Thyroid (Nature®, ½ grain)

324

New product

100x 32.5mg Tablets

We stock a comprehensive range of both synthetic and natural thyroids.

We advocate taking a natural supplement over a synthetic because products such as Armour Thyroid contain a full spectrum of Thyroid hormones (T1, T2, T3 and T4) unlike synthetic thyroid products such as Titre or Tiromel, which typically only contain one.

We also have the first synthetic T3 and T4 combination IBSA from Italy.

US$79.99

- +

Add to compare

  • Nature-Thyroid™ (Thyroid USP) Tablets

    DESCRIPTION

    Nature-Throid™ (Thyroid USP) Tablets, micro-coated, easy to swallow with a reduced odor, 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.

    Each Clear Coated Container Contains:

    Thyroid U.S.P.                 0.5 gr. (32.5mg)

    Liothyronine (T3)            4.5 mcg

    Levothyroxine (T4)         19 mcg

    Calcium                         9 mg

    Magnesium, Sodium (each) less than 1 mg

    INACTIVE INGREDIENTS

    Colloidal Silicon Dioxide, Dicalcium Phosphate, Lactose Monohydrate*, Magnesium Stearate,

    Microcrystalline Cellulose, Croscarmellose Sodium, Stearic Acid, Opadry II 85F19316 Clear.

    *Present in traceable amount as part of Thyroid USP (diluent)

    INDICATIONS AND USAGE

    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.

    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.

    CONTRAINDICATIONS

    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 in the literature of true allergic or idiosyncratic reactions to thyroid hormone.

    WARNINGS

    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.

    PRECAUTIONS

    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, whom have a greater likelihood of occult cardiac disease. With these patients, therapy should be initiated with low doses, i.e. 16.25 - 32.5 mg. 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. Thyroid hormone therapy in patients with concomitant diabetes mellitus or diabetes 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 glucorticoids.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 should be adjusted on the basis of frequent prothrombin time determinations. In infants, excessive doses of thyroid hormone preparations may produce craniosynostosis.

    Information for the Patient

    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 children in the first few months of thyroid therapy, but this is usually a transient phenomenon and later recovery is usually the rule.

    Drug Interactions

    Oral Anticoagulants-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 that 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 Hypoglycemic-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 hypoglycemic should be closely watched during initiation of thyroid replacement therapy. Cholestyramine or Colestipol- Cholestyramine or Colestipol binds both levothyroxine (T4) and liothyronine (T3) in the intestine, thus impairing absorption of these thyroid hormones. In vitro studies indicate that the binding is not easily removed. Therefore, four to five hours should elapse between administration of Cholestyramine or Colestipol and thyroid hormones.

    Estrogen, Oral Contraceptives- 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 (T4) may be decreased when estrogens are started thus increasing thyroid requirements.

    However, if the patient’s thyroid gland has sufficient function, the decreased free levothyroxine (T4) will result in a compensatory increase in levothyroxine (T4) 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.

    Pregnancy

    Category A: 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.

    Nursing Mothers: 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.

    Pediatric Use: Pregnant mothers provide little or no thyroid hormone to the fetus. The incidence of congenital hypothyroidism is relatively high (1:4,000) and the hypothyroid fetus would not derive any benefit from the small amounts of hormone crossing the placental barrier. Routine determination of

    serumT4 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.

    Geriatric use: Clinical studies of Thyroid Tablets, USP 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.

    ADVERSE REACTIONS

    Adverse reactions other than those indicative of hyperthyroidism because of therapeutic overdosage, either initially or during the maintenance period, are rare.

    OVERDOSAGE

    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.

    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.

    Thyroid hormones are given orally. In acute, emergency conditions, injectable levothyroxine sodium (T4) may be given intravenously when oral administration is not feasible or desirable (as in the treatment of

    myxedema coma, or during parenteral nutrition). Intramuscular administration is not advisable because of reported poor absorption.

    Hypothyroidism

    Therapy is usually instituted using low doses, with increments which depend on the cardiovascular status of the patient. The usual starting dose is 32.5 mg, with increment of 16.25 mg every 2 to 3 weeks. A lower starting dosage, 16.25 mg/day, is recommended in patients with longstanding myxedema, particularly if cardiovascular impairment is suspected, in which case extreme caution is recommended. The appearance of angina is an indication for reduction in dosage. Most patients require 65 - 130 mg/day. Failure to respond to doses of 195 mg suggests lack of compliance or malabsorption.

    Maintenance dosages 65 - 130 mg/day usually result in normal serum T4 and T3 levels. Adequate therapy usually results in normal TSH and T4 levels after 2 or 3 weeks of therapy. Readjustment of thyroid hormone dosage should be made within the first four weeks of therapy, after proper clinical and laboratory evaluations, including serum levels of T4, bound and free, and TSH.

    Liothyronine (T3) may be used in preference to levothyroxine (T4) during radio-isotope 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 levothyroxine (T4) and

    liothyronine (T3) is suspected.

    Myxedema Coma

    Myxedema coma is usually precipitated in the hypothyroid patient of longstanding by

    intercurrent illness or drugs such as sedatives and anesthetics and should be considered a medical emergency. Therapy should be directed at the correction of electrolyte disturbances and possible infection, besides the administration of thyroid hormones. Corticosteroids should be administered routinely. Levothyroxine (T4) and Liothyronine (T3) may be administered via a nasogastric tube, but the preferred route of administration of both hormones is intravenous. Levothyroxine sodium (T4) is given at a starting dose of 400 mcg (100 mcg/mL) given rapidly, and is usually well tolerated, even in the elderly. This initial dose is followed by daily supplements of 100 to 200 mcg given IV. Normal T4 levels are achieved in 24 hours, followed in 3 days by threefold elevation of T3. Oral therapy with thyroid hormone would be resumed as soon as the clinical situation has been stabilized and the patient is able to take oral medication.

    Thyroid Cancer

    Exogenous thyroid hormone may produce regression of metastases from follicular and papillary carcinoma of the thyroid and is used as ancillary therapy of these conditions with radioactive iodine. TSH should be suppressed to low or undetectable levels. Therefore, larger amounts of thyroid hormone than those used for replacement therapy are required. Medullary carcinoma of the thyroid is usually unresponsive to this therapy.

    Thyroid Suppression 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 base line laboratory tests appear normal, or to demonstrate thyroid gland autonomy in patients with Grave’s ophthalmopathy. 131I uptake is determined before and after the administration of the exogenous hormone. A fifty percent or greater suppression of uptake indicates a normal thyroid pituitary axis, and thus rules out thyroid gland autonomy. For adults, the usual suppressive dose of levothyroxine (T4) is 1.56 mg/kg of body weight per day given for 7 to 10 days. These doses usually yield normal serum T4 and T3 levels and lack of response to TSH. Thyroid hormones should be administered cautiously to patients in whom there is strong suspicion of thyroid gland autonomy, in view of the fact that the exogenous hormone effects will be additive to the endogenous source.

    Pediatric Dosage

    Pediatric dosage should follow these recommendations. In infants with congenital hypothyroidism, therapy with full doses should be instituted as soon as the diagnosis has been made.

    Recommended Pediatric Dosage for Congenital Hypothyroidism

    Age

    Dose per day

    Daily dose per KG of body weight

    0-6 months

    16.25-32.5 mg

    4.8-6.0 mg

    6-12 months

    32.5-48.75 mg

    3.6-4.8 mg

    1-5 years

    48.75-65 mg

    3.0-3.6 mg

    6-12 years

    65-97.5 mg

    2.4-3.0 mg

    Over 12 years

    Over 97.5 mg

    1.2-1.8 mg

    STORAGE: Store at controlled room temperature; 15°-30°C (59°-86°F)

    Dispense in tight, light-resistant containers as defined in the USP/NF

    MADE IN USA

Customers who bought this product also bought:

Recently Viewed

Menu

Top
Compare 0