The clinical presentation in PPT varies from patient to patient, depending upon duration of inflammatory reaction, degree of damage to thyroid gland and presence of temporary or permanent complication. In most cases, the symptoms are presented after several months of delivery. As described earlier, the autoimmune process in thyroid gland typically leads to initial, temporary hyperthyroidism followed by hypothyroidism in the later course, which can either be temporary or permanent. 

The clinical signs and symptoms associated with temporary hyperthyroidism in PPT are usually mild and transient and patients often fail to identify them by associating the symptoms to stress and mood disorders. Common symptoms related to an overactive thyroid gland include intolerance to heat, tremors, increased heart rate, muscular weakness, lack of concentration and weight loss due to increased metabolism. These symptoms often persist for a short period and are followed by episodes of hypothyroidism. Symptoms associated with an underactive thyroid gland comprise muscle cramps, lethargy, intolerance to cold, generalized body weakness, constipation and weight gain due to reduced metabolism. 

Establishment of diagnosis is usually based on disease stage. According to ATA, thyroid levels must be aggressively monitored in patients suspected with PPT since 80% of the patients remain asymptomatic for 1-1.5 years after initial onset of symptoms.

In the presence of symptoms related to hyperthyroidism during early stage of the disease, a radioactive iodine uptake test is performed. The test can help in differentiating hyperthyroidism due to PPT from Graves disease. In the presence of symptoms associated with an underactive thyroid gland during the later stage of the disease, estimation of serum T4 and TSH levels is required to confirm hypothyroidism. Moreover, the likelihood of developing permanent hypothyroidism is indicated by persistently elevated serum TPO levels, TSH levels exceeding 20 mIU/L and sole presence of hypothyroidism with the absence of any preceding initial hyperthyroid phase.   

Treatment of PPT depends on patients's medical history, health status, age, disease severeness and most importantly the phase of the disease. 

Symptoms of hyperthyroidism that commonly occur in the initial phase of the disease are managed differently compared to those of hypothyroidism. Rapid heart rate and presence of tremors resulting from sympathetic stimulation are controlled by beta blockers. 

During the hypothyroid phase of the disease, hormone replacement therapy is required to compensate for thyroid hormones deficit. Normally, daily dose of levothyroxine, a synthetic alternative to natural thyroid hormone is prescribed for about six months. During this period, patient's serum TSH and T4 levels are continuously monitored. It has been estimated that about 25%-30% women develop permanent hypothyroidism following PPT. In such cases, maintenance of thyroid hormone levels requires daily intake of levothyroxine for the rest of life. 

Indefinite prescribing of levothyroxine is discouraged as it increases the likelihood of developing hyperthyroidism-like symptoms in successive pregnancies. The ATA recommends yearly follow-up of PPT patients to monitor serum thyroid levels.

Women who have had PPT in preceding pregnancies are at an increased risk of developing the same in the ensuing pregnancies. Regular follow up and assessment of serum TPO, TSH, and T4 levels is required. The likelihood of developing permanent hypothyroidism is about 25%. 

The exact cause of development of PPT is not known. The ATA has enlisted certain risk factors that can contribute to inflammation of thyroid gland. These include a previous history of thyroid gland disorder, coexisting type 1 diabetes mellitus, presence of antithyroid antibodies in blood and a prior history of postpartum thyroiditis. 

PPT is a common condition. Epidemiological studies have revealed the occurrence of PPT in 8.3% of women globally whereas in the US, the percentage is found to be 5.8% [2]. The prevalence of PPT has been estimated to be approximately 5.9%-7.4% within 12 months following birth [3]. The consecutive episodes of both hyperthyroidism and hypothyroidism occur in about 16% women with no disease history [4]. 

However, certain disease conditions can contribute to the risk of developing PPT. In the presence of type 1 diabetes mellitus, positive antithyroid antibodes or an autoimmune thyroid disorder, the risk increases dramatically with about three times higher risk in women with type 1 diabetes mellitus [3] [5]. Women who have had a family history of autoimmune disorders are more prone to suffer from thyroid dysfunction although personal history of rheumatoid arthritis or scleroderma does not predispose a woman to suffer from PPT in future [6] [7]. Moreover, women with previous history of PPT in preceding pregnancies are at an extremely high risk for developing PPT in succeeding pregnancies with a prevalence rate of up to 69% [8].

The inflammation of the thyroid gland in PPT occurs in response to an autoimmune reaction. The activation of antigen-specific helper T cells provokes the inflammatory response. However, the exact triggering factor for T cell activation is not completely understood [9]. Once the T cells are activated, they induce B lymphocytes [10] to secrete thyroid peroxidase antibodies (TPO). TPO then cause apoptopic damage to thyrocytes and a cascade of inflammatory reactions occurs which leads to the release of thyroxine (T4) and triiodothyronine (T3) due to cytotoxic damage to thyrocytes, thus mimicking symptoms of hyperthyroidism. The sudden rise in levels of serum thyroid hormones causes the pituitary gland to reduce the secretion of thyroid stimulating hormone (TSH) through a negative feedback mechanism and the ensuing drop in TSH levels in blood ultimately halts the production and release of new thyroid hormones by thyroid gland, leading to temporary hypothyroidism. Once the inflammatory reaction subsides and undergoes complete resolution, the normal levels of thyroid hormones and TSH are restored. Alternatively, significant damage to the thyroid gland coupled with persistent inflammation can complicate the condition leading to permanent hypothyroidism.

PPT is not preventable although timely diagnosis of the phenomena can help in avoiding the ensuing adverse effects to health. Pregnant women should be counseled about reporting any unusual symptoms after delivery. Women who have had PPT in earlier pregnancies carry risk of recurrence in subsequent pregnancies and require regular follow ups along with close monitoring of their thyroid levels.

Postpartum thyroiditis (PPT) is a short-term, autoimmune disorder characterized by inflammation of thyroid gland that occurs after delivery. According to the American Thyroid Association (ATA), about 5%-10% of women experience inflamed thyroid gland after birth. The symptoms of postpartum thyroiditis may appear several months following birth and are manifested as hyperthyroidism, hypothyroidism or episodes of both [1]. However, the condition usually subsides and thyroid gland returns to its normal function within a year after undergoing inflammation with a few exceptional cases which lead to the development of lifelong complications. 

Thyroid gland plays a major role in fetal development and optimum levels of thyroid hormones are important in regulating normal body functions and preventing occurrence of certain postpartum complications. The exact of cause PPT still remains unknown but certain factors can increase the likelihood of developing the condition. Risks of recurrence are high in women who have had PPT in preceding pregnancies. Additionally, women with a personal or family history of thyroid dysfunction are more prone to develop PPT. 

Diagnosis, clinical presentation and treatment of the disease depend upon the phase of the disease. In initial phase with suspected hyperthyroidism, evaluation of symptoms linked to hyperactive thyroid gland along with radioactive uptake iodine test are used to confirm diagnosis. Treatment at this stage is largely symptomatic. Alternatively, symptoms of hypothyroidism require measurement of serum TSH and T4 levels to establish the diagnosis. The low blood levels of thyroid hormones are compensated with prolonged administration of levothyroxine until the levels are normalized. 

The thyroid gland is a butterfly-shaped organ present on the front side of the neck. The gland produces and releases thyroid hormones in blood which regulate different body functions in the brain, heart, muscles and digestive system. Therefore, disturbance in levels of thyroid hormones or any damage to the thyroid gland consequently impacts all such body functions adversely. 

Postpartum thyroiditis (PPT) is an inflammation of the thyroid gland that occurs in women after childbirth due to some unknown mechanism. PPT is quite common and affects about 5%-10% of women in the US after childbirth. The possibility of developing PPT is increased in women already suffering from preexisting autoimmune disorders such as diabetes mellitus type I, presence of antithyroid antibodies in blood, previous history of PPT or thyroid dysfunction and family history of thyroid dysfuntion.

The inflammatory reaction occurs due to an autoimmune reaction in which formation of antithyroid antibodies inside body causes damage to thyroid hormone producing cells in the thyroid gland, resulting in imbalance in thyroid hormone levels in the blood. As a result, the levels of thyroid hormones are fluctuating from being very high to considerably low, although some women may only suffer from either stage throughout the illness. In the initial stage of the disease the levels of thyroid hormones are abnormally high and the condition is known as hyperthyroidism (overactive thyroid gland). In the later stage the levels start depleting to exceptionally low values causing hypothyroidism (denoted by an underactive thyroid gland). The symptoms of the disease differ completely in both stages. In hyperthyroidism, patients complain of hot flushes, agitation, tremors, rapid heart beat, anxiety, difficulty in concentrating, muscle weakness and weight loss. These symptoms usually subside within 1-3 months. On the other hand, the symptoms in hypothyroidism may persist for 9-12 months and are presented by cold sensation occurring due to intolerance to cold, overall body weakness, constipation and weight gain. About 20% of women with PPT may develop permanent hypothyroidism. 

Diagnosis of PPT is based on the symptoms as both phases of the disease require different diagnostic tests. In suspected hyperthyroidism, a radioactive uptake iodine test is performed to rule out other causes of an overactive thyroid gland. In the presence of symptoms associated with hypothyroidism, analysis of blood levels of thyroid hormones (particularly thyroid stimulating hormone and T4) is performed to confirm diagnosis. 

Treatment in the hyperthyroid stage of PPT is mainly based on relieving symptoms occurring from increased thyroid hormones in blood. A class of medications called beta-blockers are used to control hyperactive symptoms such as increased heart rate and tremors. In the case of an underactive thyroid gland characterized by low levels of functional thyroid hormones, synthetic thyroid hormone levothyroxine is prescribed daily until the condition resolves. 

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