Thyroid Disorders
Clinical Snapshot
Thyroid disease is extremely common and often presents with vague, nonspecific symptoms, so a high index of suspicion combined with a low threshold for TSH testing is what actually catches most affected patients.[1] Hypothyroidism is a state of thyroid hormone deficiency — most often autoimmune (Hashimoto thyroiditis) in an iodine-sufficient country like Canada — treated with lifelong levothyroxine replacement dosed and monitored to normalize TSH. Hyperthyroidism (thyrotoxicosis) is a state of thyroid hormone excess, most often Graves disease, managed with thionamides, radioactive iodine, or surgery depending on patient factors and preference.[2] Both conditions range from mild, largely asymptomatic biochemical abnormalities (subclinical disease) to true endocrine emergencies — myxedema coma and thyroid storm — and both need individualized management across pregnancy, older age, and cardiac disease. This chapter focuses on hypothyroidism and hyperthyroidism; thyroid nodules and goitre are a separate clinical pathway not covered here.
Recognize the Condition
Symptoms of both hypothyroidism and hyperthyroidism are frequently nonspecific and develop gradually, so patients — and sometimes clinicians — often attribute them to aging, stress, or another chronic condition rather than the thyroid.
Two presentations, opposite direction
Hypothyroidism
Fatigue, cold intolerance, constipation, weight gain, dry skin and coarse hair, hoarse voice, impaired memory or concentration, menstrual irregularities, and depressive symptoms. Exam findings include bradycardia, diastolic hypertension, delayed relaxation phase of deep tendon reflexes, non-pitting edema (myxedema), and a goitre in some autoimmune or iodine-deficiency cases. The extreme end of the spectrum is myxedema coma — hypotension, hypothermia, and a decreasing level of consciousness (see Red Flags & Refer).
Hyperthyroidism (thyrotoxicosis)
Unintentional weight loss despite a normal or increased appetite, palpitations, heat intolerance, diarrhea, anxiety, tremor, and insomnia. Exam findings include tachycardia (often atrial fibrillation in older adults), lid lag and stare, hyperreflexia, warm and moist skin, and a goitre or thyroid bruit. Graves disease specifically can also produce orbitopathy (proptosis, periorbital edema, diplopia) and, less commonly, pretibial myxedema (thickened, non-pitting skin over the shins). The extreme end of the spectrum is thyroid storm — severe tachycardia, hyperthermia, and altered mental status (see Red Flags & Refer).
Subclinical disease is common and, by definition, produces few or no symptoms — an elevated TSH with a normal free T4 defines subclinical hypothyroidism, and a suppressed TSH with normal free T3/T4 defines subclinical hyperthyroidism (see Assessment & Diagnosis for when to treat).
Risk Factors
- Female sex, and a personal or family history of autoimmune thyroid disease or another autoimmune condition (type 1 diabetes, celiac disease, vitiligo, pernicious anemia).
- Prior thyroid surgery, radioactive iodine therapy, or prior external neck/upper-chest irradiation.
- The postpartum period — postpartum thyroiditis can cause a transient hyperthyroid phase, a transient hypothyroid phase, or both in sequence.
- Drugs that can cause hypothyroidism: amiodarone, lithium, iodinated contrast agents, sulfonylureas, and immune checkpoint inhibitors or other immunotherapy.
- Drugs and exposures that can cause or unmask hyperthyroidism: excess iodine intake, including amiodarone, iodinated contrast, and kelp/seaweed supplements — and, rarely, overtreatment with thyroid hormone itself.
- Iodine deficiency (rare in Canada) or iodine excess.
- Older age — a risk factor for thyroid dysfunction generally, and a population where the threshold to treat subclinical hyperthyroidism is lower given atrial fibrillation and bone risk.
- Pregnancy and the immediate postpartum period, given the physiologic rise in thyroid-binding globulin and hCG-driven TSH suppression in the first trimester.
Red Flags & Refer
Both extremes of thyroid dysfunction have a true medical emergency — recognize them early and escalate immediately rather than managing them as routine hypo- or hyperthyroidism.
- Myxedema coma — altered mental status (confusion, lethargy, coma), hypothermia, and bradycardia/hypotension in a patient with severe, usually longstanding untreated hypothyroidism. This is a true endocrine emergency requiring immediate hospital transfer, intravenous levothyroxine, and intravenous corticosteroid — do not manage as outpatient hypothyroidism.
- Thyroid storm — severe tachycardia (often with atrial fibrillation), hyperthermia, and altered mental status or agitation in a patient with severe thyrotoxicosis, frequently triggered by infection, surgery, trauma, iodinated contrast, or abrupt thionamide discontinuation. This is a true endocrine emergency requiring immediate hospital transfer and urgent multi-drug therapy in a monitored setting — do not manage as outpatient hyperthyroidism.
- Agranulocytosis on thionamide therapy — any sore throat, fever, or mouth ulcers in a patient taking methimazole or propylthiouracil requires the patient to stop the drug and get an immediate CBC; do not wait for a scheduled follow-up. Most cases occur within the first 90 days of treatment but can occur at any time.
- Propylthiouracil-associated hepatotoxicity — jaundice, dark urine, pale stools, right-upper-quadrant pain, or unexplained fatigue in a patient taking propylthiouracil requires stopping the drug immediately and urgent liver function testing; this reaction can progress to fulminant liver failure.
- New or worsening Graves orbitopathy (proptosis, diplopia, visual change) — refer to ophthalmology urgently; vision-threatening orbitopathy needs specialist management independent of thyroid hormone control.
- New atrial fibrillation or another new arrhythmia in a thyrotoxic patient.
- TSH persistently out of target range despite appropriate dose adjustment, or any thyroid dysfunction in pregnancy requiring antithyroid drug therapy — refer to or consult endocrinology.
Assessment & Diagnosis
History and physical examination
Ask specifically about the symptom clusters above, the pace of onset, family history of thyroid or other autoimmune disease, current medications (amiodarone, lithium, biotin-containing supplements), pregnancy status/plans, and — for suspected hyperthyroidism — eye symptoms and any recent iodine exposure (contrast, amiodarone). Examine for goitre, nodules, tremor, reflexes, heart rate and rhythm, and — when Graves disease is suspected — orbitopathy and pretibial skin changes.
Laboratory testing
TSH alone is the correct initial test for suspected primary thyroid dysfunction — it is far more sensitive than free T4 for picking up mild disease, and is the single test needed to screen. Add free T4 (and free T3 for suspected hyperthyroidism) only once TSH is abnormal.[1]
Order anti-TPO antibodies only when the result will actually change management (for example, confirming an autoimmune cause when it affects a shared decision about treating subclinical disease) — do not order it reflexively with every abnormal TSH.
Order thyrotropin receptor antibodies (TRAb) when the cause of confirmed thyrotoxicosis is not clear on history and exam; a clearly positive TRAb in a patient with typical Graves features can substitute for a radioactive iodine uptake scan. Thyroid scintigraphy and radioactive iodine uptake are contraindicated in pregnancy and lactation.
Discontinue biotin supplements at least 48 hours before thyroid testing — biotin interferes with many common immunoassay platforms and can produce a falsely low TSH with falsely elevated free T4/T3, mimicking hyperthyroidism.
When testing is not indicated
Routine population screening for thyroid dysfunction in asymptomatic, average-risk, nonpregnant adults is not recommended — reserve testing for patients with symptoms, risk factors, or a specific indication such as preconception or early pregnancy assessment.[3] A thyroid scan is rarely needed when TSH is normal or high, since scintigraphy is a test for the cause of thyrotoxicosis, not for hypothyroidism.
Subclinical disease — definitions and when to treat
Subclinical hypothyroidism is an elevated TSH with a normal free T4. Treatment is not routinely recommended for most adults, since randomized evidence does not show a consistent symptom or outcome benefit — but treatment should be considered specifically for a TSH over 10 mU/L, significant hypothyroid symptoms, an abnormal lipid profile, or a patient who is pregnant or planning pregnancy.[4]
Subclinical hyperthyroidism is a suppressed TSH with normal free T3 and free T4. It is a recognized risk factor for atrial fibrillation and for bone loss, so treatment is generally indicated for older or frail patients, those with other atrial fibrillation risk factors, those with osteoporosis, or those with hyperthyroid symptoms — even though free hormone levels are technically normal.[2]
Recognizing the two emergencies clinically
Myxedema coma and thyroid storm are clinical diagnoses made at the bedside — there is no single lab value that confirms either one, and severe biochemical hypothyroidism or hyperthyroidism can exist without either syndrome being present. The Burch-Wartofsky point scale is a validated bedside scoring tool that can support, but not replace, the clinical diagnosis of thyroid storm when the picture is ambiguous.[5]
Treatment Targets
- Normalize TSH (and free T4/T3 in hyperthyroidism) and resolve symptoms — in pregnancy, target free hormone levels and trimester-specific TSH ranges rather than the standard non-pregnant reference range.
- Avoid overtreatment in both directions — over-replaced hypothyroidism causes iatrogenic thyrotoxicosis and, in older adults, increased fracture risk; under-treated hyperthyroidism risks thyroid storm, arrhythmia, and bone loss.
- Prevent, and promptly recognize, the two thyroid emergencies — myxedema coma and thyroid storm.
- Protect fertility and fetal/neonatal outcomes in patients who are pregnant or planning pregnancy.
- Select a definitive strategy for hyperthyroidism — long-term thionamide, radioactive iodine, or surgery — that matches the patient's goals, orbitopathy status, and pregnancy plans.
Choose Initial Treatment
Confirm the diagnosis and direction before treating
Base initial therapy on a confirmed elevated or suppressed TSH with the corresponding free hormone abnormality — never start levothyroxine or a thionamide on symptoms alone.
Two treatment tracks
Hypothyroidism — levothyroxine replacement
1st line start levothyroxine at a full weight-based replacement dose of about 1.6 mcg/kg/day PO once daily in most otherwise healthy adults under about 60-65 years of age.[1]
Older adults, or known/suspected coronary artery disease start low — 12.5-25 mcg/day PO — and titrate slowly, since a full replacement dose can precipitate angina or arrhythmia in an undiagnosed or unstable coronary patient.
Administration timing (a major, frequently tested counselling point): take levothyroxine on an empty stomach with a full glass of water, 30-60 minutes before breakfast — or, as a consistent alternative, at bedtime at least 3 hours after the last meal. Pick one approach and keep it the same every day; food, coffee, and proximity to a meal all measurably reduce absorption.
Drug-interaction spacing: separate levothyroxine by at least 4 hours from calcium carbonate/calcium supplements, iron salts, sucralfate, and aluminum- or magnesium-containing antacids, and from cholestyramine or colestipol (ideally take levothyroxine 4-5 hours before, or at least 1 hour after, a bile-acid resin) — all of these reduce levothyroxine absorption through chelation or binding in the gut. A proton pump inhibitor does not need a fixed-hour separation but reduces the gastric acidity needed for tablet dissolution, so recheck TSH after starting or stopping one.
Retitration recheck TSH 6-8 weeks after starting therapy or after any dose change — it takes about 6 weeks to reach a new steady state — adjust the dose based on that result, recheck again 6-8 weeks after any further change until stable, then at least annually once stable or sooner if new symptoms arise.
Hyperthyroidism — thionamide, beta-blocker, and definitive therapy
1st line thionamide methimazole 10-30 mg/day PO in 2-3 divided doses (once-daily dosing is often adequate for milder disease) — preferred over propylthiouracil for most adults and children given a lower risk of serious hepatotoxicity.[2]
Use propylthiouracil instead only in the first trimester of pregnancy, in thyroid storm, or when a patient cannot tolerate methimazole and drug therapy is still required — the hepatotoxicity risk means it is never a routine first choice.
Add a beta-blocker — propranolol or a cardioselective alternative — for symptomatic control of tachycardia, tremor, and anxiety while the thionamide takes effect over the following weeks; beta-blockers control symptoms but do not lower thyroid hormone production themselves.
Definitive therapy radioactive iodine or surgery are specialist-directed options for Graves disease, a toxic nodule, or a toxic multinodular goitre once the patient is euthyroid or near-euthyroid on a thionamide; radioactive iodine is contraindicated in pregnancy, and surgery is preferred when pregnancy is planned in the near term or significant orbitopathy is present.
Non-Pharmacologic Treatment
- Reinforce consistent levothyroxine timing and, where possible, a consistent product/manufacturer — switching between brand and generic (or between generics) can shift bioavailability enough to warrant a TSH recheck after any switch.
- Counsel on iodine intake: adequate but not excessive. Discourage high-dose iodine or kelp/seaweed supplements, especially in Graves disease, since excess iodine can worsen or trigger thyrotoxicosis.
- Smoking cessation is a specific, high-yield counselling point in Graves orbitopathy — smoking significantly worsens the severity and treatment response of thyroid eye disease, more than for almost any other modifiable factor.
- Advise patients with mild Graves orbitopathy to discuss selenium supplementation with their eye-care specialist as an adjunct — see Drug Tables.
- Discuss fitness to drive if fatigue, impaired concentration, or tremor is significant enough to impair judgment or motor skills.
- Educate every patient started on a thionamide, before symptoms occur, about the specific warning symptoms — sore throat, fever, mouth sores, jaundice, dark urine — that require stopping the drug and seeking immediate care.
- Support adherence counselling for lifelong levothyroxine therapy — hypothyroidism symptoms often return gradually enough that patients underestimate the impact of missed doses.
Special Populations
Pregnancy — hypothyroidism
Levothyroxine is safe and important throughout pregnancy; reassure patients accordingly. Patients already on levothyroxine should increase their dose by about 2 extra tablets per week (roughly a 29% increase) as soon as pregnancy is confirmed, then adjust further based on TSH.[6] Requirements commonly rise by up to 50% overall during pregnancy because thyroid-binding globulin increases; recheck TSH every 4 weeks through the first trimester, then every 6 weeks until about 32 weeks gestation, and again 4-6 weeks after any dose change. In a patient not yet on levothyroxine, treat if TSH is confirmed over 4 mU/L (using a local pregnancy-specific reference range where available), or start regardless of trimester at a TSH over 10 mU/L. Postpartum, thyroid hormone requirements return to prepregnancy levels — plan to reduce the dose back down and recheck.
Pregnancy — hyperthyroidism
Propylthiouracil is preferred over methimazole specifically in the first trimester given a lower risk of methimazole-associated congenital malformations; switch back to methimazole after the first trimester if disease control allows, to reduce cumulative hepatotoxicity risk. Use the lowest antithyroid drug dose that controls the disease, and target free T4/free T3 near the upper limit of normal rather than titrating to TSH, since TSH is expected to stay low even with adequate control. Measure TRAb at the time pregnancy is confirmed and again around 18-22 weeks; if positive, repeat at 30-34 weeks and arrange specialist fetal monitoring, since a high titre carries a real risk of fetal or neonatal hyperthyroidism.[6] Radioactive iodine and thyroid scintigraphy are contraindicated throughout pregnancy.
Breastfeeding
Levothyroxine is safe during breastfeeding at usual replacement doses. For hyperthyroidism, methimazole is preferred over propylthiouracil during breastfeeding — the reverse of the first-trimester-pregnancy preference — because of propylthiouracil's hepatotoxicity risk with more prolonged use; propylthiouracil can still be used if methimazole is not tolerated. Radioactive iodine is contraindicated while breastfeeding and must be postponed until breastfeeding has stopped.
Older adults
Start levothyroxine low (12.5-25 mcg/day) and titrate slowly regardless of cardiac history, since subclinical coronary disease is common in this group. Treat subclinical hyperthyroidism more readily than in younger adults, given the added atrial fibrillation and osteoporosis risk. Watch specifically for over-replacement, since a suppressed TSH from excess levothyroxine is itself linked to increased fracture risk in older patients.
Cardiac disease
Start levothyroxine at the lowest end of the dosing range (as low as 12.5 mcg/day) with slow titration to avoid precipitating angina or arrhythmia. Use beta-blockers cautiously in decompensated heart failure. Untreated hyperthyroidism itself drives high-output heart failure and atrial fibrillation, so undertreatment carries its own real cardiac risk — the goal is careful, monitored correction in either direction, not avoidance of treatment.
Renal and hepatic impairment
Reduce the propylthiouracil dose in significant renal impairment. Use thionamides cautiously in hepatic impairment given their intrinsic hepatotoxicity risk, and obtain baseline liver function tests before starting either agent.
Pediatrics
Newborn levothyroxine replacement — for example, in congenital hypothyroidism — is dosed much higher per kilogram than in adults, at about 10-15 mcg/kg/day. Methimazole is preferred over propylthiouracil in children of any age; propylthiouracil should be avoided in children given its hepatotoxicity risk relative to the benefit in this population.
Monitoring & Follow-Up
For hypothyroidism, recheck TSH 6-8 weeks after starting levothyroxine or after any dose change, then at least annually once stable, or sooner if new symptoms arise. In pregnancy, recheck every 4 weeks in the first trimester, then every 6 weeks to about 32 weeks gestation, and 4-6 weeks after any dose adjustment.
For hyperthyroidism, obtain a baseline CBC and liver function tests (ALT, bilirubin) before starting a thionamide. Routine periodic repeat testing for neutropenia or hepatic injury is not required in an asymptomatic patient, but suspect either complication — and check immediately — within the first 3-4 months of starting therapy, or whenever fever, sore throat, or jaundice develops. Hepatic enzymes are frequently mildly elevated in untreated hyperthyroidism itself, independent of any drug effect. Monitor TSH, free T3, and free T4 every 4-6 weeks until stable, then every 3 months; expect TSH to remain suppressed for some time even after free hormone levels normalize, so trend free T4/T3 rather than TSH early in treatment.
Reassess fitness to drive at follow-up if cardiac, neurologic, or muscular symptoms remain uncontrolled.
Common Errors to Avoid
- Taking levothyroxine with food, coffee, or too close to calcium, iron, or a proton pump inhibitor — the single most common preventable cause of an apparently inadequate response.
- Rechecking TSH before 6 weeks after a dose change and over-adjusting based on a value that has not yet reached a new steady state.
- Continuing propylthiouracil past the first trimester of pregnancy without revisiting the option of switching back to methimazole.
- Dismissing a sore throat or fever in a patient on a thionamide as just a cold instead of stopping the drug and getting an immediate CBC.
- Treating subclinical hypothyroidism reflexively in every patient with a mildly elevated TSH, without checking the TSH threshold, symptoms, lipid profile, or pregnancy status first.
- Using liothyronine alone as thyroid hormone replacement in pregnancy — it does not cross the placenta.
- Giving iodine solution before the thionamide in thyroid storm — giving it first, or without a thionamide already on board, can worsen thyrotoxicosis by providing substrate for new hormone synthesis; it must follow the thionamide dose by at least 1 hour.
- Using ASA or another NSAID for fever in thyroid storm — these displace protein-bound thyroid hormone and raise free hormone levels; use acetaminophen instead.
- Ordering thyroid function tests without asking about biotin supplement use, risking a falsely reassuring or falsely alarming result.
Clinical Decision Algorithm
Drug Tables
How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment. Select any drug name to open its complete Pharmasist Drug Database page.
Thyroid hormones
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Levothyroxine | Adults (standard replacement): About 1.6 mcg/kg/day PO once daily Elderly or known/suspected coronary artery disease (starting dose): 12.5-25 mcg/day PO, titrated upward every 4-6 weeks as tolerated Newborns/infants (e.g., congenital hypothyroidism): 10-15 mcg/kg/day PO Pregnancy: Increase by about 2 extra tablets/week immediately after a positive pregnancy test, then adjust by TSH every 4 weeks in the first trimester and every 6 weeks to about 32 weeks Myxedema coma (emergency): 200-400 mcg IV loading dose, then 1.6 mcg/kg/day IV or PO, with concomitant IV hydrocortisone | Symptoms of overtreatment if the dose is too high (palpitations, tremor, insomnia, heat intolerance, worsened angina); over-replacement is linked to increased fracture risk in older adults. | Absorption reduced by calcium, iron, antacids, sucralfate, and bile-acid resins (see the interaction table below); requirements can rise with estrogen therapy, proton pump inhibitors, phenytoin, carbamazepine, or rifampin; can potentiate warfarin; glycemic control may need adjustment after starting. | Take on an empty stomach, 30-60 minutes before food, or at bedtime at least 3 hours after the last meal - pick one and keep it consistent. Recheck TSH 6-8 weeks after any dose change. |
| Liothyronine | Adjunct to levothyroxine: 5-12.5 mcg/day PO added to levothyroxine, with a small levothyroxine dose reduction as needed to keep TSH in range Thyroid cancer, short-term L-T4 withdrawal preparation: Up to 25 mcg PO BID for short-term use, per specialist direction | Symptoms of overtreatment; fluctuating T3 levels with sustained-release formulations may increase atrial fibrillation risk. | Same absorption interactions as levothyroxine; not reported to interact significantly with iron salts. | Not a substitute for levothyroxine as routine monotherapy - the short half-life makes TSH control less stable. Does not cross the placenta, so it must not be used alone for replacement in pregnancy. |
Antithyroid agents (thionamides)
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Methimazole | Adults (usual): 10-30 mg/day PO in 2-3 divided doses Thyroid storm (if used instead of PTU): 20-30 mg PO/NG Q4-6H, per institutional/critical-care protocol | Rash, arthralgia, allergic reaction, agranulocytosis, rare hepatotoxicity. | Thyroid status affects warfarin response - monitor INR whenever the antithyroid drug dose changes. | Preferred first-line thionamide, including in children, except during the first trimester of pregnancy (use propylthiouracil instead) - methimazole is, conversely, preferred over propylthiouracil during breastfeeding. Warn patients to stop the drug and seek care immediately for rash, fever, sore throat, or jaundice. |
| Propylthiouracil | Adults (usual): 50-150 mg PO TID, adjusted to response Pregnancy (first trimester): Lowest dose that keeps free T4/T3 near the upper limit of normal; switch back to methimazole after the first trimester if control allows Thyroid storm: 500-1000 mg PO/NG loading dose, then 250 mg PO/NG Q4H (up to 1200 mg/day divided) | Rash, allergic reaction, agranulocytosis, severe (sometimes fatal) hepatotoxicity. | Thyroid status affects warfarin response - monitor INR whenever the antithyroid drug dose changes. | Reserve for the first trimester of pregnancy, thyroid storm, or genuine methimazole intolerance - never a routine first choice given the hepatotoxicity risk. Avoid in children. Reduce the dose in significant renal impairment. Warn patients to stop the drug and seek care immediately for rash, fever, sore throat, or jaundice. |
Beta-blockers
Used adjunctively for adrenergic symptom control in every hyperthyroid patient without a contraindication; taper once thyrotoxicosis has improved rather than stopping abruptly.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Propranolol | Hyperthyroidism, symptom control: 10-40 mg PO QID Thyroid storm: 60-80 mg PO Q4H, or 0.5-1 mg IV slowly Q4-6H if no evidence of cardiac decompensation | Bradycardia, hypotension, fatigue, dizziness, bronchospasm. | Additive bradycardia with digoxin or nondihydropyridine calcium channel blockers; additive cardiodepressant effect with amiodarone. | Also blocks peripheral conversion of T4 to T3 at these doses, which is useful in severe thyrotoxicosis and thyroid storm specifically. Avoid in asthma, decompensated heart failure, or conditions associated with bradycardia. |
| Atenolol | Adults: 25-50 mg PO daily initially, may increase to 200 mg daily | Bradycardia, hypotension, fatigue, dizziness. | Additive bradycardia with digoxin or nondihydropyridine calcium channel blockers; additive cardiodepressant effect with amiodarone. | Cardioselective alternative when a nonselective beta-blocker is unsuitable (for example, reactive airway disease); does not block peripheral T4-to-T3 conversion. |
| Metoprolol | Adults: 50 mg PO QID, may increase to 100 mg QID | Bradycardia, hypotension, fatigue, dizziness. | Additive bradycardia with digoxin or nondihydropyridine calcium channel blockers; additive cardiodepressant effect with amiodarone. | Cardioselective alternative with a faster onset in some patients than propranolol; does not block peripheral T4-to-T3 conversion. |
Corticosteroids (thyroid emergencies)
Reserved for emergency adjunctive management, in conjunction with specific antithyroid therapy - not used in routine, non-emergency hypo- or hyperthyroidism.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Dexamethasone | Thyroid storm: 2 mg IV or PO Q6H, continued until free T3 is controlled | Hyperglycemia, mood changes, and the broader range of systemic corticosteroid effects, especially with prolonged use. | Effects may be diminished by concomitant enzyme-inducing drugs such as phenytoin. | Reduces peripheral T4-to-T3 conversion and provides glucocorticoid support in thyroid storm. |
| Hydrocortisone sodium succinate | Myxedema coma: 100 mg IV Q8H, tapered once stable | Hyperglycemia, mood changes, and the broader range of systemic corticosteroid effects, especially with prolonged use. | Effects may be diminished by concomitant enzyme-inducing drugs such as phenytoin. | Given in myxedema coma because coexisting adrenal insufficiency cannot be excluded at presentation; taper once the patient is stable. |
Iodine, selenium, and antipyretics
The Database's existing iodine, iodide, and selenium monograph slugs are formulation mismatches for this chapter and are intentionally not linked here - see the class note in each row.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Iodine solution (Lugol solution, or a saturated solution of potassium iodide) | Thyroid storm: Lugol solution 4-8 drops (or saturated potassium iodide solution 5 drops) PO Q6-8H, starting at least 1 hour after the first thionamide dose Pre-thyroidectomy, if hyperthyroidism is reasonably controlled: Lugol solution 2-6 drops PO TID for 7 days before surgery | Allergy/hypersensitivity reaction; metallic taste. | None significant at this indication. | Not linked: the Database's existing iodine and iodide monograph slugs are Lipiodol Ultra Fluid, an injectable radiographic contrast oil, and Micro I, an intravenous TPN trace-element additive - neither is the oral thyroid-storm iodine solution, so linking either would misrepresent the product. Must be given at least 1 hour after the first thionamide dose to avoid providing substrate for new hormone synthesis. |
| Selenium | Mild Graves orbitopathy adjunct: 100 mcg PO BID | Generally well tolerated at this dose; long-term high-dose supplementation carries a risk of selenium toxicity. | None significant at this indication. | Not linked: the Database's existing selenium monograph slug is MICRO Se, an intravenous total parenteral nutrition trace-element additive, not an oral supplement tablet, so it is not linked here to avoid misrepresenting the product. Reserve for mild Graves orbitopathy specifically, in conjunction with the patient's eye-care specialist. |
| Acetaminophen | Thyroid storm, fever control: 650-1000 mg PO/PR Q4-6H as needed, within usual maximum daily dose limits | Hepatotoxicity in overdose; generally well tolerated at recommended doses. | None significant at this indication. | Preferred antipyretic in thyroid storm. Avoid ASA and other NSAIDs for fever in this setting - they displace protein-bound thyroid hormone from binding proteins and raise free hormone levels, worsening thyrotoxicosis. |
Drug interactions with levothyroxine
Levothyroxine has one of the richest interaction profiles a pharmacist will counsel on - most interactions are absorption interactions that are entirely preventable with correct spacing, which makes this a genuinely high-yield counselling point at every dispense and every medication review.
| Interacting drug/class | Effect on levothyroxine | Management |
|---|---|---|
| Calcium carbonate / calcium supplements | Reduces absorption through chelation in the gut. | Separate by at least 4 hours. |
| Ferrous sulfate / iron salts | Reduces absorption through chelation in the gut. | Separate by at least 4 hours. |
| Aluminum- or magnesium-containing antacids | Reduces absorption. | Separate by at least 4 hours. |
| Sucralfate | Reduces absorption. | Separate by at least 4 hours. |
| Cholestyramine resin or colestipol | Binds levothyroxine in the gut, substantially reducing absorption. | Take levothyroxine at least 4-5 hours before, or at least 1 hour after, the resin dose. |
| Omeprazole or another proton pump inhibitor | Reduced gastric acidity can impair tablet dissolution and absorption. | No fixed-hour separation required; recheck TSH after starting or stopping therapy. |
| Conjugated estrogens or other estrogen-containing therapy | Increases thyroxine-binding globulin, which can raise the levothyroxine dose requirement. | Recheck TSH after starting or stopping estrogen therapy. |
| Warfarin | Levothyroxine can potentiate the anticoagulant effect by increasing clotting-factor catabolism. | Monitor INR closely with any levothyroxine dose change. |
| Phenytoin | Induces hepatic metabolism and alters protein binding, which can raise the levothyroxine dose requirement. | Recheck TSH after starting or stopping therapy. |
| Carbamazepine | Induces hepatic metabolism, which can raise the levothyroxine dose requirement. | Recheck TSH after starting or stopping therapy. |
| Rifampin | Induces hepatic metabolism, which can raise the levothyroxine dose requirement. | Recheck TSH after starting or stopping therapy. |
| Amiodarone | A large iodine load that can independently cause either hypothyroidism or thyrotoxicosis, complicating levothyroxine dosing. | Monitor thyroid function periodically during amiodarone therapy; involve endocrinology for amiodarone-induced thyroid dysfunction. |
| Lithium carbonate | Inhibits thyroid hormone release and can cause hypothyroidism or goitre. | Monitor thyroid function periodically during lithium therapy. |
| Sertraline or another SSRI | Reported to reduce levothyroxine effectiveness in some patients through an uncertain mechanism. | Recheck TSH if hypothyroid symptoms recur after starting an SSRI. |
Evidence note: Drug inventory, dosing, adverse effects, and comments reflect current ATA hypothyroidism and hyperthyroidism guideline recommendations and standard Canadian critical-care practice for the two thyroid emergencies.[1][2][5]
References
- Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement — Thyroid (Jonklaas J, Bianco AC, Bauer AJ, et al.). Thyroid 2014;24(12):1670-1751
- 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis — Thyroid (Ross DS, Burch HB, Cooper DS, et al.). Thyroid 2016;26(10):1343-1421
- Recommendation on screening adults for asymptomatic thyroid dysfunction in primary care — CMAJ, Canadian Task Force on Preventive Health Care (Birtwhistle R, Morissette K, Dickinson JA, et al.). CMAJ 2019;191(46):E1274-E1280
- Thyroid hormones treatment for subclinical hypothyroidism: a clinical practice guideline — BMJ (Bekkering GE, Agoritsas T, Lytvyn L, et al.). BMJ 2019;365:l2006
- Thyroid emergencies — Medical Clinics of North America (Klubo-Gwiezdzinska J, Wartofsky L). Med Clin North Am 2012;96(2):385-403
- American Thyroid Association 2026 Guidelines for Thyroid Disease in Preconception, Pregnancy, and Postpartum — Thyroid (Korevaar TIM, Leung AM, Alexander EK, et al.). Thyroid 2026;36(5):481-544
Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.