What are the possible side effects of desiccated thyroid (Armour Thyroid, Nature-Throid, Westhroid)?
What is the most important information I should know about desiccated thyroid (Armour Thyroid, Nature-Throid, Westhroid)? What should I discuss with my healthcare provider before taking desiccated thyroid (Armour Thyroid, Nature-Throid, Westhroid)?
What should I avoid while taking desiccated thyroid (Armour Thyroid, Nature-Throid, Westhroid)?
What other drugs will affect desiccated thyroid (Armour Thyroid, Nature-Throid, Westhroid)? Desiccated (dried) thyroid is a combination of hormones that are normally produced by your thyroid gland to regulate the body's energy and metabolism.
Since thyroid hormone occurs naturally in the body, almost anyone can take desiccated thyroid. Gabinet Weterynaryjny Medica-Wetzaprasza do skorzystania z uslug fryzjerskich dla Twojego pupila. Disclaimer: This drug has not been found by FDA to be safe and effective, and this labeling has not been approved by FDA. Armour® Thyroid (thyroid tablets, USP)* for oral use is a natural preparation derived from porcine thyroid glands and has a strong, characteristic odor. The steps in the synthesis of the thyroid hormones are controlled by thyrotropin (Thyroid Stimulating Hormone, TSH) secreted by the anterior pituitary. The mechanisms by which thyroid hormones exert their physiologic action are not well understood. The normal thyroid gland contains approximately 200 mcg of levothyroxine (T4) per gram of gland, and 15 mcg of liothyronine (T3) per gram.
Pharmacokinetics- Animal studies have shown that levothyroxine (T4) is only partially absorbed from the gastrointestinal tract.
Depending on other factors, absorption has varied from 48 to 79 percent of the administered dose. More than 99 percent of circulating hormones are bound to serum proteins, including thyroid-binding globulin (TBg), thyroid-binding prealbumin (TBPA), and albumin (TBa), whose capacities and affinities vary for the hormones. Deiodination of levothyroxine (T4) occurs at a number of sites, including liver, kidney, and other tissues.
As replacement or supplemental therapy in patients with hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis. As pituitary TSH suppressants, in the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, subacute or chronic Iymphocytic thyroiditis (Hashimoto's), multinodular goiter, and in the management of thyroid cancer. 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. Drugs with thyroid hormone activity, alone or together with other therapeutic agents, have been used for the treatment of obesity. 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.
The active ingredient (desiccated natural thyroid) in Armour® Thyroid (thyroid tablets, USP) is derived from porcine (pig) thyroid glands of pigs processed for human food consumption and is produced at a facility that also handles bovine (cow) tissues from animals processed for human food consumption. General—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. Thyroid hormone therapy in patients with concomitant diabetes mellitus or diabetes insipidus or adrenal cortical insufficiency aggravates the intensity of their symptoms.
Hypothyroidism decreases and hyperthyroidism increases the sensitivity to oral anticoagulants. 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.
In case of concomitant diabetes mellitus, the daily dosage of antidiabetic medication may need readjustment as thyroid hormone replacement is achieved. 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. Laboratory Tests—Treatment of patients with thyroid hormones requires the periodic assessment of thyroid status by means of appropriate laboratory tests besides the full clinical evaluation. Insulin or Oral Hypoglycemics—Initiating thyroid replacement therapy may cause increases in insulin or oral hypoglycemic requirements.
Cholestyramine or Colestipol—Cholestyramine or colestipol binds both levothyroxine (T4) and liothyronine (T3) in the intestine, thus impairing absorption of these thyroid hormones. Estrogen, Oral Contraceptives—Estrogens tend to increase serum thyroxine-binding globulin (TBg).
Changes in TBg concentration should be taken into consideration in the interpretation of levothyroxine (T4) and liothyronine (T3) values.
Medicinal or dietary iodine interferes with all in vivo tests of radio-iodine uptake, producing low uptakes which may not be relative of a true decrease in hormone synthesis. The persistence of clinical and laboratory evidence of hypothyroidism in spite of adequate dosage replacement indicates either poor patient compliance, poor absorption, excessive fecal loss, or inactivity of the preparation. Carcinogenesis, Mutagenesis, and Impairment of Fertility—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.
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. Adverse reactions other than those indicative of hyperthyroidism because of therapeutic overdosage, either initially or during the maintenance period, are rare (SeeOVERDOSAGE).
Signs and Symptoms—Excessive doses of thyroid result in a hypermetabolic state resembling in every respect the condition of endogenous origin. Treatment of Overdosage—Dosage should be reduced or therapy temporarily discontinued if signs and symptoms of overdosage appear. 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.
Other adjunctive measures may include administration of cholestyramine to interfere with thyroxine absorption, and glucocorticoids to inhibit conversion of T4 to T3.
The dosage of thyroid hormones is determined by the indication and must in every case be individualized according to patient response and laboratory findings.
Hypothyroidism—Therapy is usually instituted using low doses, with increments which depend on the cardiovascular status of the patient. 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. Myxedema Coma—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. 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. 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. 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 the recommendations summarized inTable 1.
So, to pick up after the last update, I had a resurgence of all the hypo-thyroid symptoms that I had previously been managing so well while on the naturally desiccated thyroid hormone, Armour Thyroid, and found out that Forest Laboratories, the drug company producing Armour Thyroid had changed the fillers. After finding out that the thyroid medication that I relied on every day to keep me functioning no longer worked, I got busy and found that there were many thyroid patients who were switching over to Nature-Throid.
The “y” has been left off the word Thyroid, so please make note of this if you’re trying to have your pharmacy order it in for you if it is not in stock and you want to try it as an alternative to Armour Thyroid. Desiccated thyroid is given when the thyroid does not produce enough of this hormone on its own.Desiccated thyroid treats hypothyroidism (low thyroid hormone).
This hormone's secretion is in turn controlled by a feedback mechanism effected by the thyroid hormones themselves and by thyrotropin releasing hormone (TRH), a tripeptide of hypothalamic origin. These hormones enhance oxygen consumption by most tissues of the body, increase the basal metabolic rate, and the metabolism of carbohydrates, lipids, and proteins.
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). 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 and thereby make it unavailable for diffusion.
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. The conjugated hormone, in the form of glucuronide or sulfate, is found in the bile and gut where it may complete an enterohepatic circulation. There is no well-documented evidence from the literature, however, of true allergic or idiosyncratic reactions to thyroid hormone.
In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduction.
Neither is their use justified for the treatment of male or female infertility unless this condition is accompanied by hypothyroidism. As a result, a potential risk of product contamination with porcine and bovine viral or other adventitious agents cannot be ruled out. These include patients with angina pectoris or the elderly, in whom there is a greater likelihood of occult cardiac disease.
Appropriate adjustments of the various therapeutic measures directed at these concomitant endocrine diseases are required.
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.
If thyroid medication is stopped, a downward readjustment of the dosage of insulin or oral hypoglycemic agent may be necessary to avoid hypoglycemia. 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. If oral anticoagulants are also being given, compensatory increases in clotting factor synthesis are impaired. 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. 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. No confirmatory long-term studies in animals have been performed to evaluate carcinogenic potential, mutagenicity, or impairment of fertility in either males or females. The clinical experience to date does not indicate any adverse effect on fetuses when thyroid hormones are administered to pregnant women.
Thyroid is not associated with serious adverse reactions and does not have a known tumorigenic potential. 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.
Cessation of therapy is justified in patients who have maintained a normal TSH during those 2 to 8 weeks.
In normal individuals, normal hypothalamic-pituitary-thyroid axis function is restored in 6 to 8 weeks after thyroid suppression. 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. 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 total parenteral nutrition.
The usual starting dose is 30 mg Armour Thyroid, with increments of 15 mg every 2 to 3 weeks. It may also be preferred when impairment of peripheral conversion of levothyroxine (T4) and liothyronine (T3) is suspected.
Therapy should be directed at the correction of electrolyte disturbances and possible infection besides the administration of thyroid hormones. 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. In infants with congenital hypothyroidism, therapy with full doses should be instituted as soon as the diagnosis has been made.
Since I was obviously not doing well on the new reformulation, the new task at hand became on what to do about replacing Armour Thyroid. Most doctors, especially if they don’t have a good understanding of thyroid issues, or simply believe everything that their drug rep tells them, will prescribe a synthetic medication which contains only T4 hormone.
So I called my pharmacists and explained the situation and found out that because Nature-Throid and Armour are essentially the same active ingredients, that they could most likely just refill my prescription with Nature Throid without my having to schedule another doctor’s visit.
The inactive ingredients are calcium stearate, dextrose, microcrystalline cellulose, sodium starch glycolate and opadry white.
Endogenous thyroid hormone secretion is suppressed when exogenous thyroid hormones are administered to euthyroid individuals in excess of the normal gland's secretion.
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. Peripheral monodeiodination of levothyroxine (T4) at the 5 position (inner ring) also results in the formation of reverse liothyronine (T3), which is calorigenically inactive. Only 41 percent is absorbed when given in a gelatin capsule as opposed to a 74 percent absorption when given with an albumin carrier. Malabsorption syndromes, as well as dietary factors, (children's soybean formula, concomitant use of anionic exchange resins such as cholestyramine) cause excessive fecal loss.
Both protein-bound hormones exist in reverse equilibrium with minute amounts of free hormone, the latter accounting for the metabolic activity. 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. Forest is not aware of any cases of disease transmission associated with the use of Armour Thyroid. The therapy of myxedema coma requires simultaneous administration of glucocorticoids (SeeDOSAGE AND ADMINISTRATION).
Serum T4 levels can be used to test the effectiveness of all thyroid medications except T3.
Patients stabilized on oral anticoagulants who are found to require thyroid replacement therapy should be watched very closely when thyroid is started. Patients receiving insulin or oral hypoglycemics should be closely watched during initiation of thyroid replacement therapy.
Therefore four to five hours should elapse between administration of cholestyramine or colestipol and thyroid hormones.
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. Pregnancy, estrogens, and estrogen-containing oral contraceptives increase TBg concentrations.
On the basis of current knowledge, thyroid replacement therapy to hypothyroid women should not be discontinued during pregnancy.
Therefore, larger amounts of thyroid hormone than those used for replacement therapy are required.
60 mg (1 gr) are available in bottles of 100 (NDC 0456-0459-01) and unit dose cartons of 100 (NDC 0456-0459-63). Other synthetic hormone preparations may have only T3, but the bottom line is that your body produces both T3 and T4, so many thyroid patients will do better taking a medication that more closely resembles the hormones that your body would produce naturally if it could do so. My pharmacy actually ended up making a call to my doctors office for me and my doctor just went ahead and wrote out a new prescription and faxed it to the pharmacy and I was able to pick up my new Nature-Throid medication the very next day. You may need to take thyroid medication for the rest of your life.Call your doctor if you notice any signs of thyroid toxicity, such as chest pain, fast or pounding heartbeats, feeling hot or nervous, or sweating more than usual.
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. When the total serum T4 is low but TSH is normal, a test specific to assess unbound (free) T4 levels is warranted. If a patient is truly hypothyroid, it is likely that a reduction in anticoagulant dosage will be required.
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.
Levothyroxine (T4) and liothyronine (T3) may be administered via a nasogastric tube but the preferred route of administration of both hormones is intravenous. A 50 percent or greater suppression of uptake indicates a normal thyroid-pituitary axis and thus rules out thyroid gland autonomy.
The other argument that some medical practitioners use is that they will tell patients that it is perfectly acceptable to take a synthetic T4 hormone supplement only because the thyroid gland will convert some of the synthetic T4 to T3.
The hormones contained in the natural preparations are absorbed in a manner similar to the synthetic hormones. Specific measurements of T4 and T3 by competitive protein binding or radioimmunoassay are not influenced by blood levels of organic or inorganic iodine.
No special precautions appear to be necessary when oral anticoagulant therapy is begun in a patient already stabilized on maintenance thyroid replacement therapy.
Decreases in TBg concentrations are observed in nephrosis, acromegaly, and after androgen or corticosteroid therapy. 120 mg (2 gr) are available in bottles of 100 (NDC 0456-0461-01) and unit dose cartons of 100 (NDC 0456-0461-63).
This is a problem for many of us with thyroid disorders because if you are relying on an already malfunctioning thyroid gland to do conversions of hormones for you, it can be problematic to expect that you will get the proper conversions with a thyroid gland that is not working optimally. But so far, it’s been a few weeks and things are finally getting back to normal in terms of my energy, memory and other symptoms. Antiadrenergic agents, particularly propranolol, have been used advantageously in the treatment of increased sympathetic activity. Not all, because the thyroid is a complex organ, and of course, everyone’s body is different, thus the need to adjust dosages and pay attention to patient’s symptoms. Adequate therapy usually results in normal TSH and T4 levels after 2 to 3 weeks of therapy. 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.
But most patients I have interviewed and the thousands of news group postings online seem to reflect a common denominator in that most will feel much better by taking a naturally desiccated thyroid hormone.
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