DailyMed Label: Adthyza

DailyMed Label: Adthyza

2023

DailyMed Prescription

Adthyza

Levothyroxine and Liothyronine

Azurity Pharmaceuticals, Inc.

NDC: 24338-016

NDC: 24338-016

NDC: 24338-032

NDC: 24338-032

NDC: 24338-065

NDC: 24338-065

NDC: 24338-097

NDC: 24338-097

NDC: 24338-113

NDC: 24338-113

ADTHYZA™ (thyroid tablets, USP) ADTHYZA™ (thyroid tablets, USP) has not been approved by FDA as a new drug. for oral use is a natural preparation derived from porcine thyroid glands and may have a characteristic odor. ADTHYZA™ (thyroid tablets, USP) contains both tetraiodothyronine sodium (T4 levothyroxine) and triiodothyronine sodium (T3 liothyronine). T3 liothyronine is approximately four times as potent as T4 levothyroxine on a microgram for microgram basis. They provide 38 mcg levothyroxine (T4) and 9 mcg liothyronine (T3) for each 65 mg of the labeled content of thyroid. The inactive ingredients are calcium stearate, colloidal silicon dioxide, dextrose, mannitol, microcrystalline cellulose, and sodium starch glycolate. The structural formulas are below.

ADTHYZA™ (thyroid tablets, USP) are indicated: As replacement or supplemental therapy in patients with hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis. This category includes cretinism, myxedema, and ordinary hypothyroidism in patients of any age (children, adults, the elderly), or state (including pregnancy); primary hypothyroidism resulting from functional deficiency, primary atrophy, partial or total absence of thyroid gland, or the effects of surgery, radiation, or drugs, with or without the presence of goiter; and secondary (pituitary), or tertiary (hypothalamic) hypothyroidism (See WARNINGS ). As pituitary TSH suppressants, in the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, subacute or chronic lymphocytic thyroiditis (Hashimoto's), multinodular goiter, and in the management of thyroid cancer.

The dosage of thyroid hormones is determined by the indication and must in every case be individualized according to patient response and laboratory findings. Thyroid hormones are given orally. In acute, emergency conditions, injectable levothyroxine sodium (T4) may be given intravenously when oral administration is not feasible or desirable, as in the treatment of myxedema coma, or during total parenteral nutrition. Intramuscular administration is not advisable because of reported poor absorption.

Thyroid hormone preparations are generally contraindicated in patients with diagnosed but as yet uncorrected adrenal cortical insufficiency, untreated thyrotoxicosis, and apparent hypersensitivity to any of their active or extraneous constituents. There is no well-documented evidence from the literature, however, of true allergic or idiosyncratic reactions to thyroid hormone. The use of thyroid hormones in the therapy of obesity, alone or combined with other drugs, is unjustified and has been shown to be ineffective. Neither is their use justified for the treatment of male or female infertility unless this condition is accompanied by hypothyroidism.

Thyroid hormones should be used with great caution in a number of circumstances where the integrity of the cardiovascular system, particularly the coronary arteries, is suspected. These include patients with angina pectoris or the elderly, in whom there is a greater likelihood of occult cardiac disease. In these patients therapy should be initiated with low doses, i.e., 16.25-32.5 mg of ADTHYZA™ (thyroid tablets, USP). When, in such patients, a euthyroid state can only be reached at the expense of an aggravation of the cardiovascular disease, thyroid hormone dosage should be reduced. Thyroid hormone therapy in patients with concomitant diabetes mellitus or diabetes insipidus or adrenal cortical insufficiency aggravates the intensity of their symptoms. Appropriate adjustments of the various therapeutic measures directed at these concomitant endocrine diseases are required. The therapy of myxedema coma requires simultaneous administration of glucocorticoids (See DOSAGE AND ADMINISTRATION ). Hypothyroidism decreases and hyperthyroidism increases the sensitivity to oral anticoagulants. Prothrombin time should be closely monitored in thyroid-treated patients on oral anticoagulants and dosage of the latter agents adjusted on the basis of frequent prothrombin time determinations. In infants, excessive doses of thyroid hormone preparations may produce craniosynostosis.

Adverse reactions other than those indicative of hyperthyroidism because of therapeutic overdosage, either initially or during the maintenance period, are rare (See

Thyroid hormones appear to increase catabolism of vitamin K-dependent clotting factors. If oral anticoagulants are also being given, compensatory increases in clotting factor synthesis are impaired. Patients stabilized on oral anticoagulants who are found to require thyroid replacement therapy should be watched very closely when thyroid is started. If a patient is truly hypothyroid, it is likely that a reduction in anticoagulant dosage will be required. No special precautions appear to be necessary when oral anticoagulant therapy is begun in a patient already stabilized on maintenance thyroid replacement therapy.

ADTHYZA™ (thyroid tablets, USP) tablets are supplied as described in Table 2. ADTHYZA™ (thyroid tablets, USP) are off-white to tan, round tablets with convex surfaces which may contain speckles. One side is plain and the other side of the tablet has the imprint code as defined below. Note: T3 liothyronine is approximately four times as potent as T4 levothyroxine on a microgram for microgram basis. Table 2: How Supplied Strength Imprint Code NDC Code Bottle Count Size 16.25 mg (9.5 mcg of T4 2.25 mcg of T3) 16 24338-016-14 14 24338-016-90 90 32.5 mg (19 mcg of T4 4.5 mcg of T3) 32 24338-032-14 14 24338-032-90 90 65 mg (38 mcg of T4 9 mcg of T3) 65 24338-065-14 14 24338-065-90 90 97.5 mg (57 mcg of T4 13.5 mcg of T3) 97 24338-097-14 14 24338-097-90 90 130 mg (76 mcg of T4 18 mcg of T3) 130 24338-113-14 14 24338-113-90 90

The steps in the synthesis of the thyroid hormones are controlled by thyrotropin (Thyroid Stimulating Hormone, TSH) secreted by the anterior pituitary. This hormone's secretion is in turn controlled by a feedback mechanism effected by the thyroid hormones themselves and by thyrotropin releasing hormone (TRH), a tripeptide of hypothalamic origin. Endogenous thyroid hormone secretion is suppressed when exogenous thyroid hormones are administered to euthyroid individuals in excess of the normal gland's secretion. The mechanisms by which thyroid hormones exert their physiologic action are not well understood. These hormones enhance oxygen consumption by most tissues of the body, increase the basal metabolic rate, and the metabolism of carbohydrates, lipids, and proteins. Thus, they exert a profound influence on every organ system in the body and are of particular importance in the development of the central nervous system. The normal thyroid gland contains approximately 200 mcg of levothyroxine (T4) per gram of gland, and 15 mcg of liothyronine (T3) per gram. The ratio of these two hormones in the circulation does not represent the ratio in the thyroid gland, since about 80% of peripheral liothyronine (T3) comes from monodeiodination of levothyroxine (T4). Peripheral monodeiodination of levothyroxine (T4) at the 5 position (inner ring) also results in the formation of reverse liothyronine (T3), which is calorigenically inactive. Liothyronine (T3) levels are low in the fetus and newborn, in old age, in chronic caloric deprivation, hepatic cirrhosis, renal failure, surgical stress, and chronic illnesses representing what has been called the "T3 thyronine syndrome."

NDC 24338-016-90 ADTHYZA™ (thyroid tablets, USP) 16.25 mg Rx only 90 Tablets azurity ® pharmaceuticals