I recently saw a common, but perhaps under-recognised, problem in a 33-year-old postpartum woman.
The patient has a history of Raynaud's phenomenon, recurrent miscarriage and recurrent DVT.
She presented with joint pains many times in the three months postpartum. There was no objective evidence of joint swelling on examination and all joint examinations were essentially normal.
Her postpartum depression score was normal. Bloods including TFTs were normal at three months postpartum. Eventually, the expertise of a rheumatologist was sought.
When repeated by the rheumatologist, her blood tests revealed a raised T4 at 38pmol/L and a suppressed TSH at 0.01mU/L. These were wildly different from the previous results.
The patient was displaying symptoms of anxiety and weight loss, despite increasing her food intake.
One month later, bloods were repeated to find a T4 of 35.8pmol/L and TSH of <0.05mU/L. Thyroid peroxidase antibodies were markedly raised.
Four weeks on, T4 was 11.2pmol/L with a TSH of 0.17mU/L. One month after that, T4 and TSH had normalised. No treatment was given at any point.
This is a case of a transient hyperthyroid state postpartum, commonly known as postpartum thyroiditis.
Transient changes
Brief changes in thyroid function are said to occur in 1-16% (mean 7.5%) of postpartum women.1 This is much more common when other autoimmune conditions coexist.
Postpartum thyroiditis is believed to be three times more common in women with type 1 diabetes.2,3 It is also linked to thyroid disease in later life; studies show 25% of women with thyroid instability after pregnancy eventually become hypothyroid.1
Pathologically, it is thought to be a short-lived thyroiditis caused by increased immune function following the relative immunosuppression of the pregnancy.1
The classic presentation of thyroid disease is rarely seen postpartum, although there may be weight loss or painless enlargement of a goitre.4
The changes in thyroid state can take various paths; 30% of women will experience a thyrotoxic state, followed by a period of hypothyroidism with subsequent recovery;4 50% will experience a hypothyroid episode only and 30% will experience a hyperthyroid state only.2
In this case, thyroid function became unstable at four months postpartum, which is quite usual. The hyperthyroid phase often occurs at one to six months postpartum, with resolution within one to two months, as seen in this case.3
Recovery of thyroid state should be made by one year in all women;4 however, some studies suggest that 12-60% of women who enter a hypothyroid state remain hypothyroid.5
Monitoring thyroid function for a time in general practice is reasonable if the woman is experiencing problematic symptoms.
Autoimmune disease
High levels of thyroid peroxidase antibodies indicate autoimmune disease and characterise the condition.5 Increased levels of thyroid receptor antibodies indicate Graves' disease and measuring these antibody levels in general practice can give a clearer picture.4
If the diagnosis is in doubt or thyroid dysfunction fails to settle, referral is appropriate. It is important not to start antithyroid drugs in the hyperthyroid stage because there is no overproduction of T4, there is simply an increase in its release.4
In a hypothyroid phase, however, a TSH >10mU/L would be a sensible level at which to commence levothyroxine.1 Propranolol may be of use if the patient has problematic anxiety symptoms in a hyperthyroid phase.1
- Dr Brindle is a GP in Manchester
References
1. Stagnaro-Green A. Post partum thyroiditis. Best Pract Res Clin Endocrinol Metab 2004; 18(2): 303-16.
2. Stagnaro-Green A. Approach to the patient with post partum thyroiditis. J Clin Endocrinol Metab 2012; 97(2): 334-42.
3. Gaberscek S. Thyroid physiology and autoimmunity in pregnancy and after delivery. Expert Rev Clin Immunol 2011; 7(5): 697-707.
4. Roti E, Uberti ED. Post partum thyroiditis - a clinical update. Eur J Endocrinol 2002; 146: 275-9.
5. Lazarus JH. The continuing saga of post partum thyroiditis. J Clin Endocrinol Metab 2011; 96(3): 613-16.
