Digoxin therapy in low-birth-weight infants with patent ductus arteriosus

Berman, William; Dubynsky, Orest; Whitman, Victor; Friedman, Zvi; Maisels, M. Jeffrey; Musselman, Jude

doi:10.1016/s0022-3476(78)80911-1

Cited by 32 publications

(13 citation statements)

References 15 publications

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“…In the study of Pinsky et al [14], digoxin levels in the high and low dose groups were 3.5 ± 0.4 and 1.7 ± 0.2 ng/ml, respectively. But the digoxin levels of the retrospective and prospective groups in the study by Berman et al [1] were reported to be 5.9 ± 1.7 and 3.8 ± 1.4 ng/ml; in addition, the serum digoxin levels in all toxic infants in their study varied between 4.3 and 13.0 ng/ml. Hence the lower incidence of digoxin toxicity in our study could be partially due to the lower steadystate digoxin levels.…”

Section: Discussionmentioning

confidence: 82%

Total Body Digoxin Clearance and Steady-State Concentrations in Low Birth Weight Infants

Rl¹,

Pk²,

Ma³

et al. 1982

Dev Pharmacol Ther

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Serial serum digoxin concentrations were measured over a 10-day period in 15 low birth weight infants requiring digoxin therapy. The calculated total body digoxin clearance (TBDC) was found to be highly dependent on gestational age and body weight, with dose-normalized, steady-state digoxin concentrations inversely related to the same factors. Because of the decreased TBDC in low birth weight infants, our data support the recent recommendations in the literaure to reduce maintenance doses of digoxin in these infants. Our study has further demonstrated that the reduction should be proportional to both gestational age and body weight.

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Section: Discussionmentioning

confidence: 82%

Total Body Digoxin Clearance and Steady-State Concentrations in Low Birth Weight Infants

Rl¹,

Pk²,

Ma³

et al. 1982

Dev Pharmacol Ther

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“…Digoxin toxicity has been reported in LBW infants (8)(9)(10). Half-lives of elimination up to 44 h have been reported and attributed to delayed urinary excretion (8,9) and the lang half-life has frequently been incriminated as the possible reason for digoxin toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…Half-lives of elimination up to 44 h have been reported and attributed to delayed urinary excretion (8,9) and the lang half-life has frequently been incriminated as the possible reason for digoxin toxicity. In our study, mean t1/2ß was 15 .25 h with a range of 11.5 to 21.3 h. Similar values for t1/2ß of digoxin have been recorded in infants and adults (18,25), but a mean t1/2ß of 15.25 h is shorter than values for t1/2ß reported by others in neonates (9,16,18).…”

Section: Discussionmentioning

confidence: 99%

“…However, reports of pharmai::ologic closure of the PDA with prostaglandin synthetase inhibitors ( 4,5), successes with surgical ligation of the PDA ( 6,7), and reports of toxicity with relatively low doses of digoxin (8), have led us to reassess the role of digoxin therapy in these infants. Data concerning the pharmacokinetics and pharmacodynamics of digox.in in LBW infants are limited to estimates of half-life of elimination (8,9). Objective data concerning the cardiac effects of digoxin in left-to-right shunting through the PDA in LBW infants is to our knowledge not available.…”

Section: Introductionmentioning

confidence: 99%

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Pharmacokinetics and Echocardiographic Effects of Digoxin in Low Birth Weight Infants with Left-to-Right Shunting due to Patent Ductus arteriosus

Warburton¹,

Bell²,

Oh³

1980

Dev Pharmacol Ther

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Serum digoxin (DIG) levels, timed urine and M-mode echocardiograms were performed in 9 low birth weight infants with lef't-to-right shunting due to patent ductus arteriosus treated with DIG (40 μg/kg in 3 and 20 μg/kg in 6). Half the DIG was given initially and a quarter at 8-hourly intervals. Serum DIG levels at 24 h (1.8-7 .0 ng/ml) were similar in both dose groups. One infant in the 40 μg/kg dose group developed Wenckebach phenomenon. Left atrial to aortic root ratio feil within 30 min and remained reduced during the ensuing 24 h (p < 0.025). There were no significant changes in the other echocardiographic measurements. Half-life of distribution and elimination of DIG were 1.04 ± 0.46 and 15.25 ± 0.36 h. The α-phase volumes of distribution (VD) differed between the 40 and 20 μg/kg dose groups (2.28 ± 0.05 vs. 1.33 ± 0.66 liters/kg, p < 0.025). The β-phase VD (4.25 ± 0.61 and 2.76 ± 0.99, respectively) were similar. Mean urinary DIG clearance was 13.1 ± 3.2 ml/min/1.73^2.

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“…Of these interventions, only digoxin and furosemide have been systematically evaluated as a treatment for PDA. Digoxin is ineffective, 50,51 and furosemide promotes continued patency of the ductus. 52 Measures designed to reduce PBF and Q P /Q S , as discussed above, should also be effective for prevention or management of CHF.…”

Section: Managing Congestive Heart Failurementioning

confidence: 99%

Learning to live with patency of the ductus arteriosus in preterm infants

Benitz

2011

J Perinatol

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Digoxin therapy in low-birth-weight infants with patent ductus arteriosus

Cited by 32 publications

References 15 publications

Total Body Digoxin Clearance and Steady-State Concentrations in Low Birth Weight Infants

Total Body Digoxin Clearance and Steady-State Concentrations in Low Birth Weight Infants

Pharmacokinetics and Echocardiographic Effects of Digoxin in Low Birth Weight Infants with Left-to-Right Shunting due to Patent Ductus arteriosus

Learning to live with patency of the ductus arteriosus in preterm infants

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