Hypothyroidism

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

Background/Epidemiology

• 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)

Presentation

• 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

Investigations

• 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

Management

• 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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