Scott Urquhart, PA-C

Q: I frequently counsel patients on family planning, pregnancy expectations, and postpartum concerns. Would you please discuss the specifics of postpartum thyroiditis?

Postpartum thyroiditis (PPT) affects about 5% to 10% of postpartum patients, as evidenced by biochemical thyroid dysfunction. It usually presents during the first three to nine months postpartum.

The condition may present as transient hyperthyroidism, transient hypothyroidism, or hyperthyroidism resolving to transient or permanent hypothyroidism. Only one-quarter to one-third of women experience both the hyperthyroid and hypothyroid phases; one-third of patients will have only a thyrotoxic or hypothyroid phase.

Those who are at risk for or develop PPT have underlying autoimmune thyroid disease (eg, Hashimoto’s thyroiditis). During pregnancy, the maternal immune system is partially suppressed; it rebounds dramatically after delivery, leading to increased risk for autoimmune thyroid disease in patients with thyroid peroxidase antibodies (TPOAb).

Q: How do I know if my patients are at risk for thyroid disease during or following pregnancy?

We need to ascertain who is at risk for PPT so we can appropriately evaluate and screen for the condition. It is important to educate your patients prior to or during pregnancy about the risk, timeline of occurrence, and signs/symptoms of PPT.

If possible, I recommend discussing this with patients in the family-planning stages. It would be helpful to ask the prospective mother about a family history of hyperthyroid or hypothyroid disease (eg, Grave’s disease or Hashimoto’s thyroiditis). It’s also important to inquire about other autoimmune diseases in the patient or in her family.

Other autoimmune conditions that increase the risk for thyroid disease are: systemic lupus erythematosus, rheumatoid arthritis, pernicious anemia, vitiligo, type 1 diabetes, and Addison’s disease. Of note, patients with type 1 diabetes are three times more likely than those without that condition to develop PPT.

Q: Which tests will provide the best information about risk for or presence of PPT? When should I order such tests? 

The thyroid-stimulating hormone (TSH) assay is the most sensitive laboratory test for thyroid function in a patient with a normal pituitary-thyroid axis. Testing for TPOAb is the best available screening tool for postpartum thyroiditis, being widely available, economical, and reproducible. Studies evaluating the utility of TPOAb have demonstrated a sensitivity of 46% to 89%, with a specificity of 91% to 98%. Depending on the timeline of the postpartum presentation, an elevated or low TSH level in conjunction with positive TPOAb is pathognomonic for PPT.

If the prospective or expectant mother has a personal or family history of an autoimmune disease, it would be a good idea to obtain a baseline TSH level and TPOAb. If unobtainable beforehand, a baseline TSH during pregnancy is prudent, since many of the signs and symptoms of hyper/hypothyroidism can be similar to those seen in “normal” pregnancy. A normal TSH in the face of elevated TPOAb increases the patient’s likelihood of developing Hashimoto’s thyroiditis or PPT. The best time to check TPOAb is before pregnancy or after delivery, since these antibodies can decrease or even normalize during pregnancy.

Q: Since PPT can be elusive, how might one clinically evaluate the postpartum patient?

The reasons for missed diagnosis of PPT are twofold. First, it results from women reporting few to no symptoms or simply “writing off” the signs and symptoms, thinking they’re related to the significant emotional/physical demands of caring for the new baby. Second, there is a lack of clinician recognition regarding the risk factors, clinical presentation, and frequency of PPT. Since one-third of the hyperthyroidism of PPT is asymptomatic or unreported by patients, it’s easy to see how clinicians can be uncertain whether postpartum anxiety, insomnia, palpitations, increased heart rate, and fatigue reflect thyrotoxicosis or “new mother demands.” Similarly, fatigue, constipation, impaired concentration/memory, weight gain, and depression can be interpreted as hypothyroidism or the emotional and physical challenges of infant care. Since either hyperthyroid or hypothyroid symptoms can be subtle, PPT goes undiagnosed—and therefore, untreated.

Here is an example to provide a clearer understanding:

PPT can go from hyperthyroid to hypothyroid over a four- to six-month period. I like to refer to this evolving process in its three phases to foster understanding of what is going on not only symptomatically but biochemically as well. The first phase starts with a bout of hyperthyroidism from an increased release of thyroid hormone (T4 and/or T3) as a result of nonpainful/nontender thyroid inflammation.

During this first phase, it’s unfortunate that many new mothers’ symptoms are “written off” as the anxieties associated with being a new mother. If a TSH is not ordered, the woman may feel that the clinician is correct in the assessment and that this is all a natural part of the postpartum period. If her hyperthyroid symptoms worsen, she is unlikely to seek follow-up care for fear of being deemed an “anxious mother,” and as a result, the correct diagnosis is missed. 

After approximately two months, the new mother feels better, as the excess thyroid hormones normalize. This is the second (euthryoid) phase. She may now be convinced that her symptoms of anxiety, agitation, palpitations, and insomnia were from the new experience of motherhood or from the new addition to her existing family. 

After two to three months of feeling well, she begins to experience symptoms of hypothyroidism, which is the third phase of PPT. Her symptoms may include depression, constipation, fatigue, and difficulty concentrating. This is another critical time in which the patient or her clinician may attribute her symptoms to all of the emotional changes and demands of caring for her infant. The clinician may question how the mother has felt over the previous couple of months, and since she has felt well, no thyroid studies are ordered. Again, not questioning the assessment, the mother moves on, only to experience worsening symptoms.

The problem here is that if her hypothyroidism is of a permanent nature, as in the case of autoimmune thyroid disease from Hashimoto’s, she will eventually become more symptomatic but may not return for screening or treatment, thinking this is part of the “normal” postpartum period.

Nearly 20% of PPT patients will remain hypothyroid and require lifelong thyroid hormone replacement. The remaining 80% may develop temporary hypothyroidism, requiring thyroid hormone replacement for up to one year, or the thyroiditis will be mild and resolve without the need for such treatment.

Things to Keep in Mind

Understanding who is at increased risk for PPT should prompt the clinician to check the TSH level and TPOAb before pregnancy, if possible. If the patient is pregnant and has the above stated risk factors for autoimmune thyroiditis, obtaining a baseline TSH level is prudent. In order to obtain a more accurate laboratory evaluation, it would be advisable to wait until after pregnancy to check TPOAb, since the maternal immune system is partially suppressed.

If TPOAb can’t be checked until after delivery, it would make clinical sense to test TSH at the same time (around month 3). In women with positive TPOAb before pregnancy and normal thyroid function throughout pregnancy, TSH should be checked at three and six months postpartum. Clinicians should remain astute and order a TSH any time in the interim if they suspect thyroid dysfunction based on patients’ symptoms. Literature supports annual TSH assays in patients in whom PPT resolved, as they have a markedly increased risk for permanent hypothyroidism.

Suggested Reading

Abalovich M, Amino N, Barbour LA, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2007;92(8 suppl):S1-S47.

American Thyroid Association Web site. www.thyroid.org.

Stagno-Green A. Postpartum thyroiditis. J Clin Endocrinol Metab. 2002;87(9):4042-4047.

Q: I frequently counsel patients on family planning, pregnancy expectations, and postpartum concerns. Would you please discuss the specifics of postpartum thyroiditis?

Postpartum thyroiditis (PPT) affects about 5% to 10% of postpartum patients, as evidenced by biochemical thyroid dysfunction. It usually presents during the first three to nine months postpartum.

The condition may present as transient hyperthyroidism, transient hypothyroidism, or hyperthyroidism resolving to transient or permanent hypothyroidism. Only one-quarter to one-third of women experience both the hyperthyroid and hypothyroid phases; one-third of patients will have only a thyrotoxic or hypothyroid phase.

Those who are at risk for or develop PPT have underlying autoimmune thyroid disease (eg, Hashimoto’s thyroiditis). During pregnancy, the maternal immune system is partially suppressed; it rebounds dramatically after delivery, leading to increased risk for autoimmune thyroid disease in patients with thyroid peroxidase antibodies (TPOAb).

Q: How do I know if my patients are at risk for thyroid disease during or following pregnancy?

We need to ascertain who is at risk for PPT so we can appropriately evaluate and screen for the condition. It is important to educate your patients prior to or during pregnancy about the risk, timeline of occurrence, and signs/symptoms of PPT.

If possible, I recommend discussing this with patients in the family-planning stages. It would be helpful to ask the prospective mother about a family history of hyperthyroid or hypothyroid disease (eg, Grave’s disease or Hashimoto’s thyroiditis). It’s also important to inquire about other autoimmune diseases in the patient or in her family.

Other autoimmune conditions that increase the risk for thyroid disease are: systemic lupus erythematosus, rheumatoid arthritis, pernicious anemia, vitiligo, type 1 diabetes, and Addison’s disease. Of note, patients with type 1 diabetes are three times more likely than those without that condition to develop PPT.

Q: Which tests will provide the best information about risk for or presence of PPT? When should I order such tests? 

The thyroid-stimulating hormone (TSH) assay is the most sensitive laboratory test for thyroid function in a patient with a normal pituitary-thyroid axis. Testing for TPOAb is the best available screening tool for postpartum thyroiditis, being widely available, economical, and reproducible. Studies evaluating the utility of TPOAb have demonstrated a sensitivity of 46% to 89%, with a specificity of 91% to 98%. Depending on the timeline of the postpartum presentation, an elevated or low TSH level in conjunction with positive TPOAb is pathognomonic for PPT.

If the prospective or expectant mother has a personal or family history of an autoimmune disease, it would be a good idea to obtain a baseline TSH level and TPOAb. If unobtainable beforehand, a baseline TSH during pregnancy is prudent, since many of the signs and symptoms of hyper/hypothyroidism can be similar to those seen in “normal” pregnancy. A normal TSH in the face of elevated TPOAb increases the patient’s likelihood of developing Hashimoto’s thyroiditis or PPT. The best time to check TPOAb is before pregnancy or after delivery, since these antibodies can decrease or even normalize during pregnancy.

Q: Since PPT can be elusive, how might one clinically evaluate the postpartum patient?

The reasons for missed diagnosis of PPT are twofold. First, it results from women reporting few to no symptoms or simply “writing off” the signs and symptoms, thinking they’re related to the significant emotional/physical demands of caring for the new baby. Second, there is a lack of clinician recognition regarding the risk factors, clinical presentation, and frequency of PPT. Since one-third of the hyperthyroidism of PPT is asymptomatic or unreported by patients, it’s easy to see how clinicians can be uncertain whether postpartum anxiety, insomnia, palpitations, increased heart rate, and fatigue reflect thyrotoxicosis or “new mother demands.” Similarly, fatigue, constipation, impaired concentration/memory, weight gain, and depression can be interpreted as hypothyroidism or the emotional and physical challenges of infant care. Since either hyperthyroid or hypothyroid symptoms can be subtle, PPT goes undiagnosed—and therefore, untreated.

Here is an example to provide a clearer understanding:

PPT can go from hyperthyroid to hypothyroid over a four- to six-month period. I like to refer to this evolving process in its three phases to foster understanding of what is going on not only symptomatically but biochemically as well. The first phase starts with a bout of hyperthyroidism from an increased release of thyroid hormone (T4 and/or T3) as a result of nonpainful/nontender thyroid inflammation.

During this first phase, it’s unfortunate that many new mothers’ symptoms are “written off” as the anxieties associated with being a new mother. If a TSH is not ordered, the woman may feel that the clinician is correct in the assessment and that this is all a natural part of the postpartum period. If her hyperthyroid symptoms worsen, she is unlikely to seek follow-up care for fear of being deemed an “anxious mother,” and as a result, the correct diagnosis is missed. 

After approximately two months, the new mother feels better, as the excess thyroid hormones normalize. This is the second (euthryoid) phase. She may now be convinced that her symptoms of anxiety, agitation, palpitations, and insomnia were from the new experience of motherhood or from the new addition to her existing family. 

After two to three months of feeling well, she begins to experience symptoms of hypothyroidism, which is the third phase of PPT. Her symptoms may include depression, constipation, fatigue, and difficulty concentrating. This is another critical time in which the patient or her clinician may attribute her symptoms to all of the emotional changes and demands of caring for her infant. The clinician may question how the mother has felt over the previous couple of months, and since she has felt well, no thyroid studies are ordered. Again, not questioning the assessment, the mother moves on, only to experience worsening symptoms.

The problem here is that if her hypothyroidism is of a permanent nature, as in the case of autoimmune thyroid disease from Hashimoto’s, she will eventually become more symptomatic but may not return for screening or treatment, thinking this is part of the “normal” postpartum period.

Nearly 20% of PPT patients will remain hypothyroid and require lifelong thyroid hormone replacement. The remaining 80% may develop temporary hypothyroidism, requiring thyroid hormone replacement for up to one year, or the thyroiditis will be mild and resolve without the need for such treatment.

Things to Keep in Mind

Understanding who is at increased risk for PPT should prompt the clinician to check the TSH level and TPOAb before pregnancy, if possible. If the patient is pregnant and has the above stated risk factors for autoimmune thyroiditis, obtaining a baseline TSH level is prudent. In order to obtain a more accurate laboratory evaluation, it would be advisable to wait until after pregnancy to check TPOAb, since the maternal immune system is partially suppressed.

If TPOAb can’t be checked until after delivery, it would make clinical sense to test TSH at the same time (around month 3). In women with positive TPOAb before pregnancy and normal thyroid function throughout pregnancy, TSH should be checked at three and six months postpartum. Clinicians should remain astute and order a TSH any time in the interim if they suspect thyroid dysfunction based on patients’ symptoms. Literature supports annual TSH assays in patients in whom PPT resolved, as they have a markedly increased risk for permanent hypothyroidism.

Suggested Reading

Abalovich M, Amino N, Barbour LA, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2007;92(8 suppl):S1-S47.

American Thyroid Association Web site. www.thyroid.org.

Stagno-Green A. Postpartum thyroiditis. J Clin Endocrinol Metab. 2002;87(9):4042-4047.

Q: I frequently counsel patients on family planning, pregnancy expectations, and postpartum concerns. Would you please discuss the specifics of postpartum thyroiditis?

Postpartum thyroiditis (PPT) affects about 5% to 10% of postpartum patients, as evidenced by biochemical thyroid dysfunction. It usually presents during the first three to nine months postpartum.

The condition may present as transient hyperthyroidism, transient hypothyroidism, or hyperthyroidism resolving to transient or permanent hypothyroidism. Only one-quarter to one-third of women experience both the hyperthyroid and hypothyroid phases; one-third of patients will have only a thyrotoxic or hypothyroid phase.

Those who are at risk for or develop PPT have underlying autoimmune thyroid disease (eg, Hashimoto’s thyroiditis). During pregnancy, the maternal immune system is partially suppressed; it rebounds dramatically after delivery, leading to increased risk for autoimmune thyroid disease in patients with thyroid peroxidase antibodies (TPOAb).

Q: How do I know if my patients are at risk for thyroid disease during or following pregnancy?

We need to ascertain who is at risk for PPT so we can appropriately evaluate and screen for the condition. It is important to educate your patients prior to or during pregnancy about the risk, timeline of occurrence, and signs/symptoms of PPT.

If possible, I recommend discussing this with patients in the family-planning stages. It would be helpful to ask the prospective mother about a family history of hyperthyroid or hypothyroid disease (eg, Grave’s disease or Hashimoto’s thyroiditis). It’s also important to inquire about other autoimmune diseases in the patient or in her family.

Other autoimmune conditions that increase the risk for thyroid disease are: systemic lupus erythematosus, rheumatoid arthritis, pernicious anemia, vitiligo, type 1 diabetes, and Addison’s disease. Of note, patients with type 1 diabetes are three times more likely than those without that condition to develop PPT.

Q: Which tests will provide the best information about risk for or presence of PPT? When should I order such tests? 

The thyroid-stimulating hormone (TSH) assay is the most sensitive laboratory test for thyroid function in a patient with a normal pituitary-thyroid axis. Testing for TPOAb is the best available screening tool for postpartum thyroiditis, being widely available, economical, and reproducible. Studies evaluating the utility of TPOAb have demonstrated a sensitivity of 46% to 89%, with a specificity of 91% to 98%. Depending on the timeline of the postpartum presentation, an elevated or low TSH level in conjunction with positive TPOAb is pathognomonic for PPT.

If the prospective or expectant mother has a personal or family history of an autoimmune disease, it would be a good idea to obtain a baseline TSH level and TPOAb. If unobtainable beforehand, a baseline TSH during pregnancy is prudent, since many of the signs and symptoms of hyper/hypothyroidism can be similar to those seen in “normal” pregnancy. A normal TSH in the face of elevated TPOAb increases the patient’s likelihood of developing Hashimoto’s thyroiditis or PPT. The best time to check TPOAb is before pregnancy or after delivery, since these antibodies can decrease or even normalize during pregnancy.

Q: Since PPT can be elusive, how might one clinically evaluate the postpartum patient?

The reasons for missed diagnosis of PPT are twofold. First, it results from women reporting few to no symptoms or simply “writing off” the signs and symptoms, thinking they’re related to the significant emotional/physical demands of caring for the new baby. Second, there is a lack of clinician recognition regarding the risk factors, clinical presentation, and frequency of PPT. Since one-third of the hyperthyroidism of PPT is asymptomatic or unreported by patients, it’s easy to see how clinicians can be uncertain whether postpartum anxiety, insomnia, palpitations, increased heart rate, and fatigue reflect thyrotoxicosis or “new mother demands.” Similarly, fatigue, constipation, impaired concentration/memory, weight gain, and depression can be interpreted as hypothyroidism or the emotional and physical challenges of infant care. Since either hyperthyroid or hypothyroid symptoms can be subtle, PPT goes undiagnosed—and therefore, untreated.

Here is an example to provide a clearer understanding:

PPT can go from hyperthyroid to hypothyroid over a four- to six-month period. I like to refer to this evolving process in its three phases to foster understanding of what is going on not only symptomatically but biochemically as well. The first phase starts with a bout of hyperthyroidism from an increased release of thyroid hormone (T4 and/or T3) as a result of nonpainful/nontender thyroid inflammation.

During this first phase, it’s unfortunate that many new mothers’ symptoms are “written off” as the anxieties associated with being a new mother. If a TSH is not ordered, the woman may feel that the clinician is correct in the assessment and that this is all a natural part of the postpartum period. If her hyperthyroid symptoms worsen, she is unlikely to seek follow-up care for fear of being deemed an “anxious mother,” and as a result, the correct diagnosis is missed. 

After approximately two months, the new mother feels better, as the excess thyroid hormones normalize. This is the second (euthryoid) phase. She may now be convinced that her symptoms of anxiety, agitation, palpitations, and insomnia were from the new experience of motherhood or from the new addition to her existing family. 

After two to three months of feeling well, she begins to experience symptoms of hypothyroidism, which is the third phase of PPT. Her symptoms may include depression, constipation, fatigue, and difficulty concentrating. This is another critical time in which the patient or her clinician may attribute her symptoms to all of the emotional changes and demands of caring for her infant. The clinician may question how the mother has felt over the previous couple of months, and since she has felt well, no thyroid studies are ordered. Again, not questioning the assessment, the mother moves on, only to experience worsening symptoms.

The problem here is that if her hypothyroidism is of a permanent nature, as in the case of autoimmune thyroid disease from Hashimoto’s, she will eventually become more symptomatic but may not return for screening or treatment, thinking this is part of the “normal” postpartum period.

Nearly 20% of PPT patients will remain hypothyroid and require lifelong thyroid hormone replacement. The remaining 80% may develop temporary hypothyroidism, requiring thyroid hormone replacement for up to one year, or the thyroiditis will be mild and resolve without the need for such treatment.

Things to Keep in Mind

Understanding who is at increased risk for PPT should prompt the clinician to check the TSH level and TPOAb before pregnancy, if possible. If the patient is pregnant and has the above stated risk factors for autoimmune thyroiditis, obtaining a baseline TSH level is prudent. In order to obtain a more accurate laboratory evaluation, it would be advisable to wait until after pregnancy to check TPOAb, since the maternal immune system is partially suppressed.

If TPOAb can’t be checked until after delivery, it would make clinical sense to test TSH at the same time (around month 3). In women with positive TPOAb before pregnancy and normal thyroid function throughout pregnancy, TSH should be checked at three and six months postpartum. Clinicians should remain astute and order a TSH any time in the interim if they suspect thyroid dysfunction based on patients’ symptoms. Literature supports annual TSH assays in patients in whom PPT resolved, as they have a markedly increased risk for permanent hypothyroidism.

Suggested Reading

Abalovich M, Amino N, Barbour LA, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2007;92(8 suppl):S1-S47.

American Thyroid Association Web site. www.thyroid.org.

Stagno-Green A. Postpartum thyroiditis. J Clin Endocrinol Metab. 2002;87(9):4042-4047.