|Year : 2013 | Volume
| Issue : 4 | Page : 20-21
Postpartum thyroid dysfunction
|Date of Web Publication||2-Feb-2013|
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Sriram U. Postpartum thyroid dysfunction. Thyroid Res Pract 2013;10, Suppl S1:20-1
| Introduction|| |
Postpartum thyroid dysfunction is being diagnosed more often and is being increasingly (though debated) associatedwith other postpartum conditions like mood disorders and depression. Hypothyroidism associated with Sheehan's syndrome is a well-recognized disorder, while awareness and understanding regarding postpartum thyroiditis and exacerbation of autoimmune thyroid disorders like Graves' and Hashimoto's is more recent.
Postpartum thyroid dysfunction typically occurs within the first 12 months after delivery, but has been reported after miscarriages and abortions. Since the first description of transient postpartum thyroid dysfunction by Amino et al.  several groups from various parts of the globe have reported on postpartum thyroiditis with prevalence rates ranging from 1.1% to 16.7%. This wide range is primarily due to methodological differences in study designs, geographic differences with varied iodine intake, and definition of postpartum thyroiditis among other variables.
Postpartum thyroidtis typically presents as thyrotoxicosis within the first 3-4 months after delivery [it may occur as late as 10 months later] after delivery or abortion. Symptoms include fatigue, sleeplessness, palpitations, and irritability. The recognition of PPT is often delayed due to attribution of symptoms to difficulties with responsibilities associated with caring for a newborn. The thyrotoxic phase is followed by a hypothyroid phase, which may last for several months. This pattern occurs in about one-third of the patients with postpartum thyroiditis.
Diagnosis is made by clinical features, low TSH (elevated or normal free T4), and low uptake on radioactive iodine uptake. Another one-third of women develop hypothyroidism without the hyperthyroid phase. Its symptoms include fatigue, poor concentration, poor memory, aches and pains, weight gain, and depression. Majority of women fully recover and a small percentage (2-21%) may remain permanently hypothyroid. A recent study has, however, shown a much higher percentage of permanent hypothyroidism. 
Postpartum thyroidits is more prevalent in women with anti-thyroid peroxidase antibodies, certain HLA haplotypes like DR 3, DR 4, and DR5, type 1 diabetes, lupuserythematosus, rheumatoid arthritis, and scleroderma. It is likely to result in permanent hypothyroidism in women with high anti-TPO antibodies, very high TSH at presentation and presence of other autoimmune disorders. Cytopathological studies have suggestive oflymphocytic thyroiditis. Ultrasonography shows diffuse hypoechogenicity and increased volume.
Graves' thyrotoxicosis may recur immediately after delivery due to rebound in the immune status after partial suppression during pregnancy. This will have to differentiated from postpartum thyroiditis since the management is entirely different.
| Treatment|| |
Therapy of the thyrotoxic phase ranges from no treatment to use of beta blockers in the thyrotoxic phase. Hypothyroid women may be observed if they are asymptomatic and TSH is repeated in 6weeks. If the TSH is >10 miu/ml, thyroxine is initiated in doses of 50-5 mcg/day and TSH is repeated in 6-8 weeks. Women with TSH level between 5 and 10 miu/ml can be observed or treated with 25 mcg of thyroxine if they are symptomatic or are planning another pregnancy soon. Thyroxine can be withdrawn after treatment for a period of 6-12 months to assess recovery.
| Graves' Thyrotoxicosis|| |
Treatment with beta blockers and anti-thyroid drugs is the preferred first line. Radioactive iodine therapy may be considered for women not breast feeding or after weaning.
Screening (with TSH and anti-TPO antibodies) for postpartum thyroid disorders is recommended in women with symptoms suggestive of hyper or hypothyroidism, women with type 1 diabetes, prior postpartum thyroiditis (since it may recur), women with anti-TPO antibodies, women with a family history of thyroid disorders and women with autoimmune disorders. Women with normal TSH and negative anti-TPO need not be evaluated further and women with antibodies will need another TSH at 9 months.
| Prevention of PPT|| |
A recent study by Negro using selenium 200mcg throughout pregnancy and postpartum period has shown marked decrease in the incidence of PPT. Further studies are needed to validate these findings[Figure 1] and [Figure 2].
| Summary|| |
Postpartum thyroid dysfunction is common. Clinicians need to have heightened awareness to recognize the condition. Screening is recommended in high risk group and therapy is directed at the underlying cause.
| References|| |
|1.||Amino N, Mori H, Iwatani Y, Tanizawa O, Kawashima M, Tsuge I, et al. High prevalence of transient post-partum thyrotoxicosis and hypothyroidism. N Engl J Med 1982;306:849-52. |
|2.||Stagnaro-Green A, Schwartz A, Gismondi R, Tinelli A, Mangieri T, Negro R. High rate of persistent hypothyroidism in a large-scale prospective study in postpartum thyroiditis in Southern Italy. J Clin Endocrinol Metab 2011;96:652-7. |
[Figure 1], [Figure 2]