Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The principal effects of cardiac glycosides probably can be classified as parasympathomimetic or sympathomimetic. Data from animals and from man suggest that polar cardiac glycosides, such as ouabain and digoxin, possess greater parasympathomimetic (vagal) cardiac effect for a given amount of sympathomimetic (positive inotropic) cardiac effect than do less polar cardiac glycosides, such as digitoxin. Polar glycosides therefore offer some advantage in uncomplicated paroxysmal atrial tachycardia and in uncomplicated atrial flutter and atrial fibrillation when the principal desired effect is reduction in the number of atrial impulses reaching the ventricles or conversion to normal sinus rhythm. Non-polar glycosides offer an advantage when positive inotropicity is desired but when there is some degree of atrioventricular block or when inappropriate sinus bradycardia or anorexia, nausea, or vomiting are present. Ecotopic impulse formation when due to cardiac glycosides is a toxic manifestation of excessive sympathomimetic effect, but is aggravated by vagal-induced sinus bradycardia, so that both parasympathomimetic and sympathomimetic capability of cardiac glycosides must be considered when dealing with myocardial electrical instability.
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PMID:Clinical implications of differences in pharmacodynamic action of polar and nonpolar cardiac glycosides. 83 69

Survival following attempted suicide in a 50-year-old man by ingestion of 12.4 g of mexiletine, 620 mg of nifedipine and 50 to 100 tablets of sublingual nitroglycerine 1:150 is reported. Initial presentation was that of mental obtundation, vomiting, tonic-clonic seizure, high-degree atrioventricular block, profound vasodilation and cardiovascular collapse. Treatment consisted of intravenous calcium gluconate and aggressive fluid management. Maintenance of cardiovascular stability required continuous infusion phenylephrine, dopamine and epinephrine. The patient made a full recovery and was medically discharged on the fourth hospital day. This case represents the largest overdose of mexiletine to date to end in patient survival.
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PMID:Survival following severe overdose with mexiletene, nifedipine, and nitroglycerine. 189 1

A 8 day-old full-term newborn showed severe cardiac disturbances after intravenous injection of erythromycin. The neonate, suspected of having Chlamydia pneumonitis because of tachypnea and rhinitis, had been given 5 injections of erythromycin without clinical effect. Pallor, vomiting and bradycardia developed a few minutes after the 6th injection, and ECG showed ventricular arrhythmia, prolonged QT interval and an atrioventricular block. The infant died in intensive care unit. This case and the analysis of other published cases of cardiac disturbances following the parenteral use of erythromycin, indicate the potential arrhythmogenic risk of this drug. It is suggested that newborns treated with erythromycin should be monitored by ECG.
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PMID:[QT prolongation and circulatory arrest after an injection of erythromycin in a newborn infant]. 201 21

The use of digoxin-specific Fab fragments (d-Fab) to treat life-threatening digitalis intoxication has been widely substantiated in adults. This reports a case of a 2-year-old girl who ingested 90-92, 0.25 mg tablets of digoxin and within four hours, developed vomiting, lethargy, tachycardia and AV block (Mobitz type I and II). These symptoms were associated with total and free serum digoxin concentrations of 17.1 and 12.4 ng/ml, respectively. Following GI decontamination, a total dFab dose of 1280 mg (32 vials) was given with resolution of electrocardiographic abnormalities within 40 minutes and a concomitant reduction in the free serum digoxin concentration to 0.11 ng/ml. Repeated blood sampling over 19 days revealed an apparent elimination half-life (t1/2) of 134.9 and 129.9 hr for total and free digoxin, respectively. The long t1/2 for digoxin corresponded to a low apparent renal clearance of total digoxin which ranged from 0.56 to 0.82 ml/minute over four separate collection intervals. The free serum digoxin concentration never exceeded 3% of the total concentration and the patient did not develop a recurrence of toxic symptoms or any adverse effects (e.g. fever) attributable to dFab. Administration of an equimolar dFab dose to children following acute, massive digoxin intoxication represents safe, effective treatment which produces a prompt, sustained reversal of toxic effects. Digoxin specific Fab fragments should be promptly administered to any infant or child with significant, life-threatening symptoms following acute digoxin intoxication.
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PMID:Pharmacokinetics and efficacy of digoxin specific Fab fragments in a child following massive digoxin overdose. 259 82

The attempted suicide by 2 women with a kyushin overdose is reported. Kyushin caused them to produce a significant elevation of a serum digoxin-like immunoreactive substance (2.35 and 1.84 ng/ml) and symptoms of nausea, vomiting and general malaise. Their blood biochemistry and electrolytes were normal. In one patient, an electrocardiogram revealed a second degree Wenckebach atrioventricular block and T-wave change. Toad venom, a kyushin ingredient, is possibly responsible for the development of these clinical features and electrocardiographic changes.
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PMID:A digoxin-like immunoreactive substance and atrioventricular block induced by a Chinese medicine "kyushin". 260 Oct

A woman had a 40-year history of vomiting associated with syncope. Spontaneous and induced vomiting was predictably associated with sinus bradycardia, paroxysmal atrioventricular block, and ventricular asystole. The clinical and laboratory studies carried out to illustrate the mechanism of this unusual complication of vomiting demonstrated it to be due to a vagovagal reflex initiated by distension of upper esophagus.
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PMID:Recurrent paroxysmal complete heart block induced by vomiting. 329 35

Two cases of acute blindness due to quinine poisoning are presented. In both cases, the diagnosis was initially unsuspected. In addition, tinnitus, decreased hearing, vomiting, abdominal pain, and confusion were noted in one patient, and the other experienced decreased hearing, headache, confusion, tachycardia, later bradycardia, and first-degree atrioventricular block. The onset of blindness was delayed more than 12 hours after ingestion in both cases. Quinine levels of 13.6 micrograms/mL and 18.6 micrograms/mL were demonstrated (therapeutic = 1 to 3 micrograms/mL). One patient developed marked constriction of visual fields and some residual decreased acuity, while the other regained normal visual acuity.
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PMID:Acute toxic blindness: unrecognized quinine poisoning. 380 84

Clinical and pathological findings in 15 autopsy cases, 13 males and 2 females, confirming cardiac free wall rupture after AMI were reported. The incidence is 30.6% of all autopsy cases of AMI in Chinese PLA General Hospital from 1958 to 1979. The ages ranged from 46 to 79 years, 10 being above 60 years. For 73.3% it was the first AMI and 66.7% of the patients had a history of hypertension. Thirteen of the 15 patients died within 5 days after the onset of AMI and another 2 within 7 days. When the cardiac rupture occurred, the ECG generally showed bradycardia, AV-junctional rhythm, III degrees AV block or isorhythmic ventricular rhythm and cardiac arrest. Both the gross and microscopic AMI were examined in 13 cases. All of them had a septal infarct, but only 2 had an ECG diagnosis. Of the 6 patients with inferior MI on ECG, 5 had right and left coronary lesions worse than grade III. The effective prevention of cardiac rupture consists of early diagnosis, control of chest pain and vomiting, prevention or treatment of hypertension or hypotension and 1 to 2 weeks of bed rest after the onset of AMI.
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PMID:Cardiac free wall rupture after acute myocardial infarction. Clinical and pathological analysis. 383 11

Five cases of acute accidental poisoning with White Hellebore are reported. All cases occurred several minutes after the ingestion of home-made gentian wine. The clinical signs were nausea, vomiting, abdominal pain, hypotension and bradycardia. The initial ECG showed sinus bradycardia in 4 cases. In one patient, complete atrioventricular block with an ectopic atrial bradycardia and an intermittent idioventricular rhythm was recorded. Symptomatic treatment and/or atropine led to recovery within a few hours. These symptoms suggested poisoning with a veratrum alkaloid. The White Hellebore (Veratrum Album L.) and the Yellow Gentian (Gentiana Lutea L.) often grow side by side in the fields; it is easy to confuse the two plants before they flower if one is not a botanist. Each gentian wine was analysed by thin layer chromatography and chemical ionisation spectrometry. All the wines contained Veratrum alkaloids.
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PMID:[Acute dietary poisoning by white hellebore (Veratrum album L.). Clinical and analytical data. A propos of 5 cases]. 407 96

Aclacinomycin A (ACM-A), an anthracycline analog, was given to 17 patients with solid tumors and to one patient with multiple myeloma, in a phase I clinical trial. A single dose of 60-120 mg/m2 was given every 3 weeks. Dose-limiting toxicity was myelosuppression, especially thrombocytopenia. Granulocytopenia was variable and did not always recover by Day 21 in time for the next ACM-A treatment. Other toxic effects were nausea, vomiting, urticaria, and elevation of hepatic enzymes. Alopecia was not a side effect, even in patients receiving multiple courses of ACM-A. Nine patients were monitored with 24-hour continuous ECG recordings (Holter) on 19 ACM-A treatment days. The incidence of premature atrial and ventricular beats was significantly increased following ACM-A administration. In addition, one patient developed episodes of high-degree atrioventricular block and complete heart block after each of four ACM-A doses, necessitating the insertion of a pacemaker. No antitumor responses were seen in the ten patients who had measurable disease and who had received two or more courses of ACM-A. The recommended doses for solid tumor phase II studies are 100 mg/m2 as a single dose every 4 weeks for patients with high performance status and minimal prior chemotherapy and 60 mg/m2 every 4 weeks for all other patients. Until the acute cardiac effects of ACM-A are further understood, we recommend that all patients receiving ACM-A be monitored by ECG recordings.
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PMID:Phase I trial of aclacinomycin A. 695 61


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