【药物名称】碘塞罗宁钠 Liothyronine Sodium
【药物别名】三碘甲状腺氨酸钠、碘赛罗宁 T3、Liothyronine Triiodothyronin
【制剂规格】片剂：20μg。粉针剂：20μg。
【药理毒理】为人工合成的三碘甲状腺原氨酸钠，作用与甲状腺素相似，其作用是甲状腺素的3-5倍。
【药 动 学】口服易吸收，蛋白结合率高，约0.3%以游离形式存在。血中T1/2约1～2日，但甲状腺功能低下时T1/2会延长，甲状腺功能亢进时T1/2为14.4小时。
【适 应 证】需要迅速见效的甲状腺功能减退及甲状腺功能亢进症的诊断。
【不良反应】有心动过速、心悸、心绞痛、头痛、神经质、兴奋、失眠、肌无力、怕热、出汗、潮红、发热、体重减轻、腹泻、呕吐等，偶见心律失常、心衰、昏迷和死亡。
【相互作用】可增强抗凝剂的抗凝作用及三环类抗抑郁药的作用。糖尿病患者服用本品应适当增加胰岛素或口服降糖药剂量。氨碘酮、普萘洛尔可抑制甲状腺素脱碘生成本品，导致T3浓度下降与无活性的反T3浓度同时升高。
【用法用量】口服，成人甲状腺功能减退，初始剂量10μg-25μg/日，分2次-3次服用，每1周-2周递增10μg-25μg，直至甲状腺功能恢复正常；对于年龄大、心功能不全或长期甲状腺功能严重减退的病人，初始剂量要低，增加剂量时幅度要小，加量速度要慢。维持量25μg-50μg/日。诊断成人甲状腺功能亢进症，80μg/日，分3次-4次口服，连用7日-8日；服药前后进行放射性碘摄取试验，甲亢者甲状腺对碘的摄取不受抑制，而正常人碘的摄取受到抑制。粘液性水肿昏迷患者，静脉注射，初始剂量40μg-120μg，以后每6h给予5μg-15μg，直到病人清醒改为口服。
【注意事项】发生急性药物过量时，可进行洗胃或诱导呕吐以减少胃肠道吸收，并行对症治疗和支持治疗。在替代治疗中，应首选左甲壮腺素钠，而非本品。心绞痛、动脉硬化、冠状动脉病变、高血压、心肌梗死等患者慎用。60岁以上的老年患者对本品敏感，剂量应适当减小。伴有垂体前叶功能减退或肾上腺皮质功能不全的病人，应先用皮质类固醇，待肾上腺皮质功能恢复正常后再用本品。妊娠A类，孕妇和乳母用适量甲状腺激素对胎儿或婴儿无不良影响。

碘塞罗宁
Liothyronine 
中文别名：  碘塞罗宁、碘甲腺氨酸、碘甲腺氨酸钠、碘塞罗宁钠、碘赛罗宁、甲碘安、三碘甲状腺氨酸、三碘甲状腺氨酸钠、三碘甲状腺素、三碘甲状腺素钠、三碘甲状腺原氨酸、特初新
英文别名：  Liothyronine Sodium、Sodium Liothyronine、Triiodothyronin、Triiodothyronine、Triiodothyronine Sodium
生产企业：  
药品类别：  甲状腺激素及抗甲状腺药
 
 
 
药理药动
药动学
Ｔ3钠盐胃肠道吸收完全，与Ｔ4相比，Ｔ3与血浆蛋白的结合程度较低，约0.3％以游离形式存在。在甲状腺功能正常情况下，Ｔ3在血中的Ｔ1/2约为 1～2天，在甲状腺功能减退时，略延长，在甲状腺功能亢进时约为0.6天。
适 应 症 
适用于各种原因引起的甲状腺功能减退症。
用法用量
1．口服成人甲状腺功能减退，开始剂量每日 10～25ug，分2～3次口服，每 1～2周递增 10～25ug，直至甲状腺功能恢复正常。维持量每天 25～50ug。对于年龄大、心功能不全或严重长期甲状腺功能减退病人，开始剂量应小，增加剂量时幅度应小，加量速度要慢。
诊断成人甲状腺功能亢进症，一日 80ug，分 3～4次口服，连用 7～8天。服药前后进行放射性碘摄取试验，甲状腺功能亢进者。甲状腺对碘的摄取不被抑制；而正常人则受抑制。
2．静脉注射对粘液性水肿昏迷患者，首次剂量40～120ug，以后每 6小时 5～15ug，直到病人清醒改为口服。
[制剂与规格]碘塞罗宁钠片20ug
注射用碘塞罗宁钠2Oug
成人开始一日10-20ug,分2-3次服,后渐增至80-100ug.儿童体重<7kg,开始一日2.5ug,7kg以上一日5ug,后每隔周用量每日加5ug,维持量为一日15-20ug,分2-3次服.
不良反应
 
甲状腺激素如用量适当无任何不良反应。使 用过量则引起心动过速、心悸、心绞痛、心律失常、头痛、神经质、兴奋、不安、失眠、骨路肌痉挛、肌无力、震颤、出汗、潮红、怕热、发热、腹泻、呕吐、体重减轻等类似甲状腺功能亢进的症状。T3过量时，不良反应的发生较T4或甲状腺粉快。减量或停药可使所有症状消失。T4过量所致者，症状消失较缓慢。
长期大剂量可引起心悸,手震颤,多汗,体重减轻,神经兴奋性升高和失眠.老年和心脏病人可引发心绞痛,心肌梗塞,心源性虚脱,此时应停用本品。
禁忌症 
 (1)老年患者对甲状腺激素较敏感，超过 60岁者甲状腺激素替代需要量比年青人约低25％。
(2)下列情况应慎用：

①心血管疾病，包括心绞痛、动脉硬化、冠心病、高血压、心肌梗塞等患者；②对病程长、病情重的甲状腺功能减退或粘液性水肿患者使用本类药应谨慎小心，开始用小剂量，以后缓慢增加直至生理替代剂量；③伴有垂体前叶功能减退或肾上腺皮质功能不全患者应先用皮质类固醇，俟肾上腺皮质功能恢复正常后再用本类药。
老年和心脏病人可引发心绞痛,心肌梗塞,心源性虚脱,此时应停用本品.
药物相互作用 
 (1)糖尿病患者服用甲状腺激素应适当增加胰岛素或降糖药剂量。
(2)甲状腺激素与抗凝剂如双香豆素合用时，后者的抗凝作用增强，可能引起出血；应根据凝血酶原时间调整抗凝药剂量。
(3)本类药与三环类抗抑郁药合用时，两类药的作用及毒副作用均有所增强，应注意调整剂量。
(4)服用雌激素或避孕药者，因血液中甲状腺素结合球蛋白水平增加，合用时甲状腺激素剂量度适当增加。
(5)考来烯胺(cholestyramine)或考来替泊(cholestipol)可以减弱甲状腺激素的作用，两类药伍用时，应间隔4～5小时服用，并定期测定甲状腺功能。
(6)b肾上腺素受体阻滞剂可减少外周组织 T4向 T3的转化，合用时应予注意。

Liothyronine Sodium Tablets, USP

Thyroid hormone drugs are natural or synthetic preparations containing tetraiodothyronine (T, levothyroxine) sodium or triiodothyronine (T, liothyronine) sodium or both. T and T are produced in the human thyroid gland by the iodination and coupling of the amino acid tyrosine. T contains four iodine atoms and is formed by the coupling of two molecules of diiodotyrosine (DIT). T 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.

Liothyronine Sodium Tablets, USP contain liothyronine (L-triiodothyronine or LT), 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.

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 Liothyronine Sodium Tablet, USP contains liothyronine sodium equivalent to liothyronine as follows: 5 mcg debossed 5 and 220; 25 mcg scored and debossed 25 and 222; 50 mcg scored and debossed 50 and 223. Inactive ingredients consist of calcium sulfate, microcrystalline cellulose, hypromellose, talc, and colloidal silicon dioxide.

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 liothyronine sodium (T) 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 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) for both thyroid-binding globulin and thyroid-binding prealbumin as compared to triiodothyronine (T) 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.

Thyroid hormone drugs are indicated:

Liothyronine Sodium Tablets, USP 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 Liothyronine Sodium Tablets, USP 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.

Patients on thyroid hormone preparations and parents of pediatric patients on thyroid therapy should be informed that:

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 levels can be used to test the effectiveness of all thyroid medications except products containing liothyronine sodium. When the total serum T is low but TSH is normal, a test specific to assess unbound (free) T levels is warranted. Specific measurements of Tand T 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 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.

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 Tand T 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.

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.

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.

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.

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 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 Liothyronine Sodium Tablets, USP.

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.

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.

The dosage of thyroid hormones is determined by the indication and must in every case be individualized according to patient response and laboratory findings.

Liothyronine Sodium Tablets, USP 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 to 75 mcg daily.

The rapid onset and dissipation of action of liothyronine sodium (T), as compared with levothyroxine sodium (T), 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 levels that follow its administration and the possibility of more pronounced cardiovascular side effects tend to counterbalance the stated advantages.

Liothyronine Sodium Tablets, USP may be used in preference to levothyroxine (T) 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 Tto T is suspected.

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 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.

An intravenous preparation of liothyronine sodium is marketed under the trade name Triostat for use in myxedema coma/precoma.

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 ).

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 Liothyronine Sodium Tablets, USP from thyroid, L-thyroxine or thyroglobulin, discontinue the other medication, initiate Liothyronine Sodium Tablets, USP 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.

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. I 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.

Liothyronine Sodium Tablets, USP 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. Liothyronine Sodium Tablets, USP 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.

R Only

Liothyronine Sodium Tablets, USP, 5 mcg, are white to off-white, round, flat, debossed "5" over "220" on one side and plain on the other in bottles of 100.

Liothyronine Sodium Tablets, USP, 25 mcg, are white to off-white, round, flat, debossed "25" above the score and "222" below the score on one side and plain on the other in bottles of 100.

Liothyronine Sodium Tablets, USP, 50 mcg, are white to off-white, round, flat, debossed "50" above the score and "223" below the score on one side and plain on the other in bottles of 100.

5 mcg 100's: NDC 0574-0220-01 25 mcg 100's: NDC 0574-0222-01 50 mcg 100's: NDC 0574-0223-01

Store at 20° to 25°C (68° to 77°F)[see USP Controlled Room Temperature]

Distributed by:Paddock Laboratories, Inc.Minneapolis, MN 55427

Rev 11/2008

NDC 0574-0220-01

LIOTHYRONINE SODIUM TABLETS, USP

5 mcg Rx ONLY

NET CONTENTS 100 TABLETS