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Pathology Core Reference Laboratory Case Study: Postpartum Autoimmune Thyroid Syndrome

By Laurence M. Demers, PhD

A 26-year-old white female presented to her obstetrician with complaints of heart palpitations. She states that the palpitations have been constant over the past two weeks but seem worse at nighttime. When asked to describe them, she states that they are regular and it feels as if her heart is going to jump out of her chest. She denies chest pain, shortness of breath or lightheadedness. She has felt a bit warm of late but denies any frank diaphoresis. It is of note that she recently delivered a normal baby boy during an uncomplicated delivery 5 1/2 weeks before this visit. Her review of system is remarkable for loose stools occurring approximately 4 times/day. She complains of feeling tired but unable to get a good night sleep. She states that she feels as if her mind is racing. She denies any nausea, vomiting or abdominal pain. She also denies myalgias, arthralgias, fevers or chills. She denied heat or cold intolerance.

On physical examination, she presented as a thin, white female in no apparent distress. Her blood pressure was 146/90. Pulse 96 and regular and a normal temperature of 37 degrees taken orally. Her review of systems revealed clear lungs, normal heart rhythm, normal abdomen and a normal neurological response although she showed a fine tremor of the hands. Her neck was supple with no lymphadenopathy however her thyroid was approximately 1.5 times normal in size, symmetrically enlarged, firm, non-tender with carotids palpable bilaterally without bruits.

Her blood work at the time of the clinic visit included a CBC (WBC 14.2, Hct, 38.6, MCV normal, platelet count normal, differential 56% neutrophiles, 7% bands, 34% lymphocytes and 3% monocytes) and a chemistry screen that included electrolytes (NA 142, K 3.6, Cl 101, CO2 22), glucose 86, BUN 26, creatinine 1. She also had a thyroid panel that included thyroxine 16.2 (NL 4-13), T3 resin uptake 34% (NL 25 – 35%) and a TSH of <0.05 (NL 0.3 5.0). From the physical examination, the patient's history including post partum status and the abnormal thyroid function tests, the working diagnosis was postpartum thyroiditis with hyperthyroidism. The patient had a radioactive iodine uptake scan which was normal and subsequently had thyroid auto-antibodies determined which were positive for anti-thyroglobulin and anti-microsomal antibodies. A thyroid biopsy was also performed and revealed diffuse, lymphocytic infiltration, a characteristic histologic picture of post partum thyroiditis. In this case the patient was simply treated with beta blockers to reduce the heart palpitations. Inside three months, the thyroiditis had resolved and the patients' symptoms disappeared with normal thyroid function test results.

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Postpartum thyroiditis (PPT) is a relatively common disorder expressed in 5 to 15% of postpartum women. This disorder initially presents as thyrotoxicosis in the period from 6 weeks to 3 months postpartum, is associated with an auto immune component and usually resolves spontaneously after 1-2 months of expression. In some patients, the thyrotoxic phase can be followed by a hypothyroid phase before spontaneous disease resolution occurs. This thyroid disorder is a distinct variant of silent (painless) thyroiditis and is more prevalent in patients with a family history of Hashimoto’s thyroiditis. Over 50% of patients will have a mild goiter condition.

Patients with postpartum thyroiditis usually present with the onset of palpitations and fatigue. Since these symptoms can be mildly expressed in the young mother with the trials and tribulations of normal pregnancy, these symptoms can easily be overlooked. In some patients, hypertension can accompany this disorder. The symptoms of thyrotoxicosis are generally milder than that of Graves disease, another form of thyroid auto immune disease however the presenting symptoms can be similar and it is important to distinguish thyrotoxicosis due to PPT and Graves disease since the approach to treatment is quite different between the two. The radioactive iodine uptake or thyroid scan can be used to differentiate Graves disease from PPT. A normal scan or uptake is observed in patients with PPT in contrast to Graves where there is a marked elevation in radioactive iodine uptake.

Predisposing factors for postpartum thyroiditis include a family history of thyroid disease particularly Hashimoto’s thyroiditis, the presence of other endocrine auto immune disorders (Type I Diabetes Mellitus), iodide exposure and interestingly enough cigarette smoking. White and Asian races as opposed to the black population are more prone to developing PPT.

Thyroid function testing is an important part of establishing the diagnosis of postpartum thyroiditis. An elevated level of thyroxine (Total T4 or Free T4) with a suppressed TSH level occurs in the thyrotoxic phase of the disorder while an elevated TSH with normal to low FT4 levels are found in the hypothyroid phase that occurs subsequent to the thyrotoxic phase. Measurement of thyroid peroxidase (TPO), the major antigen of thyroid microsomes recognized by anti-thyroid microsomal antibodies is important in establish the differential diagnosis.

TPO antibodies are elevated as early as the first trimester in patients who will manifest this disorder and are also raised at the time of delivery. It has been suggested that screening with TPO antibodies in high risk patients could identify those patients at risk of developing post partum thyroiditis.

To distinguish PPT from Graves disease, measurement of antibodies to the TSH receptor and the use of the thyroid scan are approaches that can help confirm the diagnosis. Both are abnormal with Graves disease and normal in the patients with PPT.

Genetics, immune dysfunction and environmental factors all contribute to the expression of auto immune thyroid disorders in the postpartum period. The genetic component of PPT is well established as noted in the literature however the considerations as to what governs the susceptibility of this disorder in some patients is still unclear. Pregnancy itself can trigger alterations in the immune system which become manifest after the pregnancy itself has ended.

PPT appears to be triggered in some patients through a rebounded immune response which can cause immune alterations and injury directly affecting the thyroid gland. The immune rebound hypothesis during pregnancy has also been linked to other auto immune thyroid disorders such as Graves, Hashimoto’s and systemic auto immune conditions such as systemic lupus erythematosus and rheumatoid arthritis.

Atypical expression of a thyroid microsomal antigen reflects the auto immune expression of this disorder. TPO antibodies have been shown to reflect disease activity. The total IgG elevation in these patients is associated predominantly with the IgG subclasses 1 and 4. The cytolytic events in the thyroid gland itself appears to be due to T-cell and NK cell attack. The massive infiltration of lymphocytes leads to enhanced release of thyroid hormone presumably from thyroglobulin stores. The circulating lymphocyte has been studied in patients with PPT and shown to reflect an increase in activated T cells with helper-inducer activity.

Because postpartum thyroiditis can spontaneously resolve, treatment is often unnecessary because the manifestation of thyrotoxicosis is usually mild and self limited. In some patients, symptomatic relief of the heart palpitations is brought about with the use of beta blockers which reduce the severity of tremor, palpitations and other anxiety related symptoms. The use of anti-thyroid drugs and/or radio iodine ablation has no role in the therapy of these patients during the thyrotoxic phase. On occasion, patients who develop hypothyroidism with this disorder are put on thyroid replacement therapy. Most patients have a complete remission although some 25% of patients have a recurrence with a subsequent pregnancy.

Table 1. Differential Diagnosis of Thyrotoxicosis Between Postpartum Thyroiditis and Graves Disease

Suggested Reading

  • Walfish, PG, Chan, JYC. Post Partum Hyperthyroidism. Clin. Endocrinol. Metab.1985;14:417
  • Singer, PA, Gorsky, JE. Familial post partum transient hyperthyroidism. Arch Intern. Med 1985;145:240
  • Ramsay, I. Post Partum Thyroiditis – An Underdiagnosed Disease. Br. J. Obstet. Gynec. 1986; 93:1121.
  • Goldman, JM. Post Partum thyroid dysfunction. Arch. Intern. Med. 1986; 146:1296
  • Nikolai, TF, Turney, SL, Robert, RC. Post Partum lymphocytic thyroiditis. Prevalence, clinical course and long term follow up. Arch Intern. Med. 1987; 147:221.
  • Hayslip, CC, Fein, HG, O’Donnell, VM et al. The value of serum antimicrosomal antibody testing in screening for symptomatic post partum thyroid dysfunction. Am. J. Obstet. Gynec. 1989; 159:302.


This case study was provided by Laurence M. Demers, PhD, Professor Emeritus of Medicine and Pathology at Penn State College of Medicine, 500 University Drive, Hershey, PA 17033. This material may not be reproduced without the permission of the author.