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)

Fifty-one patients with symptomatic ventricular tachycardia who failed control on current anti-arrhythmics were studied. Seventy-four percent had ischemic heart disease and 81% had congestive heart failure. Patients underwent serial 24 Holter recordings and radionuclide ventriculography before, during dose titration and during long-term mexiletine therapy. Twenty-eight patients (55%) were successfully controlled. Of these, 17 (33%) remained controlled greater than or equal to 1 year. Early and late side effects were common but benign and included mostly gastric pain and nausea. Twenty-eight patients underwent radionuclide ventriculography before and during mexiletine therapy: there was no significant difference in heart rate, blood pressure, left ventricular ejection fraction, stroke volume and end-diastolic volumes before and during mexiletine. Left ventricular ejection fraction was 21.4 +/- 2.2%, (SD) and 21.3 +/- 2.2% (SD) before and during mexiletine respectively. Digoxin blood levels measured in 15 patients were not significantly changed by mexiletine. In conclusion, mexiletine is effective and safe in many patients with intractable ventricular tachycardia. It has no significant hemodynamic effects even in patients with congestive heart failure nor does it affect digoxin blood levels. Its usefulness is limited by a high incidence of gastric intolerance.
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PMID:Mexiletine: long-term efficacy and hemodynamic actions in patients with ventricular arrhythmia. 241 74

Digoxin acts at central neural (CNS) as well as peripheral sites after intravenous administration. In contrast, the analog, 3-beta-O(4-amino-4,6-dideoxy-beta-D-galactopyranosyl)-digitoxigenin (ASI-222), cannot cross the blood-brain barrier so it acts only at sites outside the CNS. The effects of these two agents on plasma antidiuretic hormone activity (ADH) were investigated in conscious dogs. Despite previous evidence that digoxin produces reflex decreases in sympathetic nerve activity by activating ventricular receptors with vagal afferents, no decreases in ADH were detected when either digoxin (25 and 50 micrograms/kg) or ASI-222 (38.5 micrograms/kg) were administered intravenously even with preexisting high levels of plasma ADH. In contrast, both digoxin (50 micrograms/kg) and ASI-222 (38.5 micrograms/kg) resulted in increased ADH levels, but only in association with emesis and behavioral changes suggestive of nausea. Cerebroventricular (IVT) injections of digoxin were given, starting with a dose of 0.1 microgram, that were intended to produce a comparable cerebrospinal fluid (CSF) concentration to that associated with the 50 micrograms/kg intravenous dose. Only the highest dose of digoxin, 1 micrograms, but not 0.1 and 0.3 micrograms, produced increases in ADH and emesis when given into the lateral cerebral ventricle. This is further evidence that a site accessible to blood but not to CSF was involved. These results suggest that digoxin and ASI-222 may activate pathways in the area postrema and produce increases in ADH as well as emesis.
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PMID:Effect of digoxin and amino sugar cardiac glycoside (ASI-222) on plasma antidiuretic hormone activity. 618 2

Digoxin monitoring was examined according to 13 criteria in two nursing homes: 1) an intermediate care facility (ICF) with private physicians, and 2) a skilled care (SCF) plus ICF with 3 housestaff physicians from a identify all patients receiving digoxin, 2) evaluate dosage patterns, 3) evaluate monitoring patterns, and 4) detect possible toxic reactions and determine whether management was appropriate. The calculated correct dosage of digoxin in both ICFs. More frequent monitoring of serum creatinine and potassium levels was associated with fewer symptoms of toxicity. Possible toxicity occurred in 46 percent of the SCF and in 68 and 71 percent of patients in the ICFs. Documented toxicity occurred in 18 percent of the SCF patients and in 16 and 10 percent of the ICF patients. Eighty percent of patients who had symptoms of digoxin toxicity were not examined or managed appropriately in the SCF, and 43 and 33 percent in the ICFs. Often standing orders had been assigned for drugs to treat nausea, vomiting or diarrhea. A number of possible drug interactions with digoxin were discovered. The participation of the pharmacist in nursing home care is discussed.
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PMID:Monitoring digoxin therapy in two long-term facilities. 724 Jun 13

A 70-year-old woman with a history of atrial fibrillation, on digoxin, presented with nausea, vomiting, and dizziness two days after initiation of clarithromycin therapy. Laboratory results revealed a serum digoxin level of 3.9 ng/ml (normal range 0.5-2.0) and creatinine of 1.1 mg/dl. The patient was admitted to the hospital and digoxin and clarithromycin were discontinued. The patient's symptoms were resolved within 24 hours and her serum digoxin level was 1.9 on the second hospital day. A review of recent literature suggests that clarithromycin may induce digoxin toxicity by three different mechanisms, including reduction of renal excretion of digoxin, alteration of intestinal flora, and inhibition of cytochrome P-450 in the liver. Digoxin toxicity was reported three to 17 days after the initiation of clarithromycin (8.1 +/- 4.8 days, n = 9). The wide variation in the time required for the appearance of toxicity may imply the different mechanisms involved in each case.
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PMID:Clarithromycin-induced digoxin toxicity: a case report and a review of the literature. 1167 58

In its simplest and most succinct definition, heart failure can be defined as an inability of the heart to meet the metabolic demands of the body. Despite the diverse etiologies of heart failure in the pediatric population, the presentation of heart failure represents a common constellation of symptoms, signs, and physical findings. In infants, an inability to maintain growth either secondary to decreased nutritional intake or an increased catabolic state is a hallmark of heart failure. Infants exhibit increased sympathetic tone with excessive diaphoresis and increased heart rate. Physical findings in the infants with congestive heart failure (CHF) include increased work of breathing, tachypnea and hepatomegaly. In older children, in contrast, new onset heart failure may be less overtly symptomatic. Malaise, decrease in the level of daily activity, and weight loss may be present. Symptoms of abdominal pain and nausea and anorexia can be present and sometimes divert attention from the real etiology. Physical findings include rales and peripheral edema. If there is hepatomegaly, there will likely be hepatic tenderness as well. A gallop rhythm and tachycardia are commonly present. The long-term treatment of CHF in children includes digoxin, diuretics and afterload reduction with angiotensin-converting enzyme (ACE) inhibitors. Digoxin decreases sympathetic tone and improves growth in infants. Diuretics should be used to relieve symptoms but may not be necessary in all children. ACE inhibitors are increasingly valuable in maintaining cardiac function long term. New uses of medications include the addition of spironalactone (Aldactone, G. D. Searle & Co., Chicago, IL) which, in adults, has been shown to significantly decrease both the death rate from CHF and the need for hospitalization. Beta-Blockers have been used in children in limited studies and may have a role in the treatment of patients with idiopathic dilated cardiomyopathy. Surgical treatment, such as partial vectriculectomy, has shown short-term benefit and has been used sparingly in infants.
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PMID:Treatment of heart failure in infants and children. 1172 82

A female, aged 43 and a male, aged 66, experienced gastrointestinal and cardiovascular symptoms after a meal including snail stew. Twelve hours after the ingestion, they presented with nausea, vomiting, diarrhea, and cardiovascular symptoms typical of acute toxic digoxin ingestion and were hospitalized. The man's electrocardiogram was altered, and the woman's was normal. Serum digoxin levels, measured on a Roche COBAS Integra 800 with the Roche On-Line Digoxin reagent, were 1.14 and 1.00 nmol/L, respectively. Potassium levels were normal in both patients. The serum digoxin concentration decreased on the second day, and symptoms resolved on the third day with patients fully recovered (i.e., reversion to a normal sinus rhythm). Cardiac-glycoside-like intoxication symptoms follow the ingestion of leaves or flowers of Nerium oleander. The consumed snails were suspected to be responsible for the intoxication. In the homogenized snail tissue, the concentration expressed in digoxin equivalents was 0.282 nmol/g. The presence of oleandrin and oleandrigenin in the snails was confirmed by liquid chromatography-tandem mass spectrometry analysis, which was performed on a ionic-trap Finnigan LXQ instrument using an electrospray ionization interface. High-pressure liquid chromatographic separation was performed on a C18 column with a gradient of methanol/water. An extract of oleander leaves was used as reference.
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PMID:Unexpectedly dangerous escargot stew: oleandrin poisoning through the alimentary chain. 1713 29

Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) are potentially lethal plants after ingestion. Poisoning by these plants is a common toxicological emergency in tropical and subtropical parts of the world and intentional self-harm using T. peruviana is prevalent in South Asian countries, especially India and Sri Lanka. All parts of these plants are toxic, and contain a variety of cardiac glycosides including neriifolin, thevetin A, thevetin B, and oleandrin. Ingestion of either oleander results in nausea, vomiting, abdominal pain, diarrhoea, dysrhythmias, and hyperkalemia. In most cases, clinical management of poisoning by either N. oleander or T. peruviana involves administration of activated charcoal and supportive care. Digoxin specific Fab fragments are an effective treatment of acute intoxication by either species. However, where limited economic resources restrict the use of such Fab fragments, treatment of severely poisoned patients is difficult. Data from case reports and clinical studies were reviewed to identify treatments supported by evidence for the management of poisoning by N. oleander and T. peruviana.
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PMID:A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning. 2043 43

Nerium oleander is potentially lethal plants after ingestion. We report a case of poisoning by these plants. Our patient complained of nausea, vomiting, and diarrhoea. He had bradycardia during first twelve hours. He was discharge after 3 days. All parts of these plants are toxic and contain a variety of cardiac glycosides including oleandrin. In most cases, clinical management of poisoning by N. oleander involves administration of activated charcoal and supportive care. Digoxin specific Fab fragments are an effective treatment.
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PMID:[A non-fatal Nerium oleander self-poisoning: case report and discussion]. 2189 Jan 4

Digitalis glycosides are among the oldest drugs used in cardiology. Nowadays, due to the limited indications for their use (advanced heart failure, usually concomitant with atrial fibrillation), cases of poisoning induced by this class of drugs are rarely observed. Digoxin produces a positive inotropic and bathmotropic effect on the heart, but has a negative chronotropic and dromotropic effect. Cardiac glycosides have a narrow therapeutic window, so digitalis treatment can easily lead to symptoms of overdose. In patients taking digoxin, the drug therapeutic level should be maintained at 1-2 ng/ml; the toxic effects occur at concentrations > 2.8 ng/ml and are mainly related to disturbances of cardiac function and of the circulatory system, as well as gastrointestinal symptoms and CNS disturbances. We present, a 45-years-old patient who was hospitalized following the ingestion with suicidal intent of 100 0.25 mg tablets of digoxin. In spite of rapidly applied gastric irrigation and administration of activated charcoal, the drug level in the patient's blood was estimated at 12.0 ng/ml. During her stay on the ward, typical symptoms of severe poisoning were observed: from gastric symptoms (severe nausea, vomiting) to numerous severe arrhythmias and conduction disturbances. Type I, II and III AV blocks were detected, as well as numerous ventricular and supraventricular extrasystoles. These conduction disorders required the use of temporary endocardial pacing. Due to the unavailability of specific antidotes (antidigitalis antibodies) and lack of efficient methods of extracorporeal elimination of the drug, symptomatic treatment comprising the correction of electrolyte disturbances and heart rate control remains the most effective.
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PMID:[Severe digoxin poisoning a case study]. 2201 Apr 53

Digoxin toxicity can emerge during long-term therapy as well as after an overdose. It can occur even when the serum digoxin concentration is within the therapeutic range. Toxicity causes anorexia, nausea, vomiting and neurological symptoms. It can also trigger fatal arrhythmias. There is a range of indications for using digoxin-specific antibody fragments. The amount ingested and serum digoxin concentration help to determine the dose required, but are not essential. Digoxin-specific antibody fragments are safe and effective in severe toxicity. Monitoring should continue after treatment because of the small risk of rebound toxicity. Restarting therapy should take into account the indication for digoxin and any reasons why the concentration became toxic.
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PMID:Management of digoxin toxicity. 2704 2


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