Comparative Pharmacology
Head-to-head clinical analysis: VI DOM A versus VITAMIN A.
Peer-Reviewed Evidence
Head-to-head clinical analysis: VI DOM A versus VITAMIN A.
VI-DOM-A vs VITAMIN A
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Retinol binds to retinoic acid receptors (RARs) and retinoid X receptors (RXRs), modulating gene transcription involved in cell growth, differentiation, and immune function.
Vitamin A (retinol) is converted to retinal and retinoic acid, which bind to nuclear receptors (RARs and RXRs) to regulate gene expression involved in cell growth, differentiation, and vision.
1 mL intramuscular injection once weekly; each mL contains 100,000 IU vitamin A (as retinyl palmitate) and 50,000 IU vitamin D (as ergocalciferol).
Adults: 10000-50000 IU/day orally for deficiency; up to 100000 IU/day for severe deficiency short-term. Intramuscular: 50000 IU daily for 3 days, then 50000 IU weekly for 2-3 months.
None Documented
None Documented
Clinical Note
moderateVitamin A + Digoxin
"Vitamin A may decrease the cardiotoxic activities of Digoxin."
Clinical Note
moderateVitamin A + Digitoxin
"Vitamin A may decrease the cardiotoxic activities of Digitoxin."
Clinical Note
moderateVitamin A + Deslanoside
"Vitamin A may decrease the cardiotoxic activities of Deslanoside."
Clinical Note
moderateVitamin A + Acetyldigitoxin
"Vitamin A may decrease the cardiotoxic activities of Acetyldigitoxin."
The terminal elimination half-life of vitamin A is 10-12 hours for retinol, but due to hepatic storage and enterohepatic recirculation, the overall body half-life can extend to 2-3 weeks with chronic dosing.
The terminal elimination half-life of vitamin A is variable, ranging from 10 to 100 days due to extensive storage in the liver; in individuals with adequate hepatic stores, the half-life is approximately 50–100 days, but in deficiency states, it may be shorter (10–20 days). Clinically, this long half-life supports once-daily dosing for chronic therapy.
Vitamin A is primarily excreted via bile and feces as metabolites. Renal excretion accounts for less than 5% of an oral dose. Unchanged vitamin A is not significantly excreted in urine.
Vitamin A is eliminated primarily via biliary excretion into feces as metabolites (approximately 80–90%), with renal excretion accounting for less than 10% of unchanged drug and metabolites. A small fraction undergoes enterohepatic circulation.
Category C
Category C
Vitamin A
Vitamin A