Hypothyroidism

What is hypothyroidism: types and causes

Hypothyroidism is a state in which the thyroid gland cannot produce sufficient T3 and T4 hormones to regulate metabolism. There are two main forms: primary hypothyroidism (originating in the gland itself — elevated TSH, low T4) and secondary hypothyroidism (pituitary origin — TSH inappropriately low or normal, low T4 — rare). Primary hypothyroidism dominates in clinical practice.

The most common cause is autoimmune Hashimoto thyroiditis, in which anti-TPO and anti-thyroglobulin antibodies attack thyroid tissue. Follicular destruction progresses gradually, and hormone output declines. Other important causes: (1) surgical hypothyroidism following total or subtotal thyroidectomy, (2) permanent gland damage after radioactive iodine therapy, (3) iodine deficiency (reduced in Turkey by iodised salt programmes, but still possible in mountainous regions), (4) drug-induced — lithium (blocks hormone release), amiodarone (contains 37% iodine; can trigger both hypo- and hyperthyroidism), interferon-alfa, tyrosine kinase inhibitors.

Subclinical hypothyroidism is an intermediate state where TSH is elevated but free T4 remains within normal limits; it affects 5–10% of the population. Treatment is generally initiated when TSH exceeds 10 mIU/L or the patient is symptomatic. In pregnancy the TSH target is stricter (<2.5 mIU/L), as maternal hypothyroidism can impair foetal neurological development.

Recognising the symptoms: from fatigue to hoarseness

The symptoms of hypothyroidism reflect a general slowing of metabolism. The most common include: chronic fatigue and drowsiness, unintentional weight gain (driven by fluid and salt retention), cold intolerance, constipation, dry and pale skin, brittle nails, and diffuse hair loss. On the neuropsychiatric spectrum, difficulty concentrating, memory problems, and a depressive syndrome are prominent features of hypothyroidism.

Cardiovascular findings include bradycardia (slow heart rate) and diastolic hypertension. In severe, long-standing cases, myxoedema may develop: marked swelling from protein-mucinous accumulation in the skin, face, and eyelids. Myocardial effusion and conduction abnormalities have also been reported in myxoedematous patients.

An important ENT-related finding is hoarseness (dysphonia). Thyroid hormone deficiency can cause myxoedematous changes in the vocal cord mucosa, leading to a thickening and deepening of the voice. In Prof. Özdoğan's practice, thyroid function tests are routinely ordered for patients presenting with hoarseness. Hypothyroidism can also worsen obstructive sleep apnoea: myxoedematous thickening of the tongue base and oropharyngeal tissues increases airway resistance. Improvement in obstructive sleep apnoea with thyroid treatment has been well documented in the literature.

Diagnosis: TSH testing and interpretation

TSH (thyroid-stimulating hormone) is the most sensitive test for diagnosing hypothyroidism. When the thyroid gland under-produces, the pituitary secretes more TSH to stimulate production — hence an elevated TSH is an early, reliable marker of primary hypothyroidism. The reference range varies by laboratory but is generally accepted as 0.4–4.0 mIU/L; 4.0–10.0 mIU/L is subclinical, ≥10 mIU/L is overt hypothyroidism.

Free T4 (fT4) is interpreted alongside TSH. Elevated TSH + low fT4 = overt primary hypothyroidism; elevated TSH + normal fT4 = subclinical hypothyroidism. Anti-TPO antibodies are requested when Hashimoto is suspected; they are positive at high titre in most cases. Anti-thyroglobulin antibody provides additional information. Thyroid ultrasonography is an important complementary imaging tool for gland-related causes (goitre, nodule, parenchymal heterogeneity).

In pregnancy, trimester-specific TSH reference values are used: 1st trimester 0.1–2.5 mIU/L, 2nd trimester 0.2–3.0 mIU/L, 3rd trimester 0.3–3.5 mIU/L. The thyroid's demand increases by 50% during pregnancy; accordingly, the levothyroxine dose usually needs to be raised from the start of pregnancy. Postpartum thyroiditis covers a transient hypo- or hyperthyroid phase in the first 12 months after delivery — follow-up is important.

Treatment with levothyroxine: what to expect

The standard treatment for hypothyroidism is levothyroxine (LT4), a synthetic T4. It is absorbed in the small intestine and converted peripherally to the active form, T3. It is recommended to take it in the morning on an empty stomach, ideally 30–60 minutes before rising and with water; coffee, milk, calcium, iron, and antacids reduce absorption. The starting dose is based on the patient's weight (typically 1.6–1.7 µg/kg/day) and cardiovascular status; in elderly patients and those with cardiac disease, a low starting dose (12.5–25 µg/day) is used.

TSH targets: 0.5–2.5 mIU/L for the general population; 1–4 mIU/L is acceptable above 60 years; trimester-specific lower limits apply in pregnancy. Dose adjustments are made by TSH check every 4–6 weeks; once target TSH is reached, annual follow-up is sufficient. Symptom improvement typically begins within 4–8 weeks; some patients may take 3–6 months for full recovery.

Patients who have undergone thyroid surgery under Prof. Özdoğan's care — typically total thyroidectomy — require permanent hormone replacement. More frequent monitoring in the first year is recommended for early TSH control and dose optimisation in this group. Additional note: both psychiatric patients on lithium and cardiac patients on amiodarone may require shared follow-up between ENT and cardiology or psychiatry for thyroid monitoring.

Frequently Asked Questions

• Does hypothyroidism require lifelong medication?+
  It depends on the cause. Hypothyroidism from Hashimoto thyroiditis or total thyroidectomy is usually permanent and requires lifelong levothyroxine. By contrast, drug-induced hypothyroidism (e.g., from lithium or amiodarone) or hypothyroidism from transient thyroiditis may allow dose reduction or cessation. With postpartum thyroiditis, 70–80% of patients return to euthyroidism within 12 months.
• Are there foods I should avoid while taking levothyroxine?+
• Can hypothyroidism cause hoarseness — is this an ENT issue?+
• Should subclinical hypothyroidism be treated?+
• Is hypothyroidism inevitable after thyroid surgery, and when does it start?+

References

• ATA/AACEGarber JR et al. Clinical Practice Guidelines for Hypothyroidism in Adults. Thyroid. 2012;22(12):1200-1235.
• ETAPearce SH et al. 2013 ETA Guideline: Management of Subclinical Hypothyroidism. Eur Thyroid J. 2013;2(4):215-228.
• ATAAlexander EK et al. 2017 Guidelines of the American Thyroid Association for Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum. Thyroid. 2017;27(3):315-389.