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Thyroid Disease In Pregnancy

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It is usual for the thyroid gland to hypertrophy in normal pregnancies. There is also an increase in thyroid-binding globulin and albumin due to increased hepatic synthesis.1

In pregnancy:

  • Total T4 and T3 increase.
  • Free T4 and T3 remain within normal range.
  • Thyroid stimulating hormone (TSH) does not change.

Thyroid peroxidase antibodies (TPAs) are present in 10% of women at 14 weeks' gestation and are associated with:2

  • An increased rate of pregnancy failure.
  • An increased incidence of gestational thyroid dysfunction.
  • A predisposition to postpartum thyroiditis.

Thyroid function should be measured in women with severe hyperemesis gravidarum but not in every patient with nausea and vomiting during pregnancy.


Hypothyroidism

Epidemiology

Hypothyroidism (including sub-clinical hypothyroidism) occurs in 2.5% of pregnant women.3

Aetiology:

  • Autoimmune thyroiditis, e.g. Hashimoto's thyroiditis
  • Radiotherapy or surgery
  • Congenital
  • Drugs, e.g. lithium, amiodarone
  • Iodine deficiency
  • Infiltrative diseases
  • Pituitary or hypothalamic disease

Presentation

  • Dry skin with yellowing especially around eyes.
  • Weakness, tiredness, hoarseness, hair loss, intolerance to cold, constipation, sleep disturbance.
  • Goitre, delayed relaxation of deep tendon reflexes.
  • Anaemia, low T4, raised TSH.
  • In sub-clinical form TSH raised, but free T4 and T3 normal. Antibodies to thyroid peroxidase, TSH receptor or thyroglobulin.

Management

  • Thyroxine at increasing dosages until TSH brought to normal-low range.4
  • Hypothyroidism in pregnancy is treated with a larger dose of thyroxine than in the non-pregnant state.
  • Dose will need to be reduced as necessary after delivery, but postpartum thyroid dysfunction (PPTD) occurs in 50% of women found to have thyroid peroxidase antibodies in early pregnancy. The hypothyroid phase of PPTD is symptomatic and requires thyroxine therapy.
  • A high incidence (25-30%) of permanent hypothyroidism has been noted in these women.2 Women having transient PPTD with hypothyroidism should be monitored frequently, as there is a 50% chance of these patients developing hypothyroidism during the next 7 years.

Complications

Congestive heart failure most significant potential problem.
Women may also develop megacolon, adrenal crisis, organic psychosis, myxoedema coma, hyponatraemia (due to syndrome of inappropriate secretion of antidiuretic hormone).

Prognosis

  • Prognosis for mother and fetus is excellent with appropriate treatment.
  • However there is a small increase in stillbirth rate, and fetal assessment in third trimester is necessary.
  • Recent research has suggested increased risk of lower IQ of children of women with hypothyroidism, even with euthyroid fetus as maternal thyroid hormone needed for neuronal development until 12-13 weeks.5


Hyperthyroidism

Covered in separate article: Hyperthyroidism in Pregnancy


Thyroiditis

Aetiology

  • Acute: usually caused by infection of piriform sinus in younger patients.
  • Sub-acute thyroiditis: de Quervain's or granulomatous thyroiditis and includes postpartum thyroiditis and infection with bacteria or mycobacteria.
  • Chronic thyroiditis: 3 types are autoimmune thyroiditis, e.g. Hashimoto's thyroiditis, Riedel's thyroiditis (occurs in middle-aged pregnant women) and parasitic thyroiditis.

Presentation

  • Sub-acute thyroiditis: tender thyroid enlarged on one side and may have pain in throat or otalgia. May have history of earlier malaise and upper respiratory tract infection. Patients may show signs of thyrotoxicosis due to release of hormones from follicular destruction.
    At this point
    • TSH low with free T4 elevated
    • This is followed by raised TSH and low free T4
  • Postpartum thyroiditis: silent thyroiditis often presents 3-6 months postpartum and is usually painless with positive test for thyroid peroxidase antibodies and normal ESR.
  • Chronic thyroiditis: Hashimoto's disease is characterised by antibodies to several components of thyroid tissue and uniform goitre eventually developing into hypothyroidism. Riedel's thyroiditis presents as a hard, asymmetrical fixed thyroid gland, may cause symptoms by compressing the oesophagus or trachea.
    • Thyroid function test normal
    • ESR raised
    • Leucocytosis

Associations

Hashimoto's disease may be associated with other autoimmune diseases, e.g. Addison's disease, pernicious anaemia also shows increased incidence of mitral valve prolapse. Rarely, autoantibodies cross placenta to cause thyroiditis in the fetus.

Management

  • Sub-acute thyroiditis: usually resolves spontaneously. Patients may need treatment if prolonged hypothyroidism.
  • Postpartum thyroiditis: does not usually require treatment, may benefit from yearly reassessment.
  • Chronic thyroiditis: Hashimoto's disease may cause hypothyroidism requiring treatment with thyroxine. Reidel's thyroiditis may require rescue surgery for severe compression symptoms on trachea or oesophagus.6

Complications

Hashimoto's thyroiditis is associated with an increased risk of miscarriage. The patient may be left hypothyroid in the long-term.


Document references
  1. Glinoer D; What happens to the normal thyroid during pregnancy? Thyroid. 1999 Jul;9(7):631-5. [abstract]
  2. Lazarus JH; Thyroid disorders associated with pregnancy: etiology, diagnosis, and management. Treat Endocrinol. 2005;4(1):31-41. [abstract]
  3. Lazarus JH; Epidemiology and prevention of thyroid disease in pregnancy. Thyroid. 2002 Oct;12(10):861-5. [abstract]
  4. Lazarus JH, Kokandi A; Thyroid disease in relation to pregnancy: a decade of change. Clin Endocrinol (Oxf). 2000 Sep;53(3):265-78. [abstract]
  5. Delange F; Iodine deficiency as a cause of brain damage. Postgrad Med J. 2001 Apr;77(906):217-20. [abstract]
  6. Lorenz K, Gimm O, Holzhausen HJ, et al; Riedel's thyroiditis: impact and strategy of a challenging surgery. Langenbecks Arch Surg. 2007 Apr 3;. [abstract]

Internet and further reading
  • de Swiet M. Medical Disorders in Obstetric Practice. Fourth Edition. Blackwell. London. 2002
Acknowledgements EMIS is grateful to Dr Hayley Willacy for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2009.
Document ID: 2866
Document Version: 22
Document Reference: bgp294
Last Updated: 31 Jul 2009
Planned Review: 31 Jul 2011

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

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