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)

A 35-year-old man was hospitalized after a sudden onset of transient syncopal attack without accompanying complaints of headache or nausea. He was slightly disorientated but neurologically normal. He had a blood pressure of 150/90mmHg and a pulse rate of 40/min. An ECG showed marked sinus brady-cardia with ventricular escaped rhythm followed by advanced atrioventricular (AV) block. Some components of conducted ventricular beats showed aberration. There was no significant ST or T wave abnormality in normally captured QRS components except for prominent T in leads II, III and aVF. At first, we thought that he might require temporary pacing because of Adams-Stokes attack. However, after administration of atropine sulfate, the ECG returned to normal sinus rhythm with heart rate of 88/min. Then he began to complain of headache followed by a convulsive seizure. A CT scan and angiogram revealed a ruptured aneurysm at the top of the basilar artery, which was successfully clipped. A wide spectrum of ECG changes can be demonstrated in practically all patients with subarachnoid hemorrhage (SAH). Prolonged QT interval, ST-T changes, U wave, sinus tachycardia, or ventricular premature complex are the common abnormalities probably caused by increased circulating catecholamine. As bradyarrhythmia in patients with SAH is an uncommon finding, its mechanism has not yet been defined. Transient sinus bradycardia with advanced AV block in this patient might have been caused not by elevated intracranial pressure (Cushing phenomenon) but by drastic discharge of the parasympathetic nerve. This case serves to illustrate the vigilance required in determining whether abnormalities of cardiac rhythm are instrumental in causing neurological symptoms and signs or a disorder of cerebral function.
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PMID:[A case of subarachnoid hemorrhage with sick sinus and advanced AV block]. 151 79

A total of 20 patients with histologically proven primary hepatocellular carcinoma (PHC) received mitoxantrone IV at a dose of 10-16 mg/m2 every 3 weeks. All patients had previous hepatitis B infection. None underwent remission after treatment; 2 had stable disease and 18 progressive disease. The median overall survival was 13 weeks (range, 1-59 weeks). There was no evidence of significant antitumor activity for mitoxantrone in our patients with PHC. Hematotoxicity occurred in 100% of the patients with grades 2-4 leukopenia, 89% of those with grades 1-4 anemia, and 26% of those with grades 2-3 thrombocytopenia. Cardiotoxicity occurred in 20% of the patients after 14-30 mg/m2 mitoxantrone; these included complete heart block with fatal outcome in one case, decreased ventricular ejection fraction in one, and sinus tachycardia in two. Nausea, vomiting, fever, diarrhea, and alopecia were mild and occurred in 15%-45% of the patients Therefore, patients with PHC following hepatitis B infection may be less tolerant to mitoxantrone, resulting in the apparent increase in toxicities.
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PMID:Phase II study of mitoxantrone in unresectable primary hepatocellular carcinoma following hepatitis B infection. 253 94

A young woman with acute intermittent porphyria is described. She was admitted in a prolonged attack and had developed a flaccid quadriplegia. During the course she showed various manifestations of the autonomic nervous system, including pupils, gastrointestinal tract, cardiovascular system and others. On admission her pupils were equally mydriatic, and reacted to light sluggishly. Dilation of the pupils was seen when cocaine was instilled, but not when adrenalin. It was suggested that the parasympathetic control of pupils was disturbed. She complained repeatedly abdominal pain, nausea, vomiting, and constipation. However, diarrhea was rarely found. Radiological examinations revealed that her bowel movements were markedly impaired. Sinus tachycardia and elevation of blood pressure were frequently observed with attacks, and they correlated with the clinical course. With tachycardia the coefficient variance of R-R interval was markedly decreased, and large dose of atropine failed to accelerate the heart rate. These indicate that the vagal function was markedly impaired with attacks. The effects of isoproterenol and of propranolol on the heart rate were normal. Phenylephrine and phentolamine changed the blood pressure normally. From these it was concluded that the sympathetic nervous function was not so impaired at the time examined. However, with the elevation of blood pressure plasma and urinary noradrenaline were markedly increased. Other autonomic and related manifestations observed during the course included disorders of sweating, loss of sphincter control, fever of unknown cause and amenorrhea.
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PMID:[Autonomic dysfunctions in acute intermittent porphyria]. 258 92

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Premature uterine contractions were treated by intravenous beta-mimetics in 190 patients during a 2-year period. History and physical examination were directed toward identification of patients with cardiac problems. Unexpected cardiac pathology was discovered in 14 patients, all of whom exhibited severe and continuous nausea, retrosternal pain, or dyspnea during beta-mimetic administration. Treatment was immediately discontinued in the presence of S-T depression, supraventricular tachycardia, nonspecific T wave changes, and sinus tachycardia with right axis deviation. Further investigation revealed obstructive cardiac myopathy in one case and atrial septal defect in another. Such changes might be identified earlier by more extensive screening procedures (such as electrocardiogram) before drug administration. Administration of beta-mimetic agents may uncover previously unexpected cardiac pathology. Continuation of ritodrine in such cases is contraindicated and potentially hazardous.
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PMID:Unexpected cardiac pathology in pregnant women treated with beta-adrenergic agents (ritodrine). 668 69

A total of 221 cases of deliberate acute overdose with fluvoxamine reported to the Paris Poison Centre, and 78 cases collected by the International Drug Safety Department of Duphar BV were analysed. Other agents, mainly benzodiazepines, neuroleptics, other antidepressants and alcohol, were also taken in 77% of the cases. The acute toxicity that could be attributed to fluvoxamine alone was rarely severe. The symptoms observed were always benign when the dose of fluvoxamine was below 1000 mg and included drowsiness, tremor, nausea, vomiting, abdominal pain, bradycardia and/or anticholinergic effects (dry mouth, mydriasis, sinus tachycardia, urinary retention). Seizures occurred in a few cases after high doses (generally > 1500 mg). Cardiotoxicity was not a serious problem; sinus bradycardia was noted with doses of less than 1000 mg, but was always moderate and required no treatment. Conduction abnormalities were rare.
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PMID:Acute fluvoxamine poisoning. 790 58

To study acute organophosphorus (OP) poisoning cases, 190 OP-intoxicated cases admitted to Civil Hospital, Ahmedabad, were investigated in depth. The group consisted of subjects ranging from 11 to 60 years of age, with the maximum number of cases in the age group 21-30 years and a male-to-female ratio of 2.1:1. Most of the subjects (71.61%) were partially educated, 24.2% of the cases were illiterate, and only 4.2% of the cases were highly educated. Socioeconomically, 21.1% of the subjects were of low economic status, 52.6% were low middle class, 16.8% were upper middle class, and only 9.5% were upper class. With regard to marital status of the subjects, 98 cases were married and 92 were unmarried. About 67.4% of the cases had the intention of committing suicide, 16.8% of the cases were the result of occupational exposure, and 15.8% of the cases were from accidental poisoning. Social and domestic problems (37.5%), marital friction (15.6%), financial stress (15.6%), love affairs (14.1%), job problems (10.9%), chronic illness (4.7%), and failure in examination (1.6%) were observed as the precipitating factors. Muscarinic manifestations such as vomiting (96.8%), nausea (82.1%), miosis (64.2%), excessive salivation (61.1%), and blurred vision (54.7%) and CNS manifestations such as giddiness (93.7%), headache (84.2%), disturbances of consciousness (44.2%), and typical pungent odor from mouth and clothes (77.9%) were the main presenting symptoms. Cardiac manifestations such as sinus tachycardia (25.3%), sinus bradycardia (6.3%), and depression of ST segments with T-wave inversion (6.3%) were observed electrocardiographically, with hypertension (10.5%) and muscular twitching in some (2.1%) cases. Biochemical changes such as albuminuria (12.6%) and azotemia (18.9%) with inhibition of acetylcholinesterase enzyme activity in blood were recorded in 78.9% of the cases. About 89.5% of the cases recovered completely, 4.2% of the cases absconded after partial recovery, and 6.3% of the cases died. The mortality rate (6.3%) depended on various factors such as the organophosphorus compound consumed, the amount ingested, the time interval for hospitalization, and the general health of the patient. Chances of recovery were higher when the patient was hospitalized at the earliest indication.
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PMID:A clinical, biochemical, neurobehavioral, and sociopsychological study of 190 patients admitted to hospital as a result of acute organophosphorus poisoning. 832 67

A 42-year-old man came to our emergency room hyperthermic (oral temperature, 42.4 degrees C), diaphoretic, and delirious. Other findings included labile blood pressure, sinus tachycardia (heart rate, 138/min), tachypnea (respiratory rate 34/min), muscle rigidity, and incontinence. Two days earlier, he had gone to a local clinic with complaints of abdominal pain, nausea, and vomiting. Promethazine was prescribed, and this was the patient's only medication on admission. Laboratory studies showed leukocytosis, hypernatremia, metabolic acidosis, elevated creatinine phosphokinase level, elevated transaminase levels, azotemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobulinuria. The clinical and laboratory findings were characteristic of the neuroleptic malignant syndrome, with promethazine as the offending agent.
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PMID:Neuroleptic malignant syndrome due to promethazine. 1054 78

The authors present the case of a 65 year-old female who was admitted to the emergency room with epigastric pain, headache, palpitations, nausea, vomiting and sweating. The laboratory tests performed showed elevation of CK and CK-MB and the ECG presented sinus tachycardia. T-wave inversion and prolonged QT interval. The echocardiogram was normal. The patient was admitted to the ICU and during the standard myocardial infarction treatment (including beta-blocker) a wide range of the arterial pressure (230/140 to 70/40 mm Hg) was registered. In view of these new data, the hypothesis of pheochromocytoma and catecholamine induced myocarditis was suggested and later confirmed by high levels of plasmatic and urinary catecholamines. The abdominal echography. CT and MRI showed a large retroperitonal and para-aortic mass. The administration of phenoxybenzamine (30 mg/day) led to the normalization of the ECG and arterial pressure and the respective clinical improvement. The anatomopathological exam, after surgical removal, confirmed our hypothesis. Sixteen months after the surgical procedure the patient is assymptomatic, with normal arterial pressure and normal levels of plasmatic and urinary catecholamines.
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PMID:[Extra-adrenal pheochromocytoma simulating acute myocardial infarction]. 1060 62

Cardiac arrhythmias are a well known cause of mortality for patients with heart disease. However, sinus tachycardia is a more unusual arrhythmia which can lead to serious heart damage or death. Even young patients with structurally normal hearts may become gravely ill. This case study outlines the condition of sinus tachycardia, and associated changes in heart function, altered cellular structure of the myocardium and compensatory mechanisms in the body. Treatment modalities, including electro-physiological studies and drug therapies to moderate the tachycardia and myocardial oxygen demand of the heart, are discussed. Fourteen year old 'Ben' was previously a well, active and outgoing youth who suddenly became critically ill. He endured weeks of hospitalisation, numerous serious complications including Torsade de pointes arrhythmia, Cheyne-Stokes respirations, nausea and dizziness during this acute phase. Despite challenges, Ben's severely compromised heart muscle recovered at a remarkable rate.
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PMID:Tachycardia's toll: tachycardia induced cardiomyopathy--a case study. 1259 74


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