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{{Postpartum thyroiditis}}
{{Postpartum thyroiditis}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{SKA}}
==Overview==
==Overview==
The exact pathogenesis of postpartum thyroiditis 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 hypothroid 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 a rapid Se sequences leading to appearance of thyroiditis. Studies are going on in search of exact autoantibody and autoantigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum thyroiditis. TPO autoantibody is significantly linked to occurrence of postpartum thyroiditis.
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.


==Pathophysiology==
==Pathophysiology==


===Pathogenesis===
=== Pathophysiology: ===
=== Physiology: ===
The normal physiology of thyroid gland and thyroid hormones can be understood as under:
*Thyroid is endocrine gland which synthase and secretes thyroid hormones in bloodstream directly. It is regulated by hypothalamus and pituitary gland. Thyroid hormones are of two biochemical structures. , triiodothyronine (T<sub>3</sub>), which is true and potent form and its prohormone, thyroxine (T<sub>4</sub>) majorly is secretory form later converted to T3 in peripheral tissues by deiodinase enzyme. Thyroid hormones has negative feedback on thyroid receptors located on hypothalamus and pituitary gland. Thyroid hormones majorly effects every part of body and maintains metabolic rate by acting on thyroid receptors which are nuclear receptors mediating gene expression.  
*[[Thyroid]] is an [[endocrine gland]] which synthesizes and secretes [[thyroid hormones]] directly in the bloodstream.  
*
*[[Thyroid hormone|Thyroid hormones]] regulated by [[hypothalamus]] and [[pituitary gland]].  
*[[Thyroid hormone|Thyroid hormones]] are of two biochemical structures. [[Triiodothyronine]] (T<sub>3</sub>), which is true as well as potent form of thyroid hormone. [[Thyroxine]] ([[T4|T<sub>4</sub>]]), which is a pro-hormone, primarily found in secretory form later converted to [[T3]] in peripheral tissues by deiodinase enzyme.  
*[[Thyroid hormone|Thyroid hormones]] have a negative feedback on [[Thyroid hormone receptor|thyroid hormone receptors]] located on the [[hypothalamus]] and [[pituitary gland]].  
*Thyroid hormones may effect any part of body and maintain metabolic rate by acting on thyroid receptors which are nuclear receptors mediating gene expression.
*Functional unit of [[thyroid gland]] are thyroid follicles, which are aliened in continuous circular pattern forming a hollow cavity (thyroid cavity) between them. Connective tissue containing blood vessels is seen on the basal side of thyroid follicle and is responsible for the transport of thyroid hormone, blood cells, and iodine. Apical side of thyroid follicle faces towards thyroid cavity where [[Thyroid peroxidase|TPO]] [[enzymes]] are located, which help in the conversion of [[iodide]] to [[iodine]].
*Iodine is organified to [[tyrosine]] residue of [[thyroglobulin]], which is synthesized and stored in thyroid follicle cavity.
*This leads to the formation of mono-idodo or di-iodo [[thyroglobulin]] which combine to form tri-iodo or tetra-iodo thyroglobulin.
*On demand, thyroglobin is proteolysed to release [[T3]] and [[T4]] in blood stream across the thyroid follicle. 


*
=== Pathogenesis: ===
*[[Pregnancy]] is associated with a modification of immune system making it possible to accept [[alloantigen|alloantigens]] of paternal origin. 
*This challenge is overcome by dormant set of [[Regulatory T cell|regulatory T cells,]] CD25 CD4 positive, a subset of [[T helper cell|T helper cells]], which withholds [[T cell]] sensitization to fetal [[Antigen|antigens]].<ref name="pmid24996040">{{cite journal| author=La Rocca C, Carbone F, Longobardi S, Matarese G| title=The [[immunology]] of [[pregnancy]]: regulatory [[T cells]] control maternal immune tolerance toward the [[fetus]]. | journal=Immunol Lett | year= 2014 | volume= 162 | issue= 1 Pt A | pages= 41-8 | pmid=24996040 | doi=10.1016/j.imlet.2014.06.013 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24996040  }}</ref><ref name="pmid28618983">{{cite journal| author=Lima J, Martins C, Nunes G, Sousa MJ, Branco JC, Borrego LM| title=Regulatory T Cells Show Dynamic Behavior During Late Pregnancy, Delivery, and the Postpartum Period. | journal=Reprod Sci | year= 2017 | volume= 24 | issue= 7 | pages= 1025-1032 | pmid=28618983 | doi=10.1177/1933719116676395 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28618983  }}</ref>
*This does not suppress immunity but modulates immune response to fetal [[alloantigen]]. 
*Successful implantation of [[fetus]] in [[uterine]] cavity requires adequate [[NK cell]], [[dendritic cell]], [[macrophages]], [[T cell]], and [[B cells]].<ref name="pmid20367629">{{cite journal| author=Mor G, Cardenas I| title=The immune system in pregnancy: a unique complexity. | journal=Am J Reprod Immunol | year= 2010 | volume= 63 | issue= 6 | pages= 425-33 | pmid=20367629 | doi=10.1111/j.1600-0897.2010.00836.x | pmc=3025805 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20367629  }}</ref> 
*Subsequently on first postpartum day there is a significant decline in T regulatiory cells leading to the elevation of [[CD4 T cells]].  [[CD4 T cells]] potentiate immune as well as autoimmune responses to foreign and self-antigens.<ref name="pmid286189832">{{cite journal| author=Lima J, Martins C, Nunes G, Sousa MJ, Branco JC, Borrego LM| title=Regulatory T Cells Show Dynamic Behavior During Late Pregnancy, Delivery, and the Postpartum Period. | journal=Reprod Sci | year= 2017 | volume= 24 | issue= 7 | pages= 1025-1032 | pmid=28618983 | doi=10.1177/1933719116676395 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28618983  }}</ref>
*Role of anti-[[Thyroid peroxidase|TPO]] antibodies and anti-thyroglobulin antibodies:
**[[Thyroid peroxidase|TPO]] is found inside the [[thyroid]] follicles. Anti-[[Thyroid peroxidase|TPO]] [[antibodies]] have therefore been associated with [[Postpartum thyroiditis|PPT]]. 
**Rebound escalation of immunity in [[postpartum]] period leads to the development of anti TPO antibodies and immune complex formation of anti-TPO [[antibody]]-[[antigen]]. Subsequent activation of inflammatory response targeted against these antibodies leads to destruction of [[thyroid]] tissue. 
**In contrast to [[Hashimoto's thyroiditis|Hashimoto throiditis]], the presence of anti-[[thyroglobulin]] antibody is inconsistent with occurrence of [[Postpartum thyroiditis|PPT]]. 
**The level of anti-[[Thyroid peroxidase|TPO]] antibodies is not proportional to [[thyroid]] destruction. 
**Anti-[[Thyroid peroxidase|TPO]] antibodies are [[IgG]] antibodies containng 4 subgroups:
***[[IgG]] subset 1 is seen with activation of [[complement]] and destructive lysis of [[thyroid]] follicular cells.<ref name="pmid2090668">{{cite journal| author=Briones-Urbina R, Parkes AB, Bogner U, Mariotti S, Walfish PG| title=Increase in antimicrosomal antibody-related IgG1 and IgG4, and titers of antithyroid peroxidase antibodies, but not antibody dependent cell-mediated cytotoxicity in post-partum thyroiditis with transient hyperthyroidism. | journal=J Endocrinol Invest | year= 1990 | volume= 13 | issue= 11 | pages= 879-86 | pmid=2090668 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2090668  }}</ref> 
***Subsets 2 and 3 are not well understood till date. 
***[[IgG]] subset 4 has not been found with [[Postpartum thyroiditis|PPT]].<ref name="pmid3754185">{{cite journal| author=Jansson R, Thompson PM, Clark F, McLachlan SM| title=Association between thyroid microsomal antibodies of subclass IgG-1 and hypothyroidism in autoimmune postpartum thyroiditis. | journal=Clin Exp Immunol | year= 1986 | volume= 63 | issue= 1 | pages= 80-6 | pmid=3754185 | doi= | pmc=1577331 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3754185  }}</ref> 
**The level of [[hypothyroidism]] is related to the activation of complement cascade by IgG anti-TPO [[antibody]]-[[antigen]] complexes, either by [[complement fixation]] or direct activation of C3 esterase.<ref name="pmid8045954">{{cite journal| author=Parkes AB, Othman S, Hall R, John R, Richards CJ, Lazarus JH| title=The role of complement in the pathogenesis of postpartum thyroiditis. | journal=J Clin Endocrinol Metab | year= 1994 | volume= 79 | issue= 2 | pages= 395-400 | pmid=8045954 | doi=10.1210/jcem.79.2.8045954 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8045954  }}</ref> 
**An increase in the levels of anti-TPO [[antibodies]] has also been observed with subsequent pregnancies.<ref name="pmid23049819">{{cite journal| author=Chan WF, Gurnot C, Montine TJ, Sonnen JA, Guthrie KA, Nelson JL| title=Male microchimerism in the human female brain. | journal=PLoS One | year= 2012 | volume= 7 | issue= 9 | pages= e45592 | pmid=23049819 | doi=10.1371/journal.pone.0045592 | pmc=3458919 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23049819  }}</ref> 
 
*'''Role of T-cell:''' 
**In [[pregnancy]], [[cortisol]], [[progesterone]], and [[estrogen]] levels are high.
**These hormones modify the levels of [[Lymphocyte|lymphocytes]] such as [[TH1]], [[TH2-cells|TH2]], T reg, and [[NK-cells]]. Around 36th week of [[pregnancy]], [[cortisol]] levels decline leading to increase in [[lymphocytes]].<ref name="pmid25434070">{{cite journal| author=Argatska AB, Nonchev BI| title=Postpartum thyroiditis. | journal=Folia Med (Plovdiv) | year= 2014 | volume= 56 | issue= 3 | pages= 145-51 | pmid=25434070 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25434070  }}</ref>
**In [[Postpartum thyroiditis|PPT]] an increased ratio of [[CD4+]] to [[CD8+ T cells|CD8+]]  and  increased activation of [[T cell|T-cells]] is found.<ref name="pmid9824577">{{cite journal| author=Stallmach A, Schäfer F, Hoffmann S, Weber S, Müller-Molaian I, Schneider T et al.| title=Increased state of activation of CD4 positive T cells and elevated interferon gamma production in pouchitis. | journal=Gut | year= 1998 | volume= 43 | issue= 4 | pages= 499-505 | pmid=9824577 | doi= | pmc=1727291 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9824577  }}</ref> 
**However, [[T cell]] secretes [[Interleukin 4|IL4]], [[Interleukin 10|IL10]], and [[Interferon-gamma|interferon gamma]] which carry out destruction of [[thyroid]] gland.
**Interestingly, T reg secreting [[TGF beta|TGF-beta]] is found in high levels in [[Hyperthyroidism|thyrotoxicosis]] stage of [[Postpartum thyroiditis|PPT]], preventing [[T helper cell|CD4 T cells]] and [[Cytotoxic T lymphocytes|CD8  T]] cells from further destruction.<ref name="pmid12629119">{{cite journal| author=Olivieri A, De Angelis S, Vaccari V, Valensise H, Magnani F, Stazi MA et al.| title=Postpartum thyroiditis is associated with fluctuations in transforming growth factor-beta1 serum levels. | journal=J Clin Endocrinol Metab | year= 2003 | volume= 88 | issue= 3 | pages= 1280-4 | pmid=12629119 | doi=10.1210/jc.2002-020990 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12629119  }}</ref>


==Genetics==
==Genetics==
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
[[Genes]] involved in the pathogenesis of PPT include:<ref name="pmid9219408">{{cite journal| author=Lazarus JH, Ammari F, Oretti R, Parkes AB, Richards CJ, Harris B| title=Clinical aspects of recurrent postpartum thyroiditis. | journal=Br J Gen Pract | year= 1997 | volume= 47 | issue= 418 | pages= 305-8 | pmid=9219408 | doi= | pmc=1313006 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9219408  }}</ref>
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
*CT- 60 [[Cytotoxic T cell|cytotoxic T- cel]]<nowiki/>l [[lymphocyte]] antigen-4 CTLA-4 gene polymorphisum ([[Hypothyroidism|hypothyroid]])<ref name="pmid20408864">{{cite journal| author=Zaletel K, Krhin B, Gaberscek S, Bicek A, Pajic T, Hojker S| title=Association of CT60 cytotoxic T lymphocyte antigen-4 gene polymorphism with thyroid autoantibody production in patients with Hashimoto's and postpartum thyroiditis. | journal=Clin Exp Immunol | year= 2010 | volume= 161 | issue= 1 | pages= 41-7 | pmid=20408864 | doi=10.1111/j.1365-2249.2010.04113.x | pmc=2940147 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20408864  }}</ref><nowiki/>
*The development of [disease name] is the result of multiple genetic mutations.
*[[HLA-DR4]]
*[[HLA-DR3]]  
*[[HLA-DR5]]
 
==Associated Conditions==
==Associated Conditions==
*[[Diabetes mellitus type 1|DM type -1]]
*[[Grave's disease]]
*[[Autoimmune thyroiditis]]
*[[Postpartum thyroid dysfunction]]
*[[Postpartum depression]]
*Postpartum psychosis


==Gross Pathology==
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
On gross pathology, mild enlargement and absence of nodules are characteristic of [[postpartum thyroiditis]].<ref name="pmid10634366">{{cite journal| author=Premawardhana LD, Parkes AB, Ammari F, John R, Darke C, Adams H et al.| title=Postpartum thyroiditis and long-term thyroid status: prognostic influence of thyroid peroxidase antibodies and ultrasound echogenicity. | journal=J Clin Endocrinol Metab | year= 2000 | volume= 85 | issue= 1 | pages= 71-5 | pmid=10634366 | doi=10.1210/jcem.85.1.6227 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10634366  }}</ref>


==Microscopic Pathology==
==Microscopic Pathology==
*On microscopic histopathological analysis it hs rer sermblance to Hishimoto thyriodtis but less degree of fibrosis and atrophy , [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
On microscopy, focal or diffuse [[Lymphocyte|lymphocytic]] infiltration, follicular destruction, and [[hyperplasia]] of follicles are characteristic findings of [[Postpartum thyroiditis|PPT]].<ref name="pmid11588143">{{cite journal| author=Muller AF, Drexhage HA, Berghout A| title=Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences for antenatal and postnatal care. | journal=Endocr Rev | year= 2001 | volume= 22 | issue= 5 | pages= 605-30 | pmid=11588143 | doi=10.1210/edrv.22.5.0441 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11588143  }}</ref>
 
*Degree of destruction and [[hyperplasia]] of follicles varies with stages of [[postpartum thyroiditis]]
*Absence of fibrosis ( seen in Ridel's tyroiditis) and [[Hurthle cells]] (seen in Hashimoto's thyroiditis) 
*[[Hyperplasia]] ([[Hypothyroidism|hypothyroid]] stage)
*[[Lymphocyte|Lymphocytes]] found inside the follicles are not destructed
*[[T cell|T-cell]] activation levels and T reg cell levels are found on histopatholog of the specimen (determinant of [[thyroid]] functional status)
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}

Latest revision as of 21:15, 27 October 2017

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

Overview

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.

Pathophysiology

Pathophysiology:

The normal physiology of thyroid gland and thyroid hormones can be understood as under:

  • Thyroid is an endocrine gland which synthesizes and secretes thyroid hormones directly in the bloodstream.  
  • Thyroid hormones regulated by hypothalamus and pituitary gland.  
  • Thyroid hormones are of two biochemical structures. Triiodothyronine (T3), which is true as well as potent form of thyroid hormone. Thyroxine (T4), which is a pro-hormone, primarily found in secretory form later converted to T3 in peripheral tissues by deiodinase enzyme.  
  • Thyroid hormones have a negative feedback on thyroid hormone receptors located on the hypothalamus and pituitary gland.  
  • Thyroid hormones may effect any part of body and maintain metabolic rate by acting on thyroid receptors which are nuclear receptors mediating gene expression.
  • Functional unit of thyroid gland are thyroid follicles, which are aliened in continuous circular pattern forming a hollow cavity (thyroid cavity) between them. Connective tissue containing blood vessels is seen on the basal side of thyroid follicle and is responsible for the transport of thyroid hormone, blood cells, and iodine. Apical side of thyroid follicle faces towards thyroid cavity where TPO enzymes are located, which help in the conversion of iodide to iodine.
  • Iodine is organified to tyrosine residue of thyroglobulin, which is synthesized and stored in thyroid follicle cavity.
  • This leads to the formation of mono-idodo or di-iodo thyroglobulin which combine to form tri-iodo or tetra-iodo thyroglobulin.
  • On demand, thyroglobin is proteolysed to release T3 and T4 in blood stream across the thyroid follicle. 

Pathogenesis:

  • Pregnancy is associated with a modification of immune system making it possible to accept alloantigens of paternal origin.
  • This challenge is overcome by dormant set of regulatory T cells, CD25 CD4 positive, a subset of T helper cells, which withholds T cell sensitization to fetal antigens.[1][2]
  • This does not suppress immunity but modulates immune response to fetal alloantigen.
  • Successful implantation of fetus in uterine cavity requires adequate NK cell, dendritic cell, macrophages, T cell, and B cells.[3]
  • Subsequently on first postpartum day there is a significant decline in T regulatiory cells leading to the elevation of CD4 T cells. CD4 T cells potentiate immune as well as autoimmune responses to foreign and self-antigens.[4]
  • Role of anti-TPO antibodies and anti-thyroglobulin antibodies:
    • TPO is found inside the thyroid follicles. Anti-TPO antibodies have therefore been associated with PPT.
    • Rebound escalation of immunity in postpartum period leads to the development of anti TPO antibodies and immune complex formation of anti-TPO antibody-antigen. Subsequent activation of inflammatory response targeted against these antibodies leads to destruction of thyroid tissue.
    • In contrast to Hashimoto throiditis, the presence of anti-thyroglobulin antibody is inconsistent with occurrence of PPT.
    • The level of anti-TPO antibodies is not proportional to thyroid destruction.
    • Anti-TPO antibodies are IgG antibodies containng 4 subgroups:
      • IgG subset 1 is seen with activation of complement and destructive lysis of thyroid follicular cells.[5]
      • Subsets 2 and 3 are not well understood till date.
      • IgG subset 4 has not been found with PPT.[6]
    • The level of hypothyroidism is related to the activation of complement cascade by IgG anti-TPO antibody-antigen complexes, either by complement fixation or direct activation of C3 esterase.[7]
    • An increase in the levels of anti-TPO antibodies has also been observed with subsequent pregnancies.[8]

Genetics

Genes involved in the pathogenesis of PPT include:[12]

Associated Conditions

Gross Pathology

On gross pathology, mild enlargement and absence of nodules are characteristic of postpartum thyroiditis.[14]

Microscopic Pathology

On microscopy, focal or diffuse lymphocytic infiltration, follicular destruction, and hyperplasia of follicles are characteristic findings of PPT.[15]

References

  1. ↑ La Rocca C, Carbone F, Longobardi S, Matarese G (2014). "The [[immunology]] of [[pregnancy]]: regulatory [[T cells]] control maternal immune tolerance toward the [[fetus]]". Immunol Lett. 162 (1 Pt A): 41–8. doi:10.1016/j.imlet.2014.06.013. PMID 24996040. URL–wikilink conflict (help)
  2. ↑ Lima J, Martins C, Nunes G, Sousa MJ, Branco JC, Borrego LM (2017). "Regulatory T Cells Show Dynamic Behavior During Late Pregnancy, Delivery, and the Postpartum Period". Reprod Sci. 24 (7): 1025–1032. doi:10.1177/1933719116676395. PMID 28618983.
  3. ↑ Mor G, Cardenas I (2010). "The immune system in pregnancy: a unique complexity". Am J Reprod Immunol. 63 (6): 425–33. doi:10.1111/j.1600-0897.2010.00836.x. PMC 3025805. PMID 20367629.
  4. ↑ Lima J, Martins C, Nunes G, Sousa MJ, Branco JC, Borrego LM (2017). "Regulatory T Cells Show Dynamic Behavior During Late Pregnancy, Delivery, and the Postpartum Period". Reprod Sci. 24 (7): 1025–1032. doi:10.1177/1933719116676395. PMID 28618983.
  5. ↑ Briones-Urbina R, Parkes AB, Bogner U, Mariotti S, Walfish PG (1990). "Increase in antimicrosomal antibody-related IgG1 and IgG4, and titers of antithyroid peroxidase antibodies, but not antibody dependent cell-mediated cytotoxicity in post-partum thyroiditis with transient hyperthyroidism". J Endocrinol Invest. 13 (11): 879–86. PMID 2090668.
  6. ↑ Jansson R, Thompson PM, Clark F, McLachlan SM (1986). "Association between thyroid microsomal antibodies of subclass IgG-1 and hypothyroidism in autoimmune postpartum thyroiditis". Clin Exp Immunol. 63 (1): 80–6. PMC 1577331. PMID 3754185.
  7. ↑ Parkes AB, Othman S, Hall R, John R, Richards CJ, Lazarus JH (1994). "The role of complement in the pathogenesis of postpartum thyroiditis". J Clin Endocrinol Metab. 79 (2): 395–400. doi:10.1210/jcem.79.2.8045954. PMID 8045954.
  8. ↑ Chan WF, Gurnot C, Montine TJ, Sonnen JA, Guthrie KA, Nelson JL (2012). "Male microchimerism in the human female brain". PLoS One. 7 (9): e45592. doi:10.1371/journal.pone.0045592. PMC 3458919. PMID 23049819.
  9. ↑ Argatska AB, Nonchev BI (2014). "Postpartum thyroiditis". Folia Med (Plovdiv). 56 (3): 145–51. PMID 25434070.
  10. ↑ Stallmach A, Schäfer F, Hoffmann S, Weber S, Müller-Molaian I, Schneider T; et al. (1998). "Increased state of activation of CD4 positive T cells and elevated interferon gamma production in pouchitis". Gut. 43 (4): 499–505. PMC 1727291. PMID 9824577.
  11. ↑ Olivieri A, De Angelis S, Vaccari V, Valensise H, Magnani F, Stazi MA; et al. (2003). "Postpartum thyroiditis is associated with fluctuations in transforming growth factor-beta1 serum levels". J Clin Endocrinol Metab. 88 (3): 1280–4. doi:10.1210/jc.2002-020990. PMID 12629119.
  12. ↑ Lazarus JH, Ammari F, Oretti R, Parkes AB, Richards CJ, Harris B (1997). "Clinical aspects of recurrent postpartum thyroiditis". Br J Gen Pract. 47 (418): 305–8. PMC 1313006. PMID 9219408.
  13. ↑ Zaletel K, Krhin B, Gaberscek S, Bicek A, Pajic T, Hojker S (2010). "Association of CT60 cytotoxic T lymphocyte antigen-4 gene polymorphism with thyroid autoantibody production in patients with Hashimoto's and postpartum thyroiditis". Clin Exp Immunol. 161 (1): 41–7. doi:10.1111/j.1365-2249.2010.04113.x. PMC 2940147. PMID 20408864.
  14. ↑ Premawardhana LD, Parkes AB, Ammari F, John R, Darke C, Adams H; et al. (2000). "Postpartum thyroiditis and long-term thyroid status: prognostic influence of thyroid peroxidase antibodies and ultrasound echogenicity". J Clin Endocrinol Metab. 85 (1): 71–5. doi:10.1210/jcem.85.1.6227. PMID 10634366.
  15. ↑ Muller AF, Drexhage HA, Berghout A (2001). "Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences for antenatal and postnatal care". Endocr Rev. 22 (5): 605–30. doi:10.1210/edrv.22.5.0441. PMID 11588143.

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