Thyroid Disease In Pregnancy

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

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 of gestation and are associated with:[2][3]

  • 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.

The need for screening of all women in early pregnancy, thyroid hormone placental physiology and thyroid hormone gestational reference ranges are areas of research which are currently being investigated.[4]


Hypothyroidism (including subclinical hypothyroidism) occurs in 2.5% of pregnant women. However, only 1-3 per 1,000 pregnancies are complicated by overt hypothyroidism.[5]

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  • Autoimmune thyroiditis - eg, Hashimoto's thyroiditis (also known as Hashimoto's disease).
  • Radiotherapy or surgery.
  • Congenital.
  • Drugs - eg, lithium, amiodarone.
  • Iodine deficiency.
  • Infiltrative diseases.
  • Pituitary or hypothalamic disease.


  • Dry skin with yellowing especially around the 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 the subclinical form TSH is raised but free T4 and T3 are normal. Antibodies to thyroid peroxidase, TSH receptor and/or thyroglobulin are positive. It is important to appreciate that TSH ranges in pregnancy differ from those in non-pregnant women and vary from trimester to trimester. Guidance from the local laboratory/thyroid specialist should be sought as to the normal range.[6]

Management [5][6]

  • Thyroxine at increasing dosages until TSH is brought to a normal-low range. The starting dose is usually 0.10-0.15 mg/day and should be adjusted according to TSH levels every four weeks.
  • Hypothyroidism in pregnancy is treated with a larger dose of thyroxine than in the non-pregnant state.
  • Women already on thyroxine before pregnancy should have their dose increased by approximately 30% at the beginning of pregnancy and have TSH and T4 levels checked every eight weeks.
  • Levothyroxine dose will need to be returned to pre-pregnancy levels after delivery and the TSH checked 6-8 weeks postpartum.
  • 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. Women having transient PPTD with hypothyroidism should be monitored frequently, as there is a 50% chance of these patients developing permanent hypothyroidism subsequently.[7]


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


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

This is covered in the separate article Hyperthyroidism in Pregnancy.


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


  • Subacute thyroiditis: tender thyroid enlarged on one side and may have pain in the throat or otalgia. May have a 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 a 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, and may cause symptoms by compressing the oesophagus or trachea.
    • TFT normal
    • ESR raised
    • Leukocytosis


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


  • Subacute thyroiditis: this usually resolves spontaneously. Patients may need treatment if there is  prolonged hypothyroidism.
  • Postpartum thyroiditis: this does not usually require treatment, and may benefit from yearly reassessment.
  • Chronic thyroiditis: more than 50% of women with Hashimoto's thyroiditis require an increase in thyroxine in the postpartum period.[8] Reidel's thyroiditis may require rescue surgery for severe compression symptoms on the trachea or oesophagus.[9]


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

Further reading & references

  1. Bowen R, Thyroid Hormones: Pregnancy and Fetal Development, 2012
  2. Lazarus JH; Thyroid disorders associated with pregnancy: etiology, diagnosis, and management. Treat Endocrinol. 2005;4(1):31-41.
  3. Budenhofer BK, Ditsch N, Jeschke U, et al; Thyroid (dys-)function in normal and disturbed pregnancy. Arch Gynecol Obstet. 2013 Jan;287(1):1-7. doi: 10.1007/s00404-012-2592-z. Epub 2012 Oct 27.
  4. Lazarus JH; Thyroid function in pregnancy. Br Med Bull. 2011;97:137-48. doi: 10.1093/bmb/ldq039. Epub 2010 Dec 23.
  5. El Baba KA, Azar ST; Thyroid dysfunction in pregnancy. Int J Gen Med. 2012;5:227-30. doi: 10.2147/IJGM.S27009. Epub 2012 Mar 6.
  6. Stagnaro-Green A, Abalovich M, Alexander E, et al; Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and postpartum. Thyroid. 2011 Oct;21(10):1081-125. doi: 10.1089/thy.2011.0087. Epub 2011 Jul 25.
  7. Lazarus JH; The continuing saga of postpartum thyroiditis. J Clin Endocrinol Metab. 2011 Mar;96(3):614-6. doi: 10.1210/jc.2011-0091.
  8. Galofre JC, Haber RS, Mitchell AA, et al; Increased postpartum thyroxine replacement in Hashimoto's thyroiditis. Thyroid. 2010 Aug;20(8):901-8. doi: 10.1089/thy.2009.0391.
  9. Lorenz K, Gimm O, Holzhausen HJ, et al; Riedel's thyroiditis: impact and strategy of a challenging surgery. Langenbecks Arch Surg. 2007 Apr 3;.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Hayley Willacy
Current Version:
Peer Reviewer:
Prof Cathy Jackson
Document ID:
2866 (v23)
Last Checked:
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