ral hypoglycemics should be closely watched during initiation of thyroid replacement therapy. cholestyramine or colestipol—cholestyramine or colestipol binds both levothyroxine (t4) and liothyronine (t3) in the intestine, thus impairing absorption of these thyroid hormones. in vitro studies indicate that the binding is not easily removed. therefore four to five hours should elapse between administration of cholestyramine or colestipol and thyroid hormones. estrogen, oral contraceptives—estrogens tend to increase serum thyroxine-binding globulin (tbg). in a patient with a nonfunctioning thyroid gland who is receiving thyroid replacement therapy, free levothyroxine (t4) may be decreased when estrogens are started thus increasing thyroid requirements. however, if the patient’s thyroid gland has sufficient function, the decreased free levothyroxine (t4) will result in a compensatory increase in levothyroxine (t4) output by the thyroid. therefore, patients without a functioning thyroid gland who are on thyroid replacement therapy may need to increase their thyroid dose if estrogens or estrogen-containing oral contraceptives are given.

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.

dministration ). 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.

angina is an indication for a reduction in dosage. most patients require 60 to 120 mg/day. failure to respond to doses of 180 mg suggests lack of compliance or malabsorption. maintenance dosages 60 to 120 mg/day usually result in normal serum t4 and t3 levels. adequate therapy usually results in normal tsh and t4 levels after 2 to 3 weeks of therapy. readjustment of thyroid hormone dosage should be made within the first four weeks of therapy, after proper clinical and laboratory evaluations, including serum levels of t4, bound and free, and tsh. liothyronine (t3) may be used in preference to levothyroxine (t4) during radio-isotope scanning procedures, since induction of hypothyroidism in those cases is more abrupt and can be of shorter duration. it may also be preferred when impairment of peripheral conversion of levothyroxine (t4) and liothyronine (t3) is suspected. myxedema coma— myxedema coma is usually precipitated in the hypothyroid patient of long-standing by intercurrent illness or drugs such as sedatives and anesthetics and should be considered a medical emergency. therapy should be directed at the correction of electrolyte disturbances and possible infection besides the administration of thyroid hormones. corticosteroids should be administered routinely. levothyroxine (t4) and liothyronine (t3) may be administered via a nasogastric tube but the preferred route of administration of both hormones is intravenous. levothyroxine sodium (t4) is given at a starting dose of 400 mcg (100 mcg/ml) given rapidly, and is usually well tolerated, even in the elderly. this initial dose is followed by daily supplements of 100 to 200 mcg given iv. normal t4 levels are achieved in 24 hours followed in 3 days by threefold elevation of t3. oral therapy with thyroid hormone would be resumed as soon as the clinical situation has been stabilized and the patient is able to take oral medication. thyroid cancer— exogenous thyroid hormone may produce regression of metastases from follicular and papillary carcinoma of the thyroid and is used as ancillary therapy of these conditions with radioactive iodine. tsh should be suppressed to low or undetectable levels. therefore, larger amounts of thyroid hormone than those used for replacement therapy are required. medullary carcinoma of the thyroid is usually unresponsive to this therapy. thyroid suppression therapy— administration of thyroid hormone in doses higher than those produced physiologically by the gland results in suppression of the production of endogenous hormone. this is the basis for the thyroid suppression test and is used as an aid in the diagnosis of patients with signs of mild hyperthyroidism in whom base line laboratory tests appear normal, or to demonstrate thyroid gland autonomy in patients with grave’s ophthalmopathy. 131i uptake is determined before and after the administration of the exogenous hormone. a 50% or greater suppression of uptake indicates a normal thyroid-pituitary axis and thus rules out thyroid gland autonomy. for adults, the usual suppressive dose of levothyroxine (t4) is 1.56 mcg/kg of body weight per day given for 7 to 10 days. these doses usually yield normal serum t4 and t3 levels and lack of response to tsh. thyroid hormones should be administered cautiously to patients in whom there is strong suspicion of thyroid gland autonomy, in view of the fact that the exogenous hormone effects will be additive to the endogenous source. pediatric dosage— pediatric dosage should follow the recommendations summarized in table 1. in infants with congenital hypothyroidism, therapy with full doses should be instituted as soon as the diagnosis has been made. table 1: recommended pediatric dosage for congenital hypothyroidism age armour thyroid (thyroid tablets, usp) dose per day daily dose per kg of body weight 0-6 months 15-30 mg 4.8-6 mg 6-12 months 30-45 mg 3.6-4.8 mg 1-5 years 45-60 mg 3-3.6 mg 6-12 years 60-90 mg 2.4-3 mg over 12 years over 90 mg 1.2-1.8 mg

ral hypoglycemics should be closely watched during initiation of thyroid replacement therapy. cholestyramine or colestipol—cholestyramine or colestipol binds both levothyroxine (t4) and liothyronine (t3) in the intestine, thus impairing absorption of these thyroid hormones. in vitro studies indicate that the binding is not easily removed. therefore four to five hours should elapse between administration of cholestyramine or colestipol and thyroid hormones. estrogen, oral contraceptives—estrogens tend to increase serum thyroxine-binding globulin (tbg). in a patient with a nonfunctioning thyroid gland who is receiving thyroid replacement therapy, free levothyroxine (t4) may be decreased when estrogens are started thus increasing thyroid requirements. however, if the patient’s thyroid gland has sufficient function, the decreased free levothyroxine (t4) will result in a compensatory increase in levothyroxine (t4) output by the thyroid. therefore, patients without a functioning thyroid gland who are on thyroid replacement therapy may need to increase their thyroid dose if estrogens or estrogen-containing oral contraceptives are given.

pproximately 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.” pharmacokinetics – animal studies have shown that levothyroxine (t4) is only partially absorbed from the gastrointestinal tract. the degree of absorption is dependent on the vehicle used for its administration and by the character of the intestinal contents, the intestinal flora, including plasma protein, and soluble dietary factors, all of which bind thyroid and thereby make it unavailable for diffusion. only 41% is absorbed when given in a gelatin capsule as opposed to a 74% absorption when given with an albumin carrier. depending on other factors, absorption has varied from 48 to 79% of the administered dose. fasting increases absorption. malabsorption syndromes, as well as dietary factors, (children’s soybean formula, concomitant use of anionic exchange resins such as cholestyramine) cause excessive fecal loss. liothyronine (t3) is almost totally absorbed, 95 % in 4 hours. the hormones contained in the natural preparations are absorbed in a manner similar to the synthetic hormones. more than 99% of circulating hormones are bound to serum proteins, including thyroid-binding globulin (tbg), thyroid-binding prealbumin (tbpa), and albumin (tba), whose capacities and affinities vary for the hormones. the higher affinity of levothyroxine (t4) for both tbg and tbpa as compared to liothyronine (t3) partially explains the higher serum levels and longer half-life of the former hormone. both protein-bound hormones exist in reverse equilibrium with minute amounts of free hormone, the latter accounting for the metabolic activity. deiodination of levothyroxine (t4) occurs at a number of sites, including liver, kidney, and other tissues. the conjugated hormone, in the form of glucuronide or sulfate, is found in the bile and gut where it may complete an enterohepatic circulation. 85% of levothyroxine (t4) metabolized daily is deiodinated.

hormones. more than 99% of circulating hormones are bound to serum proteins, including thyroid-binding globulin (tbg), thyroid-binding prealbumin (tbpa), and albumin (tba), whose capacities and affinities vary for the hormones. the higher affinity of levothyroxine (t4) for both tbg and tbpa as compared to liothyronine (t3) partially explains the higher serum levels and longer half-life of the former hormone. both protein-bound hormones exist in reverse equilibrium with minute amounts of free hormone, the latter accounting for the metabolic activity. deiodination of levothyroxine (t4) occurs at a number of sites, including liver, kidney, and other tissues. the conjugated hormone, in the form of glucuronide or sulfate, is found in the bile and gut where it may complete an enterohepatic circulation. 85% of levothyroxine (t4) metabolized daily is deiodinated.

d pestle beneath the letter “a” on the top and strength code letters on the bottom as defined below strength code ¼ grain tc ½ grain td 1 grain te 1 ½ grain tj 2 grain tf 3 grain tg (bisected) 4 grain th 5 grain ti (bisected) note: (t3 liothyronine is approximately four times as potent as t4 levothyroxine on a microgram for microgram basis.) store in a tight container protected from light and moisture. store between 15°c and 30°c (59°f and 86°f). *armour thyroid (thyroid tablets, usp) has not been approved by fda as a new drug . distributed by: allergan usa, inc. madison, nj 07940 © 2019 allergan. all rights reserved. armour® is a registered trademark of allergan sales, llc. allergan® and its designs are trademarks of allergan inc. revised: june 2018 v.1.0uspi0457

s. 4. in case of concomitant oral anticoagulant therapy, the prothrombin time should be measured frequently to determine if the dosage of oral anticoagulants is to be readjusted. 5. partial loss of hair may be experienced by children in the first few months of thyroid therapy, but this is usually a transient phenomenon and later recovery is usually the rule.