Digoxin Toxicity in Patients with High Serum Digoxin Concentrations

1987 ◽  
Vol 294 (6) ◽  
pp. 423-428 ◽  
Author(s):  
Glen D. Park ◽  
Reynold Spector ◽  
Mark J. Goldberg ◽  
Ross D. Feldman
2021 ◽  
Vol 77 (18) ◽  
pp. 2119
Author(s):  
Saadat Aleem ◽  
Mohammed Al-Sadawi ◽  
Roger Fan

PEDIATRICS ◽  
1982 ◽  
Vol 70 (6) ◽  
pp. 1011-1012
Author(s):  
DAVID S. OLANDER ◽  
MICHAEL MAURER

In their recent communication, Johnson et al suggested that conventional digoxin use may be sufficiently toxic forlow-birth-weight infants to prompt consideration of alternative therapies. This conclusion was supported by their detection of digitalis associated illness in 9/18 small premature infants receiving digoxin in doses of 0.003 to 0.005 mg/kg twice per day. The documentation of abnormally elevated serum digoxin concentrations in 7/9 patients further supports the possibility of clinically significant digoxin toxicity. Akin to the findings of Berman et al and Pinsky et al, this investigation only confirms the observation that overdosage of infants with digoxin may result in digitoxicity.


1997 ◽  
Vol 31 (7-8) ◽  
pp. 864-866 ◽  
Author(s):  
James J. Nawarskas ◽  
David M. McCarthy ◽  
Sarah A. Spinier

OBJECTIVE: To report a case of digoxin toxicity thought to be secondary to clarithromycin therapy. CASE SUMMARY: A 78-year-old white woman with congestive heart failure taking digoxin 0.25 mg po qd presented to our hospital with nausea, vomiting, and diarrhea. She had taken clarithromycin 500 mg po bid for 3 days, and a serum digoxin concentration obtained the day of admission was 4.4 μg/L. An electrocardiogram (ECG) done on admission revealed ST segment changes consistent with digoxin effect and later asymptomatic, nonsustained ventricular tachycardia (NSVT). Clarithromycin was discontinued and digoxin was withheld at admission, resulting in the resolution of symptoms, ECG abnormalities, and NSVT on day 3 of hospitalization. On day 5 her serum digoxin concentration was 1.5 μg/L and digoxin therapy was reinstituted at a dose of 0.125 mg/d po. DISCUSSION: This is the fourth published case implicating clarithromycin as the cause of digoxin toxicity. This interaction is most likely due to clarithromycin eradication of digoxinmetabolizing gut flora, thereby increasing digoxin bioavailability. CONCLUSIONS: Approximately 10% of patients are thought to be extensive presystemic metabolizers of digoxin and may therefore be most susceptible to a drug interaction with clarithromycin. Serum digoxin concentrations in such patients should be monitored closely during clarithromycin therapy.


1994 ◽  
Vol 40 (3) ◽  
pp. 487-492 ◽  
Author(s):  
M H Doolittle ◽  
K Lincoln ◽  
S W Graves

Abstract We describe a patient with unexpectedly high serum digoxin after cardiac surgery. To control atrial fibrillation in the immediate postoperative period, she was given a brief trial of digoxin (four 0.25-mg doses) over 12 h. Serum digoxin 6 h later was 2.5 micrograms/L. Two days later, the patient developed ventricular fibrillation, which progressed to cardiac arrest. During or immediately after resuscitation, blood was drawn for a digoxin measurement, and the concentration reported was 9.3 micrograms/L; this result was verified by repeated analysis. Digoxin decreased rapidly and progressively to near 4.0 micrograms/L over the next several hours and thereafter decreased slowly to 1.0 microgram/L over the next 11 days, despite no digoxin being administered. The unexpectedly high digoxin raised questions about the accuracy of the digoxin measurement, particularly about the possible influence of the digoxin-like immunoreactive factor. Analytical approaches to distinguishing true digoxin from this factor and other artifacts of digoxin measurement were applied to this patient, with unanticipated results.


BMJ ◽  
1983 ◽  
Vol 286 (6371) ◽  
pp. 1089-1091 ◽  
Author(s):  
M Sonnenblick ◽  
A S Abraham ◽  
Z Meshulam ◽  
U Eylath

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