CHOLOXIN
Clinical safety rating: caution
Comprehensive clinical and safety monograph for CHOLOXIN (CHOLOXIN).
Choloxin (dextrothyroxine sodium) is a synthetic isomer of thyroxine that reduces serum cholesterol levels by increasing hepatic cholesterol catabolism and excretion, likely through enhanced LDL receptor activity and increased conversion of cholesterol to bile acids.
| Metabolism | Primarily hepatic; undergoes deiodination and conjugation to glucuronides and sulfates. Hepatic clearance involves CYP450 enzymes, with a half-life of approximately 12-24 hours. |
| Excretion | Primarily renal excretion of conjugated metabolites (70-80% of dose); biliary/fecal excretion accounts for 10-20%; less than 5% excreted unchanged. |
| Half-life | Terminal elimination half-life is approximately 1-2 hours in euthyroid patients; may be prolonged in hypothyroidism or hepatic impairment. |
| Protein binding | Highly bound (>99%) to thyroxine-binding globulin (TBG), transthyretin, and albumin. |
| Volume of Distribution | Apparent volume of distribution is 0.10-0.20 L/kg, reflecting extensive tissue binding and distribution. |
| Bioavailability | Oral bioavailability is 50-80%, reduced by food, bile acid sequestrants, and certain drugs. |
| Onset of Action | Oral: clinical effects begin within 24-48 hours; intravenous: onset within 6-12 hours. |
| Duration of Action | Duration of action is 2-3 weeks following discontinuation due to slow tissue redistribution and conversion to liothyronine. |
50-250 mcg/kg orally once daily, adjusted to maintain T4 within normal range.
| Dosage form | TABLET |
| Renal impairment | No dose adjustment required for renal impairment as drug is hepatically cleared. |
| Liver impairment | Child-Pugh A: no adjustment. Child-Pugh B: reduce dose by 25-50%. Child-Pugh C: reduce dose by 50-75% and monitor T4 closely. |
| Pediatric use | Neonates: 10-15 mcg/kg/day orally. Infants: 5-10 mcg/kg/day. Children: 2-5 mcg/kg/day. Adjust based on T4 levels. |
| Geriatric use | Start at 25 mcg/day orally, titrate slowly (every 4-6 weeks) due to increased sensitivity and risk of cardiac adverse effects. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for CHOLOXIN (CHOLOXIN).
| Breastfeeding | Excretion into human milk is unknown. Due to potential for serious adverse effects in nursing infants, including interference with thyroid function, breastfeeding is contraindicated. M/P ratio not determined. |
| Teratogenic Risk | CHOLOXIN (dextrothyroxine) is not recommended during pregnancy. In animal studies, high doses caused fetal resorptions and anomalies. First trimester exposure may increase risk of congenital defects; second and third trimester exposure may impair fetal thyroid function and development. Risk cannot be excluded. |
■ FDA Black Box Warning
None specified in FDA labeling.
| Serious Effects |
["Absolute: Euthyroid patients with pre-existing cardiovascular disease (e.g., recent MI, unstable angina, significant arrhythmias).","Absolute: Thyrotoxicosis or iodine deficiency.","Absolute: Pregnancy (Category X).","Relative: Renal or hepatic impairment; concomitant use of anticoagulants (requires close monitoring)."]
| Precautions | ["Cardiac toxicity: Increased risk of arrhythmias, angina, and myocardial infarction, especially in patients with pre-existing cardiovascular disease.","Hyperthyroidism: Can induce thyrotoxicosis if dose is too high or in patients with iodine deficiency.","Drug interactions: Enhances effect of oral anticoagulants (reduce warfarin dose); decreases effect of antidiabetic medications; alters response to digitalis.","Use in pregnancy: Category X – contraindicated due to teratogenic effects."] |
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| Fetal Monitoring |
| Monitor maternal thyroid function (TSH, free T4) and cardiac status (heart rate, blood pressure, ECG). Monitor fetal growth and development via ultrasound and fetal heart rate monitoring. Assess newborn for thyroid dysfunction at birth. |
| Fertility Effects | May reduce fertility by altering thyroid hormone levels and metabolic state. Normalization of thyroid function with appropriate therapy may improve fertility. Dextrothyroxine use may interfere with ovulation and menstrual cycle regularity. |