Postpartum thyroiditis

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Postpartum thyroiditis Microchapters

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Postpartum Thyroiditis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

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Case #1

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunny Kumar MD [2]Sargun Singh Walia M.B.B.S.[3]

Synonyms and Keywords: PPT, puerperal thyroiditis, Post partum thyroiditis, postpartum hypothyroidism

Overview

Thyroid dysfunction was first associated with pregnancy by Dr. W.E.H. Robertson a Newzeland physician who was later awarded the Sir Charles Hastings Prize for his essay in 1946. He diagnosed postpartum patients with symptoms of Hypothyroidism after pregnancy and their improvement on treatment with thyroid extracts in 1946.There is no established system for the classification of PPT but it may be classified according to clinical course into three groups: Transient hyperthyroidism, classic triphasic, and transient/ permanent hypothyroidism. The exact parthenogenesis of postpartum thyroiditis "PPT" is not fully understood. However, studies have shown that it is an autoimmune disorder in which thyroid tissue antigens are recognized as non-self-antigens and our immune cells mediate inflammatory response to thyroid gland and destroy it, then lead to sudden release of stored thyroid hormone in blood and appearance of clinical and laboratory hyperthyroid picture transiently followed by recovery to euthyroid state or hypothyroid state depending on level of destruction of thyroid gland, persistence of inflammatory state, and recovery strength of gland. PPT is considered to be sub-acute lymphocytic thyroiditis that occurs due autoimmune response towards thyroid gland in postpartum period, miscarriage or abortion. The cause of PPT is autoimmune disorder. To review risk factors for the development of PPT, click here. PPT is caused by a mutation in the G-allele mutation of CD60 CTLA-4 gene and mutation of HLA DR-3. HLA DR-4, and HLA DR-5 gene. Postpartum thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain's thyroiditisHashimoto's thyroiditisRiedel's thyroiditis, and suppurative thyroiditis Postpartum thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As Postpartum thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis. In 2012, the incidence of PPT was estimated to be 1600 to 18200 cases per 100,000 women. Incidence of PPT increase with patients having type 1 DM up to 25000 per 100,000 women. In 2012, the prevalence of PPT was estimated to be from 1000 to 20000, with a mean prevalence of 5000 cases per 100,000 women. The most potent risk factor in the development of PPT are genetic and subsequent pregnancies. Other risk factors include smoking, increase or decreased intake of Iodinehepatitis C, radiations and medications.

Historical Perspective

Thyroid dysfunction was first associated with pregnancy by Dr. W.E.H. Robertson, physician from Newzeland, latter awarded the Sir Charles Hastings Prize for his essay in 1946. Dr. Robertson diagnosed postpartum patients with symptoms of Hypothyroidism and demonstrated their improvement on treatment with thyroid extracts in 1946.

Classification

There is no established system for the classification of postpartum thyroiditis (PPT) but it may be classified according to clinical course into three groups: transient hyperthyroidism, classic triphasic, and transient or permanent hypothyroidism.

Pathophysiology

The exact pathogenesis of postpartum thyroiditis (PPT) is not completely understood. However, studies have shown that PPT is an autoimmune disorder in which thyroid tissue antigens are recognized as non-self-antigens. The immune cells mediate inflammatory response to thyroid gland leading to its destruction. This destruction is followed by sudden release of stored thyroid hormone in blood and the appearance of clinical as well as laboratory picture of hyperthyroidism transiently. This is followed by recovery to euthyroid or hypothyroid state depending on the extent of destruction of thyroid gland, persistence of inflammatory state, and recovery strength of gland. Pregnancy is understood to be associated with reduced immunity to protect fetus from unwanted exposure to maternal immune system. At the end of pregnancy the suppressed immunity is suddenly escalated, leading to the slow evolution of autoimmune response to thyroid auto-antigens, resulting in thyroiditis. The search of exact auto-antibody and auto-antigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum thyroiditis, is still ongoing. Thyroid peroxidase (TPO) auto-antibody is significantly associated with the pathogenesis of postpartum thyroiditis.

Causes

Postpartum thyroiditis (PPT) is a type of subacute lymphocytic thyroiditis that occurs due to autoimmune response towards thyroid gland in postpartum period, miscarriage, or abortionPPT is an autoimmune disorder. PPT is caused by a mutation in the G-allele of CD60 CTLA-4 geneHLA-DR3HLA-DR4, and HLA-DR5 gene. To review details about various risk factors that contribute to the development of PPTclick here.

Differentiating Postpartum thyroiditis from other Diseases

Postpartum thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain's thyroiditisHashimoto's thyroiditisRiedel's thyroiditis, and suppurative thyroiditis. Postpartum thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As postpartum thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis.

Epidemiology and Demographics

In 2012, the incidence of postpartum thyroiditis "PPT" was estimated to be 1600 to 18200 cases per 100,000 women. Incidence of PPT increase in patients with type 1 DM up to 25000 per 100,000 women. In 2012, the prevalence of PPT was estimated to be from 1000 to 20000, with a mean prevalence of 5000 cases per 100,000 women. PPT occurs in women of child bearing age. PPT usually affects individuals of the Mediterranean and Caucasian population race. Mongolian race is usually less affected with PPT. The majority of PPT cases are reported in Europe and Japan.

Risk Factors

The most potent risk factors in the development of postpartum thyroiditis (PPT) are genetic abnormalities and subsequent pregnancies. Other risk factors for postpartum thyroiditis include smoking, increase or decreased intake of iodinehepatitis Cradiations and medications.

Screening

According to the American Journal of Obstetrics and Gynecology, screening for postpartum thyroiditis, done by measuring anti-TPO antibodies is recommended for every pregnant woman. According to the Endocrinology and Metabolism Clinics of North America, screening for postpartum thyroiditis in first trimester, by measuring anti-TPO antibodies, should be limited to every high-risk pregnant women with type 1 DM and history of postpartum thyroiditis. According to these recommendations, any patient with high risk of PPT should be followed with TSH levels in every 6th and 9th postpartum month.

Natural History, Complications and Prognosis

Prognosis for postpartum thyroiditis is generally good. If left untreated, 25 to 30% patients develop hypothyroidism, 3.5 to 8.7-years after developing postpartum thyroiditis (PPT). The symptoms of postpartum thyroiditis usually develop in the twelve months after deliveryabortion or miscarriage of fetus. The symptoms of PPT depend on its clinical course such as classic triphasic, biphasic hyerthyroidism, or biphasic hypothyroidism. Common complications of PPT include hypothyroidismpostpartum depression, and fetal mental retardation. The mother may develop overt hyperthyroidsymptoms in future pregnancies. Prognosis of PPT is generally good and 90% of patient recover to normal state after postpartum period.

Diagnosis

There are no established criteria for the diagnosis of postpartum thyroiditis (PPT). However, PPT can be diagnosed on the basis of level of TSH, free T4, free T3, radio-iodine uptake, presence of anit-TPOantibodies and absence of TSH receptor antibodies.

History and Symptoms | Physical Examination | Electrocardiogram | Laboratory Findings | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Diagnostic Studies | Other Imaging Findings

Treatment

Pharmacological medical therapy is recommended among asymptomatic and symptomatic postpartum thyroiditis (PPT) patients. The medical therapy for PPT is based upon the levels of TSH, the phase of disease, and planning of next pregnancy. PPT patients with hyperthyroid phase are treated with beta blockers, whereas patients with hypothyroid phase are treated with levothyroxine LT4. In hyperthyroid phase radioiodine and antithyroid treatment acting on the thyroid hormone production or release is not useful because the increase in serum T3 and T4 is due to release of thyroid hormone in the blood secondary to the destruction of thyroid follicles rather than increased production.

 
 
 
Prior Postpartum thyroiditis episode
 
 
Family history of autoimmune disease or thyroid disease or Postive anti-TPO antibody
 
 
 
Goiter or diabetes mellitus
 
 
 
symptoms or signs of thyroid dysfunction in postpartum period
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Check ‡TFT
Anti-TPO antibodies titres
in postpartum peroid
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Panel A
TSH>4.0
normal FT4
-/+ anti-TPO
 
 
Panel B
TSH>4.0
low FT4
-/+ anti-TPO
 
 
 
Panel C
TSH=0.3-4.0
normal FT4
+ anti-TPO
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Subclinical
hypothyroid phase of †PPT
 
 
Possible
Autoimmune thyroidits
 
 
 
 
Repeat TSH
3-6months
 
If TSH<1.0
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Treat
Levothyroxine
 
 
TSH>4.0
low FT4
 
 
 
 
TSH=0.3-4.0
normal FT4
 
 
 
 
 
 
 
 
 
Panel D
TSH<1.0
+ anti-TPO
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Repeat TSH
3-6months
 
 
 
 
 
 
 
Repeat TSH
3-6months
 
 
 
 
FT4
high
 
FT4
normal
 
FT4
low
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Consider tapering Levothyroxine
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Repeat TSH
3-6months
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Dignosed as
hyperthyroid
phase of †PPT
Subclinical
hyperthyroidisum
phase of †PPT
 
Possible hypo-pituitary hypothyroidism
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
TSH>4.0
Treat
Levothyroxine
 
TSH=0.3-4.0
Repeat TSH
3-6months

‡TFT; Thyroid function tests(TSH, T4, and T3), †PPT=Postpartum thyroiditis


Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case #1


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