Clinical consequence (symptoms or otherwise) of deficient secretion of the thyroid gland.


  • Very common- Overt hypothyroidism in 1.9% of women and 0.1% of men (incidence of 0.4% women and 0.06% men); increases with age
    • Subclinical hypothyroidism is thought to occur in 8% of women and 3% of men
    • Congenital hypothyroidism occurs in 1 in 4000 births
  • Can be classified as
    • Congenital or acquired
    • Primary (thyroid dysfunction) or Secondary (normal thyroid function but abnormal stimuli)
    • Overt or subclinical (the latter is defined as fT4 within normal range despite high TSH)


  • Symptoms can be relatively non-specific and can be insidious (may present after years)
  • Symptoms include:
    • Tiredness, lethargy
    • Intolerance to cold*
    • Dry skin and hair loss
    • Difficulty concentrating, poor memory
    • Constipation*
    • Decreased appetite with weight gain
    • Deep, hoarse voice*
    • Puffy eyes*
    • Weakness* or muscle cramps
    • Paraesthesia of the hand (carpal tunnel)
    • Low mood, sleeping problems (e.g. sleep apnoea* due to tissue swelling/enlargement)
    • Hearing loss (increased fluid in the middle ear)
    • Menorrhagia, oligomenorroea or amenorrhoea
    • Reduced libido
      • * the following symptoms are good symptoms to differentiate hypo- and euthyroid patients
  • NB There may also be a history suggestive of hyperthyroidism (e.g. with transient thyroiditis)
    • Other symptoms include thyroid pain
  • Remember to have raised suspicion of hypothyroidism in pregnancy
    • NB Pregnant women may require more close monitoring and be more likely to require treatment. (Thyroid hormone is important for foetal development)
  • On Examination
    • Dry, coarse, possibly yellowish skin; sparse, coarse hair; cool peripheries
    • Puffy face, hands and feet, periorbital oedema
      • NB Some patients (5%) can also present with eye disease similar to that in Graves i.e. proptosis, restricted eye movements, redness, etc
      • Large tongue
    • Bradycardia
    • Generalised oedema (non-pitting; myxoedema)
    • Delayed tendon reflex relaxation e.g. prolonged ankle jerk/clonus; bradykinesia
    • Carpal tunnel


  • Thyroid function tests
  • NB NICE guidelines do not recommend routinely testing for thyroid peroxidase antibodies or TRAb
    • The former is present in multiple causes of hypothyroidism and rarely helps to guide treatment
    • Indications for antibody investigations include
      • Subclinical hypothyroid where TSH levels are very low (<10mU/l)
      • Prior to amiodarone treatment (or lithium or interferon alfa)
      • Women with T1DM who are pregnant/planning pregnancy
  • Who to screen/test?
    • People with goitre, T1DM should be screened at presentation, ASAP in women who are pregnant or planning pregnancy, and at 6-8 weeks post-partum
    • People with T2DM, AF, Osteoporosis, dyslipidaemia, amenorrhoea/menorrhagia, subfertility, postpartum depression, should be screened at presentation
    • People who have had radioiodine treatment or thyroid surgery should be screened 4-8 weeks post treatments then every 3 months up to a year
    • People who have had neck irradiation/surgery, Down’s/Turner’s syndrome should be screened annually
    • People with a family/personal history of thyroid disease (autoimmune or otherwise), or with other autoimmune disorders; should be screened ASAP in women who are pregnant or planning pregnancy, and at 6-8 weeks post-partum
    • People on amiodarone, lithium or interferon alfa

Causes of Hypothyroidism

  • Worldwide, iodine-deficiency is most common (but this is rare in the UK).  Most common cause in UK is autoimmune thyroid disease or iatrogenic thyroid damage following surgery/radioactive iodine treatment for other causes
  • Primary
    • Autoimmune
      • Hashimoto’s thyroiditis
        • Most common cause (estimated to occur in between 0.3-1.5% of the general population)
          • More common in older women
          • Often associated with other autoimmune diseases e.g. Addison’s, T1DM, Pernicious anaemia, rheumatoid arthritis, SLE etc
        • There is classically aggressive destruction of thyroid cells by various autoimmune process (TPO antibodies are often present in very high titres).  The cause of which is not understood
          • Usually has periods of destruction then regeneration, which produces a goitre- often this remains even once the patient returns to a euthyroid state; it may be responsive to levothyroxine (even if the patient is euthyroid)
          • Also causes a reduction in T3/T4 secretion (in contrast to Grave’s)
      • Atrophic thyroiditis (Ord’s thyroiditis)
        • Also very common (most common in Europe).
        • Similarly caused by autoimmune processes (commonly involving TRAb and TPO antibodies)
        • In contrast to Hashimoto’s, atrophic disease rarely ever has a hyperthyroid phase and it rarely produces a goitre (almost always just atrophy/destruction)
    • Iodine deficiency
    • Drugs e.g. amiodarone, contrast, lithium, antithyroid drugs
    • Congenital hypothyroidism
    • Infiltrative e.g. amyloidosis, sarcoidosis
  • Secondary
    • TSH deficiency
    • Hypopituitarism (e.g. neoplasm, infiltrative, infection, radiotherapy)
    • Hypothalamic
  • Transient causes (do not require treatment)
    • First 6 months after subtotal thyroidectomy or radioiodine treatment of Graves’
    • Post thyrotoxic phase of subacute thyroiditis
    • Post partum thyroiditis


  • Thyroid hormone replacement (levothyroxine) is the mainstay of treatment for chronic (i.e. not transient) causes of hypothyroidism
    • Start low dose (e.g. 50μg for 3 weeks) then increase to 100μg for another 3 weeks.  Remonitor TFTs and adjust maintenance dose accordingly (100-150μg is common).
      • Aim is to keep TSH <10mU/l.  This may mean having a slightly elevated fT4 level.
  • Subclinical hypothyroid (Normal T3/4 but raised TSH)
    • Treat if TSH >10; Autoantibody positive; presence of other autoimmune conditions; previous treatment for hyperthyroidism

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