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Liothyronin is the commonly associated brand name for the synthetic thyroid hormone Liothyronine Sodium. This is a perfect replica of the naturally produced thyroid hormone triiodothyronine, or what is commonly referred to as the T3 hormone. While synthetic Cytomel has been available since the 1950’s, thyroid hormones including T3 have been used medicinally since the 1890’s. Early thyroid treatment plans were simply pure animal extracts and contained pure forms of the T3 and T4 hormone. Extracted thyroid hormones proved very useful in therapeutic treatment plans, specifically in the treatment of hypothyroidism. This is a condition in which the thyroid simply no longer produces enough thyroid hormones, which can lead to weight gain, loss of energy, hair loss and changes in the appearance and texture of the skin. With the introduction of Cytomel, the synthetic model of the T3 hormone, this has provided a much safer and sanitary hormone for such treatments.
Liothyronin is not the only synthetic thyroid hormone available. The T4 hormone, Levothyroxine Sodium is also available found under the trade name Synthroid most commonly. Both T3 and T4 are very similar in nature; however, T3 is considered 4-5 times more powerful than T4. T4, in simple terms, acts as a reserve for T3, which makes the Cytomel version the more powerful of the two popular thyroid hormones. While both are effective in treating hypothyroidism, Cytomel is the preferred thyroid hormone among performance enhancement athletes. Anabolic steroid users commonly use Cytomel in an effort to lose body fat.
Liothyronin Functions & Traits:
Liothyronin or T3 is a thyroid hormone that greatly affects the basil metabolic rate in a stimulating sense. This hormone is involved in many cellular functions including the metabolism of carbohydrates, fats and proteins. When an individual is no longer producing enough of this hormone on his own, such as when suffering from hypothyroidism, the metabolism does not function properly. When suffering from hypothyroidism, the individual will find body fat gain to be very common and fat loss becomes extremely difficult. The individual also often experiences a loss of energy and even hair loss in some cases. By supplementing with Cytomel, this provides the body with the thyroid hormone it needs and the problem is solved.
It generally only takes a low dose of Cytomel to treat hypothyroidism. This will not necessarily promote enhanced fat loss, but it should return the metabolism back to proper working order. However, many performance enhancing athletes enjoy using Cytomel to in fact enhance direct fat loss. The use of Cytomel along side a calorie restricted diet will promote significant and accelerated fat loss. While effective, generally this type of use cannot be recommended without the use of anabolic steroids. This is one of the most powerfully effective fat loss tools we have at our disposal, but we cannot call it perfect. Many performance athletes report Cytomel leaves them lethargic, which isn’t surprising. Cytomel feeds off of raw ATP. Due to the necessarily higher doses needed to promote enhanced fat loss and due to the depletion of ATP, this can promote lean tissue loss. The body will take whatever it needs from wherever it can get it to meet its energy demands. For this reason, an anabolic protectant is normally advised when supplementing with Cytomel for this purpose.
Effects of Liothyronin
The effects of Liothyronin are generally the same regardless of the purpose of use, to treat hypothyroidism or enhance fat loss in a performance setting. In both instances, the hormone functions the same as a direct replica of the T3 hormone. Regardless of the initial reason for use, both individuals should be able to enjoy fat loss. The hypothyroidism patient should now have a more properly functioning metabolism, which will help them lose fat. Often this is welcomed as the individual probably put on a fair amount of fat due to the thyroid disorder. For the performance minded, again fat loss is merely accelerated.
Regardless of the specific reason for using Cytomel, while it will enhance the metabolic rate you will still need to diet. In order to lose body fat you must burn more calories than you consume. If you are consuming more than you burn all the Cytomel in the world won’t do anything for you. However, in a performance setting with an individual who already produces adequate amounts of T3, he may find he can now keep his total caloric intake a little higher than he would without it and still lose weight. Due to Cytomel use, the rate by-which calories are burned is now enhanced due to the administration of excess T3 hormone.
Some have also found that the use of Cytomel can be beneficial when using Human Growth Hormone (HGH ), particularly when using high doses of HGH. Some data has shown that the use of HGH in high levels may reduce natural T3 production. We cannot call such Cytomel supplementation necessary, but it does appear to have some validity. Regardless, without question the individual who uses Cytomel and HGH in a fat loss plan will lose more body fat at a far more accelerated rate. This is due to HGH carrying tremendous metabolic enhancement properties. If the individual further includes a beta-2 stimulant like Clenbuterol. he will be a fat burning machine.
The final effect of Cytomel revolves around an anabolic nature. Some have suggested that Cytomel carries an anabolic advantage by enhancing the anabolic action of anabolic steroids. The idea is that anabolic steroids provide a greater utilization for carbohydrates, fats and proteins, and as discussed Cytomel promotes the metabolism of such nutrients. Conjoined, in theory this could promote a greater enhancement of the total body. However, while this theory exists and is deemed fact by some performance enhancing athletes, it lacks a lot of solid credibility. Most will find they should only rely on Liothyronin for its direct intended purposes.
Side Effects of Cytomel:
Cytomel is generally viewed as a very well-tolerated hormone for most healthy adults; healthy excluding hypothyroidism. The side effects of Cytomel are most commonly associated with high or overdoses of the hormone, but the individualistic nature of man cannot be ruled out as playing a role. The possible side effects of Cytomel include:
Increased Bowel Motility
Extremely high doses or over exposure to the T3 hormone can also lead to potential complications. The side effects of Cytomel in this category include:
Congestive Heart Failure
Generally speaking Cytomel is a very safe thyroid medication, but abuse, particular high dose long term exposure can be life threatening.
The final side effect of Cytomel that needs to be discussed is promoting hypothyroidism. Many fear using this hormone due to the idea of a possible hypothyroidism conditioning occurring once use is discontinued. The idea is that once use has come to an end the body will no longer produce enough of its own T3 and fat gain will occur. While it is possible to become dependent, it is highly unlikely with proper use. Proper use not only revolves around dosing and duration of use, but specifically how we discontinue use. Use should not be abruptly discontinued. Instead, the individual should drop down to a maintenance dose for a short period of time in order to allow his thyroid to reset. For the healthy individual who has not abused Cytomel, recovery should not be an issue.
For the purpose of treating hypothyroidism, Cytomel doses will normally begin at 25mcg per day. After a couple weeks of use, levels are normally rechecked and the dose may be increased by 25mcg. The dose may again be increased to 75mcg per day another two weeks later until a comfortable maintenance level dosing is found. 25-75mcg per day will be average with most finding 25-50mcg per day to be all that’s needed. Regardless of the dose, the entire daily dose can be taken once per day.
In a performance setting, Cytomel doses will be very similar to hypothyroidism treatment plans. The individual will normally begin with 25mcg per day and increase the total dose 12.5-25mcg every 2-4 weeks as needed. Most will find they will have no need to go above 75-100mcg per day, with the 125mcg per day range being acceptable for very short periods of time. Such a high dose might be acceptable at the end of a harsh contest diet but should not be a regular dose through the brunt of the diet. As for total use, 6-8 weeks will be the safest total duration. Longer can be acceptable, such as 8-12 weeks, but it does increase the risk of thyroid dependency. However, most healthy adults should not have an issue. Once you have reached your high end dose and it’s time to come off, you are encouraged to drop the dose down to 25mcg per day and hold at that dose for 7-10 days. This will allow the body to adjust and protect you from falling into hypothyroidism. For no reason should you discontinue use abruptly, the 7-10 day low dose is imperative.
Availability of Cytomel:
Cytomel is widely available throughout the world on both the pharmaceutical and black markets. It is also available commonly through research chemical labs (RCL’s). While it is available on the U.S. pharmaceutical market, it is not as common as Synthroid (T4). This is despite the T3 hormone proving to be far more powerful and effective. You will also find the T3 hormone is available in tablet and injectable forms. Tablets are most common and injectable forms should be avoided as they are only suitable for emergency medical conditions. Injectable Cytomel will more than likely cause severe damage to the average man or woman. Then we’re left with RCL’s. RCL’s produce Liothyronine Sodium in its liquid state, and it is almost always sold under its chemical name Liothyronine Sodium. As with many non-controlled substances, RCL’s are legally allowed to sell such items so as long as they’re for research purposes; you do not need a prescription. This is a loophole in the law many take advantage of.
Overview and History of Liothyronin (T3)
Liothyronin is a brand and trade name for T3, which is Liothyronine Sodium. Liothyronine Sodium is a synthetic variant of the human bodys own thyroid hormone. It should be understood that the human bodys own natural endogenously manufactured thyroid hormone is actually known as Triiodothyronine, which is different from Liothyronine Sodium. Liothyronine is the L-isomer of Triiodothyronine. Liothyronine and Triiodothyronine are both nearly identical with one another, but Liothyronine is a more potent variant and is also better absorbed orally, which is why it has been developed into a prescription medicine and preparation known as Cytomel, Tiromel, Tertroxin, etc. Within a medical and clinical setting, Cytomel (T3) is utilized in the treatment of hypothyroidism, which is a condition whereby an individuals thyroid gland is not secreting the proper and normal levels of thyroid hormone for proper function. In such a case, hypothyroidism is commonly diagnosed via a blood test that analyzes the serum hormone profile of thyroid hormones (T3, T4, and TSH, which is Thyroid Stimulating Hormone). Hypothyroidism also carries with it various symptoms such as a lack of energy, lethargy, weight and fat gain, hair loss, and alterations in skin colour and texture. T3 is the primary thyroid hormone used by the body.
Unfortunately, T3 is one of those compounds among the bodybuilding and athletic community that has gathered a large amount of mysticism, rumor, and lies that have been spread for years in regards to what it does, its use, and how it should be used. As a result, many within the anabolic steroid using community have become deathly afraid of T3, and shudder at the mere mention of its use. This profile will set these misconceptions straight and clarify many of the common misconceptions in regards to Cytomel.
T3 was originally formulated as a medicine by way of an extract from the thyroid gland. Many hormonal medicines originated in the same way, as being derived from the endocrine glands from the cadavers of animals and humans. The very first application of this thyroid extract was administered in 1981 to an individual who suffered from myxedema, which is a skin disorder that is normally the result of hypothyroidism. Thyroid hormones were some of the very first hormonal medicines used in the field of endocrinology and in the treatment of many disorders and diseases. The very first thyroid extracts not only contained T3, but also T4, and these extracts were utilized for over 60 years in medicine. In the 1950s, methods of creating thyroid hormones synthetically took over and the previously used thyroid extracts were done away with. Liothyronine Sodium (T3) and Levothyroxine Sodium (T4) are the two most popular currently used synthetic thyroid hormones, and are widely available both in the United States as well as internationally. Cytomel tends to be the most widely utilized and most recognized brand name of T3, especially in the United States. In The USA, Cytomel is manufactured by King Pharmaceuticals.
T3, much like many other ancillary bodybuilding drugs is widely available with very little or no laws in regards to its sale, distribution, purchase, or use in most countries throughout the world. It is manufactured by dozens of different pharmaceutical companies across the world with different brand and trade names, as well as a diverse selection of generic T3 products. Because of the vast availability and manufacture of this product, it is not uncommon to find a wide variation in different T3 dosages in the different products. For example, T3 can commonly be seen in concentrations ranging from 5mcg, 25mcg, and all the way up to 50mcg tablets.
Chemical Characteristics of Cytomel (T3)
T3 (Liothyronine Sodium) is a synthetic variant of the bodys thyroid hormone Triiodothyronine.
Properties of Liothyronin (T3)
T3 in the body is responsible for regulating the uptake of various nutrients into cells and into the mitochondria of those cells in order to effectively become utilized for the production and consumption of energy . The mitochondria of every single cell in the body utilizes carbohydrates (primarily), fat, and even protein for the production of an energy source known as ATP (Adenosine Triphosphate). Through the intake of more T3, this production of ATP will increase, leading to an increased rate of energy consumption in the form of fats, carbohydrates, and protein. Hence, this is why the consumption of too much T3 without the use of anabolic steroids can result in muscle loss.
The bodybuilding and athletic world is attracted to the use of T3 as a physique and/or performance enhancing drug because of its capability to distinctly boost the bodys metabolism in the effort to metabolize body fat at a greater rate. T3 is traditionally utilize during cutting, dieting, and/or pre-contest phases of training due to the universal goal of these phases to break down body fat, though in recent years Liothyronin has gained some popularity as a useful agent during bulking and mass gaining phases of training (normally in conjunction with anabolic steroids) in order to better efficiently process nutrients and/or to keep body fat levels down during periods of higher caloric intake. Liothyronin (T3) is commonly used with anabolic steroids due to its significant impact on the bodys metabolism as a whole. It is very important to understand that T3 is indiscriminate in its metabolism boosting properties it will increase the metabolism of fats, carbohydrates, and protein all equally. Therefore, beyond a particular dose of T3, there is an increased risk of muscle loss through increased turnover of protein. Through the use of anabolic steroids and a properly adjusted diet, this muscle loss as a result of T3 can be prevented as a result of the nitrogen-retaining and protein sparing properties of theanabolic steroids.
Liothyronin (T3) is also commonly combined with other fat loss agents in order to increase its overall effect, as it does work synergistically with other fat loss agents. Some of these include Ephedrine. Clenbuterol. Albuterol. Human Growth Hormone (HGH ) as well as other fat burning agents. The combination of T3 with anabolic steroids and other fat burning agents, as well as the possible interactions between them, will be further covered in greater detail in the Liothyronin (T3) Doses and Liothyronin ( T3 ) Cycles sections of this profile.
Thyroid hormone drugs are natural or synthetic preparations containing tetraiodothyronine (T 4. levothyroxine) sodium or Liothyronin sodium or both. T 4 and T 3 are produced in the human thyroid gland by the iodination and coupling of the amino acid tyrosine. T 4 contains four iodine atoms and is formed by the coupling of two molecules of diiodotyrosine (DIT). T 3 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 LT 3 ), 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.
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 KPI and 115; 25 mcg scored and debossed KPI and 116; 50 mcg scored and debossed KPI and 117. Inactive ingredients consist of calcium sulfate, gelatin, starch, stearic acid, sucrose and talc.
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.
Since Liothyronin sodium (T 3 ) 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.
T 3 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 (T 4 ) for both thyroid-binding globulin and thyroid-binding prealbumin as compared to triiodothyronine (T 3 ) 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:
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 ).
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.
As diagnostic agents in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy.
Liothyronin (liothyronine sodium) Tablets can be used in patients allergic to desiccated thyroid or thyroid extract derived from pork or beef.
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.
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 life-threatening 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. 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.
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 Patients
Patients on thyroid hormone preparations and parents of pediatric patients on thyroid therapy should be informed that:
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.
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.
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.
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.
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.
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 T 4 levels can be used to test the effectiveness of all thyroid medications except products containing liothyronine sodium. When the total serum T 4 is low but TSH is normal, a test specific to assess unbound (free) T 4 levels is warranted. Specific measurements of T 4 and T 3 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 T 4 by column.
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.
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 binds both T 4 and T 3 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.
Liothyronin Oral Contraceptives
Liothyronin 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.
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.
Thyroid preparations may potentiate the toxic effects of digitalis. Thyroid hormonal replacement increases metabolic rate, which requires an increase in digitalis dosage.
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.
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 and 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.
Changes in TBg concentration should be taken into consideration in the interpretation of T 4 and T 3 values. In such cases, the unbound (free) hormone shouldbemeasured. 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-thyroxine-binding-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.
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.
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, 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.
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.
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.
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.
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 T 4 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.
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.
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-thyroidaxis 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.
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.
Liothyronin (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.
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 to75 mcg daily.
The rapid onset and dissipation of action of liothyronine sodium (T 3 ), as compared with levothyroxine sodium (T 4 ), 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 T 3 levels that follow its administration and the possibility of more pronounced cardiovascular side effects tend to counterbalance the stated advantages.
Liothyronin (liothyronine sodium) Tablets may be used in preference to levothyroxine (T 4 ) 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 T 4 to T 3 is suspected.
Liothyronine is used to treat an underactive thyroid (hypothyroidism ). It replaces or provides more thyroid hormone, which is normally made by the thyroid gland. Liothyronine is a man-made form of thyroid hormone. Low thyroid hormone levels can occur naturally or when the thyroid gland is injured by radiation /medications or removed by surgery. Having enough thyroid hormone helps you stay healthy. For children, having enough thyroid hormone helps them grow and learn normally.
This medication is also used to treat other types of thyroid problems (such as certain types of goiters, thyroid cancer ). It can also be used to test for certain types of thyroid disease.
This medication should not be used to treat infertility unless it is caused by low thyroid hormone levels.
How to use Liothyronin
Take this medication by mouth with or without food as directed by your doctor, usually once daily. It is best to take it at the same time each day so your thyroid hormone level is kept at a constant level.
Take this medication regularly to get the most benefit from it. Do not stop taking it without first talking with your doctor. Thyroid replacement treatment is usually taken for life.
The dosage is based on your medical condition, age, lab test results, and response to treatment.
Certain medications can decrease the absorption of liothyronine. Examples include products that contain aluminum or magnesium. antacids, sucralfate, calcium supplements. iron, bile acid-binding resins (such as cholestyramine. colestipol. colesevelam ), simethicone. sevelamer. sodium polystyrene sulfonate, among others. If you take any of these medications, take them at least 4 hours before or after liothyronine. If you take lanthanum. take it at least 2 hours before or after liothyronine.
Symptoms of low thyroid hormone levels include tiredness, muscle aches, constipation. dry skin. weight gain, slow heartbeat, or sensitivity to cold. You may see an improvement in these symptoms within a few days. Tell your doctor if you do not get better or if you get worse.
Temporary hair loss may occur during the first few months of starting this drug, especially in children. If this effect lasts or gets worse, tell your doctor or pharmacist promptly.
Remember that your doctor has prescribed this medication because he or she has judged that the benefit to you is greater than the risk of side effects. Many people using this medication do not have serious side effects.
Though unlikely, it is possible to have too much thyroid hormone. Tell your doctor right away if you have symptoms of too much thyroid hormone, including: headache, mental/mood changes (such as irritability, nervousness), increased sweating, sensitivity to heat, diarrhea, menstrual changes.
Get medical help right away if you have any very serious symptoms of too much thyroid hormone, including: chest pain, fast/pounding/irregular heartbeat, swelling ankles/feet, trouble breathing, unusual tiredness.
Before taking liothyronine, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. This product may contain inactive ingredients, which can cause allergic reactions or other problems. Talk to your pharmacist for more details.
Before using this medication, tell your doctor or pharmacist your medical history, especially of: decreased adrenal gland function, heart disease (such as chest pain, heart failure, irregular heartbeat, heart attack), high blood pressure, diabetes, water diabetes (diabetes insipidus).
Before having surgery, tell your doctor or dentist about all the products you use (including prescription drugs, nonprescription drugs, and herbal products).
Current information shows that this drug may be used during pregnancy. Tell your doctor if you are pregnant because your doctor may need to change your dose.
Liothyronine passes into breast milk but is unlikely to harm a nursing infant. Consult your doctor before breast-feeding.
See also How to Use section.
Drug interactions may change how your medications work or increase your risk for serious side effects. This document does not contain all possible drug interactions. Keep a list of all the products you use (including prescription/nonprescription drugs and herbal products) and share it with your doctor and pharmacist. Do not start, stop, or change the dosage of any medicines without your doctor’s approval.
Some products that may interact with this drug include: “blood thinners” (such as warfarin).