Levothyroxine Sodium (levothyroxine sodium)

The dosage of levothyroxine sodium for hypothyroidism or pituitary TSH suppression depends on a variety of factors, including patient age, body weight, cardiovascular status, concomitant medical conditions (including pregnancy), concomitant medications, co-administered food, and the specific nature of the condition being treated. Dosage must be individualized to account for these factors, with dosage adjustments made based on periodic assessment of the patient's clinical response and laboratory parameters.

Levothyroxine sodium is administered orally or by IV injection. It is available for oral administration as a tablet, capsule, or oral solution; approved oral preparations may not be therapeutically equivalent to one another (consult the FDA's Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) for current information). Levothyroxine sodium is available for IV administration as a solution for injection or a powder for reconstitution and injection.

There is no enhanced messaging for this drug.

There are no contraindication interactions for this drug.

Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

Agents That Affect Iodide/Radioactive Iodide

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Many compounds can affect iodide protein binding and alter iodide pharmacokinetics and pharmacodynamics.(1)

CLINICAL EFFECTS: Compounds that affect iodide pharmacokinetics and pharmacodynamics may impact the effectiveness of radioactive iodide.(1)

PREDISPOSING FACTORS: Compounds that affect iodide pharmacokinetics and pharmacodynamics are expected to have the most impact during therapy using radioactive iodide. Diagnostic procedures would be expected to be impacted less.

PATIENT MANAGEMENT: Discuss the use of agents that affect iodide pharmacokinetics and pharmacodynamics with the patient's oncologist.(1) Because indocyanine green contains sodium iodide, the iodine-binding capacity of thyroid tissue may be reduced for at least one week following administration. Do not perform radioactive iodine uptake studies for at least one week following administration of indocyanine green.(2) The manufacturer of iopamidol states administration may interfere with thyroid uptake of radioactive iodine and decrease therapeutic and diagnostic efficacy. Avoid thyroid therapy or testing for up to 6 weeks post administration of iopamidol.(3)

DISCUSSION: Many agents interact with radioactive iodine. The average duration of effect is: anticoagulants - 1 week antihistamines - 1 week anti-thyroid drugs, e.g: carbimazole, methimazole, propylthiouracil - 3-5 days corticosteroids - 1 week iodide-containing medications, e.g: amiodarone - 1-6 months expectorants - 2 weeks Lugol solution - 3 weeks saturated solution of potassium iodine - 3 weeks vitamins - 10-14 days iodide-containing X-ray contrast agents - up to 1 year lithium - 4 weeks phenylbutazone - 1-2 weeks sulfonamides - 1 week thyroid hormones (natural or synthetic), e.g.: thyroxine - 4 weeks tri-iodothyronine - 2 weeks tolbutamide - 1 week topical iodide - 1-9 months (1)

Agents That Affect Iodide/Sodium Iodide I 131

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Many compounds can affect iodide protein binding and alter iodide pharmacokinetics and pharmacodynamics.(1,2)

CLINICAL EFFECTS: Compounds that affect iodide pharmacokinetics and pharmacodynamics may impact the effectiveness of radioactive iodide.(1,2)

PREDISPOSING FACTORS: Compounds that affect iodide pharmacokinetics and pharmacodynamics are expected to have the most impact during therapy using radioactive iodide. Diagnostic procedures would be expected to be impacted less.

PATIENT MANAGEMENT: Discuss the use of agents that affect iodide pharmacokinetics and pharmacodynamics with the patient's oncologist.(1,2) Because indocyanine green contains sodium iodide, the iodine-binding capacity of thyroid tissue may be reduced for at least one week following administration. Do not perform radioactive iodine uptake studies for at least one week following administration of indocyanine green.(3) The manufacturer of iopamidol states administration may interfere with thyroid uptake of radioactive iodine and decrease therapeutic and diagnostic efficacy. Avoid thyroid therapy or testing for up to 6 weeks post administration of iopamidol.(4)

DISCUSSION: Many agents interact with radioactive iodine. The average duration of effect is: anticoagulants - 1 week antihistamines - 1 week anti-thyroid drugs, e.g: carbimazole, methimazole, propylthiouracil - 3-5 days corticosteroids - 1 week iodide-containing medications, e.g: amiodarone - 1-6 months expectorants - 2 weeks Lugol solution - 3 weeks saturated solution of potassium iodine - 3 weeks vitamins - 10-14 days iodide-containing X-ray contrast agents - up to 1 year lithium - 4 weeks phenylbutazone - 1-2 weeks sulfonamides - 1 week thyroid hormones (natural or synthetic), e.g.: thyroxine - 4 weeks tri-iodothyronine - 2 weeks tolbutamide - 1 week topical iodide - 1-9 months (1,2)

Moderate Interaction: Assess the risk to the patient and take action as needed.

Thyroid Preparations/Carbimazole; Methimazole

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Methimazole can affect the therapeutic response to thyroid hormone therapy. It decreases thyroid hormone secretion. Thyroid hormone therapy can antagonize the pharmacologic effects of methimazole by supplying an exogenous source of thyroid hormone. Carbimazole is a prodrug of methimazole.(1)

CLINICAL EFFECTS: Concurrent use of carbimazole or methimazole and thyroid hormones may result in opposing effects.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Concurrent use of carbimazole or methimazole and thyroid hormones should be avoided.

DISCUSSION: The 2016 American Thyroid Association guidelines recommended avoiding the concurrent use of methimazole and thyroid preparations for "block and replace" therapy to make a patient euthyroid. Meta-analyses have shown that a higher prevalence of adverse events occurs with block-and-replace regimens than dose titration.(2) The 2018 European Thyroid Association guidelines state that methimazole (30 mg) may be given combined with levothyroxine supplement ion for block-and-replace therapy to avoid drug-induced hypothyroidism but methimazole dose titration is the preferred therapy.(3)

Thyroid Preparations/Estrogens

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Estrogens increase thyroxine-binding globulin (TBG) levels by increasing its biosynthesis and decreasing its clearance.(1) Hypothyroid patients who start estrogens may be unable to compensate for this increase and may have decreased serum free T4 (FT4) concentrations and increased TSH.(1,2)

CLINICAL EFFECTS: The coadministration of thyroid preparations and estrogens may result in decreased levels and clinical effects of thyroid hormones.(1-4)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Patients taking thyroid preparations and who start or stop estrogens should be monitored for changes in thyroid function. The dosage of the thyroid preparation may need to be increased.(1-4)

DISCUSSION: In a prospective observational study, 25 post-menopausal women with hypothyroidism on stable levothyroxine therapy for at least 9 months started on estrogen replacement therapy. After 12 weeks, mean serum FT4 levels decreased significantly from 1.7 +/- 0.4 ng/dL to 1.4 +/-0.3 mg/dL and TSH increased significantly from 0.9 +/-1.1 to 3.2 +/- 3.1 milli-units/L.(1)

Thyroid Preparations/Imatinib;Sunitinib

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: The suspected mechanism responsible for this phenomenon is an induction of non-deiodination clearance. The induction of uridine diphosphate-glucuronyl transferases (UGTs) by imatinib and sunitinib decreases levels of the thyroid preparations.(1)

CLINICAL EFFECTS: The coadministration of thyroid preparations and imatinib and sunitinib may result in decreased levels and clinical effects of thyroid hormones.(1-3)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Patients taking thyroid preparations and imatinib or sunitinib should be monitored for changes in thyroid function. The dosage of the thyroid preparation may need to be increased.(1-3)

DISCUSSION: In a case report, 8 patients had undergone thyroidectomy and used levothyroxine and imatinib. These patients had an increase need for levothyroxine levels and were monitored for elevations in thyrotropin indicating worsening hypothyroidism.(2) A case report of a 73 year old man who was treated with imatinib and levothyroxine developed worsening hypothyroidism. An increase in levothyroxine dosage was needed.(3) In a case report, a 59 year old woman was taking levothyroxine therapy for hypothyroidism secondary to subtotal thyroidectomy and was recently started on imatinib for chronic myeloid leukemia. The patient developed clinical signs of hypothyroidism and required an increased dose of levothyroxine.(4) In a case report, a 73 year old woman was taking levothyroxine and developed fatigue, nausea, cold-intolerance, hair-loss, brittle nails, progressive weakness, and impressive facial oedema 6 months after starting imatinib. The patient levothyroxine was increased and she remained euthyroid, but the imatinib was discontinued due to extreme fatigue and periorbital oedema. Five months later the patient was stared on sunitinib and her levothyroxine dose was increased. The patient developed similar symptoms to imatinib reaction.(5) In a case report, a patient receiving sunitinib for metastatic papillary renal cell cancer developed high thyroid stimulating hormone levels and severe symptoms despite receiving L-thyroxine.(6)

Thyroid Preparations/Rifampin

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Rifampin is an organic anion transporting polypeptide (OATP) inhibitor and has been found to decrease measured free T4 when taking thyroid replacements. The mechanism for the rifampin effect may be due to induction of hepatic metabolic and biliary clearance. It is also possible that rifampin may have increased net intestinal absorption of L-T4 through inhibition of P-glycoprotein, an intestinal efflux transporter.

CLINICAL EFFECTS: The concurrent or recent use of rifampin may result in altered levels and clinical effects of thyroid hormones. Some patients may experience increased thyroid hormone effects, while others may experience decreased effects.(1)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Patients taking thyroid preparations and rifampin should be monitored for changes in thyroid function. Symptoms of hyperthyroidism include weight loss, rapid heartbeat, nervousness, sweating, tremor, fatigue, and difficulty sleeping. Symptoms of hypothyroidism include fatigue, sluggishness, constipation, stiffness, muscle cramps, loss of appetite, excessive weight gain, or dry skin. The dosage of levothyroxine may need to be adjusted accordingly.

DISCUSSION: In a study, 8 healthy individuals received 100 mcg of levothyroxine combined with placebo or rifampin 600 mg. The coadministration of rifampin significantly increased the 4 AUC by 25% (p=0.003). Levothyroxine absorptions with rifampin was 125% compared to controls.(1) In contrast to this study, two case reports exist documenting decreased effects of levothyroxine during concurrent rifampin. In a case report, a 31 year old woman had a total thyroidectomy and was receiving levothyroxine and was recently started on rifampin. The patient did not develop symptoms of hypothyroidism, but had a decrease in serum thyroxine levels and free thyroxine index during rifampin therapy and an increase in serum thyrotropin levels.(2) In a case report of a 50 year old male, stable on levothyroxine, who exhibited significantly elevated TSH levels during therapy with rifampin. The patient's TSH levels returned to baseline 9 days after discontinuing rifampin.(3)

Thyroid Preparations/Ritonavir

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Thyroid preparations are substrates for uridine diphosphate glucuronosyltransferase (UGT). Also, levothyroxine is converted to the thyroid hormone triiodothyronine (T3) which is further metabolized via UGT.(1) Ritonavir may induce UGT and may increase metabolism of levothyroxine and T3.(1)

CLINICAL EFFECTS: The concurrent use of ritonavir may result in decreased levels and clinical effects of the thyroid preparation.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Patients taking thyroid preparations and ritonavir should be monitored for changes in thyroid function. Symptoms of hypothyroidism include fatigue, sluggishness, constipation, stiffness, muscle cramps, loss of appetite, excessive weight gain, or dry skin. The dosage of the thyroid preparation may need to be adjusted accordingly.

DISCUSSION: A case report of a 29 year old male with auto-immune thyroiditis was stabilized on levothyroxine 125 mcg daily for one year when concurrent therapy with stavudine 40 mg twice daily, lamivudine 150 mg twice daily, ritonavir 600 mg twice daily, and saquinavir 400 mg twice daily was started. One month after concurrent therapy, the patient's thyroid stimulating hormone (TSH) increased to 18.47 mIU/L (a 2.7-fold increase) requiring a dose increase of levothyroxine to 250 mcg daily. Subsequently, ritonavir was discontinued with a decrease in levothyroxine dose to 125 mcg daily with stabilization of TSH at 7.32 mIU/L.(2) A case report of a 58 year old female on zidovudine, lamivudine, and lopinavir/ritonavir underwent a total thyroidectomy with subsequent introduction of levothyroxine. Levothyroxine was titrated to 225 mcg daily along with the addition of liothyronine. Due to persistently elevated TSH values (range 47.6 - 85.1 mIU/L), lopinavir/ritonavir was then withdrawn and two months later TSH and T4 levels returned to normal, 4.1 mIU/L and 12.1 pmol/L, respectively. Eight months later lopinavir/ritonavir was reintroduced and 1 month later TSH and T4 increased to 42.9 mIU/L and 10.6 mIU/L, respectively. Again, lopinavir/ritonavir was withdrawn and TSH and T4 values returned to normal, 1.1 mIU/L and 13.4 pmol/L, respectively.(3) A case report of a 37 year old female on abacavir/lamivudine and lopinavir/ritonavir details the management course of hypothyroidism over a six year period, including during 3 pregnancies. After a total thyroidectomy, the patient was started on levothyroxine 75 mcg daily. Post-surgical levels of TSH and T4 (during patient's second pregnancy) increased to 94.3 mIU/L and 6.1 mIU/L, respectively, and peaked at 125.89 mIU/L and 7.7 mIU/L, respectively. Levothyroxine doses were increased to 175 mcg daily over the following year (during the patient's second and third pregnancies) to achieve decreased TSH and T4 values of 8.58 mIU/L and 12.8 mIU/L, respectively. TSH values rose again to 17.23 mIU/L and ritonavir was withdrawn from therapy. The patient was then maintained on levothyroxine 125 mcg daily with a TSH of 0.12 - 0.42 mIU/L over the next 2 years.(1)

Thyroid Preparations/Sertraline

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: The mechanism by which sertraline lowers serum thyroid hormone concentrations is uncertain. One reported case in which sertraline caused a low serum total thyroxine concentration is believed to be caused by sertraline increasing the clearance of the thyroxine.(1)

CLINICAL EFFECTS: The coadministration of thyroid preparations and sertraline may result in decreased levels and clinical effects of thyroid hormones.(1)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Patients taking thyroid preparations and sertraline should be monitored for changes in thyroid function. The dosage of the thyroid preparation may need to be increased.

DISCUSSION: In a case report of 9 levothyroxine treated patients with hypothyroidism, who were treated with sertraline, all were found to have elevated serum thyrotropin concentrations. Elevated thyrotropin levels are indicative of a decrease in the efficacy of levothyroxine. The dose of levothyroxine was increased for all patients. Required dosage adjustments ranged from 11% to 50%.(1) In a study, patients with major depression and hypothyroidism on adequate levothyroxine therapy were treated with either fluoxetine or sertraline. The results of this study showed no change in thyroid levels among hypothyroid patients on levothyroxine therapy who were treated with either fluoxetine or sertraline.(2)

Thyroid/Selected Anticoagulants

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Unknown. However, thyroid hormones may influence concentrations of vitamin K-dependent clotting factors.

CLINICAL EFFECTS: Concurrent use of vitamin K antagonists and thyroid hormones may increase the risk for bleeding. Hypothyroidism may increase the oral anticoagulant requirements. Administration of thyroid hormones or hyperthyroidism may decrease oral anticoagulant requirements.

PREDISPOSING FACTORS: The risk for bleeding episodes may be greater in patients with disease-associated factors (e.g. thrombocytopenia). Drug associated risk factors include concurrent use of multiple drugs which inhibit anticoagulant/antiplatelet metabolism and/or have an inherent risk for bleeding (e.g. NSAIDs).

PATIENT MANAGEMENT: Monitor prothrombin activity and adjust the anticoagulant dosage accordingly during initiation of warfarin therapy in patients receiving thyroid replacement therapy, during the initiation or titration of thyroid replacement therapy in patients receiving warfarin, or if any changes in thyroid function occur. If concurrent therapy is warranted, monitor patients receiving concurrent therapy for signs of blood loss, including decreased hemoglobin, hematocrit, fecal occult blood, and/or decreased blood pressure and promptly evaluate patients with any symptoms. When applicable, perform agent-specific laboratory test (e.g. INR, aPTT) to monitor efficacy and safety of anticoagulation. Discontinue anticoagulation in patients with active pathologic bleeding. Instruct patients to report any signs and symptoms of bleeding, such as unusual bleeding from the gums or nose; unusual bruising; red or black, tarry stools; red, pink or dark brown urine; acute abdominal or joint pain and/or swelling. The time of highest risk for a coumarin-type drug interaction is when the precipitant drug is initiated or discontinued. Contact the prescriber before initiating, altering the dose or discontinuing either drug.

DISCUSSION: Any change in thyroid status in patients stabilized on warfarin may necessitate a change in warfarin dosage requirements. Initiation of thyroid replacement therapy in patients stabilized on warfarin may result in increases in the effects of warfarin. A decrease in the dose of warfarin usually becomes necessary within one to four weeks after starting therapy with thyroid compounds. Warfarin therapy should be initiated in low doses in patients who are hyperthyroid. In a 16 year population based nested matched case control study, 10,532 hospitalizations for hemorrhage were evaluated and matched to 40,595 controls. The primary analysis showed no increase in risk of hemorrhage in older patients on warfarin initiated on levothyroxine in previous 30 days (OR 1.11, 95% CI 0.67-1.86). When patients were matched up to 90 days prior to the hemorrhage event, there was no significant association with levothyroxine 31-60 days prior to index date (OR 0.75 95% CI 0.26-2.25) or 61-90 days prior to index date (OR 0.67 95% CI 0.15-3.01). A retrospective, self-controlled study of 102 patients on chronic warfarin therapy were included if the patient had INR results 90 days before and after starting levothyroxine. The mean warfarin dose/INR ratio in the pre-period and post-period had no significant change (p=0.825). In patients who achieved euthyroid during post-period, warfarin dose/INR ratio was numerically lower in the post-period but not statistically significant (13.42 versus 12.7, respectively; p=0.338). In patients initiated on levothyroxine doses greater than 50 mcg, pre-period and post-period warfarin dose/INR ratio also had no significant difference (p>0.2).

*Uncorrected adrenal insufficiency.

*Hypersensitivity to glycerol (Tirosint-SOL(R) only).

*Hypersensitivity to glycerin and edetate disodium (Ermeza(R) only).

• Thyrotoxicosis crisis

• Myocarditis
• Primary adrenocortical insufficiency
• Thyrotoxicosis

• Coronary artery disease
• Diabetes mellitus
• Hypertension

Adverse reactions associated with oral levothyroxine are primarily those of hyperthyroidism due to therapeutic overdosage, including arrhythmia, myocardial infarction, dyspnea, muscle spasm, headache, nervousness, irritability, insomnia, tremors, muscle weakness, increased appetite, weight loss, diarrhea, heat intolerance, menstrual irregularities, and skin rash.

Adverse reactions associated with IV levothyroxine are also primarily those of hyperthyroidism due to therapeutic overdosage, including fatigue, increased appetite, weight loss, heat intolerance, fever, excessive sweating, headache, hyperactivity, nervousness, anxiety, irritability, emotional lability, insomnia, tremors, muscle weakness, muscle spasm, palpitations, tachycardia, arrhythmias, increased pulse and blood pressure, heart failure, angina, myocardial infarction, cardiac arrest, dyspnea, diarrhea, vomiting, abdominal cramps, elevations in liver function tests, flushing, and rash.

Less Frequent

• Osteopenia

Rare or Very Rare

• Abnormal hepatic function tests
• Acute myocardial infarction
• Angina
• Angioedema
• Cardiac arrest
• Cardiac arrhythmia
• Dyspnea
• Heart failure
• Idiopathic intracranial hypertension
• Mood changes
• Seizure disorder
• Skin rash
• Slipped capital epiphyses
• Tachycardia
• Urticaria

More Frequent

• Female infertility

Less Frequent

• Hypertension
• Weight loss

Rare or Very Rare

• Abdominal pain with cramps
• Alopecia
• Chest pain
• Diarrhea
• Fatigue
• Fever
• Flushing
• Headache disorder
• Heat intolerance
• Hyperhidrosis
• Increased appetite
• Increased pulse rate
• Insomnia
• Irregular menstrual periods
• Irritability
• Menstrual disorder
• Muscle spasm
• Muscle weakness
• Nervousness
• Palpitations
• Symptoms of anxiety
• Tremor
• Vomiting

No enhanced messaging available.

Safety and effectiveness of levothyroxine tablets and oral solution have been established for use as replacement therapy for primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) congenital or acquired hypothyroidism in pediatric patients from birth to <17 years of age. Safety and effectiveness have also been established for use as an adjunct to surgery and radioiodine therapy for management of thyrotropin-dependent well-differentiated thyroid cancer in pediatric patients from birth to <17 years of age.

Safety and effectiveness of levothyroxine oral capsules have been established in pediatric patients >=6 years of age.

Rapid restoration of normal serum T4 concentrations in patients with congenital hypothyroidism is essential for preventing adverse effects on cognitive development or overall growth and maturation. Levothyroxine therapy should be initiated immediately upon diagnosis; it is typically continued for life in patients with congenital hypothyroidism.

In pediatric patients without an established diagnosis of permanent hypothyroidism, discontinue levothyroxine for a trial period (after the patient is at least 3 years of age) and obtain serum T4 and TSH levels at the end of the trial period; use laboratory test results and clinical assessments to guide diagnosis and treatment, if warranted.

Closely monitor infants and children for cardiac overload, arrhythmia, and aspiration from avid suckling during the first 2 weeks of levothyroxine therapy.

Levothyroxine oral solutions contain glycerin or glycerol. These inactive ingredients may cause GI irritation resulting in vomiting and/or osmotic diarrhea; patients in the first 3 months of life may be particularly susceptible to serious fluid and electrolyte complications from glycerin- or glycerol-induced GI irritation. Closely monitor patients from birth to 3 months of age for signs and symptoms of GI irritation.

Safety and effectiveness of IV levothyroxine have not been established in pediatric patients.

Clinical experience, including data from published postmarketing studies, has not identified increased rates of major birth defects, miscarriages, or other adverse maternal or fetal outcomes in pregnant women treated with oral levothyroxine to maintain a euthyroid state. Maternal hypothyroidism during pregnancy may increase the risk of complications, including spontaneous abortion, gestational hypertension, pre-eclampsia, stillbirth, and premature delivery. Untreated maternal hypothyroidism may also adversely affect fetal neurocognitive development. Levothyroxine should not be discontinued during pregnancy, and hypothyroidism diagnosed during pregnancy should be promptly treated.

Because thyroid-stimulating hormone (TSH) levels may increase during pregnancy, levothyroxine requirements may also be increased; TSH should be monitored, and the dosage of levothyroxine should be adjusted as necessary. Postpartum TSH levels are similar to preconception values, so the levothyroxine dosage should be decreased to the pre-pregnancy dosage immediately after delivery.

There are no reported cases of IV levothyroxine being used to treat myxedema coma in pregnant patients; however, because nontreatment is associated with a high probability of significant morbidity or mortality to the maternal patient and the fetus, pregnant patients who develop myxedema should be treated with IV levothyroxine.

Published studies report that levothyroxine is present in human milk following oral administration. No adverse effects on the breast-fed infant have been reported. The effects of levothyroxine on milk production are not known; however, adequate levothyroxine treatment during lactation may normalize milk production in hypothyroid lactating mothers with low milk supply.

The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for the drug and any potential adverse effects on the breast-fed infant from levothyroxine or from the underlying maternal condition.

There are no reported cases of IV levothyroxine being used to treat myxedema coma in lactating patients; however, because nontreatment is associated with a high probability of significant morbidity or mortality, breastfeeding patients who develop myxedema should be treated with IV levothyroxine.

Geriatric patients should receive lower starting dosages of oral levothyroxine (e.g., 12.5-25 mcg/day); in these patients, the dosage of levothyroxine should be titrated every 6-8 weeks as needed based on serum TSH or free T4 until the patient is euthyroid.

Cautious use (e.g., dosages in the lower end of the recommended range) of IV levothyroxine sodium may be warranted in geriatric patients.

Because of the increased prevalence of cardiovascular disease among elderly patients, oral levothyroxine should be initiated at less than the full replacement dosage in such patients. Use caution when administering IV levothyroxine for myxedema coma in elderly patients and monitor for adverse cardiac effects. Levothyroxine overtreatment can lead to atrial arrhythmias (including atrial fibrillation) in elderly patients.