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WP Thyroid® (Thyroid USP) Tablets, for oral use, are natural preparations derived from porcine thyroid glands (T3 liothyronine is approximately four times as potent as T4 levothyroxine on a microgram for microgram basis). They provide 38 mcg levothyroxine (T4) and 9 mcg liothyronine (T3) for each 65 mg (1 Grain) of the labeled content of thyroid.
Inulin, Medium Chain Triglycerides, Lactose Monohydrate*
*Present in traceable amount as part of Thyroid USP (diluent)
The structural formulas of liothyronine (T3) and levothyroxine (T4) are as follows:
- As replacement of 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 (children, 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 TSH suppressants, in the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, subacute, or chronic lymphocytic thyroiditis (Hashimoto’s), multinodular goiter, and in the management of thyroid cancer.
- As diagnostic agents in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland anatomy.
Adverse reactions other than those indicative of hyperthyroidism because of therapeutic overdosage, either initially or during the maintenance period, are rare (See OVERDOSE).
Signs And Symptoms
Excessive doses of thyroid result in a hypermetabolic state resembling in every respect the condition of endogenous origin. The condition may be self induced.
Treatment Of Overdosage
Dosage should be reduced or therapy temporarily discontinued signs and symptoms of overdosage appear.
Treatment may be reinstituted at a lower dosage. In normal individuals, normal hypothalamic-pituitarythyroid 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, initially, especially when no contraindications exist for its use.
The steps in the synthesis of the thyroid hormones are controlled by thyrotropin (Thyroid Stimulating Hormone, TSH) secreted by the anterior pituitary. This hormone’s secretion is in turn controlled by a feedback mechanism affected by the thyroid hormones themselves and by thyrotropin releasing hormone (TRH), a tripeptide of hypothalamic origin. Endogenous thyroid hormone secretion is suppressed when exogenous thyroid hormones are administered to euthyroid individuals in excess of the normal gland’s secretion.
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.
The normal thyroid gland contains approximately 200 mcg of levothyroxine (T4) per gram of gland, and 15 mcg of liothyronine (T3) per gram. The ratio of these two hormones in the circulation does not represent the ratio in the thyroid gland, since about 80 percent of peripheral liothyronine (T3) comes from monodeiodination of levothyroxine (T4). Peripheral monodeiodination of levothyroxine (T4) at the 5 position (inner ring) also results in the formation of reverse liothyronine (T3), which is calorigenically inactive. Liothyronine (T3) levels are low in the fetus and newborn, in old age, in chronic caloric deprivation, hepatic cirrhosis, renal failure, surgical stress, and chronic illnesses representing what has been called the “T3 thyronine syndrome”.
Animal studies have shown that levothyroxine (T4) is only partially absorbed from the gastrointestinal tract. The degree of absorption is dependent on the vehicle used for its administration and by the character of the intestinal contents, the intestinal flora, including plasma protein, and soluble dietary factors, all of which bind thyroid, thereby making it unavailable for diffusion. Only 41 percent is absorbed when given in a gelatin capsule, as opposed to 74 percent absorption when given with an albumin carrier.
Depending on other factors, absorption has varied from 48 to 79 percent of the administered dose. Fasting increases absorption. Malabsorption syndromes, as well as dietary factors, (children’s soybean formula, concomitant use of anionic exchange resins such as cholestyramine) cause excessive fecal loss. Liothyronine (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.
More than 99 percent of circulating hormones are bound to serum proteins, including thyroid-binding globulin (TBg), thyroid-binding pre-albumin (TBPA), and albumin (TBa), whose capacities and affinities vary for the hormones. The higher affinity of levothyroxine (T4) for both TBg and TBPA, as compared to liothyronine (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. Deiodination of levothyroxine (T4) occurs at a number of sites, including liver, kidney, and other tissues. The conjugated hormone, in the form of glucuronide or sulfate, is found in the bile and gut where it may complete an enterohepatic circulation. Eighty-five percent of levothyroxine (T4) metabolized daily is deiodinated.