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(thyroid tablets, USP)
Armour® Thyroid (thyroid tablets, USP) for oral use is a natu-ral preparation derived from porcine thyroid glands and has astrong, characteristic odor. (T3 liothyronine is approximatelyfour times as potent as T4 levothyroxine on a microgram formicrogram basis.) They provide 38 mcg levothyroxine (T4)and 9 mcg liothyronine (T3) per grain of thyroid. The inactiveingredients are calcium stearate, dextrose, microcrystallinecellulose, sodium starch glycolate and opadry white.
The steps in the synthesis of the thyroid hormones are con-
trolled 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 physi-
ologic 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 carbo-
hydrates, lipids, and proteins. Thus, they exert a profound influ-
ence 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 liothyro-
nine (T3) per gram. The ratio of these two hormones in the cir-
culation does not represent the ratio in the thyroid gland, since
about 80 percent of peripheral liothyronine (T3) comes from
monodeiodination of levothyroxine (T4). Peripheral monodeio-
dination of levothyroxine (T4) at the 5 position (inner ring) also
results in the formation of reverse liothyronine (T3), which is
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 levothy-
roxine (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 intesti-
nal 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 percent is absorbed
when given in a gelatin capsule as opposed to a 74 percent
absorption when given with an albumin carrier.
Depending on other factors, absorption has varied from 48 to
79 percent of the administered dose. Fasting increases absorp-
tion. Malabsorption syndromes, as well as dietary factors, (chil-
dren’s soybean formula, concomitant use of anionic exchange
resins such as cholestyramine) cause excessive fecal loss.
Liothyronine (T3) is almost totally absorbed, 95 percent in 4
hours. The hormones contained in the natural preparations are
absorbed in a manner similar to the synthetic hormones.
More than 99 percent 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 affin-
ity 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 hor-
mones 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 hor-
mone, in the form of glucuronide or sulfate, is found in the bile
and gut where it may complete an enterohepatic circulation.
Eighty-five percent of levothyroxine (T4) metabolized daily is
INDICATIONS AND USAGE
Armour Thyroid tablets are indicated:1. As replacement or supplemental therapy in patients withhypothyroidism of any etiology, except transient hypothy-roidism during the recovery phase of subacute thyroiditis. Thiscategory includes cretinism, myxedema, and ordinaryhypothyroidism in patients of any age (children, adults, theelderly), or state (including pregnancy); primary hypothy-roidism resulting from functional deficiency, primary atrophy,partial or total absence of thyroid gland, or the effects ofsurgery, radiation, or drugs, with or without the presence ofgoiter; and secondary (pituitary), or tertiary (hypothalamic)hypothyroidism (See WARNINGS).
2. As pituitary TSH suppressants, in the treatment or preventionof various types of euthyroid goiters, including thyroid nodules,subacute or chronic Iymphocytic thyroiditis (Hashimoto’s),multinodular goiter, and in the management of thyroid cancer.
3. As diagnostic agents in suppression tests to differentiatesuspected mild hyperthyroidism or thyroid gland autonomy.
Thyroid hormone preparations are generally contraindicated inpatients with diagnosed but as yet uncorrected adrenal corticalinsufficiency, untreated thyrotoxicosis, and apparent hypersen-sitivity to any of their active or extraneous constituents. Thereis no well-documented evidence from the literature, however,of true allergic or idiosyncratic reactions to thyroid hormone.
Drugs with thyroid hormone activity, alone or together withother therapeutic agents, have been used for the treatment ofobesity. In euthyroid patients, doses within the range of dailyhormonal requirements are ineffective for weight reduction.
Larger doses may produce serious or even life-threateningmanifestations of toxicity, particularly when given in associ-ation with sympathomimetic amines such as those used fortheir anorectic effects.
The use of thyroid hormones in the therapy of obesity, alone orcombined with other drugs, is unjustified and has been shownto be ineffective. Neither is their use justified for the treatmentof male or female infertility unless this condition is accompa-nied by hypothyroidism.
General—Thyroid hormones should be used with great cau-
tion 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., 15-30 mg Armour Thyroid. 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 dia-
betes mellitus or diabetes insipidus or adrenal cortical insuffi-
ciency aggravates the intensity of their symptoms. Appropriate
adjustments of the various therapeutic measures directed at
these concomitant endocrine diseases are required. The thera-
py 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 anticoag-
ulants and dosage of the latter agents adjusted on the basis of
frequent prothrombin time determinations. In infants, exces-
sive doses of thyroid hormone preparations may produce
Information for the Patient—Patients on thyroid hormone
preparations and parents of children on thyroid therapy should
be informed that:
1. Replacement therapy is to be taken essentially for life, with
the exception of cases of transient hypothyroidism, usually
associated with thyroiditis, and in those patients receiving a
therapeutic trial of the drug.
2. They should immediately report during the course of thera-
py any signs or symptoms of thyroid hormone toxicity, e.g.,
chest pain, increased pulse rate, palpitations, excessive sweat-
ing, heat intolerance, nervousness, or any other unusual event.
3. In case of concomitant diabetes mellitus, the daily dosage of
antidiabetic medication may need readjustment as thyroid hor-
mone replacement is achieved. If thyroid medication is
stopped, a downward readjustment of the dosage of insulin or
oral hypoglycemic agent may be necessary to avoid hypo-
glycemia. At all times, close monitoring of urinary glucose
levels is mandatory in such patients.
4. In case of concomitant oral anticoagulant therapy, the pro-
thrombin 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 tran-
sient phenomenon and later recovery is usually the rule.
Laboratory Tests—Treatment of patients with thyroid hor-
mones requires the periodic assessment of thyroid status by
means of appropriate laboratory tests besides the full clinical
evaluation. The TSH suppression test can be used to test the
effectiveness of any thyroid preparation bearing in mind the
relative insensitivity of the infant pituitary to the negative feed-
back effect of thyroid hormones. Serum T4 levels can be used
to test the effectiveness of all thyroid medications except T3.
When the total serum T4 is low but TSH is normal, a test
specific to assess unbound (free) T4 levels is warranted.
Specific measurements of T4 and T3 by competitive protein
binding or radioimmunoassay are not influenced by blood
levels of organic or inorganic iodine.
Drug Interactions—Oral Anticoagulants—Thyroid hormones
appear to increase catabolism of vitamin K-dependent clotting
factors. If oral anticoagulants are also being given, compensa-
tory 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 stabi-
lized on maintenance thyroid replacement therapy.
Insulin or Oral Hypoglycemics—Initiating thyroid replacement
therapy may cause increases in insulin or oral hypoglycemic
requirements. The effects seen are poorly understood and
depend upon a variety of factors such as dose and type of thy-
roid preparations and endocrine status of the patient. Patients
receiving insulin or oral 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 intes-
tine, 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 administra-
tion of cholestyramine or colestipol and thyroid hormones.
Estrogen, Oral Contraceptives—Estrogens tend to increase
serum thyroxine-binding globulin (TBg). In a patient with a non-
functioning thyroid gland who is receiving thyroid replacement
therapy, free levothyroxine (T4) may be decreased when estro-
gens 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.
Drug/Laboratory Test Interactions—The following drugs or
moieties are known to interfere with laboratory tests per-
formed in patients on thyroid hormone therapy: androgens,
corticosteroids, estrogens, oral contraceptives containing
estrogens, iodine-containing preparations, and the numerous
preparations containing salicylates.
(thyroid tablets, USP)
1. Changes in TBg concentration should be taken into consid-
eration in the interpretation of levothyroxine (T4) and liothyro-
nine (T3) values. In such cases, the unbound (free) hormone
should be measured. Pregnancy, estrogens, and estrogen-
containing oral contraceptives increase TBg concentrations.
TBg may also be increased during infectious hepatitis.
Decreases in TBg concentrations are observed in nephrosis,
acromegaly, and after androgen or corticosteroid therapy.
Familial hyper- or hypothyroxine-binding-globulinemias have
been described. The incidence of TBg deficiency approximates
1 in 9,000. The binding of levothyroxine by TBPA is inhibited
2. Medicinal or dietary iodine interferes with all in vivo tests of
radio-iodine uptake, producing low uptakes which may not be
relative of a true decrease in hormone synthesis.
3. The persistence of clinical and laboratory evidence of
hypothyroidism in spite of adequate dosage replacement indi-
cates either poor patient compliance, poor absorption, exces-
sive fecal loss, or inactivity of the preparation. Intracellular
resistance to thyroid hormone is quite rare.
Carcinogenesis, Mutagenesis, and Impairment of Fertility—
A reportedly apparent association between prolonged thyroid
therapy and breast cancer has not been confirmed and patients
on thyroid for established indications should not discontinue
therapy. No confirmatory long-term studies in animals have
been performed to evaluate carcinogenic potential, mutagenic-
ity, or impairment of fertility in either males or females.
Pregnancy-Category A—Thyroid hormones do not readily
cross the placental barrier. The clinical experience to date does
not indicate any adverse effect on fetuses when thyroid hor-
mones are administered to pregnant women. On the basis of
current knowledge, thyroid replacement therapy to hypothy-
roid women should not be discontinued during pregnancy.
Nursing Mothers—Minimal amounts of thyroid hormones are
excreted in human milk. Thyroid is not associated with serious
adverse reactions and does not have a known tumorigenic
potential. However, caution should be exercised when thyroid
is administered to a nursing woman.
Pediatric Use—Pregnant mothers provide little or no thyroid
hormone to the fetus. The incidence of congenital hypothy-
roidism is relatively high (1:4,000) and the hypothyroid fetus
would not derive any benefit from the small amounts of hor-
mone crossing the placental barrier. Routine determinations of
serum T4 and/or TSH is strongly advised in neonates in view
of the deleterious effects of thyroid deficiency on growth and
Treatment should be initiated immediately upon diagnosis, and
maintained for life, unless transient hypothyroidism is suspect-
ed; in which case, therapy may be interrupted for 2 to 8 weeks
after the age of 3 years to reassess the condition. Cessation of
therapy is justified in patients who have maintained a normal
TSH during those 2 to 8 weeks.
Adverse reactions other than those indicative of hyperthy-roidism because of therapeutic overdosage, either initially orduring the maintenance period, are rare (See OVERDOSAGE).
Signs and Symptoms—Excessive doses of thyroid result in a
hypermetabolic state resembling in every respect the condition
of endogenous origin. The condition may be self-induced.
Treatment of Overdosage—Dosage should be reduced or
therapy temporarily discontinued if signs and symptoms of
Treatment may be reinstituted at a lower dosage. In normal indi-
viduals, normal hypothalamic-pituitary-thyroid axis function is
restored in 6 to 8 weeks after thyroid suppression.
Treatment of acute massive thyroid hormone overdosage is
aimed at reducing gastrointestinal absorption of the drugs and
counteracting central and peripheral effects, mainly those of
increased sympathetic activity. Vomiting may be induced initial-
ly if further gastrointestinal absorption can reasonably be pre-
vented and barring contraindications such as coma, convul-
sions, or loss of the gagging reflex. Treatment is symptomatic
and supportive. Oxygen may be administered and ventilation
maintained. Cardiac glycosides may be indicated if congestive
heart failure develops. Measures to control fever, hypoglycemia,
or fluid loss should be instituted if needed. Antiadrenergic
agents, particularly propranolol, have been used advantageous-
ly in the treatment of increased sympathetic activity.
Propranolol may be administered intravenously at a dosage of
1 to 3 mg, over a 10-minute period or orally, 80 to 160 mg/day,
initially, especially when no contraindications exist for its use.
Other adjunctive measures may include administration of
cholestyramine to interfere with thyroxine absorption, and
glucocorticoids to inhibit conversion of T4 to T3.
DOSAGE AND ADMINISTRATION
The dosage of thyroid hormones is determined by the indica-
tion and must in every case be individualized according to
patient response and laboratory findings.
Thyroid hormones are given orally. In acute, emergency condi-
tions, injectable levothyroxine sodium (T4) may be given intra-
venously 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.
Hypothyroidism—Therapy is usually instituted using low doses,
with increments which depend on the cardiovascular status of
the patient. The usual starting dose is 30 mg Armour Thyroid,
with increments of 15 mg every 2 to 3 weeks. A lower starting
dosage, 15 mg/day, is recommended in patients with long-
standing myxedema, particularly if cardiovascular impairment is
suspected, in which case extreme caution is recommended. The
appearance of 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 nor-
mal 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 induc-
tion of hypothyroidism in those cases is more abrupt and can
be of shorter duration. It may also be preferred when impair-
ment of peripheral conversion of levothyroxine (T4) and liothy-
ronine (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 con-
sidered 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 rapid-
ly, 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 carcino-
ma of the thyroid and is used as ancillary therapy of these con-
ditions with radioactive iodine. TSH should be suppressed to
low or undetectable levels. Therefore, larger amounts of thy-
roid hormone than those used for replacement therapy are
required. Medullary carcinoma of the thyroid is usually unre-
sponsive to this therapy.
Thyroid Suppression Therapy—Administration of thyroid hor-
mone in doses higher than those produced physiologically by
the gland results in suppression of the production of endoge-
nous 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
percent or greater suppression of uptake indicates a normal thy-
roid-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 recom-
mendations summarized in Table 1. In infants with congenital
hypothyroidism, therapy with full doses should be instituted as
soon as the diagnosis has been made.
Armour Thyroid tablets (thyroid tablets, USP) are supplied asfollows: 15 mg (1/4 gr) are available in bottles of 100 (NDC0456-0457-01). 30 mg (1/2 gr) are available in bottles of 100(NDC 0456-0458-01), containers of 50,000 (NDC 0456-0458-69)and unit dose cartons of 100 (NDC 0456-0458-63). 60 mg (1 gr)are available in bottles of 100 (NDC 0456-0459-01) and 5000(NDC 0456-0459-51), containers of 50,000 (0456-0459-69) andunit dose cartons of 100 (NDC 0456-0459-63). 90 mg (1 1/2 gr)are available in bottles of 100 (NDC 0456-0460-01). 120 mg (2 gr)are available in bottles of 100 (NDC 0456-0461-01), containersof 50,000 (NDC 0456-0461-69) and unit dose cartons of 100(NDC 0456-0461-63). 180 mg (3 gr) are available in bottles of100 (NDC 0456-0462-01). 240 mg (4 gr) are available in bottlesof 100 (NDC 0456-0463-01). 300 mg (5 gr) are available in bot-tles of 100 (NDC 0456-0464-01). The bottles of 100 are specialdispensing bottles with child-resistant closures.
Armour Thyroid tablets are evenly colored, light tan, roundtablets, with convex surfaces. One side is debossed with amortar and pestle beneath the letter “A” on the top andstrength code letters on the bottom as defined below Strength
Note: (T3 liothyronine is approximately four times as potent asT4 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).
A Subsidiary of Forest Laboratories, Inc.
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