scholarly journals DIGOXIN TOXICITY WITH NEGATIVE SERUM DIGOXIN LEVELS

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.


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

1980 ◽  
Vol 14 (7-8) ◽  
pp. 547-548
Author(s):  
Stephen H. Powell

A case of digoxin toxicity occurring in a patient with stable renal function and serum digoxin levels of 0.6–0.9 ng/ml is discussed. The patient is a 62-year-old black male admitted to the hospital with a chief complaint of shortness of breath. The patient's problem list included: (1) congestive heart failure, (2) coronary artery disease, (3) adult-onset diabetes mellitus, (4) cerebral vascular accident, (5) fever, and (6) anemia. The patient complained of a poor appetite and “sour stomach” while on digoxin. Serum electrolytes were normal, and the serum creatinine was essentially stable with a range of 1.2–1.6 mg% reported. Despite the “apparent” therapeutic serum digoxin levels, a probable diagnosis of digoxin toxicity was made, and the patient responded within two days of the dechallenge with improvement in the nausea and anorexia. The limitations and problems in assessing digoxin toxicity with serum digoxin levels are discussed.


1987 ◽  
Vol 294 (6) ◽  
pp. 423-428 ◽  
Author(s):  
Glen D. Park ◽  
Reynold Spector ◽  
Mark J. Goldberg ◽  
Ross D. Feldman

Sign in / Sign up

Export Citation Format

Share Document