Hypothyroidism treatment with levothyroxine is the established standard of care for the approximately 20 million Americans living with this condition. It’s the most common endocrine disorder, yet most patients don’t realize that the same medication used for hypothyroidism treatment requires vastly different dosing strategies depending on the underlying condition.
A woman who’s newly pregnant doesn’t take the same levothyroxine dose as someone who just had thyroid cancer removed. A subclinically hypothyroid patient being observed might not need treatment at all, while a newborn with congenital hypothyroidism requires high-dose therapy immediately. An elderly patient with cardiac disease starts at a fraction of what a healthy 40-year-old takes.
This guide explains how levothyroxine treats each form of hypothyroidism, and why dosing, TSH targets, and monitoring differ by condition.
Key Takeaways
- Levothyroxine is the standard treatment for most hypothyroidism, replacing missing thyroid hormone (T4) with synthetic hormone that your body converts to active T3 as needed.
- Dosing varies dramatically by condition: typical hypothyroidism targets TSH 0.4–4.0 mIU/L, while thyroid cancer may target TSH <0.1 mIU/L (intentional over-replacement to suppress tumor growth).
- During pregnancy, levothyroxine requirements increase 25–30% per American Thyroid Association (ATA) guidelines, with trimester-specific monitoring and dose adjustments critical for fetal neurodevelopment.
Additional factors that influence your treatment:
- Hashimoto’s thyroiditis (autoimmune) is the most common cause in the US; levothyroxine replaces the missing hormone but doesn’t address the underlying autoimmune attack.
- Subclinical hypothyroidism (elevated TSH, normal free T4) is increasingly common; ATA recommends treating only if TSH >10 mIU/L or if TSH 4.5–10 with symptoms or risk factors.
- Age and comorbidities matter: Elderly patients, those with heart disease, and those on multiple medications require lower starting doses and closer monitoring than younger, healthy patients.
What Is Hypothyroidism? How Does Levothyroxine Treat It?
Hypothyroidism is a state of insufficient thyroid hormone production. Specifically, your thyroid gland manufactures thyroxine (T4) and triiodothyronine (T3), hormones that regulate metabolism, energy, body temperature, and cognitive function.
When thyroid hormone production falls below what your body needs, symptoms develop: fatigue, weight gain, cold intolerance, depression, constipation, hair loss, dry skin.
Levothyroxine replaces this missing hormone. It’s a synthetic version of T4. Like all medications, proper levothyroxine dosage and administration are critical, the right dose, taken the right way, at the right time. Your body:
1. Absorbs levothyroxine from your small intestine
2. Circulates it in your bloodstream
3. Converts T4 to T3 as needed (in peripheral tissues and organs)
4. Uses T3 to regulate metabolism
The FDA approves levothyroxine specifically for “thyroid hormone replacement and supplementation in hypothyroidism.” Your healthcare provider monitors TSH (thyroid-stimulating hormone) to determine if your levothyroxine dose is right. TSH is the pituitary gland’s signal that tells your thyroid: “Make more hormone” or “Stop, enough hormone.”
When TSH is elevated, it signals low thyroid hormone. When levothyroxine dose is optimized, TSH normalizes, and you feel better.
Most treatment pathways start with one diagnosis visit and a plan that keeps evolving
Levothyroxine is used across several thyroid conditions, but the reason for treatment changes what comes next.
Hypothyroidism Treatment Overview: Conditions & Levothyroxine Protocols
Different conditions cause hypothyroidism, and the treatment protocol differs accordingly. Here’s how they compare:
| Condition | Cause | Prevalence | Levothyroxine Role | Typical TSH Target | Special Considerations |
|---|---|---|---|---|---|
| Primary Hypothyroidism (Hashimoto’s) | Autoimmune thyroid attack | ~90% of all hypothyroidism | Replace missing T4; hormone is standard | 0.4–4.0 mIU/L | Most common; lifelong replacement needed |
| Postpartum Hashimoto’s | Autoimmune flare after delivery | 5–10% of postpartum women | Temporary hormone replacement (may be transient) | 0.4–4.0 mIU/L | May resolve 6–12 months; requires re-evaluation |
| Post-Thyroidectomy | Surgical removal of thyroid | Common in cancer patients | Permanent hormone replacement | 0.4–4.0 mIU/L (or suppressed if cancer) | Doses typically higher; entire gland gone |
| Thyroid Cancer (TSH Suppression) | Post-thyroidectomy + malignancy | Cancer-specific | High-dose hormone to suppress TSH (suppress tumor growth) | <0.1 mIU/L (suppressed) | Intentional over-replacement; higher side effect burden |
| Subclinical Hypothyroidism | Early thyroid failure or normal variation | 10–15% of population | Treatment only if TSH >10 or if symptomatic + TSH 4.5–10 | 0.4–4.0 mIU/L (if treated) | Controversy: some treat all; ATA: treat selectively |
| Pregnancy-Induced Hypothyroidism | Pre-existing + pregnancy metabolic changes | ~2–5% of pregnancies | Increased replacement (25–30% more) | 0.5–2.5 mIU/L (tighter) | Critical for fetal neurodevelopment |
| Congenital Hypothyroidism | Thyroid dysgenesis or enzyme defect (newborn) | ~1 in 2,000 births | High-dose replacement (critical timing) | Age-specific targets | Screened at birth; early treatment prevents intellectual disability |
Primary Hypothyroidism Treatment: The Most Common Form
Primary hypothyroidism (most often Hashimoto’s thyroiditis) is thyroid failure originating at the thyroid level. In this case, TSH is elevated because the pituitary is correctly signaling for more hormone, but the thyroid can’t respond. As a result, hypothyroidism treatment in this setting focuses on replacing the missing T4 with levothyroxine to normalize TSH and relieve symptoms.
Diagnosis & Starting Levothyroxine
Diagnostic criteria (per ATA):
– TSH >4.0 mIU/L (or >2.5 if pregnant or planning pregnancy)
– Free T4 in lower-normal or low range
– Symptoms consistent with hypothyroidism
Clinical presentation typically includes:
– Fatigue
– Weight gain (10–20 lbs)
– Cold intolerance
– Constipation
– Hair loss or thinning
– Dry skin
– Brain fog or depression
– Menstrual irregularities (in women)
Dosing Protocol
Starting dose (per ATA guidelines): 1.6–1.8 mcg/kg/day
– For average 150-lb (68 kg) adult: 50–75 mcg daily
– Elderly or cardiac patients: Start lower (25 mcg), titrate slowly
– Pregnant women: Increase by 25–30% upon confirmation
Dose adjustment timeline:
Per ATA guidelines, TSH monitoring and dose adjustments follow a standard protocol: retest TSH every 6–8 weeks after dose changes, adjust by 12.5–25 mcg increments until TSH reaches target range, then retest annually (or whenever symptoms change, weight fluctuates significantly, or new medications are added).
Target TSH: 0.4–4.0 mIU/L
Timeline to Symptom Improvement
- TSH normalization: 4–6 weeks (biological effect visible)
- Symptom improvement begins: 4–8 weeks
- Maximum symptom relief: 3–6 months
- Full optimization: Some patients take 6–12 months to feel completely normal
Patient scenario: James was diagnosed with hypothyroidism at age 52, TSH 8.4 mIU/L. Started on levothyroxine 50 mcg daily. After 6 weeks, his TSH was 3.2, in range. But he still felt tired. His provider explained: TSH is normal, but his body is still adjusting to consistent hormone levels. At 12 weeks, his fatigue lifted. At 6 months, he had lost 12 lbs and had his energy back. Patience was key.
Why Does Hashimoto’s Thyroiditis Cause Hypothyroidism?
Hashimoto’s thyroiditis is an autoimmune disease in which your immune system attacks thyroid tissue. In fact, it accounts for ~90% of hypothyroidism cases in iodine-sufficient countries (including the US).
Why Levothyroxine Treats the Symptom, Not the Disease
This is a critical distinction that frustrates many patients:
Levothyroxine replaces the missing hormone, but does NOT treat the autoimmune attack itself.
Your immune system continues producing antibodies against your thyroid peroxidase (TPO) and thyroglobulin (TGB). Levothyroxine doesn’t reduce these antibodies. But it does replace the hormone your damaged thyroid can no longer produce.
The result: symptoms improve (because hormone is restored), but the autoimmune condition persists.
Dosing & Monitoring for Hashimoto’s Hypothyroidism Treatment
Dosing is identical to primary hypothyroidism:
– Starting dose: 1.6–1.8 mcg/kg/day (~50–75 mcg)
– Target TSH: 0.4–4.0 mIU/L
– Monitoring: Every 6–8 weeks initially, then annually once stable
Clinical Expectations
When starting levothyroxine for Hashimoto’s:
Symptoms improve: ✅ (hormone is restored)
Antibody levels decrease: ❌ (autoimmune component remains)
Disease progression slows: ✅ (by treating TSH, you reduce thyroid stress)
Condition cured: ❌ (Hashimoto’s is lifelong)
Patient perspective: Maria was diagnosed with Hashimoto’s at 38. Her TPO antibodies were 1,200 (very high). She started levothyroxine 75 mcg. After 3 months, her TSH was normal and her fatigue was gone. But her TPO antibodies were still 1,100. She was disappointed: “I thought the levothyroxine would fix my immune system.” Her provider explained: Hashimoto’s is lifelong, but levothyroxine prevents her thyroid from failing completely and manages the hormone deficiency. That’s the goal.
Pregnancy is one of the clearest examples of thyroid treatment changing quickly
The condition may be familiar, but the dose targets, urgency, and lab schedule often change as soon as pregnancy begins.
Treating Hypothyroidism During Pregnancy: ATA Protocol
Pregnancy dramatically increases levothyroxine requirements. This is one of the highest-stakes scenarios for hypothyroidism treatment.
Why Levothyroxine Needs Increase
Three factors:
1. Increased estrogen raises thyroid-binding globulin (TBG), sequestering more levothyroxine protein-bound
2. Pregnancy increases metabolic demand for thyroid hormone
3. Fetal brain development requires maternal T4 (before fetal thyroid becomes functional at 12–14 weeks)
ATA Pregnancy Protocol (Trimester-Specific)
The American Thyroid Association (ATA) recommends specific levothyroxine dosing adjustments during pregnancy to ensure adequate fetal brain development while managing maternal hormone levels. See our detailed levothyroxine dosing adjustments during pregnancy guide for more information. Following these protocols can reduce miscarriage risk and support healthy fetal neurodevelopment.
Pre-Conception (If You Have Hypothyroidism)
- TSH target: 0.5–2.5 mIU/L (tighter than non-pregnant)
- Why: Optimize hormone status before pregnancy for better outcomes
- Action: If planning pregnancy, inform your provider; likely dose increase before conception
First Trimester (Weeks 1–12)
- Dose increase: 25–30% upon confirmation of pregnancy
- Example: If you take 75 mcg, increase to 100 mcg
- TSH retest: 4–6 weeks after dose increase
- Fetal importance: Maternal T4 crosses placenta; critical for fetal brain development
- Monitoring frequency: Every 4–6 weeks through first trimester
Second Trimester (Weeks 13–27)
- Further adjustments: Based on TSH results; may need additional increase
- TSH target: 0.5–2.5 mIU/L (maintain tight range)
- Monitoring: Every 4–6 weeks
Third Trimester (Weeks 28–40)
- Continued monitoring: Every 6–8 weeks
- Dose adjustments: If TSH drifts, adjust (common as pregnancy progresses)
- Preparation: Plan for dose decrease after delivery
Postpartum
- Dose reduction: Return to pre-pregnancy dose within days to weeks after delivery
- TSH retest: 4–6 weeks postpartum
- Breastfeeding: Levothyroxine is safe while breastfeeding; minimal excretion in breast milk
Why This Matters Clinically
Untreated or undertreated hypothyroidism during pregnancy is associated with:
– Increased miscarriage risk (2–3x higher)
– Impaired fetal neurodevelopment
– Preterm delivery risk
– Postpartum depression
Treatment for hypothyroidism during pregnancy reduces these risks significantly.
Real scenario: Rachel was on levothyroxine 75 mcg for hypothyroidism. She became pregnant. Her provider increased her dose to 100 mcg and planned TSH monitoring. But Rachel didn’t increase her dose, thinking it was unnecessary. At 8 weeks, her TSH was 6.8 (elevated). Her provider explained the fetal brain development importance and adjusted her dose to 125 mcg. After that, TSH stayed in range. She delivered a healthy baby with normal newborn screening.
Should You Treat Subclinical Hypothyroidism With Levothyroxine?
Subclinical hypothyroidism is a state of elevated TSH with normal or low-normal free T4. It’s increasingly common, especially with age. Notably, whether managing hypothyroidism at this mild stage improves outcomes remains one of endocrinology’s most debated questions.
Prevalence & Controversy
Affects 10–15% of the general population, rising to 20–25% in adults >65. Yet whether to treat is genuinely controversial.
ATA’s Evidence-Based Recommendation
Treat if:
– TSH >10 mIU/L (clear recommendation)
– Levels of 4.5–10 mIU/L AND patient is symptomatic
– A reading of 4.5–10 mIU/L AND has risk factors (history of miscarriage, coronary artery disease, age >65)
Observe without treatment if:
– TSH 4.5–10 AND asymptomatic
– TSH 4.5–10 AND no risk factors
– Retest TSH annually (may progress or remain stable)
Why the Debate Exists
Arguments FOR treating all subclinical hypothyroidism:
– Early intervention prevents overt hypothyroidism
– May prevent cardiovascular events
– Fertility outcomes may also improve
– Risk of depression may be reduced with treatment
Arguments AGAINST (ATA position):
– No strong evidence all subclinical cases benefit from treatment
– Risk of overtreatment (iatrogenic hyperthyroidism from levothyroxine)
– Not all asymptomatic elevated TSH will progress
– Unnecessary medication burden for some
Clinical reality: Many primary care doctors treat all elevated TSH; specialists (endocrinologists) often follow ATA guidelines more closely. Patient expectations vary widely.
What This Means for You
If your TSH is 5.5 and you’re asymptomatic: Your provider might observe (no treatment) or treat (based on their practice pattern). Neither is “wrong”, but guidelines-based care follows ATA recommendations.
After thyroidectomy, replacement becomes a daily necessity rather than an optional adjustment
The reason for treatment changes the psychology of the medication as much as the dose itself.
How Much Levothyroxine Do You Need After Thyroidectomy?
When your thyroid is surgically removed or destroyed (radioactive iodine therapy), it can no longer produce hormone. As a result, levothyroxine becomes a permanent, lifelong replacement and is the cornerstone of hypothyroidism treatment in post-surgical patients.
Surgical Removal (Thyroidectomy)
Indications: Thyroid cancer, large goiter, hyperthyroidism (surgery), nodules with cancer risk
Dosing after surgery:
– Often higher than primary hypothyroidism (because entire gland is gone, not partially functional)
– Typical range: 100–200 mcg daily (vs. 50–75 for partial failure)
– Adjusted based on TSH monitoring
Timeline:
– TSH checked 6–12 weeks post-surgery
– Adjusted if needed; then monitored annually
TSH target: 0.4–4.0 mIU/L (unless cancer-related; see below)
Thyroid Cancer & TSH Suppression Therapy
This is a specialized scenario with intentionally DIFFERENT dosing.
When levothyroxine is used after thyroid cancer removal, the goal is TSH suppression, keeping TSH intentionally low to suppress thyroid-stimulating hormone’s effect on any remaining cancer cells.
TSH Suppression Protocol
Target TSH: <0.1 mIU/L (often completely suppressed, undetectable)
Typical dose: 150–300+ mcg daily (much higher than other hypothyroidism treatment)
Rationale: TSH stimulates thyroid cells to grow and take up iodine. Cancer cells may respond to TSH similarly. Suppressing TSH reduces this growth signal.
Side Effects of Intentional Over-Replacement
Unlike regular hypothyroidism treatment, TSH suppression therapy intentionally creates a mild hyperthyroid state. These thyroid medication side effects are a known trade-off:
– Palpitations
– Anxiety
– Tremor
– Heat intolerance
– Insomnia
However, these are accepted because cancer prevention and recurrence reduction outweigh temporary discomfort. Your oncology team monitors you closely to balance efficacy against side effect burden.
Monitoring & Specialist Care
TSH suppression therapy is specialized. Your endocrinologist manages dosing based on:
– Thyroid cancer stage and type
– Risk of recurrence
– TSH suppression level needed
– Annual thyroid ultrasound + radioactive iodine scans (for some patients)
This is not managed by primary care; it requires oncologic endocrinology expertise.
Thyroid replacement becomes more individualized when age, heart disease, or frailty enters the picture
The diagnosis may be the same, but the safe starting point and monitoring strategy can change dramatically.
How Does Hypothyroidism Treatment Change With Age & Health Conditions?
Pregnancy (Covered above)
Elderly Patients (Age 65+)
Why elderly dosing differs:
– Heart disease prevalence increases (levothyroxine can trigger arrhythmias at high doses)
– Absorption may be slightly reduced
– Comorbidities (cardiac disease, kidney disease) affect dosing
– Often on multiple medications (interaction risk)
Dosing approach:
– Start lower: 25 mcg (vs. 50 mcg in younger adults)
– Titrate slowly: Increase by 12.5 mcg every 4–6 weeks (vs. every 6 weeks in younger)
– Aim for TSH 0.4–4.0, but some guidelines accept TSH up to 5–6 mIU/L to avoid overtreatment
Monitoring: TSH checked every 6–12 months (less frequent than younger patients)
Comorbidity considerations:
– Cardiac disease: higher risk of side effects; start very low
– Kidney disease: adjusted monitoring (kidneys affect levothyroxine metabolism)
– On multiple drugs: increased interaction risk (PPIs, calcium, iron all reduce absorption)
Pediatric & Congenital Hypothyroidism
Congenital hypothyroidism (1 in 2,000–4,000 births) is screened via newborn heel-prick TSH test in all 50 US states.
Why early treatment is critical: The first 12–18 months of life are critical for brain development. Untreated hypothyroidism during this window causes intellectual disability and developmental delay. Therefore, immediate levothyroxine treatment is essential to prevent these outcomes.
Dosing in infants & children:
– Much higher on a weight basis than adults
– 10–15 mcg/kg/day (vs. 1.6–1.8 in adults)
– Requires frequent TSH monitoring (every 2–4 weeks initially, then every 3–6 months)
– Dose adjustments as child grows
Lifelong management: Congenital hypothyroidism requires levothyroxine for life.
Patients With Malabsorption Disorders
Celiac disease, Crohn’s disease, post-gastric bypass: Levothyroxine absorption is reduced.
Solutions:
– Higher levothyroxine doses needed (may need 30–50% more)
– Tirosint (soft gel capsule) formulation instead of tablets, designed to bypass absorption barriers and improve bioavailability
– Liquid levothyroxine formulation
– More frequent TSH monitoring (every 6–12 weeks until stable)
When to Contact Your Healthcare Provider
Contact your provider if:
- New symptoms of hyperthyroidism develop (palpitations, anxiety, tremor, weight loss), may indicate over-replacement
- Persistent hypothyroid symptoms despite “normal” TSH, may indicate inadequate dose or absorption issue
- You become pregnant, dose increase needed
- New medications are started, interaction potential (especially calcium, iron, PPIs, antacids)
- Significant weight change (>10 lbs), dose adjustment may be needed
- New cardiac symptoms, levothyroxine may affect heart; needs evaluation
- Older adults experiencing new symptoms should report them promptly, as age-related dosing adjustments may be needed
Frequently Asked Questions
Q: Is hypothyroidism curable?
A: No, not in most cases. Primary hypothyroidism (Hashimoto’s) and post-thyroidectomy hypothyroidism are permanent and require lifelong levothyroxine replacement. Exception: Postpartum thyroiditis may resolve 6–12 months after delivery; re-evaluation is important to determine if permanent treatment is needed.
Q: Why does my TSH target differ from my friend’s?
A: TSH targets vary by condition and circumstances. Pregnancy targets TSH 0.5–2.5 mIU/L (tighter). Thyroid cancer may target TSH <0.1 mIU/L (suppressed). General hypothyroidism targets 0.4–4.0 mIU/L. Your provider sets your specific target based on your condition.
Q: If I have Hashimoto’s, will levothyroxine stop the autoimmune disease?
A: No. Levothyroxine replaces the missing hormone but doesn’t address the underlying autoimmune attack on your thyroid. Your antibody levels won’t decrease. However, once TSH is normalized with levothyroxine, your symptoms typically improve significantly.
Q: How much levothyroxine should I take when pregnant?
A: That depends on your pre-pregnancy dose. Most pregnant women need a 25–30% dose increase per ATA guidelines. Your provider will retest TSH every 4–6 weeks during pregnancy and adjust accordingly.
Q: Can I get pregnant with hypothyroidism?
A: Yes, but untreated or undertreated hypothyroidism increases miscarriage risk. ATA recommends treating hypothyroidism before conception and maintaining TSH 0.5–2.5 during pregnancy.
Q: Is subclinical hypothyroidism worth treating?
A: It depends. ATA recommends treating if TSH >10, or if TSH 4.5–10 with symptoms or risk factors. If asymptomatic and no risk factors, many providers monitor without treating. Discuss with your provider.
Dosing, Monitoring & Special Situations
Q: After my thyroid was removed, will I always need high-dose levothyroxine?
A: Yes. Without a thyroid gland, you require permanent hormone replacement. Your dose will be higher than someone whose thyroid is partially functional. Your provider will adjust based on TSH monitoring.
Q: If I have thyroid cancer, why is my TSH target so different?
A: High-dose levothyroxine (with suppressed TSH) reduces the risk of cancer recurrence and growth. TSH suppression is an intentional strategy; side effects are accepted for cancer control.
Q: What should I expect after starting levothyroxine?
A: TSH typically normalizes in 4–6 weeks. Symptoms improve over 4–12 weeks. Full benefit may take 3–6 months. Some people feel better within days; others take longer.
Q: Will my dose stay the same forever?
A: No. Dose adjustments are common, especially with pregnancy, weight changes, new medications, or changes in absorption. Annual TSH monitoring is standard.
Q: Does levothyroxine cure postpartum thyroiditis?
A: It treats the hypothyroid phase temporarily. Postpartum thyroiditis often resolves on its own within 6–12 months. Your provider will retest TSH postpartum to determine if permanent treatment is needed.
Q: Can hypothyroidism be prevented?
A: Primary prevention: Adequate iodine intake. If you have risk factors (family history, female sex, autoimmune disease), screening may catch subclinical hypothyroidism early. Some causes (post-surgery, radioactive iodine for hyperthyroidism) are unavoidable consequences of other treatments.
Comorbidities, Pregnancy & Safety
Q: I have both diabetes and hypothyroidism. How do these interact?
A: Levothyroxine may affect insulin requirements. Notify both your endocrinologist and primary care provider. TSH and glucose monitoring may need adjustment when starting or changing levothyroxine dose.
Q: Is it safe to use levothyroxine in the first trimester?
A: Yes, absolutely. Benefits far outweigh risks. The first trimester is critical for fetal neurodevelopment, and adequate maternal thyroid hormone is essential. Untreated hypothyroidism in pregnancy carries higher risk than levothyroxine replacement.
The Key to Successful Hypothyroidism Treatment With Levothyroxine
Levothyroxine is safe and effective for treating hypothyroidism, but one size does not fit all.
Your condition, age, life stage, and comorbidities determine your dose, TSH target, and monitoring frequency. A pregnant woman’s hypothyroidism treatment protocol differs from a cancer survivor’s, which differs from an elderly patient’s.
The key to success is:
1. Clear diagnosis (TSH + free T4, not TSH alone)
2. Appropriate starting dose for your situation
3. Consistent TSH monitoring (every 6–8 weeks initially; annually once stable)
4. Patient communication (tell your provider about weight changes, new meds, pregnancy plans, symptoms)
5. Patience (symptom improvement takes weeks to months)
When managed properly, hypothyroidism treatment with levothyroxine restores thyroid hormone balance and allows you to feel better and live normally, for life.
Related Resources
Learn more about managing your hypothyroidism and levothyroxine:
- Levothyroxine Dosage & Administration Guide, How and when to take your dose for optimal absorption
- Drug & Food Interactions: Complete Guide – What interferes with levothyroxine and how to manage timing
- Side Effects & Safety Guide – What’s normal and when to contact your provider
- Brands & Cost Comparison – Synthroid vs. generic and other levothyroxine options
- Living Well With Levothyroxine, Diet, supplements, and daily routine tips
- Free Levothyroxine Reference Guide – Download our complete guide with condition charts
Sources & References
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Surks, M. I., et al. “Subclinical thyroid disease: scientific review and guidelines for diagnosis and management.” JAMA. 2004;291(2):239-243. https://pubmed. ncbi. nlm. nih. gov/14722150/
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Benvenga, S., et al. “Thyroid hormone therapy in patients with resistant symptoms of hypothyroidism.” Endocr Pract. 2012;18(3):457-466. https://pubmed. ncbi. nlm. nih. gov/22784850/
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De Groot, L., et al. “Management of Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force.” Thyroid. 2016;26(1):1-133. https://pubmed. ncbi. nlm. nih. gov/26462967/
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Abalovich, M., et al. “Management of thyroid dysfunction during pregnancy and postpartum: An Endocrine Society Clinical Practice Guideline.” J Clin Endocrinol Metab. 2007;92(8 Suppl): S1-S47. https://pubmed. ncbi. nlm. nih. gov/17948378/
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Cleveland Clinic. “Hypothyroidism: Overview, Symptoms, Diagnosis & Management.” Clevelandclinic. org. Available at: https://my. clevelandclinic. org/health/diseases/8619-hypothyroidism