Cytomel - liothyronine sodium tablets
Cytomel is a hormone pill used to treat Thyroid conditions. Andecdotally, Cytomel was also popular among bodybuilders as a way to increase metabolism and build muscle mass while eating a high calorie diet.
Warning: Cytomel / liothyronine sodium is a very powerful drug even in small dosages and is not to be taken under any circumstances without approval of a doctor and under the strict supervision of your physician.
Following is the extensive FDA approved information from Cytomel manufacturer Monarch Pharmaceuticals. This information is more easily printed from the FDA website here
DESCRIPTION
Thyroid hormone drugs are natural or synthetic preparations containing tetraiodothyronine (T4,
levothyroxine) sodium or triiodothyronine (T3, liothyronine) sodium or both. T4 and T3 are produced in the human thyroid gland by the iodination and coupling of the amino acid tyrosine. T4 contains four iodine atoms and is formed by the coupling of two molecules of diiodotyrosine (DIT). T3 contains three atoms of iodine and is formed by the coupling of one molecule of DIT with one molecule of monoiodotyrosine (MIT). Both hormones are stored in the thyroid colloid as thyroglobulin. Thyroid hormone preparations belong to two categories: (1) natural hormonal preparations derived from animal thyroid, and (2) synthetic preparations. Natural preparations include desiccated thyroid and thyroglobulin. Desiccated thyroid is derived from domesticated animals that are used for food
by man (either beef or hog thyroid), and thyroglobulin is derived from thyroid glands of the hog. The
United States Pharmacopeia (USP) has standardized the total iodine content of natural preparations.
Thyroid USP contains not less than (NLT) 0.17 percent and not more than (NMT) 0.23 percent iodine,
and thyroglobulin contains not less than (NLT) 0.7 percent of organically bound iodine. Iodine content is
only an indirect indicator of true hormonal biologic activity.
Cytomel (liothyronine sodium) Tablets contain liothyronine (L-triiodothyronine or L T3), a
synthetic form of a natural thyroid hormone, and is available as the sodium salt.
The structural and empirical formulas and molecular weight of liothyronine sodium are given
below.
2
Liothyronine Sodium
L-Tyrosine, O-(4-hydroxy-3-iodophenyl)-3,5-diiodo-, monosodium salt
Twenty-five mcg of liothyronine is equivalent to approximately 1 grain of desiccated thyroid or
thyroglobulin and 0.1 mg of L-thyroxine.
Each round, white to off-white Cytomel (liothyronine sodium) tablet contains liothyronine
sodium equivalent to liothyronine as follows: 5 mcg debossed JMI and D14; 25 mcg scored and debossed
JMI and D16; 50 mcg scored and debossed JMI and D17. Inactive ingredients consist of calcium sulfate,
gelatin, starch, stearic acid, sucrose and talc.
CLINICAL PHARMACOLOGY
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.
Pharmacokinetics
Since liothyronine sodium (T3) is not firmly bound to serum protein, it is readily available to
body tissues. The onset of activity of liothyronine sodium is rapid, occurring within a few hours.
Maximum pharmacologic response occurs within 2 or 3 days, providing early clinical response. The
biological half-life is about 2-1/2 days.
3
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.
Liothyronine sodium has a rapid cutoff of activity which permits quick dosage adjustment and
facilitates control of the effects of overdosage, should they occur.
The higher affinity of levothyroxine (T4) for both thyroid-binding globulin and thyroid-binding
prealbumin as compared to triiodothyronine (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.
INDICATIONS AND USAGE
Thyroid hormone drugs are indicated:
1. 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 (pediatric
patients, 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).
2. As pituitary thyroid-stimulating hormone (TSH) suppressants, in the treatment or prevention of
various types of euthyroid goiters, including thyroid nodules, subacute or chronic lymphocytic
thyroiditis (Hashimoto’s) and multinodular goiter.
3. As diagnostic agents in suppression tests to differentiate suspected mild hyperthyroidism or
thyroid gland autonomy.
Cytomel (liothyronine sodium) Tablets can be used in patients allergic to desiccated thyroid or
thyroid extract derived from pork or beef.
4
CONTRAINDICATIONS
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.
WARNINGS
Drugs with thyroid hormone activity, alone or together with other therapeutic agents, have been used
for the treatment of obesity. In euthyroid patients, doses within the range of daily hormonal
requirements are ineffective for weight reduction. Larger doses may produce serious or even lifethreatening
manifestations of toxicity, particularly when given in association with sympathomimetic
amines such as those used for their anorectic effects.
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, liothyronine sodium therapy should be initiated with low doses, with due
consideration for its relatively rapid onset of action. Starting dosage of Cytomel (liothyronine sodium)
Tablets is 5 mcg daily, and should be increased by no more than 5 mcg increments at 2-week intervals.
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.
Morphologic hypogonadism and nephrosis should be ruled out before the drug is administered. If
hypopituitarism is present, the adrenal deficiency must be corrected prior to starting the drug.
5
Myxedematous patients are very sensitive to thyroid; dosage should be started at a very low level
and increased gradually.
Severe and prolonged hypothyroidism can lead to a decreased level of adrenocortical activity
commensurate with the lowered metabolic state. When thyroid-replacement therapy is administered, the
metabolism increases at a greater rate than adrenocortical activity. This can precipitate adrenocortical
insufficiency. Therefore, in severe and prolonged hypothyroidism, supplemental adrenocortical steroids
may be necessary. In rare instances the administration of thyroid hormone may precipitate a hyperthyroid
state or may aggravate existing hyperthyroidism.
PRECAUTIONS
General – Thyroid hormone therapy in patients with concomitant diabetes mellitus or 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.
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.
Information for the Patient – Patients on thyroid hormone preparations and parents of pediatric
patients 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 therapy any signs or symptoms of thyroid
hormone toxicity, e.g., chest pain, increased pulse rate, palpitations, excessive sweating, heat
intolerance, nervousness, or any other unusual event.
6
3. In case of concomitant diabetes mellitus, the daily dosage of antidiabetic medication may need
readjustment as thyroid hormone 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 hypoglycemia. At all times, close monitoring of urinary glucose levels is mandatory in such
patients.
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 pediatric patients in the first few months of thyroid
therapy, but this is usually a transient phenomenon and later recovery is usually the rule.
Laboratory Tests – Treatment of patients with thyroid hormones 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 feedback effect of thyroid hormones. Serum
T4 levels can be used to test the effectiveness of all thyroid medications except products containing
liothyronine sodium. 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 and have essentially
replaced older tests of thyroid hormone measurements, i.e., PBI, BEI and T4 by column.
Drug Interactions
OralAnticoagulants – 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
7
appear to be necessary when oral anticoagulant therapy is begun in a patient already stabilized 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 thyroid preparations and endocrine status of the patient.
Patients receiving insulin or oral hypoglycemics should be closely watched during initiation of thyroid
replacement therapy.
Cholestyramine – Cholestyramine binds both T4 and T3 in the intestine, thus impairing absorption
of these thyroid hormones. In vitro studies indicate that the binding is not easily removed. Therefore, 4 to
5 hours should elapse between administration of cholestyramine 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 may be decreased when estrogens are started thus increasing thyroid requirements.
However, if the patient’s thyroid gland has sufficient function, the decreased free thyroxine will result in a
compensatory increase in thyroxine 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.
Tricyclic Antidepressants – Use of thyroid products with imipramine and other tricyclic
antidepressants may increase receptor sensitivity and enhance antidepressant activity; transient cardiac
arrhythmias have been observed. Thyroid hormone activity may also be enhanced.
Digitalis – Thyroid preparations may potentiate the toxic effects of digitalis. Thyroid hormonal
replacement increases metabolic rate, which requires an increase in digitalis dosage.
Ketamine – When administered to patients on a thyroid preparation, this parenteral anesthetic
may cause hypertension and tachycardia. Use with caution and be prepared to treat hypertension, if
necessary.
8
Vasopressors – Thyroxine increases the adrenergic effect of catecholamines such as epinephrine
and norepinephrine. Therefore, injection of these agents into patients receiving thyroid preparations
increases the risk of precipitating coronary insufficiency, especially in patients with coronary artery
disease. Careful observation is required.
Drug/Laboratory Test Interactions – The following drugs or moieties are known to interfere
with laboratory tests performed in patients on thyroid hormone therapy: androgens, corticosteroids,
estrogens, oral contraceptives containing estrogens, iodine-containing preparations and the numerous
preparations containing salicylates.
1. Changes in TBg concentration should be taken into consideration in the interpretation of T4 and
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 hypo-thyroxinebinding-
globulinemias have been described. The incidence of TBg deficiency approximates 1 in
9000. The binding of thyroxine by thyroxine-binding prealbumin (TBPA) is inhibited by
salicylates.
2. Medicinal or dietary iodine interferes with all in vivo tests of radioiodine uptake, producing low
uptakes which may not be reflective of a true decrease in hormone synthesis.
3. The persistence of clinical and laboratory evidence of hypothyroidism in spite of adequate dosage
replacement indicates either poor patient compliance, poor absorption, excessive 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, mutagenicity, or impairment of fertility in either
males or females.
9
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 hormones are
administered to pregnant women. On the basis of current knowledge, thyroid replacement therapy to
hypothyroid 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.
Geriatric Use – Clinical studies of liothyronine sodium did not include sufficient numbers of
subjects aged 65 and over to determine whether they respond differently from younger subjects. Other
reported clinical experience has not identified differences in responses between the elderly and younger
patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low
end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function,
and of concomitant disease or other drug therapy. This drug is known to be substantially excreted by the
kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function.
Because elderly patients are more likely to have decreased renal function, care should be taken in dose
selection, and it may be useful to monitor renal function.
Pediatric Use – Pregnant mothers provide little or no thyroid hormone to the fetus. The incidence
of congenital hypothyroidism is relatively high (1:4000) and the hypothyroid fetus would not derive any
benefit from the small amounts of hormone 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 development.
Treatment should be initiated immediately upon diagnosis and maintained for life, unless
transient hypothyroidism is suspected, 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.
10
ADVERSE REACTIONS
Adverse reactions, other than those indicative of hyperthyroidism because of therapeutic
overdosage, either initially or during the maintenance period are rare (see OVERDOSAGE).
In rare instances, allergic skin reactions have been reported with Cytomel (liothyronine sodium)
Tablets.
OVERDOSAGE
Signs and Symptoms – Headache, irritability, nervousness, sweating, arrhythmia (including
tachycardia), increased bowel motility and menstrual irregularities. Angina pectoris or congestive heart
failure may be induced or aggravated. Shock may also develop. Massive overdosage may result in
symptoms resembling thyroid storm. Chronic excessive dosage will produce the signs and symptoms of
hyperthyroidism.
Treatment Of Overdosage – Dosage should be reduced or therapy temporarily discontinued if
signs and symptoms of overdosage appear. Treatment may be reinstituted at a lower dosage. In normal
individuals, 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 initially if further gastrointestinal absorption can
reasonably be prevented and barring contraindications such as coma, convulsions, 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 advantageously 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, especially when no contraindications exist for its use.
11
DOSAGE AND ADMINISTRATION
The dosage of thyroid hormones is determined by the indication and must in every case be
individualized according to patient response and laboratory findings.
Cytomel (liothyronine sodium) Tablets are intended for oral administration; once-a-day dosage is
recommended. Although liothyronine sodium has a rapid cutoff, its metabolic effects persist for a few
days following discontinuance.
Mild Hypothyroidism: Recommended starting dosage is 25 mcg daily. Daily dosage then may
be increased by up to 25 mcg every 1 or 2 weeks. Usual maintenance dose is 25 to75mcg daily.
The rapid onset and dissipation of action of liothyronine sodium (T3), as compared with
levothyroxine sodium (T4), has led some clinicians to prefer its use in patients who might be more
susceptible to the untoward effects of thyroid medication. However, the wide swings in serum T3 levels
that follow its administration and the possibility of more pronounced cardiovascular side effects tend to
counterbalance the stated advantages.
Cytomel (liothyronine sodium) Tablets may be used in preference to levothyroxine (T4) during
radioisotope 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 T4 to T3
is suspected.
Myxedema: Recommended starting dosage is 5 mcg daily. This may be increased by 5 to 10 mcg
daily every 1 or 2 weeks. When 25 mcg daily is reached, dosage may be increased by 5 to 25 mcg every 1
or 2 weeks until a satisfactory therapeutic response is attained. Usual maintenance dose is 50 to 100 mcg
daily.
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.
12
An intravenous preparation of liothyronine sodium is marketed by Jones Pharma Incorporated,
under the trade name Triostat® for use in myxedema coma/precoma.
Congenital Hypothyroidism: Recommended starting dosage is 5 mcg daily, with a 5 mcg
increment every 3 to 4 days until the desired response is achieved. Infants a few months old may require
only 20 mcg daily for maintenance. At 1 year, 50 mcg daily may be required. Above 3 years, full adult
dosage may be necessary (see PRECAUTIONS, Pediatric Use).
Simple (non-toxic) Goiter: Recommended starting dosage is 5 mcg daily. This dosage may be
increased by 5 to 10 mcg daily every 1 or 2 weeks. When 25 mcg daily is reached, dosage may be
increased every week or two by 12.5 or 25 mcg. Usual maintenance dosage is 75 mcg daily.
In the elderly or in pediatric patients, therapy should be started with 5 mcg daily and increased
only by 5 mcg increments at the recommended intervals.
When switching a patient to Cytomel (liothyronine sodium) Tablets from thyroid, Lthyroxine
or thyroglobulin, discontinue the other medication, initiate Cytomel at a low dosage, and
increase gradually according to the patient's response. When selecting a starting dosage, bear in mind that
this drug has a rapid onset of action, and that residual effects of the other thyroid preparation may persist
for the first several weeks of 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 baseline laboratory tests appear normal or to demonstrate thyroid
gland autonomy in patients with Graves’ 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.
Cytomel (liothyronine sodium) Tablets are given in doses of 75 to 100 mcg/day for 7 days, and
radioactive iodine uptake is determined before and after administration of the hormone. If thyroid
function is under normal control, the radioiodine uptake will drop significantly after treatment. Cytomel
13
(liothyronine sodium) Tablets should be administered cautiously to patients in whom there is a strong
suspicion of thyroid gland autonomy, in view of the fact that the exogenous hormone effects will be
additive to the endogenous source.
HOW SUPPLIED
Cytomel (liothyronine sodium) Tablets: 5 mcg in bottles of 100;
25 mcg in bottles of 100; and 50 mcg in bottles of 100.
5 mcg 100’s: NDC 52604-3414-1
25 mcg 100’s: NDC 52604-3416-1
50 mcg 100’s: NDC 52604-3417-1
Store between 15° and 30°C (59° and 86°F).
DATE OF ISSUANCE November 2001
Manufactured by:
Schering Canada, Inc., 3535 Trans-Canada Highway, Pointe Claire, Quebec H9R 1B4 Canada
Distributed by:
Monarch Pharmaceuticals, Inc., Bristol, TN 37620
83-481648 Rev. 11/01
