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Liothyronine dosing

Liothyronine (T3) 25-50 meg IV bolus. Use 10-20 meg IV bolus in patients with CAD. Subsequent doses (e.g., 2.5-10 meg IV q6-8h) should be administered between 4—12 h after the initial bolus dose and continued until signs and symptoms resolve... [Pg.108]

A single dose of liothyronine administered IV produces a detectable metabolic response in as little as 2 to 4 hours and a maximum therapeutic response within 2 days. [Pg.345]

Tri-iodothyronine (synonym liothyronine) is rarely used orally for maintenance therapy. Its half-life is only 24 hours and multiple daily doses are required. Its high potency carries a greater risk for car-diotoxicity. It is mainly used for diagnostic purposes. [Pg.392]

Although liothyronine (T3) is three to four times more potent than levothyroxine, it is not recommended for routine replacement therapy because of its shorter half-life (24 hours), which requires multiple daily doses its higher cost and the greater difficulty of monitoring its adequacy of replacement by conventional laboratory tests. Furthermore, because of its greater hormone activity and consequent greater risk of cardiotoxicity, T3 should be avoided in patients with cardiac disease. [Pg.862]

The use of desiccated thyroid rather than synthetic preparations is never justified, since the disadvantages of protein antigenicity, product instability, variable hormone concentrations, and difficulty in laboratory monitoring far outweigh the advantage of low cost. Significant amounts of T3 found in some thyroid extracts and liotrix may produce significant elevations in T3 levels and toxicity. Equivalent doses are 100 mg (1.5 g) of desiccated thyroid, 100 Mg of levothyroxine, and 37.5 ug of liothyronine. [Pg.891]

Disposition in the Body. Incompletely and variably absorbed after oral administration. It is metabolised by de-iodination to liothyronine (tri-iodothyronine) which is the principal active form of thyroxine further de-iodination to thyroacetic acid (4-/7-hydroxyphenoxyphenylacetic acid), and conjugation with glucuronic acid and sulphate also occur. About 30 to 55% of a dose is excreted in the urine and 20 to 40% is eliminated in the faeces of the urinary material about 40% is thyroacetic acid and 20% is liothyronine. [Pg.1024]

Tj (liothyronine) is about 5 times as biologically potent as T a single dose reaches its maximum effect in about 24 h (its binding to plasma proteins is weak) and passes off in one week (t) 2d in euthyroid subjects). [Pg.700]

Liothyronine Tabs. Liothyronine is the most rapidly effective thyroid hormone, a single dose giving maximum effect within 24 h and passing off over 24—48 h. It is not used in routine treatment of hypothyroidism because its rapid onset of effect can induce heart failure. Its main uses are in myxoedema coma and psychosis, both rare conditions. A specialised use is during the withdrawal of levothyroxine replacement (to permit diagnostic radioiodine scanning) in patients with thyroid carcinoma. [Pg.701]

Thyroid extract is partially absorbed from the gastrointestinal tract. Up to 79% of a therapeutic dose is absorbed. Approximately 99% is protein bound. Thyroid extract contains both levothyroxine (T4) and liothyronine (T3). T4 is deiodinated in the liver, kidney, and tissues to form active T3 and inactive T2. The half-life of T4 is 5.3-9.4 days. T3 has a half-life of 2.5 days. [Pg.2577]

The synthetic preparations used are the sodium salts of the natural isomers of the thyroid hormones. Levothyroxine sodium (L-T, synthroid, levoxyl, levothroid, unithroid, others) is available in tablets in a variety of doses and as a lyophilized powder for injection. L-T has a narrow therapeutic index, and the FDA has mandated demonstration of bioequivalence for brand and generic preparations by the various producers. Liothyronine sodium (L-Tft is available in tablets (cytomel) and in an injectable form (triostat). A mixture of L-T and L-T is marketed as liotrix (thyroiar). Desiccated thyroid preparations, derived from whole animal thyroids and containing both T and T have highly variable biologic activity and are much less desirable. [Pg.987]

A patient with myxoedema required a gradual reduction in his dosage of phenindione from 200 to 75 mg daily as his thyroid status was corrected by liothyronine. A similar patient required a reduction in acenocoumarol dose from 16 mg daily to 5 mg daily when hypothyroidism was corrected with Uothyronine. ... [Pg.455]

Uses Thyroid hormones (levothyroxine, T4, and liothyronine, T3) are used to treat overt hypothyroidism. In addition, supra-physiological doses of levothyroxine are widely used to reduce the risk of thyroid cancer recurrence by suppressing serum TSH concentrations. The use of levothyroxine suppressive therapy to induce shrinkage of benign thjnoid nodules remains controversial and its routine use is not recommended in view of its low efficacy and potential long-term effects on the cardiovascular system and the skeleton caused by the induction of subchnical hjrper-thyroidism [5 ]. [Pg.881]

Two separate reports have suggested that supraphysiological doses of liothyronine may be beneficial in refractory major depression when combined with both tricyclic antidepressants and SSRIs [8, 9 ]. Preliminary evidence suggests that the presence of a functional polymorphism in the type 1 de-iodinase enzyme, resulting in reduced peripheral conversion of T4 to T3, may be associated with increased benefit from combination therapy of antidepressants with liothyronine [10 ]. [Pg.882]


See other pages where Liothyronine dosing is mentioned: [Pg.207]    [Pg.221]    [Pg.866]    [Pg.207]    [Pg.708]    [Pg.3002]    [Pg.1384]    [Pg.1385]    [Pg.207]    [Pg.455]   
See also in sourсe #XX -- [ Pg.1383 ]




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