The actions of thyroid hormones are extensive. In general, thyroid hormones influence the growth and maturation of tissues, increase energy expenditure, and affect the turnover of essentially all substrates. These effects are mediated through control of DNA transcription and, ultimately, protein synthesis. Thyroid hormones play an integral role in both anabolic and catabolic processes and are particularly important to the development of the central nervous system in newborns. They regulate cell differentiation and proliferation, and aid in the myelination of nerves and the development of axonal and dendritic processes in the nervous system. Thyroid hormones, along with somatotropin, are responsible for regulating growth, particularly of bones and teeth. Thyroid hormones also decrease cholesterol concentrations in the liver and the bloodstream, and have a direct cardiostimulatory action. Cardiac consumption is increased by the administration of thyroid hormone, resulting in an increased cardiac output. Administration of exogenous thyroid hormone to patients with hypothyroidism increases the metabolic rate by enhancing protein and carbohydrate metabolism, increasing gluconeogenesis, facilitating the mobilization of glycogen stores, and increasing protein synthesis. In response to reestablishing physiologic levels of thyroid hormone, thyroid-stimulating hormone (TSH) concentrations correct if the primary disorder is at the level of the thyroid.

The release of T3 and T4 from the thyroid gland into the systemic circulation is regulated by TSH (thyrotropin), which is secreted by the anterior pituitary gland. Thyrotropin release is controlled by the secretion of thyroid-releasing hormone (TRH) from the hypothalamus and by a feedback mechanism dependent on the concentrations of circulating thyroid hormones. Because of this feedback mechanism, the administration of pharmacologic doses of exogenous thyroid hormone to patients with a normal thyroid suppresses endogenous thyroid hormone secretion.

Exogenously administered thyroid hormone is deiodinated in peripheral tissues, with small amounts metabolized in the liver and excreted in the bile. Iodine liberated during metabolism is used for hormone synthesis in the thyroid gland or is excreted in the feces or urine. The half-life of thyroid hormone varies with the concentrations of T3 and T4 in the preparation and typically will fall somewhere between their half-life values, which are approximately 2 days and about 6—7 days, respectively.

Although hypersensitivity is not common, desiccated thyroid should not be used in patients with a suspected hypersensitivity to thyroid hormones. In particular, because most desiccated thyroid is produced from porcine thyroid glands, it should not be used in patients with known porcine protein hypersensitivity.

Desiccated thyroid is contraindicated in patients with untreated thyrotoxicosis of any etiology. Caution should be used when administering thyroid agents to patients with autonomous thyroid tissue to prevent precipitation of thyrotoxicosis.

Administration of desiccated thyroid to patients with uncontrolled adrenal insufficiency can cause adrenal crisis and thus administration of thyroid hormones is contraindicated. Adrenal insufficiency should be corrected during concomitant administration of desiccated thyroid since the thyroid hormones increase the body’s demand for adrenal hormones. Symptoms of adrenal insufficiency can be unmasked or exacerbated by the administration of thyroid hormones.

Other causes of hypothyroidism (e.g., morphologic hypogonadism and nephroses) should be ruled out prior to beginning treatment with desiccated thyroid. Patients with hypothyroidism secondary to hypopituitarism are likely to have suppressed adrenal function as well, which should be corrected prior to initiating thyroid replacement therapy. Symptoms of hypopituitarism can be unmasked or exacerbated by the administration of thyroid hormones.

Desiccated thyroid should be used with extreme caution in patients with an acute myocardial infarction (MI) that is not associated with hypothyroidism; small amounts of thyroid hormones may be used only if the MI is complicated or caused by hypothyroidism. Thyroid agents are cardiostimulatory and should be used with great caution in patients with angina pectoris or other preexisting cardiac disease, including uncontrolled hypertension, cardiac arrhythmias, coronary artery disease, or a previous myocardial infarction. Many authorities recommend lower initial dosages and slower titration of thyroid hormones in patients with heart disease. If adverse cardiac symptoms develop or worsen, desiccated thyroid dosages should be reduced or withheld and cautiously restarted at a lower dose. Overtreatment with thyroid hormones may cause cardiac stimulation and lead to increased heart rate, cardiac wall thickening and increased cardiac contractility, which may precipitate angina or cardiac arrhythmias. Concomitant administration of desiccated thyroid with sympathomimetic agents in patients with coronary artery disease may precipitate coronary insufficiency and associated symptoms. Patients with coronary artery disease who are receiving thyroid hormones may be at a higher risk for developing arrhythmias, particularly during surgery.

Caution should be used in geriatric patients since they may be more sensitive to the cardiac effects of desiccated thyroid replacement. Lower initial dosages and slower titration are recommended. Thyroid hormone requirements are typically 25% lower than in younger adults. Individualization of dosage is recommended. According to the Beers Criteria, desiccated thyroid is considered a potentially inappropriate medication (PIM) for use in geriatric patients and should be avoided due to concerns about adverse cardiac effects and the availability of safer alternatives, like levothyroxine.1

Symptoms of diabetes mellitus can be unmasked or exacerbated by the administration of thyroid agents. The use of desiccated thyroid may require alteration in the dosage of antidiabetic regimens. Blood glucose should be monitored closely during concomitant therapy. In addition, withdrawal of thyroid hormones may cause hypoglycemia in susceptible patients.

Thyroid hormones are considered FDA pregnancy risk category A drugs. Desiccated thyroid hormones undergo minimal placental transfer and human experience does not indicate adverse fetal effects; do not discontinue needed replacement during pregnancy.2Also, hypothyroidism diagnosed during pregnancy should be promptly treated. Measure TSH during each trimester to gauge adequacy of thyroid replacement dosage since during pregnancy thyroid requirements may increase. Immediately after obstetric delivery, dosage should return to the pre-pregnancy dose, monitor a serum TSH or other thyroid function tests 6—8 weeks postpartum to assess for needed adjustments.

Thyroid hormones, like desiccated thyroid, are generally compatible with breast-feeding; minimal amounts of thyroid hormones are excreted in breast milk.3 Thyroid hormones do not have a known tumorigenic potential and are not associated with serious adverse reactions in nursing infants. However, use caution when administering desiccated thyroid to a nursing woman 2; changes in thyroid status in the post-partum period may require careful monitoring and maternal dosage adjustment. It should be noted that in general, adequate thyroid status is needed to maintain normal lactation, and there is no reason maternal replacement should be halted due to lactation alone. Levothyroxine is often the preferential drug to treat hypothyroidism and is considered compatible with breast feeding.3

Desiccated thyroid is not indicated for obesity treatment. Normal replacement doses are not effective, and large doses that would be required for reducing weight in euthyroid patients could lead to serious or even life-threatening toxicity. This is particularly dangerous when thyroid hormones are administered along with sympathetic amines that are also often used for weight loss.

The use of desiccated thyroid for treatment of female or male infertility is only justified if such infertility is accompanied by hypothyroidism.

Long-term use of thyroid hormones has been associated with decreased bone mineral density, particularly in postmenopausal females on greater than replacement doses or in women of any age receiving suppressive doses. Patients should be given the minimum dose necessary for desired clinical and biochemical response to limit risks for osteoporosis.

Studies performed to date in children, infants, and neonates have not shown problems that would limit the usefulness of thyroid hormones in these types of patients. Caution is necessary in interpreting results of thyroid function tests in neonates since serum T4concentrations are transiently elevated and T3 concentrations are transiently low. In addition, the immature pituitary gland is relatively insensitive to the negative feedback effect of thyroid hormones.

This list may not include all possible contraindications.

Many drugs affect thyroid hormone pharmacokinetics, metabolism or in vivopharmacodynamics; such drugs may alter the therapeutic response to thyroid hormone replacement. The following medication list is not complete, consult specialized resources for drug-thyroidal axis interactions that may occur.
Antithyroid agents should not be administered with the thyroid hormones due to their opposing effects.4 However, iodide and drugs that contain pharmacological amounts of iodine including radiopaque contrast agents that contain iodine (e.g., iohexol, ioversol, iopamidol, and iodixanol) may cause either hypothyroidism or hyperthyroidism in previously euthyroid patients. Patients receiving thyroid hormones and drugs that contain iodine should be monitored for changes in thyroid function.5
Certain foods, beverages, and enteral feedings can inhibit the absorption of thyroid hormones.5 6 To minimize the risk of an interaction, thyroid hormones should be administered on an empty stomach with a glass of water at least 30—60 minutes prior to food or enteral feedings. Foods that may decrease thyroid hormone absorption include soybean flour and soy-based infant formulas or enteral feedings, as well as high fiber diets, cottonseed meal, and walnuts. In addition to decreasing the oral absorption of thyroid hormones, limited data indicate that soy containing foods and supplements may also influence thyroid physiology. Concentrated soy isoflavones (e.g., genistein and daidzein) may interfere with thyroid peroxidase catalyzed iodination of thyroglobulin, resulting in a decreased production of thyroid hormones and an increased secretion of TSH endogenously.7 More studies are required to assess the exact mechanism of this interaction. Caution should be used in administering soy isoflavone supplements concurrently with thyroid hormones.5 Limited data show that coffee has the potential to impair T4 intestinal absorption. In one report, T4 intestinal absorption was evaluated after the administration of 200 mcg L-thyroxine (L-T4) swallowed with coffee/espresso, water, or water followed 60 minutes later by coffee/espresso. Researchers found that administration with coffee/espresso significantly lowered average serum T4 (p<0.001) and peak serum T4 concentrations (p<0.05) when compared to L-T4 taken with water alone. Coffee/espresso taken 60 minutes after L-T4 ingestion had no significant effect on T4 intestinal absorption. It is prudent to remind patients that thyroid hormones should be separated from food and beverages (other than water), including coffee, by at least 30—60 minutes.6
Cholestyramine and colestipol have also been shown to decrease the absorption of thyroid hormones.8 9 Administration should be separated by at least 4—6 hours.
Oral aluminum hydroxide, magnesium salts, calcium salts, calcium carbonate, and antacids, containing any of these electrolyte salts have been reported to chelate oral levothyroxine within the GI tract when administered simultaneously, leading to decreased absorption. Some case reports have described clinical hypothyroidism resulting from coadministration of levothyroxine with oral calcium supplements and aluminum hydroxide. To be prudent and to minimize this interaction, administer thyroid hormones at least 4 hours before or after antacids or other drugs containing aluminum, magnesium, or calcium.10 115
Concurrent use of sucralfate may reduce the efficacy of levothyroxine and other thyroid hormones by binding and delaying or preventing absorption, potentially resulting in hypothyroidism. Administer levothyroxine at least 4 hours apart from a dose of sucralfate. Patients treated concomitantly with these drugs should be monitored for changes in thyroid function. Consider an alternative to sucralfate, if appropriate.12
Polysaccharide-iron complex and other oral iron salts have been reported to chelate oral thyroid hormones within the GI tract when administered simultaneously, leading to decreased thyroid hormone absorption. Some case reports have described clinical hypothyroidism resulting from co-administration of thyroid hormones with oral iron supplements.13 To minimize the risk of interaction, oral thyroid hormones should be administered at least 4 hours before or after the ingestion of iron supplements.5
Cation exchange resins like sodium polystyrene sulfonate (i.e., Kayexalate®) can bind desiccated thyroid in the GI tract and inhibit thyroid hormone absorption. Administer thyroid hormones at least 4 hours apart from any of these agents.5
Sympathomimetic amines should be used with caution in patients with thyrotoxicosis since these patients who are unusually responsive to sympathomimetic amines. Based on the cardiovascular stimulatory effects of sympathomimetic drugs 14, the concomitant use of sympathomimetics and thyroid hormones can enhance the effects on the cardiovascular system. Patients with coronary artery disease have an increased risk of coronary insufficiency from either agent. Concomitant use of these agents may increase this risk further.
Drugs that possess hepatic enzyme-inducing properties can increase the catabolism of levothyroxine and, thus, should be used cautiously with desiccated thyroid.5 These include barbiturates 15, carbamazepine 16, hydantoins (i.e., fosphenytoin, phenytoin, or ethotoin) 17, and rifamycins (e.g., rifabutin or rifampin) 18 19. Clinicians should be alert for a decreased response to thyroid hormones if any of these agents are used during thyroid hormone therapy.
The pharmacodynamic effects of thyroid agents in the diabetic patient are poorly understood. Close monitoring of blood glucose is necessary for individuals who use insulin or oral hypoglycemics whenever there is a change in thyroid treatment therapy. Because the addition of other thyroid agents (i.e., levothyroxine, liothyronine) may require adjusted doses of antidiabetic agents when coadministered 5, it is advisable to carefully monitor the patients’ blood glucose concentrations and alter the doses of antidiabetic agents if desiccated thyroid is added or discontinued.
The coadministration of ketamine and levothyroxine has been reported to cause marked hypertension and tachycardia.5 Use caution when coadministering ketamine with any thyroid hormone.
The administration of estrogens and oral contraceptives can increase circulating concentrations of thyroxine-binding globulin. Increased amounts of thyroxine-binding globulin may result in a reduced clinical response to thyroid hormones.5 Some hypothyroid patients on estrogen may require larger doses of thyroid hormones.
The effects of indandione- or coumarin-derivative anticoagulants can be altered when thyroid agents are administered concomitantly. It has been shown that by accelerating the metabolic degradation of vitamin K-dependent clotting factors, hyperthyroidism augments the response to warfarin.20 It is possible that exogenously administered thyroid hormones may augment the response to warfarin or dicumarol. INRs should be monitored carefully in patients receiving warfarin and thyroid hormones concomitantly and the dose of the anticoagulant should be adjusted as needed.
The metabolism of corticosteroids and corticotropin (ACTH) are increased in patients with hyperthyroidism and decreased in patients with hypothyroidism. Additionally, short-term administration of large corticosteroid doses (i.e., dexamethasone) may decrease serum T3 concentrations by 30%, and long-term corticosteroid therapy may result in decreased thyroid binding globulin production, causing slightly decreased T3 and T4 concentrations.5 Therefore, caution should be taken when initiating, changing or discontinuing thyroid agents.
Amiodarone has a complex effect on the metabolism of thyroid hormones and can alter thyroid function tests in many patients. Since approximately 37% of amiodarone (by weight) is iodine, maintenance doses of 200—600 mg of amiodarone/day result in ingestion of 75—225 mg/day of organic iodide, resulting in much higher total iodine stores in the body. In addition, amiodarone decreases T4 5′-deiodinase activity, which decreases the peripheral conversion of T4 to T3, leading to decreased serum T3. Serum T4 levels are usually normal but may be slightly increased. TSH concentrations usually increase during amiodarone therapy, but after 3 months of continuous administration, TSH concentrations often return to normal. However, amiodarone can cause hypothyroidism or hyperthyroidism, including life-threatening thyrotoxicosis. Therefore, patients receiving thyroid hormones and amiodarone should be monitored for changes in thyroid function; because of the slow elimination of amiodarone and its metabolites, abnormal thyroid function tests may persists for weeks or months after amiodarone drug discontinuation.21 5
Thyroid disease is known to alter the response to digoxin. Digoxin toxicity is more likely to occur in patients with hypothyroidism, while the response to digoxin is diminished in patients with hyperthyroidism. These reactions should be kept in mind when therapy with thyroid hormones is begun or interrupted. When hypothyroid patients are administered thyroid hormone, the dose requirement of digoxin may be increased.22
Thyroid hormones may increase receptor sensitivity and enhance the effects of tricyclic antidepressants and related drugs (e.g., amoxapine 23, and maprotiline 24). Older literature describes a variety of responses when tricyclic antidepressants are used concomitantly with thyroid hormones. Thyroid hormones may accelerate the onset of action of tricyclic antidepressants; however, several case reports have described cardiovascular toxicity as a result of this drug combination; other reports describe no interaction. Although this drug combination appears to be safe, clinicians should be aware of the remote possibility of exaggerated cardiovascular side effects such as arrhythmias and CNS stimulation.
Correction of hypothyroidism to the euthyroid state may precipitate certain drug interactions. For example, hypothyroidism causes decreased clearance of theophylline, which returns to normal in the euthyroid state. Theophylline dosage adjustments may be needed with thyroid hormone replacement.5
Because thyroid hormones cause cardiac stimulation including increased heart rate and increased contractility 5, the effects of beta-blockers may be reduced by thyroid hormones. The reduction of effects may be especially evident when a patient goes from a hypothyroid to a euthyroid state or when excessive amounts of thyroid hormone are given to the patient. In addition, because liothyronine (T3) has more pronounced cardiovascular side effects when compared to levothyroxine (T4), the effects on beta-blockers may be more common in patients treated with liothyronine.
Thyroid hormones are susceptible to drug interactions with buffers/antacids containing aluminum or calcium, which may chelate thyroid hormones within the GI tract and decrease oral thyroid hormone absorption. Certain didanosine, ddI formulations contain buffers (e.g., chewable/dispersible tablets and oral powder for solution) or are mixed with antacids (e.g., pediatric oral powder for solution).25 Thyroid hormones should be administered at least 2 hours before the administration of these ddI formulations to avoid an interaction. The delayed-release didanosine capsules (e.g., Videx® EC) do not contain a buffering agent and would not be expected to interact with thyroid hormones.
Closely monitor the thyroid status of any patient taking thyroid hormones concurrently with indinavir. Hyperthyroidism was reported in a patient when indinavir was added to a stable levothyroxine dosing regimen. Indinavir inhibits UDP-glucuronosyl transferase, which may have decreased the metabolism of the thyroid hormone and may explain the increased thyroxine levels observed.26Theoretically, similar interactions may occur between indinavir and other thyroid hormones, given that both T4 and T3 are metabolized to some degree via hepatic UDP-glucuronosyl transferase.
Raloxifene may delay and reduce the oral absorption of levothyroxine (T4). In a case report, a patient with chronic but treated hypothyroidism was taking a stable dose of levothyroxine. The patient required increasing doses of levothyroxine when raloxifene was co-administered; the TSH level remained elevated and serum T4 remained decreased despite an increase in oral levothyroxine dosage. An absorption interaction was suspected and the patient rechallenged on two occasions; a decrease in serum T4 was observed whenever raloxifene and levothyroxine were administered concurrently. The patient’s levothyroxine dosage requirements returned to baseline and the TSH value normalized when levothyroxine and raloxifene were administered 12 hours apart rather than simultaneously. The mechanism for the observed interaction is unknown. In theory, raloxifene might cause malabsorption of any thyroid hormone containing T4 (e.g., desiccated thyroid, levothyroxine, liotrix) if administered at the same time. Patients prescribed raloxifene while taking these thyroid hormones should be advised to take the drugs at separate times (e.g., 12 hours apart) until more data are available.27
The concomitant use of systemic tretinoin, ATRA and thyroid hormones should be done cautiously due to the potential for increased intracranial pressure and an increased risk of pseudotumor cerebri (benign intracranial hypertension).28 Early signs and symptoms of pseudotumor cerebri include papilledema, headache, nausea, vomiting, and visual disturbances.29 30
In order to increase thyroid uptake and optimize exposure of thyroid tissue to the radionucleotide sodium iodide I-131, patients must discontinue all medications and supplements that may interfere with iodide uptake into thyroid tissue prior to therapy with sodium iodide I-131. Although various protocols are used, a procedure guideline published by the Society of Nuclear Medicine in February 2002 recommends that all T4 thyroid hormones, such as levothyroxine, be discontinued 4—6 weeks and that all T3 thyroid hormones, such as liothyronine, be discontinued 2 weeks prior to sodium iodide I-131 therapy.31
The manufacturer for colesevelam suggests monitoring serum drug concentrations and/or clinical effects for those drugs for which alterations in serum blood concentrations have a clinically significant effect on safety or efficacy.32 To minimize potential for interactions, consider administering oral drugs with a narrow therapeutic index, such as desiccated thyroid, at least 4 hours before colesevelam. There have been rare reports of elevated thyroid stimulating hormone (TSH) concentrations in patients who have received colesevelam coadministered with thyroid hormone replacement therapy.32
Excessive use of thyroid hormones with growth hormone (somatropin, rh-GH) may accelerate epiphyseal closure. However, untreated hypothyroidism may interfere with growth response to somatropin. Patients receiving concomitant therapy should be monitored closely to ensure appropriate therapeutic response to somatropin.5
Lithium therapy can result in goiter in up to 50% of patients, and subclinical or overt hypothyroidism in up to 20% of patients. Lithium decreases thyroid hormone synthesis and secretion leading to hypothyroidism after long-term use. Prevalence of hypothyroidism appears to be highest in women and in those patients over the age of 50, with a family history of hypothyroidism.33 Patients receiving thyroid hormones should be monitored for changes in thyroid function when lithium is either initiated or discontinued.5
Simethicone has been reported to chelate oral thyroid hormones within the GI tract when administered simultaneously, leading to decreased thyroid hormone absorption. To minimize the risk of interaction, oral thyroid hormones should be administered at least 4 hours before or after the ingestion of simethicone.5
Sevelamer could potentially decrease the oral absorption of other medications; the alteration can be clinically significant for drugs with a narrow therapeutic window such as the thyroid hormones.34 In one study of normal volunteers, the subjects (n=7) ingested orally levothyroxine sodium, either taken separately or co-administered with sevelamer. Serum thyroxine was measured at intervals over a 6-hour period following drug ingestion. Sevelamer significantly (p <0.05) decreased the area under the serum thyroxine concentration curve. The authors concluded that patients should be advised to separate the time of ingestion of sevelamer from their thyroid hormone preparation.35 Administering levothyroxine 4 hours before or after sevelamer may minimize the potential for an interaction.34
Chromium could potentially decrease the oral absorption of thyroid hormones. In one study of normal volunteers, the subjects (n=7) ingested orally levothyroxine sodium, either taken separately or co-administered with chromium picolinate. Serum thyroxine was measured at intervals over a 6-hour period following drug ingestion. Chromium picolinate significantly (p <0.05) decreased the area under the serum thyroxine concentration curve. The authors concluded that patients should be advised to separate the time of ingestion of chromium from their thyroid hormone preparation.35 Administering levothyroxine 1 hours before or 3 hours after chromium picolinate ingestion, for example, should minimize the potential for an interaction.
This list may not include all possible drug interactions.  Give your health care provider a list of all the medicines, herbs, non-prescription drugs, or dietary supplements you use. Also tell them if you smoke, drink alcohol, or use illegal drugs. Some items may interact with your medicine.

Monitor for signs and symptoms of hypothyroidism that could require an upward adjustment of the desiccated thyroid dosage. Signs or symptoms of underdosage or hypothyroidism include constipation, cold intolerance, dry skin (xerosis) or hair, fatigue, impaired intellectual performance or other mental status changes (e.g., depression), deepening of voice, lethargy, weight gain, tongue enlargement, and, eventually, myxedema coma.
Adverse reactions to desiccated thyroid are rare. Adverse reactions usually indicate inappropriate dosage of the hormone. No well-documented evidence from the literature of true allergic or idiosyncratic reactions to thyroid hormone exist.36
Transient partial alopecia may occur in children in the first few months of desiccated thyroid treatment, but normal hair growth usually recovers.36 Alopecia may be due to hyperthyroidism from therapeutic overdosage or to hypothyroidism from therapeutic underdosage.12
Many of the signs and symptoms of thyroid hormone imbalance are subtle and insidious. Manifestations of desiccated thyroid excessive dosage or hyperthyroidism include anorexia, diaphoresis, diarrhea, dyspnea, elevated hepatic enzymes, emotional lability, fatigue, fever, flushing, headache, heat intolerance, hyperactivity, appetite stimulation, infertility, irritability, insomnia, menstrual irregularity (e.g., amenorrhea), muscle weakness, muscle cramps, nausea, vomiting, nervousness or anxiety, tremor, and weight loss. The clinician should be alert to constellations of symptoms that gradually worsen over time.12
Pseudotumor cerebri has been reported in patients receiving thyroid hormone replacement therapy such as desiccated thyroid.12 Symptoms such as headache, papilledema, and elevated opening pressures on lumbar puncture may occur within weeks of starting thyroid hormone replacement therapy and must be differentiated from brain metastases, if applicable. 37
In infants, excessive doses of thyroid hormone preparations such as desiccated thyroid may produce craniosynostosis.36 Also, undertreatment may result in slowed reduced adult height, and overtreatment may accelerate the bone age and result in premature epiphyseal closure and compromised adult stature (growth inhibition). Slipped capital femoral epiphysis has been reported in children receiving levothyroxine.12
Overtreatment with thyroid hormone such as desiccated thyroid may have adverse cardiovascular effects such as an increase in heart rate, cardiac wall thickness, and cardiac contractility and may precipitate angina or arrhythmias. Symptoms may include palpitations, sinus tachycardia, arrhythmias, hypertension, heart failure, angina, myocardial infarction, and cardiac arrest.12 Peripheral edema may also occur. Patients with subclinical hyperthyroidism, either from excessive thyroid hormone replacement or other, may also be at an increased risk for atrial fibrillation. One study compared elderly patients (mean age 65 years) with subclinical hyperthyroidism to euthyroid subjects for 2 years; atrial fibrillation was initially recorded in 8 patients and 3 additional patients developed atrial fibrillation during follow-up; the data correspond to a total incidence of atrial fibrillation of 28% in subclinical hyperthyroidism patients compared to 10% in euthyroid subjects.38 Lower initial doses of desiccated thyroid are advised for patients where compromised integrity of the cardiovascular system, particularly the coronary arteries, is suspected or known such as patients with angina pectoris or the elderly. Also, reduce the dose in such patients if a euthyroid state can only be reached at the expense of an aggravation of the cardiovascular disease. Closely monitor infants for cardiac overload, arrhythmias, and aspiration from avid suckling during the first 2 weeks of thyroid hormone replacement.12 36
Administration of too much desiccated thyroid may lead to osteopenia and osteoporosis. Suppressed serum thyrotropin (TSH) concentrations by use of another thyroid hormone levothyroxine was associated with bone loss and the potential increased risk for osteopenia and the premature development of osteoporosis. Because estrogen plays a protective role against bone loss, this increased risk is thought to be relevant in postmenopausal women receiving prolonged thyroid therapy. In a meta-analysis that pooled study data on the effects of slight over treatment with levothyroxine on pre- and postmenopausal women, a significant reduction in bone mass was observed in the postmenopausal study groups. Pooled study data contained skeletal measurements of the distal forearm, femoral neck, and lumbar spines of postmenopausal women. For all postmenopausal women, a theoretical bone consisting of 11.3% distal forearm, 42% femoral neck, and 46.7% lumbar spine was constructed (n = 317 measurements). Data showed that a postmenopausal woman at an average age of 61.2 years and treated with levothyroxine for 9.93 years (leading to suppressed serum TSH) would have an excess loss of bone mass of 9.02%; corresponding to an excess annual loss of 0.91% after 9.93 years of levothyroxine treatment as compared to healthy postmenopausal women.3940
This list may not include all possible adverse reactions or side effects. Call your health care provider immediately if you are experiencing any signs of an allergic reaction: skin rash, itching or hives, swelling of the face, lips, or tongue, blue tint to skin, chest tightness, pain, difficulty breathing, wheezing, dizziness, red, a swollen painful area/areas on the leg.

11. Singh N, Weisler SL, Hershman JM. The acute effect of calcium carbonate on the intestinal absorption of levothyroxine. Thyroid 2001;11:967—71.

12. Synthroid (levothyroxine) tablets. North Chicago, IL: Abbott Pharmaceuticals; 2012 Sep.

13. Campbell N. Ferrous sulfate reduces thyroxine efficacy in patients with hypothyroidism. Ann Int Med Gericke KR. Possible interaction between warfarin and fluconazole. Pharmacotherapy 1993;13:508—9.2;117:1010.

14. Hoffman BB, Lefkowitz RJ. Catecholamines and sympathomimetic drugs. Gilman AG, Rall TW, Nies AS, Taylor P, (eds.) In: Goodman and Gilman’s Pharmacological Basis of Therapeutics. 8th ed., New York, Pergamon Press. Gericke KR. Possible interaction between warfarin and fluconazole. Pharmacotherapy 1993;13:508—9.0. 187—91.

15. Hansten P, Horn J. The Top 100 Drug Interactions: A Guide to Patient Management. includes table of CYP450 and drug transporter substrates and modifiers (appendices). H & H Publications, LLP 2014 edition.

16. Tegretol® (carbamazepine) package insert. East Hanover, NJ. Novartis Pharmaceuticals; 2003 Sept.

17. Dilantin® Kapseals® (extended phenyotin sodium capsules, USP) package insert. Morris Plains, NJ: Parke Davis; Gericke KR. Possible interaction between warfarin and fluconazole. Pharmacotherapy 1993;13:508—9.9 Aug.

18. Finch CK, Chrisman CR, Baciewicz AM, et al. Rifampin and rifabutin drug interactions: an update. Arch Intern Med 2002;162:985—92.

19. Rifampin Injection package insert. Bedford, OH: Bedford Laboratories; 2000 Nov.

20. Gericke KR. Possible interaction between warfarin and fluconazole. Pharmacotherapy 1993;13:508—9.

21. Cordarone® (amiodarone) package insert. Philadelphia, PA: Wyeth Laboratories; 2007 Mar.

22. Lanoxin® (digoxin) package insert. Research Triangle Park, NC: Glaxo Smith Kline; 2001 Aug.

23. Amoxapine package insert. Corona, CA: Watson Laboratories, Inc.; 2007 Aug.

24. Ludiomil (maprotiline hydrochloride) package insert. Summit, NJ: Ciba-Geigy Corporation; 1996 Nov.

25. Videx® (didanosine chewable/dispersible buffered tablets and pediatric powder for oral solution) package insert. Princeton, NJ: Bristol-Myers Squibb Company; 2006 Jan.

26. Lanzafame M, Trevenzoli M, Faggian F, et al. Interaction between levothyroxine and indinavir in a patient with HIV infection. Infection 2002;30:54—5.

27. Siraj ES, Gupta MK, Reddy SK. Raloxifene causing malabsorption of levothyroxine. Arch Intern Med 2003;163:1367—70.

28. Vesanoid® (tretinoin) capsules package insert. Nutley, NJ: Roche Laboratories Inc.; 2004 Oct.

29. Griffin JP. A review of the literature on benign intracranial hypertension associated with medication. Adverse Drug React Toxicol Rev 1992;11:41—57. Review.

30. Lee AG. Pseudotumor cerebri after treatment with tetracycline and isotretinoin for acne. Cutis 1995;55:165—8. Review.

31. Meier DA, Brill DR, Becker DV, et al. Society of Nuclear Medicine procedure guideline for therapy of thyroid disease with iodide-131 (sodium iodide). Retrieved January 26, 2006. Available on the World Wide Web at http://interactive.snm.org/docs/Therapy%20of%20Thyroid%20Disease%20with%20Iodine-131%20v2.0.pdf

32. Welchol® (colesevelam) tablets package insert. Parsipanny, NJ: Daiiki Sankyo; 2006 Sept

33. Freeman MP, Freeman SA. Lithium: clinical considerations in internal medicine. Am J Med 2006;119:478—81.

34. Renagel® (sevelamer) package insert. Cambridge, MA: Genzyme Corporation; 2004 Feb.

35. Kalarickal J, Pearlman G, Carlson HE. New medications which decrease levothyroxine absorption. Thyroid 2007;17:763—5.

36. Armour Thyroid (thyroid tablets) package insert. St. Louis, MO: Forest Pharmaceuticals, Inc.; 2011 Jan.

37. Panza N, DeRosa M, Lombardi G, et al. Pseudotumor cerebri and thyroid-replacement therapy in patients affected by differentiated thyroid carcinoma. J Endocrinol Invest 1985;8:357-358.

38. Tenerz A, Forberg R, Jansson R. Is a more active attitude warranted in patients with subclinical thyrotoxicosis? J Int Med 1990;228:229-233.

39. Samuels MH. Subclinical thyroid disease in the elderly. Thyroid 1998;8:803-13.

40. Faber J, Galloe AM. Changes in bone mass during prolonged subclinical hyperthyroidism due to L-thyroxine treatment: a meta-analysis. Eur J Endocrinol 1994;130:350-6.