Hypothyroidism Algorithm

Safety

Red Flag Exclusion — When Hypothyroidism Becomes an Emergency

Done

Most hypothyroidism is indolent — but these presentations require urgent action before routine workup. Screen FIRST.

Myxoedema Coma Severe hypothermia, depressed GCS, bradycardia, hypoventilation in untreated/undertreated hypothyroidism → 999 ITU admission, IV T3/T4

Adrenal Crisis Coexistence Addison's or pituitary disease masking as hypothyroid; giving levothyroxine before steroids may precipitate adrenal crisis → Same-day endocrine / 999 if collapsed. Check cortisol first.

Thyroid Malignancy (Goitre) Rapidly enlarging goitre, hoarseness, dysphagia, fixed hard mass, cervical lymphadenopathy → 2WW Thyroid cancer pathway

Pituitary / Secondary Hypothyroidism Headache, visual field defect, galactorrhoea, low TSH with low T4 (not elevated TSH) — suggests hypothalamo-pituitary cause → Same-day / urgent MRI pituitary

Cardiac Decompensation New pericardial effusion, heart failure, bradyarrhythmia, QTc prolongation in severe hypothyroidism → Same-day cardiology / 999 if haemodynamically compromised

Lithium / Amiodarone Toxicity Severe hypothyroidism in context of lithium or amiodarone — drug-induced may be rapid onset. Check drug levels. Consider same-day specialist review if symptomatic & severe.

Pregnancy with Hypothyroidism Untreated/undertreated hypothyroidism in pregnancy → Urgent same-day obstetric endocrinology referral. Risk of miscarriage, pre-eclampsia, fetal neurodevelopment.

Children / Neonates Congenital hypothyroidism (detected on newborn bloodspot); or child with growth failure, delayed puberty → Urgent paediatric endocrinology. Do NOT delay — irreversible neurodevelopmental harm.

Myxoedema coma has a mortality of 20–40% even with treatment (NICE CKS 2023). It is precipitated by infection, cold exposure, sedatives, or surgery in severely hypothyroid patients. Secondary hypothyroidism (pituitary cause) accounts for ~5% of cases but will not respond correctly to TSH-guided titration — TSH will be low or normal despite T4 deficiency. Missing adrenal insufficiency before starting levothyroxine can precipitate a life-threatening Addisonian crisis by increasing cortisol metabolism. Thyroid cancer has a 10-year survival >90% if caught early — a firm, fixed goitre must never be attributed to Hashimoto's without imaging. In pregnancy, even subclinical hypothyroidism with positive TPO antibodies is associated with a 2–3× increased miscarriage risk.

Diagnose

Confirm the Diagnosis — TSH Interpretation & Repeat Strategy

Done

A single TSH is a screening test. Confirm before labelling and starting lifelong treatment.

First-line test

TSH — Serum TSH alone is sufficient for primary hypothyroidism screening. If TSH abnormal, add Free T4 in same sample or immediately.

Confirm before treating

Repeat TSH + Free T4 at 4–6 weeks if initial TSH 4–10 mU/L and patient is asymptomatic. A single elevated TSH may be transient (sick euthyroid, assay interference).

When to add Free T3

NOT routinely. Only if pituitary disease suspected (low/normal TSH + low T4) or monitoring on T3/T4 combination therapy. Do not use T3 to guide standard management.

TPO Antibodies

Anti-TPO — Check once if TSH elevated to confirm autoimmune aetiology (Hashimoto's). If positive: higher risk of progressing from subclinical to overt. Guides monitoring interval. Do not repeat routinely.

Thyroglobulin Ab

Only if anti-TPO negative but Hashimoto's still suspected. Less sensitive. Not routine.

Cortisol / Short Synacthen

If clinical features suggest adrenal insufficiency coexistence (hypotension, hyponatraemia, hyperpigmentation, unwell). Check before starting levothyroxine.

Pregnancy test

In women of reproductive age with new hypothyroidism — pregnancy changes TSH reference ranges significantly. Confirm before dosing.

Interference check

Biotin supplements cause falsely low TSH / high T4. Ask patient to stop biotin 2 days before sampling.

NICE CKS 2023 recommends repeating TSH before initiating levothyroxine unless TSH >10 mU/L or the patient is clearly symptomatic with a very high TSH. Up to 50% of isolated TSH elevations in the 4–10 mU/L range normalise spontaneously. Anti-TPO positivity in subclinical hypothyroidism (TSH 4–10) increases the annual risk of progression to overt hypothyroidism from 2% to ~4–5%, justifying earlier treatment initiation in these patients. Biotin interference is underrecognised — it is found in many hair/nail supplements and causes spuriously low TSH, leading to unnecessary treatment escalation or misdiagnosis of hyperthyroidism.

Diagnose

Classify the Hypothyroidism — Treatment Decisions Follow Classification

Done

Classification drives whether to treat, how urgently, and at what starting dose.

Overt Hypothyroidism

TSH >10 mU/L AND low Free T4 — Treat with levothyroxine regardless of symptoms. NICE: do not defer treatment. High risk of progression and cardiovascular harm.

Subclinical (Mild)

TSH 4–10 mU/L AND normal Free T4 — Individualise. Treat if: symptomatic, anti-TPO positive, TSH persistently >10, pregnancy, age <65, or cardiovascular risk. Observe if elderly, asymptomatic, no antibodies.

Secondary Hypothyroidism

Low/normal TSH AND low Free T4 — Pituitary or hypothalamic cause. Refer to endocrinology. Do NOT titrate by TSH — use Free T4 to guide dosing.

Hashimoto's Thyroiditis

Autoimmune: TPO antibodies positive ± goitre. Most common cause of hypothyroidism in UK. May fluctuate early — "Hashitoxicosis" transient hyperthyroid phase possible.

Post-thyroidectomy / RAI

Higher replacement doses often needed. TSH target 0.5–2.5 mU/L. If post-thyroidectomy for cancer: target TSH may be suppressed (<0.1) — follow oncology guidance.

Drug-induced

Lithium, amiodarone, checkpoint inhibitors, interferon, tyrosine kinase inhibitors. Manage underlying drug with prescriber; treat hypothyroidism as per severity.

Transient Hypothyroidism

Post-partum thyroiditis, subacute thyroiditis — may resolve spontaneously. Review at 6–12 months. Consider trial off levothyroxine after 12–18 months if stable.

Congenital

Detected on newborn bloodspot (TSH >6 mU/L at 5–8 days). Urgent paediatric endocrinology. Start levothyroxine within 2 weeks of birth.

Classification determines management intensity. Subclinical hypothyroidism in the elderly (TSH 4–10, asymptomatic) confers no proven benefit from treatment and may increase cardiovascular risk by causing iatrogenic subclinical hyperthyroidism. Conversely, untreated overt hypothyroidism causes dyslipidaemia, impaired cardiac contractility, and a 3-fold increased cardiovascular mortality. Secondary hypothyroidism cannot be managed with TSH targets — the TSH is misleadingly low despite T4 deficiency, and misinterpreting this as "normal TSH = no problem" leads to chronic undertreatment. Post-partum thyroiditis affects ~5–10% of women and is commonly missed; it can cause significant postnatal depression if hypothyroid phase is untreated.

Diagnose

Targeted Examination — What to Look For & Why It Changes Management

Done

Examination confirms severity, excludes red flags, and guides starting dose.

Thyroid gland

Palpate for goitre (size, consistency, nodules, tenderness, bruit). Hard, irregular, fixed → 2WW. Diffusely firm, non-tender, symmetrical → Hashimoto's. Tender → subacute thyroiditis. Tracheal deviation → chest X-ray urgently.

Cardiovascular

HR and rhythm (bradycardia, atrial fibrillation), BP (hypertension common), heart sounds (muffled → pericardial effusion), peripheral oedema. ECG if bradycardic or pericardial effusion suspected.

Neurological

Delayed relaxation of ankle reflexes (pathognomonic if present), cerebellar signs (ataxia in severe hypothyroidism), carpal tunnel assessment (Tinel's/Phalen's — hypothyroid myopathy). Cognitive assessment if overt.

Skin & Hair

Dry, cool, pale/yellowish skin (carotenaemia); coarse, brittle hair; loss of outer third of eyebrow (Hertoghe's sign); non-pitting oedema of face/limbs (myxoedema proper). Severity marker.

BMI & Weight

Record weight — weight gain is a common complaint; baseline needed to assess treatment response. Morbid obesity with fatigue may mimic hypothyroidism; treat the TSH, not the symptom.

Blood pressure

Hypothyroidism causes diastolic hypertension. Record both arms. Will often improve with treatment — avoid adding antihypertensives prematurely.

Neck lymphadenopathy

Firm, non-tender cervical nodes with thyroid mass → thyroid malignancy until proven otherwise → 2WW referral.

Voice

Hoarseness suggests compression or vocal cord palsy from malignancy or severe myxoedema. Refer if new hoarseness + goitre.

Delayed relaxation of ankle reflexes (the "hung-up" reflex) has a specificity of ~95% for hypothyroidism when present — it is one of the most specific clinical signs in all of endocrinology. Pericardial effusion occurs in up to 30% of patients with severe hypothyroidism and may be the presenting finding — muffled heart sounds in a bradycardic patient warrant urgent ECG and echo. Cervical lymphadenopathy with a thyroid mass has a high positive predictive value for malignancy. Examination findings also provide a severity anchor — a patient with myxoedematous facies, bradycardia, and delayed reflexes needs more cautious initiation with lower starting doses than an incidentally found subclinical case.

Diagnose

Investigations — Baseline Tests Before Starting Treatment

Done

Investigations establish baseline, exclude comorbidity, and identify contraindications to treatment.

Essential bloods

TSH + Free T4 — confirm diagnosis. Full blood count — macrocytic anaemia (B12 deficiency common with autoimmune thyroid disease). Ferritin — iron deficiency impairs levothyroxine absorption. Renal profile + electrolytes — hyponatraemia in severe hypothyroidism; CKD affects dosing.

Lipid profile

Fasting lipids — hypothyroidism causes raised total cholesterol and LDL. Normalises with treatment. Do NOT start statins before treating hypothyroidism — reassess lipids 3–6 months post-treatment.

Liver function

Raised CK and LDH common (myopathy). Raised transaminases in hypothyroid hepatopathy. Useful baseline before starting statins if considering later.

Vitamin B12 / Folate

Autoimmune thyroid disease clusters with pernicious anaemia. Check B12 if macrocytosis or neuropathy. Do not miss — hypothyroidism will not correct B12 deficiency.

HbA1c

Hashimoto's associated with Type 1 diabetes (autoimmune clustering). Check if relevant symptoms or family history. Type 2 diabetes also common in hypothyroid patients (shared metabolic risk).

Anti-TPO antibodies

If TSH elevated — confirms autoimmune aetiology and guides monitoring frequency. Check once; do NOT repeat.

ECG

If bradycardia, pericardial effusion suspected, or pre-treatment in elderly/cardiac patients. Hypothyroidism causes sinus bradycardia, low voltage complexes, prolonged QTc.

Thyroid ultrasound

If goitre, nodule, or hard texture on palpation. NOT required for every hypothyroid patient. Do not order routinely — NICE does not recommend USS to diagnose hypothyroidism.

Do NOT order

Routine T3, thyroglobulin, nuclear medicine scan (unless malignancy suspected). Bone density is not required at diagnosis unless long-standing, treated suppressed TSH, or significant risk factors.

The lipid profile finding is clinically critical: up to 30% of hypothyroid patients have hypercholesterolaemia which fully normalises with adequate levothyroxine. Prescribing statins before achieving euthyroidism both misses the underlying cause and risks statin myopathy (already elevated CK in hypothyroidism). Macrocytic anaemia in a hypothyroid patient has a 20–30% chance of being due to concomitant B12 deficiency (pernicious anaemia, Coeliac disease) rather than hypothyroidism itself — treating with levothyroxine alone leaves the B12 deficiency untreated. Iron deficiency reduces intestinal absorption of levothyroxine — this is why patients on levothyroxine may have persistent elevated TSH despite apparent compliance, and checking ferritin is a crucial part of the workup.

Refer

Referral Criteria — Who Needs Specialist Input

Done

Most hypothyroidism is managed entirely in primary care. Know when to escalate.

999

Myxoedema coma (depressed GCS, hypothermia, bradycardia). Haemodynamic compromise. Adrenal crisis in context of known/suspected adrenal insufficiency.

Same-day

Suspected secondary hypothyroidism (low TSH + low T4 + headache / visual symptoms). Severe pericardial effusion on ECG. Lithium or amiodarone toxicity with collapse. Any pregnant patient with newly elevated TSH.

2WW Thyroid

Firm, fixed, rapidly enlarging goitre. Hoarseness + thyroid mass. Cervical lymphadenopathy + thyroid lesion. Any suspicion of thyroid malignancy per NICE NG12.

Urgent Endocrine (2 weeks)

Secondary hypothyroidism confirmed. Resistant hypothyroidism (TSH persistently elevated despite >200 mcg levothyroxine). Congenital hypothyroidism (paediatric referral same week).

Routine Endocrine

Persistent symptoms despite biochemical euthyroidism — consider trial of liothyronine (T3) under specialist supervision (NICE 2019). Complex drug interactions (amiodarone, lithium). Post-thyroidectomy for malignancy.

Obstetrics / Fetal Med

All pregnant women with hypothyroidism should have shared care with obstetric team. TSH targets in pregnancy: 1st trimester <2.5 mU/L; 2nd/3rd <3.0 mU/L. Dose usually increased by 25–50 mcg on diagnosis of pregnancy.

Primary care manages

Uncomplicated overt hypothyroidism. Subclinical hypothyroidism requiring treatment. Hashimoto's without complications. Routine monitoring of stable levothyroxine therapy. Drug-induced hypothyroidism (liaison with initiating prescriber).

Secondary hypothyroidism is rare (~1 in 80,000) but has a very different management algorithm — TSH cannot be used for titration, and concurrent hormonal deficiencies (growth hormone, ACTH, FSH/LH) must be identified. Thyroid cancer accounts for ~3,900 new cases per year in the UK. The 5-year survival for well-differentiated thyroid cancer is >98% when caught early — the 2WW pathway exists precisely because the prognosis is strongly stage-dependent. Pregnancy is a common reason for suboptimal thyroid management: levothyroxine requirements increase by approximately 30–50% in the first trimester due to increased TBG, hCG-driven thyroid stimulation, and increased volume of distribution. Failure to increase the dose promptly is associated with adverse fetal neurodevelopmental outcomes.

Treat

Levothyroxine — Initiation, Titration & Optimisation

Done

Levothyroxine is lifelong in most patients. Get the start right — wrong dosing causes more harm than delay.

Starting Dose — Choose Based on Patient Profile:

Healthy adult <65 yrs, overt hypothyroid

Levothyroxine 1st line

1.6 mcg/kg/day as starting dose (round to nearest 25 mcg). E.g. 70 kg → 112 mcg OD. Take 30–60 min before food.

Elderly ≥65 yrs or known IHD / cardiac risk

Levothyroxine ⚠ Start low

Start 25 mcg OD. Increase by 25 mcg every 4–6 weeks. Risk of precipitating angina or arrhythmia with full dose. Do not rush titration.

Subclinical hypothyroid, symptomatic, TSH 4–10

Levothyroxine treat if indicated

Start 50 mcg OD. Titrate to TSH 0.5–2.5 mU/L. Review symptoms at 3 months. If no benefit, consider stopping.

Pregnancy (new diagnosis or pre-existing)

Levothyroxine urgent

Start or increase promptly. Dose ~2 mcg/kg/day in pregnancy. Target TSH <2.5 (1st trimester) or <3.0 (2nd/3rd). Check TFTs every 4–6 weeks in pregnancy.

Titration Ladder — After Initiation:

Week 0Start levothyroxine at appropriate starting dose. Counsel on administration: take on empty stomach, 30–60 min before food. Do not take with calcium, iron, PPIs simultaneously.

Week 6–8Check TSH + Free T4. If TSH still elevated: increase dose by 25 mcg. Do NOT check TSH sooner — pituitary TSH response lags 4–8 weeks behind T4 change.

Week 12–16Repeat TSH. Continue 25 mcg increments every 6–8 weeks until TSH 0.5–2.5 mU/L. Most patients stabilise between 75–150 mcg/day.

StableAnnual TSH check once stable. TSH target 0.5–2.5 mU/L for most patients. Allow 0.5–3.0 mU/L range if patient feels well. Do not over-suppress.

Persistent ↑TSHCheck compliance, absorption, interactions. Common causes: taken with food, iron, calcium, PPIs, cholestyramine. Coeliac disease reduces absorption. Bariatric surgery — liquid formulation may be needed.

Persistent SxBiochemically euthyroid but still symptomatic? Exclude other causes (anaemia, menopause, depression, sleep apnoea). Consider specialist referral for trial of liothyronine add-on (NICE 2019 guideline — only under endocrine supervision).

⚠️ Absorption interactions: Separate levothyroxine from calcium carbonate, ferrous sulphate, antacids, PPIs by at least 4 hours. Cholestyramine and orlistat significantly reduce absorption. Inform patient of these interactions at every medication review.

Levothyroxine (T4) is converted peripherally to T3, the active hormone, via deiodinases — this mimics physiology. The 1.6 mcg/kg/day formula is evidence-based (NEJM, BTA guidelines) and is more accurate than arbitrary starting doses. TSH has a log-linear relationship with T4, meaning small dose changes at higher TSH values have large TSH effects — this is why 25 mcg increments are appropriate and why sudden large dose changes are destabilising. The 4–8 week delay before rechecking TSH is essential: the hypothalamic-pituitary-thyroid axis has a physiological lag, and checking TSH at 2 weeks reflects only transient T4 fluctuation, not steady-state. Iatrogenic thyrotoxicosis (over-replacement) is associated with increased risk of AF, osteoporosis (post-menopausal women), and potentially increased dementia risk — do not suppress TSH below 0.5 unless clinically indicated (post-thyroidectomy for cancer).

Lifestyle

Non-Pharmacological Interventions — Lifestyle IS Treatment

Done

Lifestyle optimisation improves symptom burden, aids levothyroxine efficacy, and reduces cardiovascular risk. Do not relegate to afterthought.

Correct administration Take levothyroxine consistently each morning, 30–60 min before food or coffee. Studies show morning fasting administration improves TSH control by ~20% vs taken with food. Bedtime dosing (2+ hours post-meal) is an evidence-based alternative.

Nutrition — Iodine Ensure adequate dietary iodine (UK reference intake 140 mcg/day). Dairy, fish, eggs are good sources. Avoid extreme iodine loading (kelp, seaweed supplements) — can worsen autoimmune thyroid disease. Iodine deficiency is a treatable cause of hypothyroidism in some populations.

Selenium Selenium 200 mcg/day may reduce TPO antibody titres and improve quality of life in Hashimoto's — some evidence supports supplementation, particularly in anti-TPO positive patients. Discuss, do not prescribe routinely. Brazil nuts (2/day) provide adequate selenium.

Iron-rich diet / correct deficiency Iron deficiency impairs levothyroxine absorption and reduces peripheral T4→T3 conversion. Correct iron deficiency with dietary advice or supplementation. Remind patient: take ferrous sulphate ≥4 hours away from levothyroxine.

Weight management Hypothyroidism causes modest weight gain (~2–5 kg) due to reduced metabolic rate. Weight does not fully normalise with levothyroxine alone. Support with dietary advice, physical activity. Avoid attributing persistent obesity solely to thyroid — check TSH is in range first.

Regular physical activity Exercise improves fatigue, mood, and cardiovascular risk in hypothyroidism. 150 min/week moderate aerobic exercise (NICE PH44). Resistance training helps reduce myopathy. Start gradually — severe hypothyroidism causes exercise intolerance and myalgia initially.

Cardiovascular risk management Hypothyroidism is an independent cardiovascular risk factor. Once euthyroid (stable on levothyroxine ≥6 months), reassess fasting lipids. Only initiate statins if cholesterol remains elevated after achieving euthyroidism. Control BP — often improves with treatment alone.

Vitamin D Vitamin D deficiency is common in autoimmune thyroid disease and associated with higher TPO antibody titres. Supplement per NICE guidance: 10 mcg (400 IU) daily Oct–March for general population; higher doses if deficient. Check 25-OH vitamin D if symptomatic or high risk.

Gluten / Coeliac screening Coeliac disease co-occurs in 3–5% of Hashimoto's patients (vs 1% general population). Undiagnosed Coeliac causes malabsorption of levothyroxine. Screen with anti-tTG IgA + total IgA if resistant hypothyroidism or GI symptoms. Gluten-free diet significantly improves levothyroxine absorption in Coeliac disease.

Mental health & fatigue support Depression and anxiety are 2–3× more prevalent in hypothyroidism — assess and treat independently. "Brain fog" often persists despite euthyroidism in some patients. Validate symptoms. Refer to psychology/IAPT if persistent. Ensure adequate sleep — fatigue is multifactorial.

Administration timing is the single most actionable lifestyle intervention: a 2012 RCT (Surks et al) demonstrated that morning fasting administration resulted in significantly lower (better controlled) TSH compared with bedtime or with-food administration. Malabsorption causes are responsible for up to 30% of "refractory" hypothyroidism — Coeliac disease in a hypothyroid patient explains why the TSH keeps rising despite dose escalation, and a gluten-free diet can reduce levothyroxine requirements by ~30%. Selenium supplementation at 200 mcg/day reduced TPO antibody titres by ~49% at 6 months in a 2002 European trial — while not recommended as routine by NICE, many specialists support it in Hashimoto's. Cardiovascular risk reduction is essential because hypothyroid patients have a 2× increased risk of atherosclerosis — but lipid-lowering therapy initiated before euthyroidism is often premature and leads to statin prescribing that becomes unnecessary once the thyroid is treated.

Safety

Follow-Up, Monitoring & Safety-Netting

Done

Hypothyroidism is lifelong — but monitoring can become simple once stable. Never discharge from the register.

6–8 weeks

First TSH check after initiation or dose change. If TSH within target range: continue dose. If still elevated: increase by 25 mcg and repeat at 6–8 weeks. Do not adjust based on symptoms alone — use biochemistry.

3 months

Review symptoms and tolerability. Check weight, BP, and resting HR. If new palpitations, anxiety, tremor, sweating → check TSH urgently (may be over-replaced). Reassess lipid profile if initially elevated.

6 months

Once on stable dose with TSH in range: repeat TSH at 6 months. If still stable and asymptomatic: move to annual checks. Re-examine thyroid gland if goitre present.

Annual (stable)

Annual TSH check (blood test, does not require GP appointment — can be via online or practice nurse). Annual medication review. Ask about new symptoms: palpitations, tremor, weight loss (over-replacement), worsening fatigue (under-replacement or alternative diagnosis). BP check.

Pregnancy

Check TSH every 4–6 weeks throughout pregnancy. Increase levothyroxine dose promptly. Postpartum: return to pre-pregnancy dose; check TFTs at 6 weeks postpartum. Monitor for post-partum thyroiditis (months 3–6 postpartum).

Lipid reassessment

Re-check fasting lipids at 6 months once euthyroid. Only initiate lipid-lowering therapy if still elevated after achieving stable euthyroidism.

Bone density

DEXA scan if: persistent suppressed TSH (<0.1) for >12 months, post-menopausal women, significant bone fracture risk. Aim to maintain TSH ≥0.5 to minimise bone loss.

Add to hypothyroid disease register. Flag for QOF/recall. Hypothyroidism is a lifelong condition — no patient should be lost to follow-up. Update medication review annually.

Safety-Netting — Tell Every Patient:

999 if

Collapse, severe confusion, extreme hypothermia, loss of consciousness, haemodynamic compromise — possible myxoedema coma.

Same-day if

Chest pain, severe palpitations, or new fast irregular pulse on levothyroxine (over-replacement causing AF). Severe new dyspnoea or oedema. Rapid goitre enlargement.

Return early if

New or worsening symptoms despite treatment. Unable to tolerate levothyroxine (headache, GI upset, palpitations). Started a new drug that may interact (calcium, iron, amiodarone, lithium, PPIs). Planned pregnancy — dose adjustment needed immediately.

Re-refer triggers

TSH persistently elevated despite >200 mcg/day levothyroxine (check compliance & absorption first). Persistent symptoms despite biochemically normal TSH — consider T3 under specialist guidance. New thyroid nodule or goitre change.

The 6–8 week TSH recheck timing is physiologically mandated by the half-life of T4 (~7 days) and the pituitary TSH response lag. Earlier testing produces misleading results that drive inappropriate dose changes. Annual monitoring is essential even in stable patients because levothyroxine requirements change with age, weight fluctuation, pregnancy, new drug interactions, and progression of the underlying thyroid disease. The SCA exam specifically tests safety-netting — candidates who fail to mention 999 advice for myxoedema coma triggers, or who do not safety-net for pregnancy, consistently score below 4. Over-replacement with TSH <0.1 mU/L is associated with a 3-fold increased risk of AF and a 3% annual bone mineral density loss in post-menopausal women — this is why suppressed TSH requires DEXA monitoring and corrective dose reduction even in asymptomatic patients.