocardial infarction. In order to avoid high morbidity and death from complications such as arrhythmias, heart failure, rupture and aneurysm formation it is important that a patient who has had a myocardial infarction should be treated as soon as possible, preferably by reperfusion therapy.
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PMID:[Complications of an unrecognized myocardial infarction]. 1635 69

The coughing paroxysms of patients with cystic fibrosis may occasion neurological symptoms. Although cough syncope is well-known, and is associated with headache and paralysis, a migrainous mechanism has not been reported. We reviewed the medical records, autonomic testing results, and responses to treatment in two cystic fibrosis patients with similar presentations of cough-induced impairment of consciousness followed by headache and paralysis. A 24-year-old woman and an unrelated 38-year-old man, both with cystic fibrosis, developed post-tussive neurologic deficits. Both patients reported infrequent dramatic spells, always preceded by major hemoptysis, and associated with left-sided paralysis, transient blindness, nausea, and severe pulsating headaches. Autonomic testing demonstrated only postural tachycardia and a near-vasodepressor episode in the woman, and mild, generalized sympathetic dysfunction in the man. Treatment for presumptive migraine with aura with verapamil nearly eradicated symptoms in both patients. Discontinuation of verapamil in the woman was associated with symptom recurrence and a stroke, with significant persistent residual left hemiparesis. In conclusion, cough-induced neurologic deficits were previously reported with cystic fibrosis, without clear understanding of the mechanism of impairment of consciousness. Based on the hemiparesis, nausea, and throbbing headache, which repeatedly followed the events in both patients, and based on the response to verapamil, we hypothesize a migrainous mechanism in both of our patients. The pathophysiology that links the hemoptysis to the spells deserves further investigation.
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PMID:Cough-induced hemiplegic migraine with impaired consciousness in cystic fibrosis. 1637 53


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