Hypothyroidism

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138 Hypothyroidism

Instruction

Obtain a history and perform relevant general examination.

Salient features

History

• Dryness of skin

• Hair dryness or loss (Fig. 138.1)

• Cold intolerance

• Change in the voice (hoarse, husky)

• Lethargy, undue tiredness

• Constipation

• Moderate weight gain in spite of loss of appetite

• Menstrual irregularity especially menorrhagia

• Infertility

• Muscle cramps

• Radioiodine therapy for previous Graves’ disease (the patient may have associated eye signs of Graves’ disease)

• Medications and other compounds such as lithium carbonate and iodine-containing compounds (e.g. amiodarone, radiocontrast agents, expectorants containing potassium iodide and kelp)

• Family history of thyroid dysfunction, pernicious anaemia, diabetes mellitus, primary adrenal insufficiency

• Obtain history of hypercholesterolaemia, angina pectoris and hypertension (remember hypertension occurs in 10% of these patients and disappears with thyroxine replacement).

Fig. 138.1 Myxedema facies: dull, puffy, yellowed skin; coarse, sparse hair; temporal loss of eyebrows; periorbital oedema; prominent tongue.

(With permission from Seidel et al. 2004.)

Diagnosis

This patient has delayed ankle jerks, puffy lower eyelids, slow pulse and hoarse husky voice (lesions), indicating that he has hypothyroidism (functional status); the cause needs to be determined (aetiology).

Questions

How is delayed relaxation best elicited in the ankle?

Get the patient to kneel on a chair with his hands holding the back of the chair and then elicit the jerks on either side.

What are the causes of goitre?

• Idiopathic (majority)

• Hashimato’s thyroiditis

• Graves’ disease

• Iodine deficiency (simple goitre)

• Puberty, pregnancy, subacute thyroiditis, goitrogens (lithium, phenylbutazone).

What is the thyroid status in Hashimato’s disease?

Hypothyroidism (usually).

What is the single best clinical indicator for hypothyroidism?

Delayed ankle jerks.

What is the best laboratory indicator for hypothyroidism?

Elevated serum thyroid-stimulating hormone (TSH). When there is a suspicion of pituitary or hypothalamic disease, the serum free thyroxine (T₄) should be measured in addition to serum TSH. Serum triiodothyronine (T₃) is a poor indicator of hypothyroid state and should not be used.

What are the laboratory changes in hypothyroidism?

• Hypercholesterolaemia

• Hyponatraemia

• Elevation of serum creatinine phosphokinase and lactate dehydrogenase

• Hyperprolactinaemia.

What are the causes of isolated thyroid-stimulating hormone elevation?

• Mild (subclinical) hypothyroidism

• Recovery from hypothyroxinaemia of non-thyroidial illnesses

• Medications such as amiodarone or lithium (Arch Intern Med 2000;160:1573–5).

What are the causes of isolated thyroid-stimulating hormone suppression?

• Mild (subclinical) hyperthyroidism

• Recovery from overt hyperthyroidism

• Non-thyroidal illness, which cause low serum free T₄

• Pregnancy during first trimester

• Medications such as dopamine and glucocorticoids.

How would you investigate a simple goitre?

Estimation of serum T₄, T₃, TSH and thyroid antibodies (presence of anti-thyroid peroxidise antibodies suggests Hashimato’s thyroditis).

Remember: One does not know what free T₄ value is normal for an individual person unless the serum TSH is measured.

What is the cause for delayed relaxation in hypothyroidism?

The exact cause is not known. It is probably caused by decreased muscle metabolism.

How would you manage this patient with hypothyroidism?

Oral T₄ replacement therapy for life. The therapeutic dose varies between 100 and 200 µg/day taken as a single dose. It is taken on an empty stomach (1 h before or 2–3 h after food). Dose adjustments are made once in 3 weeks. The dose is adjusted depending on the clinical response and suppression of raised serum TSH. Lack of response to T₄ suggests:

• non-thyroid related disease

• poor compliance

• underlying psychiatric abnormalities

• presence of pernicious anaemia

• associated autoimmune disease such as Addison’s disease.

In hypothyroid patients who become pregnant, T₄ requirements go up by ~50% in the first half of pregnancy.

What is the hazard in treating the elderly?

Rapid T₄ replacement may precipitate angina and myocardial infarction. The starting dose in the elderly is 25–50 µg/day.

What are the cardiovascular manifestations of hypothyroidism?

• Bradycardia

• Mild hypertension

• Pericarditis and pericardial effusion

• High LDL, low HDL levels, hypercholesterolaemia

• Diminished cardiac output and cardiac failure

• Coronary artery disease

• ECG changes: low-voltage T and P waves, prolongation of QT interval.

What do you understand by subclinical hypothyroidism?

This is a condition where there is low normal serum T₄ and there is moderately raised serum TSH (grade 1:5–10, grade 2:10.1–20, grade 3: >20 mIU/l). All these patients should be treated.

What do you understand by the term sick euthyroid syndrome?

In severe acute non-thyroidal illness or following surgery, changes in pituitary–thyroid function result in altered thyroid indices but, despite this, patients remain euthyroid. On recovery from the illness, the indices of thyroid function return to normal (N Engl J Med 1995;333:1562–3). The changes in thyroidal indices include:

• decrease in extrathyroidal conversion of T₄ to T₃, the active form of the thyroid hormone

• a decrease in TSH secretion, which causes decreased thyroidal secretion and, in time, decreases in serum T₄ concentrations and further decreases in serum T₃ concentrations—the latter as a result of both decreased secretion of T₄ by the thyroid and diminished availability of T₄ for peripheral conversion to T₃

• decreased production or diminished affinity for thyroidal hormones of one or more major serum thyroid hormone-binding proteins: thyroxine-binding globulin, transthyretin and albumin. These decreases can result in decreased serum total T₄ levels but not in free T₄ or T₃. Serum concentrations of reverse T₃ (which is inactive) are increased because its deiodination is impaired.

What is the prevalence of hypothyroidism?

The prevalence is 2% of the adult population, whereas mild (sublinical) hypothyroidism is 5–17% (subclinical hypothyroidism is when serum TSH is elevated with a normal free T₄ concentration).

What are the components of Grover’s disease?

• Hypothyroidism

• Autoimmune alopecia

• Transient acantholytic dermatosis.

Laterally truncated eyebrows came to be associated with Anne of Denmark (1574–1619), James I’s Queen Consort, likely because a contemporaneous portrait of her by Paul van Somer shows a woman with fair and abbreviated brows (J Med Biogr 2007;15:97–101). The sign is named after Eugene Hertoghe of Antwerp, is a pioneer in thyroid function research.

WW Gull (1816–1890), FRS, graduated from Guy’s Hospital in London and was created a Baronet when he treated the then Prince of Wales, who had typhoid. He was a good teacher and said that ‘Savages explain, science investigates’. In 1873, he described several previously healthy women who acquired clinical features similar to those in cretinism. He coined the term myxoedema to describe a syndrome in five women with coarse features, mental dullness, dry skin, hypothermia and oedema (Gull WW. On a cretinoid state supervening in adult life in women. Trans Clin Soc London 1873;7:180–185).

Ord in 1878 coined the word myxoedema when, at postmortem, he found extensive deposits of mucin in the skin of the feet (Ord WM. On myxoedema, a term proposed to be applied to an essential condition in the ‘cretinoid’ affection occasionally observed in middle-aged women. Med Chir Trans 1878;61:57).

Treatment for hypothyroidism with sheep thyroid extract was first reported by Murray in 1891.

Emil Theodor Kocher (1841–1917), Swiss Professor of Surgery in Berne, was awarded the Nobel Prize in 1909 for his work on the physiology, pathology and surgery of the thyroid gland. He was the first to excise the thyroid gland for goitre and described myxoedema following thyroidectomy: ‘cachexia strumipriva’. His name is associated with: Kocher forceps, Kocher’s transverse cervical incision for thyroidectomy, Kocher’s operation for the wrist, Kocher’s oblique right subcostal incision for gallbladder surgery, Kocher manoeuvre for reduction of a dislocated shoulder, and Kocher syndrome describing splenomegaly and lymphadenopathy with thyrotoxicosis.

In 1912, Hashimoto (1881–1934), a Japanese surgeon, described autoimmune thyroiditis in four women with goitres that seemed to have turned into lymphoid tissue (struma lymphomatosa).

Johann Hoffmann (1857–1919), a German neurologist.

In 1914 Thyroid hormone was crystallised by Kendall.

In 1927 Harington and Barger reported the synthesis of thyroxine; its initial physiological testing was reported in 1927.

R Debré and G Sémélaigne were both French physicians (Debré R, Sémélaigne G. Syndrome of diffuse muscular hypertrophy in infants causing athletic appearance. Its connection with congenital myxoedema. Am J Dis Child 1935;50:1351).

In 1948, HEW Roberton, a general practitioner in New Zealand, was the first to recognize postpartum thyroid disease; he successfully treated lassitude and other symptoms of hypothyroidism related to the postpartum period with thyroid extract.

In 1952, triiodothyronine was discovered by Pitt-Rivers and Gross.

In 1956, Roitt and colleagues reported the presence of circulating thyroid autoantibodies in Hashimoto thyroiditis.

In 1963, Condliffe purified thyrotrophin (TSH), and soon thereafter Odell and Utiger both reported the first immunoassays for human TSH.

In 1970, the endogenous generation of T₃ from T₄ was described by Ingbar, Sterling and Braverman.

In 1971, Mayberry and Hershman simultaneously described use of TSH immunoassays for diagnosis of hypothyroidism.

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