Postpartum thyroiditis overview: Difference between revisions
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{{Postpartum thyroiditis}} | {{Postpartum thyroiditis}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}}{{SKA}} | ||
==Overview== | ==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 [[Postpartum thyroiditis|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 [[Antigen|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 [[Inflammation|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 [[Pericarditis causes#Overview|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 thyroiditis]], [[Hashimoto's thyroiditis]], [[Riedel's thyroiditis]], and [[suppurative thyroiditis]] [[Postpartum thyroiditis]] must also be differentiated from other diseases which cause [[hypothyroidism]]. As [[Postpartum thyroiditis]] may cause transient [[Hyperthyroidism|thyrotoxic]] symptoms, the diseases causing [[Hyperthyroidism|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 [[Diabetes mellitus type 1|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 [[Genetics|genetic]] and subsequent [[Pregnancy|pregnancies]]. Other risk factors include smoking, increase or decreased intake of [[Iodine]], [[hepatitis C]], radiations and medications. | |||
==Historical Perspective== | ==Historical Perspective== | ||
Thyroid dysfunction was first associated | [[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. | ||
==Classification== | ==Classification== | ||
There is no established system for the classification of PPT but it may be classified according to clinical course into three groups: Transient hyperthyroidism, | 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|hypothyroidism.]] | ||
==Pathophysiology== | ==Pathophysiology== | ||
The exact | 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 [[Antigen|antigens]] are recognized as non-self-antigens and our [[White blood cells|immune cells]] mediate [[Inflammation|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 [[Inflammation|inflammatory]] state, and recovery strength of gland. Studies have also shown that [[pregnancy]] is stage of reduced immunity to protect fetus from unwanted exposure of [[Immunity (medical)|immunity]] which at the end of [[pregnancy]] escalate sudden [[Immunity (medical)|immunity]], leading to beginning of slowly evolving [[Autoimmunity|autoimmune]] response to thyroid auto-antigens, in rapid sequences and appearance of [[thyroiditis]]. Studies are going on in search of exact auto-antibody and auto-antigens triggering an [[Autoimmunity|autoimmune]] response, which correlates with a clinical and pathological picture of [[postpartum thyroiditis]]. [[Thyroid peroxidase|TPO]] auto-antibody is significantly linked to occurrence of [[Postpartum thyroiditis|postpartum thyroiditis.]] | ||
==Causes== | ==Causes== | ||
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 [[Pericarditis causes#Overview|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. | 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 [[Pericarditis causes#Overview|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. | ||
==Differentiating Postpartum thyroiditis from Other Diseases== | ==Differentiating Postpartum thyroiditis from Other Diseases== | ||
Postpartum thyroiditis must be differentiated from other causes of thyroiditis, such as | [[Postpartum thyroiditis]] must be differentiated from other causes of [[thyroiditis]], such as [[de Quervain's thyroiditis]], [[Hashimoto's thyroiditis]], [[Riedel's thyroiditis]], and suppurative thyroiditis. [[Postpartum thyroiditis]] must also be differentiated from other diseases which cause [[hypothyroidism]]. As [[Postpartum thyroiditis]] may cause transient [[Thyrotoxicosis|thyrotoxic]] symptoms, the diseases causing [[thyrotoxicosis]] must also be considered in the differential diagnosis. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
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. PPT occurs in women in child bearing age. PPT usually affects individuals of the Mediterranean and Caucasians population race. Mongolian race is usually less affected. The majority of PPT cases are reported Europe and Japan. | 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 diabetes|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 in child bearing age. PPT usually affects individuals of the Mediterranean and Caucasians population race. Mongolian race is usually less affected. The majority of PPT cases are reported Europe and Japan. | ||
==Risk Factors== | ==Risk Factors== | ||
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 Iodine, hepatitis C, radiations and medications. | The most potent risk factor in the development of PPT are genetic and subsequent [[Pregnancy|pregnancies]]. Other risk factors include smoking, increase or decreased intake of [[Iodine]], [[hepatitis C]], radiations and medications. | ||
==Screening== | ==Screening== | ||
There is insufficient evidence to recommend routine screening for PPT. According to the American Journal of Obstetrics and Gynecology screening for postpartum thyroiditis by measuring anti-TPO antibodies is recommended every pregnant women. 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, history of postpartum thyroiditis and any patient with high risk should be followed with TSH levels every 6th and 9th postpartum period. | There is insufficient evidence to recommend routine [[Screening (medicine)|screening]] for [[Postpartum thyroiditis|PPT.]] According to the American Journal of Obstetrics and Gynecology screening for [[postpartum thyroiditis]] by measuring anti-[[Thyroid peroxidase|TPO]] [[antibodies]] is recommended every [[Pregnancy|pregnant]] women. According to the Endocrinology and Metabolism Clinics of North America screening for [[postpartum thyroiditis]] in first trimester by measuring anti-[[Thyroid peroxidase|TPO]] [[antibodies]] should be limited to every high-risk pregnant women with [[Type 1 diabetes|type 1 DM]], history of [[postpartum thyroiditis]] and any patient with high risk should be followed with TSH levels every 6th and 9th postpartum period. | ||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
Prognosis is generally good, 25-30% in 3.5 to 8.7-year patients with [[postpartum thyroiditis]] PPT develop [[hypothyroidism]]. The symptoms of postpartum thyroiditis, PPT usually develop in the twelve months after delivery, abortion or miscarriage of fetus and start with symptoms depending on clinical course that it follows. Common complications of include hypothyroidism, postpartum depression, fetal mental retardation in future pregnancies in diagnosed cases and overt hyperthyroid symptoms in future pregnancies. Prognosis is generally good and 90% of patient recover to normal state after 12 months of postpartum. | [[Prognosis]] is generally good, 25-30% in 3.5 to 8.7-year patients with [[postpartum thyroiditis]] PPT develop [[hypothyroidism]]. The symptoms of [[postpartum thyroiditis]], PPT usually develop in the twelve months after delivery, abortion or [[miscarriage]] of fetus and start with symptoms depending on clinical course that it follows. Common complications of include [[hypothyroidism]], [[Postpartum depression (patient information)|postpartum depression]], fetal [[mental retardation]] in future pregnancies in diagnosed cases and overt [[Hyperthyroidism|hyperthyroid]] symptoms in future [[Pregnancy|pregnancies]]. [[Prognosis]] is generally good and 90% of patient recover to normal state after 12 months of postpartum. | ||
==Diagnosis== | ==Diagnosis== | ||
===Diagnostic Criteria=== | ===Diagnostic Criteria=== | ||
There are no established criteria for the diagnosis of PPT but it can be diagnosed on basis of level of TSH, free | There are no established criteria for the diagnosis of PPT but it can be diagnosed on basis of level of [[TSH]], free [[T4]], free [[T3]], radio-iodine uptake, presence of anit-[[Thyroid peroxidase|TPO]] [[antibodies]] and absence of [[TSH]] receptor [[antibodies]] depending on the phase of disease. | ||
===History and Symptoms=== | ===History and Symptoms=== | ||
The majority of patients with Postpartum thyroiditis | The majority of patients with [[postpartum thyroiditis]], [[Postpartum thyroiditis|PPT]] are asymptomatic. The hallmark of PPT is lassitude. A positive history of [[fatigue]] and [[depression]] is suggestive of [[Postpartum thyroiditis|PPT]]. The most common symptoms of [[Postpartum thyroiditis|PPT]] include [[depression]], [[fatigue]], and [[anxiety]]. | ||
===Physical Examination=== | ===Physical Examination=== | ||
The presence of signs of hyperthyroidism or hypothyroidism in postpartum period on physical examination is highly suggestive of PPT. | The presence of signs of [[hyperthyroidism]] or [[hypothyroidism]] in postpartum period on physical examination is highly suggestive of [[Postpartum thyroiditis|PPT]]. | ||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
Laboratory findings consistent with the diagnosis of PPT depend on the phase of disease and include screening of serum TSH, serum free T4, serum free T3, serum Anti-TPO anitbodies, serum TSH-receptor abs, serum ESR, serum thyroglobulin | Laboratory findings consistent with the diagnosis of [[Postpartum thyroiditis|PPT]] depend on the phase of disease and include screening of serum [[Thyroid-stimulating hormone|TSH]], serum free [[Thyroxine|T4]], serum free [[Triiodothyronine|T3]], serum Anti-[[Thyroid peroxidase|TPO]] anitbodies, serum [[Thyrotropin receptor|TSH-receptor abs]], serum [[Erythrocyte sedimentation rate|ESR]], serum [[thyroglobulin]] and radio-iodine uptake. Some patients with [[Postpartum thyroiditis|PPT]] may have elevated concentration of Serum Anti-[[Thyroid peroxidase|TPO]] abs, which is usually suggestive of future [[hypothyroidism]]. | ||
===Electrocardiogram=== | ===Electrocardiogram=== | ||
There are no ECG findings associated with PPT. An ECG may be helpful in the excluding the causes of [[palpitation]] in PPT. Findings on an ECG suggestive of PPT include sinus rhythm tachycardia in hyperthyroid phase. | There are no [[ECG]] findings associated with [[Postpartum thyroiditis|PPT]]. An [[ECG]] may be helpful in the excluding the causes of [[palpitation]] in [[Postpartum thyroiditis|PPT]]. Findings on an ECG suggestive of [[Postpartum thyroiditis|PPT]] include sinus rhythm [[tachycardia]] in [[Hyperthyroidism|hyperthyroid]] phase. | ||
===X-ray=== | ===X-ray=== | ||
There are no x-ray findings associated with PPT. However radiation is one of risk factor for PPT. | There are no x-ray findings associated with [[Postpartum thyroiditis|PPT]]. However radiation is one of risk factor for [[Postpartum thyroiditis|PPT]]. | ||
===Ultrasound=== | ===Ultrasound=== | ||
Ultrasound Thyroid may be helpful in the diagnosis of PPT. Findings on an ultrasound thyroid suggestive of PPT include diffuse or multi-focal echogenicity which correlates with lymphocytic infiltration of thyroid gland. | Ultrasound Thyroid may be helpful in the diagnosis of PPT. Findings on an ultrasound [[thyroid]] suggestive of [[Postpartum thyroiditis|PPT]] include diffuse or multi-focal echogenicity which correlates with lymphocytic infiltration of [[thyroid gland]]. | ||
===CT scan=== | ===CT scan=== | ||
There are no CT findings associated with PPT. However radiation is one of risk factor for PPT. | There are no [[CT]] findings associated with PPT. However radiation is one of risk factor for PPT. | ||
===MRI=== | ===MRI=== | ||
There are no MRI findings associated with PPT. | There are no [[MRI]] findings associated with PPT. | ||
===Other Imaging Findings=== | ===Other Imaging Findings=== | ||
Radio-iodine uptake may be helpful in the diagnosis o | Radio-iodine uptake may be helpful in the diagnosis o [[Postpartum thyroiditis|PPT.]] Findings on an decreased Radio-iodine uptake by [[thyroid gland]] [[Inflammation|inflammatory]] areas is suggestive of PPT. | ||
===Other Diagnostic Studies=== | ===Other Diagnostic Studies=== | ||
There are no other diagnostic studies associated with PPT. | There are no other diagnostic studies associated with [[Postpartum thyroiditis|PPT]]. | ||
==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
Pharmacological medical therapy is recommended among PPT with asymptomatic and symptomatic patients according to levels of TSH, the phase of disease and planning of pregnancy. Patients of PPT 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 is not useful because the increase in serum T3 and T4 is due to release of thyroid hormone in the blood due to the destruction of thyroid follicle rather than increased production. | Pharmacological medical therapy is recommended among [[Postpartum thyroiditis|PPT]] with asymptomatic and symptomatic patients according to levels of [[Thyroid-stimulating hormone|TSH]], the phase of disease and planning of [[pregnancy]]. Patients of PPT with [[hyperthyroid]] phase are treated with [[beta blockers]], whereas patients with [[Hypothyroidism|hypothyroid]] phase are treated with [[levothyroxine]] LT4. In [[Hyperthyroidism|hyperthyroid]] phase radioiodine and antithyroid treatment is not useful because the increase in serum [[T3]] and [[T4]] is due to release of [[thyroid hormone]] in the blood due to the destruction of [[thyroid]] follicle rather than increased production. | ||
===Surgery=== | ===Surgery=== | ||
Surgical intervention is not recommended for the management of Postpartum thyroidits. | Surgical intervention is not recommended for the management of [[Postpartum thyroiditis|Postpartum thyroidits.]] | ||
===Primary Prevention=== | ===Primary Prevention=== | ||
There are no established measures for the primary prevention of [[Postpartum thyroiditis]]. However, the common risk factors which increase chances of PPT are subsequent [[Pregnancy|pregnancies]], smoking, intake of [[iodine]], radiation, and medications such as [[lithium]], [[amiodarone]], [[Interferon alpha-n3|interferon alpha]], [[interleukin 2]], and the highly active [[AIDS antiretroviral drugs|antiretroviral therapy.]] | |||
===Secondary Prevention=== | ===Secondary Prevention=== | ||
Effective measures for the secondary prevention of [[Postpartum thyroiditis]] are same as primary prevention measures. Studies have shown that 200 µg/day of PO [[Selenium|selenomethionine]] started from 12th week and till the end of postpartum period significantly declines recurrence of [[postpartum thyroiditis]] cases. | |||
==References== | ==References== | ||
Latest revision as of 11:56, 19 October 2017
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Postpartum thyroiditis Microchapters |
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Postpartum thyroiditis overview On the Web |
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American Roentgen Ray Society Images of Postpartum thyroiditis overview |
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Risk calculators and risk factors for Postpartum thyroiditis overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunny Kumar MD [2]
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 thyroiditis, Hashimoto's thyroiditis, Riedel'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 Iodine, hepatitis C, radiations and medications.
Historical Perspective
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.
Classification
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.
Pathophysiology
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. Studies have also shown that pregnancy is stage of reduced immunity to protect fetus from unwanted exposure of immunity which at the end of pregnancy escalate sudden immunity, leading to beginning of slowly evolving autoimmune response to thyroid auto-antigens, in rapid sequences and appearance of thyroiditis. Studies are going on in search of exact auto-antibody and auto-antigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum thyroiditis. TPO auto-antibody is significantly linked to occurrence of postpartum thyroiditis.
Causes
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.
Differentiating Postpartum thyroiditis from Other Diseases
Postpartum thyroiditis must be differentiated from other causes of thyroiditis, such as de Quervain's thyroiditis, Hashimoto's thyroiditis, Riedel'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 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. PPT occurs in women in child bearing age. PPT usually affects individuals of the Mediterranean and Caucasians population race. Mongolian race is usually less affected. The majority of PPT cases are reported Europe and Japan.
Risk Factors
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 Iodine, hepatitis C, radiations and medications.
Screening
There is insufficient evidence to recommend routine screening for PPT. According to the American Journal of Obstetrics and Gynecology screening for postpartum thyroiditis by measuring anti-TPO antibodies is recommended every pregnant women. 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, history of postpartum thyroiditis and any patient with high risk should be followed with TSH levels every 6th and 9th postpartum period.
Natural History, Complications, and Prognosis
Prognosis is generally good, 25-30% in 3.5 to 8.7-year patients with postpartum thyroiditis PPT develop hypothyroidism. The symptoms of postpartum thyroiditis, PPT usually develop in the twelve months after delivery, abortion or miscarriage of fetus and start with symptoms depending on clinical course that it follows. Common complications of include hypothyroidism, postpartum depression, fetal mental retardation in future pregnancies in diagnosed cases and overt hyperthyroid symptoms in future pregnancies. Prognosis is generally good and 90% of patient recover to normal state after 12 months of postpartum.
Diagnosis
Diagnostic Criteria
There are no established criteria for the diagnosis of PPT but it can be diagnosed on basis of level of TSH, free T4, free T3, radio-iodine uptake, presence of anit-TPO antibodies and absence of TSH receptor antibodies depending on the phase of disease.
History and Symptoms
The majority of patients with postpartum thyroiditis, PPT are asymptomatic. The hallmark of PPT is lassitude. A positive history of fatigue and depression is suggestive of PPT. The most common symptoms of PPT include depression, fatigue, and anxiety.
Physical Examination
The presence of signs of hyperthyroidism or hypothyroidism in postpartum period on physical examination is highly suggestive of PPT.
Laboratory Findings
Laboratory findings consistent with the diagnosis of PPT depend on the phase of disease and include screening of serum TSH, serum free T4, serum free T3, serum Anti-TPO anitbodies, serum TSH-receptor abs, serum ESR, serum thyroglobulin and radio-iodine uptake. Some patients with PPT may have elevated concentration of Serum Anti-TPO abs, which is usually suggestive of future hypothyroidism.
Electrocardiogram
There are no ECG findings associated with PPT. An ECG may be helpful in the excluding the causes of palpitation in PPT. Findings on an ECG suggestive of PPT include sinus rhythm tachycardia in hyperthyroid phase.
X-ray
There are no x-ray findings associated with PPT. However radiation is one of risk factor for PPT.
Ultrasound
Ultrasound Thyroid may be helpful in the diagnosis of PPT. Findings on an ultrasound thyroid suggestive of PPT include diffuse or multi-focal echogenicity which correlates with lymphocytic infiltration of thyroid gland.
CT scan
There are no CT findings associated with PPT. However radiation is one of risk factor for PPT.
MRI
There are no MRI findings associated with PPT.
Other Imaging Findings
Radio-iodine uptake may be helpful in the diagnosis o PPT. Findings on an decreased Radio-iodine uptake by thyroid gland inflammatory areas is suggestive of PPT.
Other Diagnostic Studies
There are no other diagnostic studies associated with PPT.
Treatment
Medical Therapy
Pharmacological medical therapy is recommended among PPT with asymptomatic and symptomatic patients according to levels of TSH, the phase of disease and planning of pregnancy. Patients of PPT 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 is not useful because the increase in serum T3 and T4 is due to release of thyroid hormone in the blood due to the destruction of thyroid follicle rather than increased production.
Surgery
Surgical intervention is not recommended for the management of Postpartum thyroidits.
Primary Prevention
There are no established measures for the primary prevention of Postpartum thyroiditis. However, the common risk factors which increase chances of PPT are subsequent pregnancies, smoking, intake of iodine, radiation, and medications such as lithium, amiodarone, interferon alpha, interleukin 2, and the highly active antiretroviral therapy.
Secondary Prevention
Effective measures for the secondary prevention of Postpartum thyroiditis are same as primary prevention measures. Studies have shown that 200 µg/day of PO selenomethionine started from 12th week and till the end of postpartum period significantly declines recurrence of postpartum thyroiditis cases.