Cytomel

Cytomel brand of liothyronine is the synthetic levo form of triiodothyronine, with all pharmacologic activities of the natural substance. Its onset of action is rapid, occurring within a few hours. Maximum pharmacological response occurs within two or three days, providing early clinical response.

Following oral administration, about 95% of the dose of liothyronine is absorbed from the gastrointestinal tract in 4 hours. Liothyronine, not firmly bound to serum protein, is readily available to body tissues. Its biologic half-life is about 2.5 days.

Liothyronine has a rapid cut-off of activity, which permits quick dosage adjustment and facilitates control of the effects of overdosage, should they occur.

There are two principal naturally occurring thyroid hormones, L-tetraiodothyronine (T₄, levothyroxine, L-thyroxine) and L-triiodothyronine (T₃, liothyronine).

The mechanisms by which thyroid hormones exert their physiologic actions are not well understood. It is generally believed that they exert most if not all of their actions through control of protein sythesis.

At moderate concentrations, thyroid hormones increase the synthesis of RNA and protein, followed by an increase in basal metabolic rate (BMR). They stimulate oxidative enzyme systems generally, and enhance the release of free fatty acids from adipose tissue. They also increase the intestinal absorption and peripheral utilization of glucose.

At higher concentrations, thyroid hormones decrease protein synthesis, uncouple oxidative phosphorylation and increase the breakdown of glycogen, lipids and protein.

See Precautions.

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. Treatment should be initiated immediately upon diagnosis and maintained for life, unless transient hypothyroidism is suspected, in which case therapy may be interrupted for two to eight weeks after the age of three years to reassess the condition. Cessation of therapy is justified in patients who have maintained a normal TSH level during those two to eight weeks.

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.

Since liothyronine is not as firmly bound to serum protein as thyroxine, the PBI usually remains at levels below normal during full replacement therapy. As with all thyroid preparations, thyroid gland function reflected by I¹³¹ uptake may be depressed by Cytomel, particularly when dosage exceeds 75 µg daily. This effect disappears rapidly, and useful I¹³¹ thyroid uptake values may be obtained usually within 2 weeks following discontinuance of the drug.

The following drugs or moieties are known to interfere with laboratory tests performed in patients on thyroid hormone therapy: androgens, corticosteroids, estrogens and estrogen-containing oral contraceptives, iodine-containing preparations and salicylates.

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.

Cholestyramine binds orally administered thyroid hormones in the intestine, impairing their absorption. In vitro studies indicate that the binding is not easily overcome. Therefore, 4 to 5 hours should elapse between administration of cholestyramine and thyroid hormones.

Thyroid preparations may potentiate the toxic effects of digitalis. Thyroid hormonal replacement increases metabolic rate, which requires an increase in digitalis dosage.

Thyroid hormones are excreted in human milk in minimal amounts which are not associated with serious adverse reactions. Thyroid hormones do not have a known tumorigenic potential. Nevertheless, caution should be exercised when thyroid is administered to a nursing woman.

Thyroid hormones increase 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.

In infants, excessive doses of thyroid hormone preparations may produce craniosynostosis.

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.

Estrogens tend to increase serum thyroxine-binding globulin (TBG) and may require, depending on the level of thyroid gland function, adjustment of (supplemental or replacement) thyroid hormone dosage.

Thyroid hormones appear to increase catabolism of vitamin K-dependent clotting factors. Patients stabilized on oral anticoagulants may require dosage adjustment, through close monitoring of prothrombin time, when thyroid hormone therapy is started. No special precautions appear to be necessary when oral anticoagulant therapy is begun in a patient already stabilized on maintenance thyroid therapy.

Initiating thyroid replacement therapy may require 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.

Each round, flat-faced, bevel-edged, white, compressed tablet, debossed with KPI on one side and 115 on the other side, contains: liothyronine 5 µg (present as liothyronine sodium 5.18 µg). Nonmedicinal ingredients: calcium sulfate, gelatin, starch, stearic acid, sucrose and talc. Bottles of 100.

Each round, flat-faced, bevel-edged, white, compressed tablet, debossed with KPI 116 on one side and scored on the other side, contains: 25 µg (present as liothyronine sodium 25.9 µg). Nonmedicinal ingredients: calcium sulfate, gelatin, starch, stearic acid, sucrose and talc. Bottles of 100.

25 µg of liothyronine is equivalent to approximately 65 mg of desiccated thyroid or thyroglobulin and 0.1 mg of L-thyroxine.

Headache, irritability, nervousness, sweating, tachycardia, increased bowel motility and menstrual irregularities. Because of liothyronine's rapid cut-off of activity, such symptoms will generally disappear within a few days after dosage is reduced. 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.

General supportive measures. Sedation if indicated. If tachycardia is present, reserpine may be helpful. Measures should be instituted to control shock if present, such as intravenous fluids, oxygen. Intravenous hydrocortisone should be considered for the treatment of unrecognized adrenal insufficiency.

Recommended starting dosage is 25 µg daily. Daily dosage then may be increased by 12.5 or 25 µg every 1 or 2 weeks. Usual maintenance dosage is 25 to 75 µg daily. Smaller doses may be fully effective in some patients, while 100 µg may be required in others.

Since the mother provides little or no thyroid hormone to the fetus, infants with thyroid dysfunction will require replacement therapy from birth. Treatment should be initiated as early as possible to avoid permanent physical and mental changes. Recommended starting dosage is 5 µg daily, with a 5 µg increment every 3 to 4 days until the desired response is achieved. Infants a few months old may require only 20 µg daily for maintenance. At 1 year, 50 µg daily may be required. Above 3 years, full adult dosage may be necessary.

Recommended starting dosage is 5 µg daily. Based on sperm count and motility, daily dosage may be increased by 5 or 10 µg every 2 to 4 weeks. Daily dosage will usually not exceed 25 µg and rarely should dosage exceed 50 µg daily in this indication.

Recommended starting dosage is 5 µg daily. This dosage my be increased by 5 to 10 µg daily every 1 to 2 weeks. When 25 µg daily is reached, dosage may be increased every week or two by 12.5 or 25 µg. Usual maintenance dosage is 75 µg daily.

In the elderly or in children, therapy should be started with 5 µg daily and increased only by 5 µg increments at the recommended intervals.

When switching a patient to Cytomel from thyroid, L-thyroxine 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.

Myxedematous patients are very sensitive to thyroid substances; dosage should be started at a very low level and increased gradually. Recommended starting dose is 5 µg daily. This may be increased by 5 or 10 µg daily every 1 or 2 weeks. Usual maintenance dosage is 50 to 100 µg daily.

When I¹³¹ thyroid uptake is in the borderline high range, administer 75 to 100 µg of Cytomel daily for 7 days, then repeat I¹³¹ thyroid uptake test. In the hyperthyroid patient, 24-hour I¹³¹ thyroid uptake will not be affected significantly. In the euthyroid patient, 24-hour I¹³¹ thyroid uptake will drop to less than 20%.