LEVOXYL PACKAGE INSERT PDF

Furosemide has been shown to inhibit the protein binding of T4 to TBG and albumin, causing an increased free-T4 fraction in serum. Furosemide competes for T4-binding sites on TBG, prealbumin, and albumin, so that a single high dose can acutely lower the total T4 level. Closely monitor thyroid hormone parameters. Drug or Drug Class Phenobarbital Rifampin Phenobarbital has been shown to reduce the response to thyroxine. Changes in thyroid status may occur if barbiturates are added or withdrawn from patients being treated for hypothyroidism.

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Non-Steroidal Anti-inflammatory Drugs - Fenamates These drugs may cause protein-binding site displacement. Furosemide has been shown to inhibit the protein binding of T4 to TBG and albumin, causing an increase free T4 fraction in serum. Furosemide competes for T4-binding sites on TBG, prealbumin, and albumin, so that a single high dose can acutely lower the total T4 level. Closely monitor thyroid hormone parameters.

Table 2: Drugs That May Alter Hepatic Metabolism of T4 Hypothyroidism Potential impact: Stimulation of hepatic microsomal drug-metabolizing enzyme activity may cause increased hepatic degradation of levothyroxine, resulting in increased levothyroxine requirements. Drug or Drug Class Phenobarbital Rifampin Phenobarbital has been shown to reduce the response to thyroxine.

Changes in thyroid status may occur if barbiturates are added or withdrawn from patients being treated for hypothyroidism. Rifampin has been shown to accelerate the metabolism of levothyroxine. However, serum T4 levels are usually normal but may occasionally be slightly increased.

Drug or Drug Class Beta-adrenergic antagonists e. It should be noted that actions of particular beta-adrenergic antagonists may be impaired when the hypothyroid patient is converted to the euthyroid state. Glucocorticoids e. However, long-term glucocorticoid therapy may result in slightly decreased T3 and T4 levels due to decreased TBG production See above.

Other drugs: Amiodarone Amiodarone inhibits peripheral conversion of levothyroxine T4 to triiodothyronine T3 and may cause isolated biochemical changes increase in serum free-T4, and decreased or normal free-T3 in clinically euthyroid patients.

Antidiabetic Therapy Addition of levothyroxine to antidiabetic or insulin therapy may result in increased antidiabetic agent or insulin requirements. Careful monitoring of glycemic control is recommended. Oral Anticoagulants Levothyroxine increases the response to oral anticoagulant therapy.

Therefore, a decrease in the dose of anticoagulant may be warranted with correction of the hypothyroid state. Closely monitor coagulation tests to permit appropriate and timely dosage adjustments. Digitalis Glycosides Levothyroxine may reduce the therapeutic effects of digitalis glycosides. Serum digitalis glycoside levels may be decreased when a hypothyroid patient becomes euthyroid, necessitating an increase in the dose of digitalis glycosides. Antidepressant Therapy Concurrent use of tricyclic e.

Toxic effects may include increased risk of cardiac arrhythmias and central nervous system stimulation. Levothyroxine may accelerate the onset of action of tricyclics.

Administration of sertraline in patients stabilized on levothyroxine may result in increased levothyroxine requirements. Ketamine Concurrent use of ketamine and levothyroxine may produce marked hypertension and tachycardia.

Closely monitor blood pressure and heart rate in these patients. Sympathomimetics Concurrent use may of sympathomimetics and levothyroxine may increase the effects of sympathomimetics or thyroid hormone. Thyroid hormones may increase the risk of coronary insufficiency when sympathomimetic agents are administered to patients with coronary artery disease. Pregnancy, infectious hepatitis, estrogens, estrogen containing oral contraceptives, and acute intermittent porphyria increase TBG concentrations.

Nephrosis, severe hypoproteinemia, severe liver disease, acromegaly, androgens, and corticosteroids decrease TBG concentration.

Familial hyper- or hypo-thyroxine binding globulinemias have been described, with the incidence of TBG deficiency approximating 1 in 9, The clinical data in pregnant women treated with oral levothyroxine to maintain a euthyroid state have not reported increased rates of major birth defects, miscarriages, or adverse maternal or fetal outcomes see Data. There are risks to the mother and fetus associated with myxedema coma in pregnancy see Clinical Considerations. Animal reproduction studies have not been conducted with levothyroxine sodium.

The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. In the U. Delaying treatment in pregnant women with myxedema coma increases the risk of maternal and fetal morbidity and mortality. Life-sustaining therapy for the pregnant woman should not be withheld due to potential concerns regarding the effects of Levothyroxine Sodium Injection on the fetus.

Oral levothyroxine is approved for use as a replacement therapy in hypothyroidism. There is a long experience of oral levothyroxine use in pregnant women that has not reported increased rates of fetal malformations, miscarriages or other adverse maternal or fetal outcomes associated with levothyroxine use in pregnant women.

Lactation Risk Summary Published studies report that levothyroxine is present in human milk following the administration of oral levothyroxine. However, there is insufficient information to determine the effects of levothyroxine on the breastfed infant and no available information on the effects of levothyroxine on milk production.

There is no available data with use of Levothyroxine Sodium Injection in lactating women. Pediatric Use The safety and efficacy of Levothyroxine Sodium Injection have not been established in pediatric patients. Geriatric Use Because of the increased prevalence of cardiovascular disease among the elderly, initiate Levothyroxine Sodium Injection with lower doses in elderly patients and in patients with underlying cardiovascular disease and closely monitor for cardiac adverse reactions.

Atrial arrhythmias can occur in elderly patients. Atrial fibrillation is the most common of the arrhythmias observed with levothyroxine overtreatment in the elderly [see Dosage and Administration 2. Overdosage The signs and symptoms of overdosage are those of hyperthyroidism [see Warnings and Precautions 5 and Adverse Reactions 6 ]. In addition, confusion and disorientation may occur. Cerebral embolism, shock, coma, and death have been reported. Reduce the Levothyroxine Sodium Injection dose or temporarily discontinue if signs or symptoms of overdosage occur.

Levothyroxine Injection Description Levothyroxine Sodium Injection contains synthetic crystalline levothyroxine T4 in sodium salt form. Levothyroxine Sodium Injection is in single dose clear glass vials.

Levothyroxine Injection - Clinical Pharmacology Mechanism of Action Thyroid hormones exert their physiologic actions through control of DNA transcription and protein synthesis. Triiodothyronine T3 and levothyroxine T4 diffuse into the cell nucleus and bind to thyroid receptor proteins attached to DNA. This hormone nuclear receptor complex activates gene transcription and synthesis of messenger RNA and cytoplasmic proteins. Pharmacodynamics Levothyroxine sodium is a synthetic T4 hormone that exerts the same physiologic effect as endogenous T4, thereby maintaining normal T4 levels when a deficiency is present.

Protein bound thyroid hormones exist in reverse equilibrium with small amounts of free hormone. Only unbound hormone is metabolically active. Many drugs and physiologic conditions affect the binding of thyroid hormones to serum proteins [see Drug Interactions 7 ].

Thyroid hormones do not readily cross the placental barrier [see Use in Specific Populations 8. Metabolism T4 is slowly eliminated. The major pathway of thyroid hormone metabolism is through sequential deiodination. Approximately eighty percent of circulating T3 is derived from peripheral T4 by monodeiodination. The liver is the major site of degradation for both T4 and T3, with T4 deiodination also occurring at a number of additional sites, including the kidney and other tissues.

T3 and rT3 are further deiodinated to diiodothyronine. Thyroid hormones are also metabolized via conjugation with glucuronides and sulfates and excreted directly into the bile and gut where they undergo enterohepatic recirculation. Excretion Thyroid hormones are primarily eliminated by the kidneys.

A portion of the conjugated hormone reaches the colon unchanged, where it is hydrolyzed and eliminated in feces as the free hormones. Urinary excretion of T4 decreases with age. Table 1: Pharmacokinetic Parameters of Thyroid Hormones in Euthyroid Patients T4: Levothyroxine 1 3 to 4 days in hyperthyroidism, 9 to 10 days in hypothyroidism.

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