Postpartum thyroiditis: Difference between revisions

	Postpartum thyroiditis Microchapters
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Overview
Historical Perspective
Classification
Pathophysiology
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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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VisualWikitext

Latest revision as of 23:07, 13 December 2017

For patient information, click here

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 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, 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 abortion. PPT is an autoimmune disorder. PPT is caused by a mutation in the G-allele of CD60 CTLA-4 gene, HLA-DR3, HLA-DR4, and HLA-DR5 gene. To review details about various risk factors that contribute to the development of PPT, click here.

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 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 iodine, hepatitis C, radiations 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 delivery, abortion 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 hypothyroidism, postpartum 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-TPO antibodies and absence of TSH receptor antibodies.

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

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

Case Studies

Case #1

@@ Line 1: / Line 1: @@
-{{Infobox_Disease |
+__NOTOC__
-  Name           = {{PAGENAME}} |
+{{Postpartum thyroiditis}}
-  Image          = |
+'''For patient information, click [[Postpartum thyroiditis (patient information)|here]]'''
-  Caption        = |
-  DiseasesDB     = 10441 |
-  ICD10          = {{ICD10|O|90|5|o|85}} |
-  ICD9           = |
-  ICDO           = |
-  OMIM           = |
-  MedlinePlus    = |
-  eMedicineSubj  = |
-  eMedicineTopic = |
-  MeshID         = D050032 |
-}}
-'''Postpartum thyroiditis''' is usually a transient phenomenon observed following [[pregnancy]] and may involve [[hyperthyroidism]], [[hypothyroidism]] or the two sequentially.  It affects about 5% of all women within a year after giving birth. The first phase is typically [[hyperthyroidism]]. Then, the [[thyroid]] either returns to normal or a woman develops [[hypothyroidism]]. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring life-long treatment.
+{{CMG}}; {{AE}} {{SKA}}{{SSW}}
-Postpartum thyroiditis is believed to result from the modifications to the [[immune system]] necessary in [[pregnancy]], and histologically is a [[lymphocytic thyroiditis]]. The process is normally self-limiting, but when conventional antibodies are found there is a high chance of this proceeding to permanent hypothyroidism. Postpartum thyroiditis is a member of the group of thyroiditis conditions known as [[resolving thyroiditis]].
+{{SK}} PPT, puerperal thyroiditis, Post partum thyroiditis, postpartum hypothyroidism
-{{Pathology of pregnancy, childbirth and the puerperium}}
+==[[Postpartum thyroiditis 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.
+==[[Postpartum thyroiditis historical perspective|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.
-[[de:Postpartum-Thyreoiditis]]
+==[[Postpartum thyroiditis classification|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]].
+==[[Postpartum thyroiditis pathophysiology|Pathophysiology]]==
+The exact pathogenesis of [[postpartum thyroiditis]] ([[Postpartum thyroiditis|PPT]]) is not completely understood. However, studies have shown that [[Postpartum thyroiditis|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 [[Hyperthyroid|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 (medical)|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|Thyroid peroxidase (TPO)]] auto-antibody is significantly associated with the pathogenesis of postpartum thyroiditis.
+==[[Postpartum thyroiditis causes|Causes]]==
+[[Postpartum thyroiditis|Postpartum thyroiditis (PPT)]] is a type of subacute [[Lymphocyte|lymphocytic]] [[thyroiditis]] that occurs due to [[Autoimmunity|autoimmune]] response towards thyroid gland in [[postpartum]] period, [[miscarriage]], or [[abortion]]. [[Postpartum thyroiditis|PPT]] is an [[autoimmune]] disorder. [[Postpartum thyroiditis|PPT]] is caused by a [[mutation]] in the G-allele of CD60 CTLA-4 [[gene]], [[HLA-DR3]], [[HLA-DR4]], and [[HLA-DR5]] gene. To review details about various risk factors that contribute to the development of [[Postpartum thyroiditis|PPT]], [[Postpartum thyroiditis risk factors|'''click here.''']]
+==[[Postpartum thyroiditis differential diagnosis|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.
+==[[Postpartum thyroiditis epidemiology and demographics|Epidemiology and Demographics]]==
+In 2012, the [[incidence]] of [[Postpartum thyroiditis|postpartum thyroiditis "PPT"]] was estimated to be 1600 to 18200 cases per 100,000 women. [[Incidence]] of [[Postpartum thyroiditis|PPT]] increase in patients with [[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. PPT occurs in women of child bearing age. [[Postpartum thyroiditis|PPT]] usually affects individuals of the Mediterranean and Caucasian population race. Mongolian race is usually less affected with PPT. The majority of [[Postpartum thyroiditis|PPT]] cases are reported in Europe and Japan.
+==[[Postpartum thyroiditis risk factors|Risk Factors]]==
+The most potent risk factors in the development of [[Postpartum thyroiditis|postpartum thyroiditis (PPT)]] are [[Genetics|genetic]] abnormalities and subsequent pregnancies. Other risk factors for postpartum thyroiditis include [[smoking]], increase or decreased intake of [[iodine]], [[hepatitis C]], [[Radiation exposure|radiations]] and [[medications]].
+==[[Postpartum thyroiditis screening|Screening]]==
+According to the American Journal of Obstetrics and Gynecology, screening for [[postpartum thyroiditis]], done by measuring anti-[[Thyroid peroxidase|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-[[Thyroid peroxidase|TPO]] [[antibodies]], should be limited to every high-risk pregnant women with [[Diabetes mellitus type 1|type 1 DM]] and history of [[postpartum thyroiditis]]. According to these recommendations, any patient with high risk of PPT should be followed with [[Thyroid-stimulating hormone|TSH]] levels in every 6th and 9th postpartum month.
+==[[Postpartum thyroiditis natural history, complications and prognosis|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]] [[Postpartum thyroiditis|(PPT)]]. The symptoms of [[postpartum thyroiditis]] usually develop in the twelve months after [[delivery]], [[abortion]] 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 [[hypothyroidism]], [[Postpartum depression (patient information)|postpartum depression]], and [[Mental retardation|fetal mental retardation]]. The mother may develop overt [[Hyperthyroidism|hyperthyroid]]<nowiki/>symptoms 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]] ([[Postpartum thyroiditis|PPT]]). However, PPT can be diagnosed on the basis of level of [[Thyroid-stimulating hormone|TSH]], free [[Thyroxine|T4]], free [[Triiodothyronine|T3]], radio-iodine uptake, presence of anit-[[Thyroid peroxidase|TPO]][[antibodies]] and absence of [[TSH receptor]] antibodies.
+[[Postpartum thyroiditis history and symptoms|History and Symptoms]] | [[Postpartum thyroiditis physical examination|Physical Examination]] | [[Postpartum thyroiditis electrocardiogram|Electrocardiogram]] | [[Postpartum thyroiditis laboratory findings|Laboratory Findings]] | [[Postpartum thyroiditis x ray|X-Ray Findings]] | [[Postpartum thyroiditis echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Postpartum thyroiditis CT scan|CT-Scan Findings]] | [[Postpartum thyroiditis MRI|MRI Findings]] | [[Postpartum thyroiditis other diagnostic studies|Other Diagnostic Studies]] | [[Postpartum thyroiditis other imaging findings|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.
+{{familytree/start|summary=Sample 1}}
+{{familytree | | | | X01 | | | X02 | | | | X03 | | | | X04 |X01=Prior [[Postpartum thyroiditis]] episode|X02=Family history of [[autoimmune]] disease or [[thyroid]] disease or Postive [[anti-TPO antibody]]|X03=[[Goiter]] or [[diabetes mellitus]]|X04=symptoms or signs of [[thyroid dysfunction in postpartum period]]}}
+{{familytree | | | | |!| | | | |!| | | | | |!| | | | | |!}}
+{{familytree | | | | |`|-|-|-|-|^|-|-|v|-|-|^|-|-|-|-|-|'}}
+{{familytree | | | | | | | | | | | | Z01 | | | Z01=Check ‡TFT<br>Anti-TPO antibodies titres<br>in postpartum peroid}}
+{{familytree | | | | |,|-|-|-|-|v|-|-|^|-|-|v|-|-|-|-|-|-|-|-|-|-|-|.| | | | }}
+{{familytree | | | | A01 | | | A02 | | | | A03 | | | | | | | | | | |!|A01=Panel A<br>TSH>4.0<br>normal FT4 <br>-/+ anti-TPO|A02=Panel B<br>TSH>4.0 <br> low FT4 <br> -/+ anti-TPO|A03=Panel C<br>TSH=0.3-4.0 <br> normal FT4 <br> + anti-TPO}}
+{{familytree | | | | |!| | | | |!| | | | | |!| | | | | | | | | | | |!}}
+{{familytree | | | | B01 | | | B02 | |,|-| B03 |-| B04|-|-|-|-|-|-|(|B01=Subclinical<br>[[hypothyroid]] phase of †[[PPT]]|B02=Possible<br>[[Autoimmune thyroidits]]|B03=Repeat TSH<br>3-6months|B04=If TSH<1.0}}
+{{familytree | | | | |!| | | | |!| | |!| | |!| | | | | | | || | | |!| | | || |}}
+{{familytree | | | | |)|-|-|-|-|'| | |!| | |!| | | | | | | || | | |!| | | || |}}
+{{familytree | | | |C01|-|-|C02|-|'| |C03| | | | | | | | | |C04| |C01=Treat<br>[[Levothyroxine]]|C02=TSH>4.0 <br>low FT4|C03=[[TSH]]=0.3-4.0 <br>normal FT4|C04=Panel D<br>[[TSH]]<1.0 <br>+ anti-TPO}}
+{{familytree | | | | |!| | | | | | | | || |!|| | | | | | | |,|-|-|+|-|-|-|.| }}
+{{familytree | | | | D01 | | | | | | | ||D02 | | | | ||D03| |D04| |D05|D01=Repeat [[TSH]]<br>3-6months|D02=Repeat [[TSH]]<br>3-6months|D03=[[FT4]]<br>high|D04=[[FT4]]<br>normal|D05=[[FT4]]<br>low}}
+{{familytree | | | | |!| | | | | | | | | | | | | | | | | | |!| | | |!| | ||!|}}
+{{familytree | | | |E01| | | | | | | | | | | | | | | | | |!| | | |!| | ||!|E01=Consider tapering [[Levothyroxine]]}}
+{{familytree | | | ||!|| | | | | | | | | | | | | | | | | |!| | | |!| | ||!|}}
+{{familytree | | | |F01| | | | | | | | | | | | | | | | |F02||F03| |F04|F01=Repeat TSH<br>3-6months|F02=Dignosed as<br> hyperthyroid<br>phase of †[[PPT]]|F03=Subclinical<br>hyperthyroidisum<br>phase of †[[PPT]]|F04=Possible hypo-pituitary [[hypothyroidism]]}}
+{{familytree | | | ||)|-|-|.| }}
+{{familytree | | | |J01| |J02 |J01=TSH>4.0 <br>Treat<br>[[Levothyroxine]]|J02=TSH=0.3-4.0<br>Repeat [[TSH]]<br>3-6months}}
+{{familytree/end}}
+<small>‡TFT; Thyroid function tests(TSH, T4, and T3), †PPT=[[Postpartum thyroiditis]] </small>
+[[Postpartum thyroiditis medical therapy|Medical Therapy]] | [[Postpartum thyroiditis surgery|Surgery]] | [[Postpartum thyroiditis primary prevention|Primary Prevention]] | [[Postpartum thyroiditis secondary prevention|Secondary Prevention]] | [[Postpartum thyroiditis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Postpartum thyroiditis future or investigational therapies|Future or Investigational Therapies]]
+==Case Studies==
+[[Postpartum thyroiditis case study one|Case #1]]
+[[Category: (name of the system)]]

Postpartum thyroiditis: Difference between revisions

Latest revision as of 23:07, 13 December 2017

Diagnosis

Treatment

Case Studies

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