SYNTHROID- levothyroxine sodium tablet

If so, advise them to stop biotin supplementation at least 2 days before assessing TSH and/or T4 levels see Dosage and Administration (2.4) and Drug Interactions (7.10). SYNTHROID is not indicated for suppression of benign thyroid nodules and nontoxic diffuse goiter in iodine-sufficient patients, as there are no clinical benefits and overtreatment with SYNTHROID may induce hyperthyroidism. Levothyroxine is one of the ten NTI drug classes most commonly prescribed.

HYPOTHYROIDISM MEDICATION1,2*

Initiation of thyroid hormone therapy prior to initiating glucocorticoid therapy may precipitate an acute adrenal crisis in patients with adrenal insufficiency. Treat patients with adrenal insufficiency with replacement glucocorticoids prior to initiating treatment with levothyroxine sodium tablets see Contraindications (4). This may be a life-threatening emergency, therefore, symptomatic and supportive therapy should be instituted immediately. If not contraindicated (e.g., by seizures, coma, or loss of the gag reflex), the stomach should be emptied by emesis or gastric lavage to decrease gastrointestinal absorption. Activated charcoal or cholestyramine may also be used to decrease absorption.

• Studies in women taking levothyroxine sodium during pregnancy have not shown an increased risk of congenital abnormalities.
• Toxic effects may include increased risk of cardiac arrhythmias and central nervous system stimulation.
• Administer levothyroxine sodium tablets at least 4 hours apart from these agents.
• The importance of writing “Dispense as Written,” or using the state-specific language for SYNTHROID, is something I discuss with my staff as well.
• Therefore, oral thyroid hormone drug products are not recommended to treat this condition.
• TSH, in turn, is the physiologic stimulus for the synthesis and secretion of thyroid hormones, L-thyroxine (T4) and L-triiodothyronine (T3), by the thyroid gland.

That is primary, secondary, or tertiary hypothyroidism, either due to congenital or acquired state. It is not indicated for the suppression of benign thyroid nodules, or for non-toxic defuse goiter in iodine-sufficient patients. It is also not indicated for the treatment of hypothyroidism during the recovery phase of subacute thyroiditis. There are safety considerations as SYNTHROID should not be used for treatment of obesity or for weight loss. And SYNTHROID is contraindicated in patients who have uncorrected adrenal insufficiency.

Prothrombin time should be closely monitored to permit appropriate and timely dosage adjustments (see Table 2). Thyroid hormone synthesis and secretion is regulated by the hypothalamic-pituitary-thyroid axis. Thyrotropin-releasing hormone (TRH) released from the hypothalamus stimulates secretion synthroid sintomas of thyrotropin-stimulating hormone, TSH, from the anterior pituitary. TSH, in turn, is the physiologic stimulus for the synthesis and secretion of thyroid hormones, L-thyroxine (T4) and L-triiodothyronine (T3), by the thyroid gland. Circulating serum T3 and T4 levels exert a feedback effect on both TRH and TSH secretion.

Warnings and Precautions

• Biotin supplementation is known to interfere with thyroid hormone immunoassays that are based on a biotin and streptavidin interaction, which may result in erroneous thyroid hormone test results.
• Monitor patients treated concomitantly with orlistat and levothyroxine sodium tablets for changes in thyroid function.
• Titrate the dosage (every 2 weeks) as needed based on serum TSH or free-T4 until the patient is euthyroid see Dosage and Administration (2.2) .
• The therapeutic effects of digitalis glycosides may be reduced by levothyroxine.

The levothyroxine sodium tablets dosage is based on the target level of TSH suppression for the stage and clinical status of thyroid cancer. Do not administer in foods that decrease absorption of levothyroxine sodium tablets, such as soybean-based infant formula see Drug Interactions (7.9) . Levothyroxine therapy is usually initiated at full replacement doses, with the recommended dose per body weight decreasing with age (see Table 3). However, in children with chronic or severe hypothyroidism, an initial dose of 25 mcg/day of levothyroxine sodium is recommended with increments of 25 mcg every 2-4 weeks until the desired effect is achieved. Many drugs and physiologic conditions affect the binding of thyroid hormones to serum proteins (see PRECAUTIONS – Drug Interactions and Drug-Laboratory Test Interactions).

These consequences include, among others, effects on growth and development, cardiovascular function, bone metabolism, reproductive function, cognitive function, emotional state, gastrointestinal function, and on glucose and lipid metabolism. Many drugs interact with levothyroxine sodium necessitating adjustments in dosing to maintain therapeutic response (see Drug Interactions ). Use the serum free-T4 level to titrate SYNTHROID dosing until the patient is clinically euthyroid and the serum free-T4 level is restored to the upper half of the normal range see Dosage and Administration (2.3).

• Use the serum free-T4 level to titrate SYNTHROID dosing until the patient is clinically euthyroid and the serum free-T4 level is restored to the upper half of the normal range see Dosage and Administration (2.3).
• Animal studies have not been performed to evaluate the carcinogenic potential, mutagenic potential or effects on fertility of levothyroxine.
• Failure to do so may precipitate an acute adrenal crisis when thyroid hormone therapy is initiated, due to increased metabolic clearance of glucocorticoids by thyroid hormone.
• Dosing must be individualized and adjustments made based on periodic assessment of the patient’s clinical response and laboratory parameters (see PRECAUTIONS – Laboratory Tests).

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. Approximately 80% of the daily dose of T4 is deiodinated to yield equal amounts of T3 and reverse T3 (rT3). Thyroid hormones are also metabolized via conjugation with glucuronides and sulfates and excreted directly into the bile and gut where they undergo enterohepatic recirculation. Levothyroxine, at doses individualized according to patient response, is effective as replacement or supplemental therapy in hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis. Approximately 80% of circulating T3 is derived from peripheral T4 by monodeiodination. Serum TSH levels should be monitored and the SYNTHROID dosage adjusted during pregnancy.

Drug Interactions

Undertreatment and overtreatment should be avoided (see PRECAUTIONS – Pediatric Use). SYNTHROID may be administered to infants and children who cannot swallow intact tablets by crushing the tablet and suspending the freshly crushed tablet in a small amount (5-10 mL or 1-2 teaspoons) of water. Foods that decrease absorption of levothyroxine, such as soybean infant formula, should not be used for administering levothyroxine sodium tablets (see PRECAUTIONS – Drug-Food Interactions).

Overtreatment may accelerate the bone age and result in premature epiphyseal closure and compromised adult stature. Thyroid hormones cross the placental barrier to some extent as evidenced by levels in cord blood of athyreotic fetuses being approximately one-third maternal levels. Transfer of thyroid hormone from the mother to the fetus, however, may not be adequate to prevent in utero hypothyroidism. Infants with congenital hypothyroidism appear to be at increased risk for other congenital anomalies, with cardiovascular anomalies (pulmonary stenosis, atrial septal defect, and ventricular septal defect) being the most common association.

The mechanisms by which thyroid hormones exert their physiologic actions are not completely understood, but it is thought that their principal effects are exerted through control of DNA transcription and protein synthesis. T3 and 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.