Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
DIGOXIN PEDIATRIC vs PARSABIV
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Inhibits sodium-potassium ATPase, increasing intracellular sodium, which promotes calcium influx via sodium-calcium exchanger, enhancing cardiac contractility. Also increases vagal tone, slowing AV conduction.
Calcium-sensing receptor (Ca SR) agonist; increases the sensitivity of the Ca SR to extracellular calcium, thereby decreasing parathyroid hormone (PTH) secretion.
Heart failure (FDA-approved for pediatric patients with heart failure),Atrial fibrillation (off-label for rate control in pediatric patients)
Secondary hyperparathyroidism in adults with chronic kidney disease on hemodialysis
For pediatric patients, digoxin pediatric dosing is weight-based; no standard adult dose. Typical pediatric loading dose: 10-12 mcg/kg orally divided every 6-8 hours, with maintenance: 5-10 mcg/kg/day divided every 12 hours. For infants <1 month, loading: 10-15 mcg/kg, maintenance: 4-6 mcg/kg/day. For children 1-24 months, loading: 15-20 mcg/kg, maintenance: 5-8 mcg/kg/day. For children >2 years, loading: 10-15 mcg/kg, maintenance: 3-5 mcg/kg/day.
Initial dose 5 mg intravenously three times per week, titrated by 2.5 or 5 mg increments every 4 weeks to a maximum of 15 mg three times per week to achieve target parathyroid hormone levels.
Terminal elimination half-life in neonates is 35-70 hours, infants 18-30 hours, children 12-30 hours, and adults 36-48 hours; prolonged in renal impairment and hypothyroidism.
Terminal elimination half-life of 3-5 days, supporting once-weekly subcutaneous dosing.
Primarily renally excreted unchanged; minimal hepatic metabolism (mostly via reduction, hydrolysis, and conjugation in older children).
Primarily metabolized via amide hydrolysis and oxidation, with involvement of CYP3A4, CYP2D6, and CYP1A2 as minor pathways.
Renal excretion accounts for 50-70% of elimination as unchanged drug; biliary/fecal excretion accounts for 30-40%, primarily as metabolites; enterohepatic recirculation occurs.
Renal: negligible (<2% unchanged); fecal: primary route via biliary elimination of intact drug and metabolites; not dialyzable.
25% bound to serum albumin; binding decreases in uremia and hyperbilirubinemia.
Approximately 90-95% bound to albumin.
Vd: 6-10 L/kg in infants and children, 5-7 L/kg in adults; large Vd indicates extensive tissue binding, particularly to cardiac muscle (Na+/K+-ATPase).
Approximately 0.29-0.46 L/kg, indicating distribution limited to extracellular fluid.
Oral: 60-80% (elixir 70-85%, tablets 60-75%); IM: 70-85% (but erratic absorption and pain limit use); IV: 100%.
Subcutaneous: approximately 50% (range 40-60%).
Digoxin is primarily renally excreted. For pediatric patients, if GFR <30 m L/min/1.73m2, reduce maintenance dose by 50% and monitor serum levels. For GFR 30-60, reduce dose by 25-50%. In neonates with renal impairment, dose reduction proportional to creatinine clearance.
Contraindicated in patients with estimated glomerular filtration rate (e GFR) less than 15 m L/min/1.73 m². No dose adjustment required for e GFR ≥ 15 m L/min/1.73 m².
Digoxin is minimally hepatically metabolized; no dose adjustment required for hepatic impairment. However, in Child-Pugh class C, monitor levels due to potential altered distribution.
No specific guidelines available; use with caution in severe hepatic impairment (Child-Pugh class C) due to lack of data.
See standard_dosing. Weight-based dosing: total digitalizing dose (TDD) and maintenance as above. For premature infants, TDD 10-15 mcg/kg, maintenance 3-5 mcg/kg/day divided q12h. For full term neonates, TDD 15-20 mcg/kg, maintenance 5-7 mcg/kg/day. For infants 1-24 months, TDD 20-25 mcg/kg, maintenance 7-10 mcg/kg/day. For children 2-10 years, TDD 10-15 mcg/kg, maintenance 5-7 mcg/kg/day. For children >10 years, TDD 10-15 mcg/kg, maintenance 3-5 mcg/kg/day. Divide TDD into 3-4 doses every 6-8 hours. Maintenance started 12 hours after last loading dose.
Safety and efficacy not established in pediatric patients; no approved dosing recommendations.
Not applicable for pediatric formulation. For elderly, use adult digoxin dosing with caution: reduced renal function may require lower maintenance doses. Typical adult maintenance: 0.0625-0.25 mg daily based on renal function and lean body mass.
No specific dose adjustments recommended; clinical studies included patients aged 65 years and older; no overall differences in safety or efficacy observed.
Toxicity can be life-threatening. Use caution in renal impairment, electrolyte disturbances (hypokalemia, hypomagnesemia, hypercalcemia). Narrow therapeutic index requires monitoring.
None.
Monitor serum digoxin levels, renal function, electrolytes (potassium, magnesium, calcium). Risk of arrhythmias (including ventricular fibrillation, bradycardia, AV block). Use with caution in patients with thyroid disease, acute myocardial infarction, or myocarditis.
Hypocalcemia,Seizures potentially due to severe hypocalcemia,QT interval prolongation,Gastrointestinal bleeding,Adynamic bone disease
Ventricular fibrillation, hypersensitivity to digitalis preparations, hypokalemia (uncorrected), hypercalcemia (uncorrected), AV block (second or third degree) unless pacemaker present.
Hypocalcemia
High-fiber foods may decrease absorption; take digoxin 1 hour before or 2 hours after meals. Avoid natural licorice, which can cause hypokalemia and increase toxicity. Maintain consistent dietary potassium intake.
No specific food interactions. However, patients should adhere to a renal diet as prescribed, which may include restrictions on phosphorus and calcium intake. Avoid calcium-containing supplements or binders without medical advice due to risk of hypercalcemia.
Digoxin crosses the placenta. First trimester: No increased risk of major malformations reported in human studies. Second/third trimester: Potential for fetal toxicity (e.g., bradycardia, cardiac arrhythmias) at maternal toxic doses. No known teratogenicity at therapeutic doses.
In animal reproduction studies, intravenous etelcalcetide administered to pregnant rats during organogenesis at doses 2.5 times the maximum recommended human dose (MRHD) based on AUC caused increased incidences of fetal skeletal variations and reduced fetal body weight. In rabbits, no adverse fetal effects were observed at doses up to 0.7 times the MRHD. No adequate and well-controlled studies in pregnant women exist. In the first trimester, exposure poses unknown but potential teratogenic risk. During the second and third trimesters, the drug may cause fetal hypocalcemia due to PTH suppression. Use only if potential benefit justifies potential risk.
Digoxin is excreted into breast milk in low concentrations. M/P ratio approximately 0.6–0.9. Infant dose via milk is <1% of maternal weight-adjusted dose, unlikely to cause adverse effects in term infants. Caution in preterm or neonates with renal impairment.
No data on etelcalcetide presence in human milk, effects on breastfed infants, or milk production. Animal studies show etelcalcetide is present in rat milk. M/P ratio unknown. Because of the potential for serious adverse reactions including hypocalcemia in nursing infants, advise patients not to breastfeed during treatment and for two weeks after the last dose.
During pregnancy, increased volume of distribution and renal clearance may reduce serum digoxin levels. Dose adjustments may be required based on therapeutic drug monitoring; typical dose increase of 20–30% in third trimester. Postpartum, reduce dose to prepregnancy level to avoid toxicity.
No specific dosage adjustments are recommended for pregnancy due to lack of pharmacokinetic data in pregnant women. However, because of the potential for hypocalcemia, more frequent monitoring of serum calcium is advised, and dose adjustments may be needed to maintain calcium levels within target range. The effect of pregnancy on etelcalcetide pharmacokinetics is unknown.
Monitor serum digoxin levels (therapeutic range 0.5-2 ng/m L) and renal function, especially in neonates. Correct hypokalemia, hypomagnesemia, and hypercalcemia before administration to reduce toxicity risk. Use with caution in patients with WPW, hypertrophic cardiomyopathy, or incomplete heart block. Dosing in infants and children is based on weight and renal function.
Monitor serum calcium closely; PARSABIV (etelcalcetide) is a calcimimetic that lowers PTH and serum calcium. Initiate only if corrected serum calcium is above the lower limit of normal. Administer intravenously three times per week during hemodialysis. Dose adjustments needed based on serum calcium and PTH levels. Avoid use with other calcimimetics. May cause significant hypocalcemia, especially in patients with adynamic bone disease.
Take exactly as prescribed; do not double up doses.,Monitor for signs of toxicity: nausea, vomiting, vision changes (yellow-green halos), arrhythmias.,Keep medication out of reach of children; immediate medical attention if overdose suspected.,Do not stop abruptly without consulting healthcare provider.,Inform healthcare provider of all medications, including OTC and herbal supplements.
This medication is given intravenously during your dialysis sessions three times a week.,It works by lowering parathyroid hormone (PTH) levels to help manage secondary hyperparathyroidism.,You will need regular blood tests to monitor your calcium and PTH levels.,Report symptoms of low calcium such as muscle cramps, numbness, tingling around the mouth, or seizures.,Do not take any other medications for secondary hyperparathyroidism unless prescribed by your doctor.
"Eflornithine, an ornithine decarboxylase inhibitor used in the treatment of African trypanosomiasis and hirsutism, may reduce the therapeutic efficacy of digoxin, a cardiotonic glycoside used for heart failure and atrial fibrillation. The proposed mechanism involves eflornithine-induced alterations in gastrointestinal motility or absorption, potentially decreasing digoxin bioavailability. This could lead to subtherapeutic digoxin levels, diminished inotropic and chronotropic effects, and increased risk of arrhythmias or worsening heart failure."
"Osimertinib, a tyrosine kinase inhibitor used in non-small cell lung cancer, can inhibit P-glycoprotein (P-gp) transport in the gastrointestinal tract and kidneys, leading to increased absorption and reduced renal clearance of digoxin. This elevation in serum digoxin concentration heightens the risk of digoxin toxicity, including cardiac arrhythmias (e.g., bradycardia, atrial tachycardia with block) and gastrointestinal symptoms such as nausea and vomiting. Clinical monitoring for digoxin toxicity is warranted, especially when initiating or adjusting osimertinib therapy."
"Lenvatinib, a tyrosine kinase inhibitor, may reduce the therapeutic efficacy of digoxin by interfering with its cardiotonic effects. This interaction could lead to decreased inotropic support in patients with heart failure, potentially worsening cardiac function and clinical outcomes. The clinical consequence is a possible loss of rate control in atrial fibrillation or diminished contractility in systolic dysfunction."
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about DIGOXIN PEDIATRIC vs PARSABIV, answered by our medical review team.
DIGOXIN PEDIATRIC is a Cardiac Glycoside that works by Inhibits sodium-potassium ATPase, increasing intracellular sodium, which promotes calcium influx via sodium-calcium exchanger, enhancing cardiac contractility. Also increases vagal tone, slowing AV conduction.. PARSABIV is a Calcimimetic that works by Calcium-sensing receptor (Ca SR) agonist; increases the sensitivity of the Ca SR to extracellular calcium, thereby decreasing parathyroid hormone (PTH) secretion.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between DIGOXIN PEDIATRIC and PARSABIV depend on the specific clinical indication. These are agents from distinct pharmacological classes and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of DIGOXIN PEDIATRIC is: For pediatric patients, digoxin pediatric dosing is weight-based; no standard adult dose. Typical pediatric loading dose: 10-12 mcg/kg orally divided every 6-8 hours, with maintenance: 5-10 mcg/kg/day divided every 12 hours. For infants <1 month, loading: 10-15 mcg/kg, maintenance: 4-6 mcg/kg/day. For children 1-24 months, loading: 15-20 mcg/kg, maintenance: 5-8 mcg/kg/day. For children >2 years, loading: 10-15 mcg/kg, maintenance: 3-5 mcg/kg/day.. The standard adult dose of PARSABIV is: Initial dose 5 mg intravenously three times per week, titrated by 2.5 or 5 mg increments every 4 weeks to a maximum of 15 mg three times per week to achieve target parathyroid hormone levels.. Dosing should always be individualized based on indication, renal and hepatic function, age, and other patient factors.
No direct drug-drug interaction has been formally documented between DIGOXIN PEDIATRIC and PARSABIV in current clinical databases. However, individual patient risk factors including other medications, organ function, and comorbidities should always be evaluated by a qualified healthcare provider.
The maternal-fetal safety profiles differ. DIGOXIN PEDIATRIC is classified as Category A/B. Digoxin crosses the placenta. First trimester: No increased risk of major malformations reported in human studies. Second/third trimester: Potential for fetal toxicity (e.g., brady. PARSABIV is classified as Category C. In animal reproduction studies, intravenous etelcalcetide administered to pregnant rats during organogenesis at doses 2.5 times the maximum recommended human dose (MRHD) based on A. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.