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Biology of Reproduction Nov 2018Thyroid hormones are vital for the proper functioning of the female reproductive system, since they modulate the metabolism and development of ovarian, uterine, and... (Review)
Review
Thyroid hormones are vital for the proper functioning of the female reproductive system, since they modulate the metabolism and development of ovarian, uterine, and placental tissues. Therefore, hypo- and hyperthyroidism may result in subfertility or infertility in both women and animals. Other well-documented sequelae of maternal thyroid dysfunctions include menstrual/estral irregularity, anovulation, abortion, preterm delivery, preeclampsia, intrauterine growth restriction, postpartum thyroiditis, and mental retardation in children. Several studies have been carried out involving prospective and retrospective studies of women with thyroid dysfunction, as well as in vivo and in vitro assays of hypo- and hyperthyroidism using experimental animal models and/or ovarian, uterine, and placental cell culture. These studies have sought to elucidate the mechanisms by which thyroid hormones influence reproduction to better understand the physiology of the reproductive system and to provide better therapeutic tools for reproductive dysfunctions that originate from thyroid dysfunctions. Therefore, this review aims to summarize and update the available information related to the role of thyroid hormones in the morphophysiology of the ovary, uterus, and placenta in women and animals and the effects of hypo- and hyperthyroidism on the female reproductive system.
Topics: Female; Humans; Pregnancy; Reproduction; Reproductive Health; Thyroid Hormones
PubMed: 29767691
DOI: 10.1093/biolre/ioy115 -
Endocrine Reviews Oct 2001Postpartum thyroiditis is a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery and based on an autoimmune inflammation of... (Review)
Review
Postpartum thyroiditis is a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery and based on an autoimmune inflammation of the thyroid. The prevalence ranges from 5-7%. We discuss the role of antibodies (especially thyroid peroxidase antibodies), complement, activated T cells, and apoptosis in the outbreak of postpartum thyroiditis. Postpartum thyroiditis is conceptualized as an acute phase of autoimmune thyroid destruction in the context of an existing and ongoing process of thyroid autosensitization. From pregnancy an enhanced state of immune tolerance ensues. A rebound reaction to this pregnancy-associated immune suppression after delivery explains the aggravation of autoimmune syndromes in the puerperal period, e.g., the occurrence of clinically overt postpartum thyroiditis. Low thyroid reserve due to autoimmune thyroiditis is increasingly recognized as a serious health problem. 1) Thyroid autoimmunity increases the probability of spontaneous fetal loss. 2) Thyroid failure due to autoimmune thyroiditis-often mild and subclinical-can lead to permanent and significant impairment in neuropsychological performance of the offspring. 3) Evidence is emerging that as women age subclinical hypothyroidism-as a sequel of postpartum thyroiditis-predisposes them to cardiovascular disease. Hence, postpartum thyroiditis is no longer considered a mild and transient disorder. Screening is considered.
Topics: Adult; Female; Humans; Postnatal Care; Pregnancy; Pregnancy Complications; Prenatal Care; Puerperal Disorders; Thyroiditis; Thyroiditis, Autoimmune
PubMed: 11588143
DOI: 10.1210/edrv.22.5.0441 -
Journal of the Indian Medical... May 1995
Review
Topics: Female; Humans; India; Pregnancy; Prevalence; Puerperal Disorders; Thyroiditis
PubMed: 8834140
DOI: No ID Found -
Endokrynologia Polska 2008Postpartum thyroiditis is a form of autoimmune thyroiditis developing during the first 12 months postpartum as a consequence of the immunologic flare following the... (Review)
Review
Postpartum thyroiditis is a form of autoimmune thyroiditis developing during the first 12 months postpartum as a consequence of the immunologic flare following the immune suppression of pregnancy. This disease, found in 5-10% of women in a general population and even more frequently in patients suffering from other autoimmune disorders, may re-occur in about 70% of women after a subsequent pregnancy. Postpartum thyroiditis is strongly associated with antithyroid peroxidase antibodies. Patients may present with symptoms of either thyrotoxicosis or hypothyroidism which may be transient or, in some (20-30%) cases of hypothyroidism, permanent in nature. A thyrotoxic phase of postpartum thyroiditis is usually brief and often unnoticed before a more long-lasting hypothyroid phase occurs. The diagnosis of postpartum thyroiditis is based on the observation of abnormal thyroid function tests in a postpartum antithyroid peroxidase- positive woman. In this paper, we discuss the etiopathogenesis, clinical picture, diagnosis, prognosis and treatment of postpartum thyroiditis and provide the reader with some practical guidance concerning dealing with a patient suffering from this disorder.
Topics: Diagnosis, Differential; Female; Humans; Postpartum Period; Postpartum Thyroiditis; Pregnancy; Risk Factors; Thyroxine
PubMed: 18465693
DOI: No ID Found -
The Medical Clinics of North America Mar 2012Subacute, silent, and postpartum thyroiditis are temporary forms of thyroid dysfunction caused by thyroid gland inflammation. They classically present with a triphasic... (Review)
Review
Subacute, silent, and postpartum thyroiditis are temporary forms of thyroid dysfunction caused by thyroid gland inflammation. They classically present with a triphasic course: a brief period of thyrotoxicosis due to release of preformed thyroid hormone that lasts for 1 to 3 months, followed by a more prolonged hypothyroid phase lasting up to 6 months, and eventual return to a euthyroid state. However, the types and degree of thyroid dysfunction are variable in these disorders, and individual patients may present with mild or more severe cases of thyrotoxicosis alone, hypothyroidism alone, or both types of thyroid dysfunction.
Topics: Diagnosis, Differential; Female; Humans; Male; Pregnancy; Puerperal Disorders; Risk Factors; Sex Factors; Thyroiditis, Autoimmune; Thyroiditis, Subacute; Thyroiditis, Suppurative; Women's Health
PubMed: 22443972
DOI: 10.1016/j.mcna.2012.01.003 -
Endocrinology and Metabolism Clinics of... Jun 2000Postpartum thyroiditis is the most common endocrinologic disorder, with an incidence that varies geographically from 5% to 10%. It has important clinical sequelae... (Review)
Review
Postpartum thyroiditis is the most common endocrinologic disorder, with an incidence that varies geographically from 5% to 10%. It has important clinical sequelae including symptoms of hyperthyroidism, hypothyroidism, and depression. Long-term follow-up of women who experience postpartum thyroiditis reveals a high recurrence rate in subsequent pregnancies. Postpartum thyroiditis is an autoimmune disorder, and thyroid antibody-positive women in the first trimester have a 33% to 50% chance of developing thyroiditis in the postpartum period. Whether or not to screen for postpartum thyroiditis remains controversial.
Topics: Autoimmune Diseases; Depression, Postpartum; Female; Humans; Hyperthyroidism; Hypothyroidism; Puerperal Disorders; Thyroiditis; Thyroiditis, Autoimmune; Ultrasonography
PubMed: 10874538
DOI: 10.1016/s0889-8529(05)70140-7 -
Nederlands Tijdschrift Voor Geneeskunde Apr 1989
Review
Topics: Clinical Protocols; Female; Humans; Pregnancy; Puerperal Disorders; Thyroiditis
PubMed: 2657443
DOI: No ID Found -
The Journal of Clinical Endocrinology... Aug 2012The aim was to update the guidelines for the management of thyroid dysfunction during pregnancy and postpartum published previously in 2007. A summary of changes between... (Review)
Review
OBJECTIVE
The aim was to update the guidelines for the management of thyroid dysfunction during pregnancy and postpartum published previously in 2007. A summary of changes between the 2007 and 2012 version is identified in the Supplemental Data (published on The Endocrine Society's Journals Online web site at http://jcem.endojournals.org).
EVIDENCE
This evidence-based guideline was developed according to the U.S. Preventive Service Task Force, grading items level A, B, C, D, or I, on the basis of the strength of evidence and magnitude of net benefit (benefits minus harms) as well as the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system to describe both the strength of recommendations and the quality of evidence.
CONSENSUS PROCESS
The guideline was developed through a series of e-mails, conference calls, and one face-to-face meeting. An initial draft was prepared by the Task Force, with the help of a medical writer, and reviewed and commented on by members of The Endocrine Society, Asia and Oceania Thyroid Association, and the Latin American Thyroid Society. A second draft was reviewed and approved by The Endocrine Society Council. At each stage of review, the Task Force received written comments and incorporated substantive changes.
CONCLUSIONS
Practice guidelines are presented for diagnosis and treatment of patients with thyroid-related medical issues just before and during pregnancy and in the postpartum interval. These include evidence-based approaches to assessing the cause of the condition, treating it, and managing hypothyroidism, hyperthyroidism, gestational hyperthyroidism, thyroid autoimmunity, thyroid tumors, iodine nutrition, postpartum thyroiditis, and screening for thyroid disease. Indications and side effects of therapeutic agents used in treatment are also presented.
Topics: Evidence-Based Medicine; Female; Humans; Hyperthyroidism; Postpartum Period; Practice Guidelines as Topic; Pregnancy; Pregnancy Complications; Puerperal Disorders; Thyroid Diseases; Thyroiditis
PubMed: 22869843
DOI: 10.1210/jc.2011-2803 -
Thyroid : Official Journal of the... May 2001Iodine is an essential element for thyroid hormone synthesis. The thyroid gland has the capacity and holds the machinery to handle the iodine efficiently when the... (Review)
Review
Iodine is an essential element for thyroid hormone synthesis. The thyroid gland has the capacity and holds the machinery to handle the iodine efficiently when the availability of iodine becomes scarce, as well as when iodine is available in excessive quantities. The latter situation is handled by the thyroid by acutely inhibiting the organification of iodine, the so-called acute Wolff-Chaikoff effect, by a mechanism not well understood 52 years after the original description. It is proposed that iodopeptide(s) are formed that temporarily inhibit thyroid peroxidase (TPO) mRNA and protein synthesis and, therefore, thyroglobulin iodinations. The Wolff-Chaikoff effect is an effective means of rejecting the large quantities of iodide and therefore preventing the thyroid from synthesizing large quantities of thyroid hormones. The acute Wolff-Chaikoff effect lasts for few a days and then, through the so-called "escape" phenomenon, the organification of intrathyroidal iodide resumes and the normal synthesis of thyroxine (T4) and triiodothyronine (T3) returns. This is achieved by decreasing the intrathyroidal inorganic iodine concentration by down regulation of the sodium iodine symporter (NIS) and therefore permits the TPO-H202 system to resume normal activity. However, in a few apparently normal individuals, in newborns and fetuses, in some patients with chronic systemic diseases, euthyroid patients with autoimmune thyroiditis, and Graves' disease patients previously treated with radioimmunoassay (RAI), surgery or antithyroid drugs, the escape from the inhibitory effect of large doses of iodides is not achieved and clinical or subclinical hypothyroidism ensues. Iodide-induced hypothyroidism has also been observed in patients with a history of postpartum thyroiditis, in euthyroid patients after a previous episode of subacute thyroiditis, and in patients treated with recombinant interferon-alpha who developed transient thyroid dysfunction during interferon-a treatment. The hypothyroidism is transient and thyroid function returns to normal in 2 to 3 weeks after iodide withdrawal, but transient T4 replacement therapy may be required in some patients. The patients who develop transient iodine-induced hypothyroidism must be followed long term thereafter because many will develop permanent primary hypothyroidism.
Topics: Amiodarone; Drug Synergism; Female; Goiter; Humans; Hypothyroidism; Infant, Newborn; Iodides; Iodine; Pregnancy; Prenatal Diagnosis; Thyroid Diseases; Thyroid Gland
PubMed: 11396709
DOI: 10.1089/105072501300176462 -
American Family Physician May 2006Thyroiditis is an inflammation of the thyroid gland that may be painful and tender when caused by infection, radiation, or trauma, or painless when caused by autoimmune...
Thyroiditis is an inflammation of the thyroid gland that may be painful and tender when caused by infection, radiation, or trauma, or painless when caused by autoimmune conditions, medications, or an idiopathic fibrotic process. The most common forms are Hashimoto's disease, subacute granulomatous thyroiditis, postpartum thyroiditis, subacute lymphocytic thyroiditis, and drug-induced thyroiditis (caused by amiodarone, interferon-alfa, interleukin-2, or lithium). Patients may have euthyroidism, hyperthyroidism, or hypothyroidism, or may evolve from one condition to another over time. Diagnosis is by clinical context and findings, including the presence or absence of pain, tenderness, and autoantibodies. In addition, the degree of radioactive iodine uptake by the gland is reduced in most patients with viral, radiation-induced, traumatic, autoimmune, or drug-induced inflammation of the thyroid. Treatment primarily is directed at symptomatic relief of thyroid pain and tenderness, if present, and restoration of euthyroidism.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Female; Humans; Hyperthyroidism; Hypothyroidism; Postpartum Thyroiditis; Pregnancy; Thyroiditis; Thyroiditis, Subacute; Thyroiditis, Suppurative
PubMed: 16734054
DOI: No ID Found