1 / 55

Thyrotoxicosis in Pregnancy: A Detailed Overview

Learn about transient thyrotoxicosis of pregnancy, Graves' disease during pregnancy, and changes in thyroid physiology. Understand the prevalence, pathogenesis, and role of human chorionic gonadotropin in causing hyperthyroidism during gestation.

maloneh
Download Presentation

Thyrotoxicosis in Pregnancy: A Detailed Overview

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Thyrotoxicosis in pregnancy DrHashemipour.S QUMS

  2. Outline • Transient thyrotoxicosis of pregnancy • Graves disease during pregnancy

  3. Changes in thyroid physiology in pregnancy

  4. Physiologic changes during pregnancy

  5. Transient thyrotoxicosis of pregnancy (TTP)

  6. TTP: Prevalence • Close to 20%of pregnant women have a suppressed TSH and normal free T4 • In about 2.4% pregnant women had low TSH ( less than 0.20 mU/liter) and high free T4 index concentration.

  7. Racial differences

  8. In some studies (Yeo et al., 2001) the frequency of transient gestational hyper thyroid-ism reached 11% for Asian women

  9. Prevalence Gestational thyrotoxicosisis at least 10-fold more frequent than hyperthyroid ism due to graves disease

  10. Pathogenesis Human chorionic gonadotropin (hCG) is a weak TSH agonist The etiology of thyroid stimulation during pregnancy is related to hCG action

  11. Action of HCG on thyroid cells In thyroid cells, hCG increases CAMP, iodide transport , and cell growth and hormone synthesis.

  12. Mirror curve of TSH and HCG concentrations Glinoer et al., 1990,The Endocrine Society

  13. TTP:Role of HCG • In normal pregnancy, when hCG levels are highest at 10–12 wk gestation, there is suppression of serum TSH levels, presumably due to slight increases in free thyroxine concentration driven by high hCG values De Groot et al. JCEM 2012, 2543–2565,

  14. HCG level and thyrotoxicosis (cont) These abnormalities are exaggerated in hyperemesisgravidarumand more so in gestational Hyperthyroidism , especially if peak hCG values exceed 75–100,000 IU/ml with a duration of the peak that exceeds the normal situation (which is less than 1 wk).

  15. HCG level and thyrotoxicosis (cont) In twin pregnancies, HCG levels tend to be higher and suppressed TSH levels are more frequentand more prolonged.

  16. HCG level and thyrotoxicosis: Trophoblastic thyrotoxicosis The reported prevalence of hyperthyroidism in patients with hydatidiform mole is 25–64% .However, most patients with hydatidiform mole have either none or very few clinical signs of excess thyroid hormone secretion despite elevated levels of thyroxine (T4) and triiodothyronine (T3) It has been reported that about 5% have clinical hyperthyroidism

  17. Role of HCG quality • Elevations of thyroid hormone and suppression of TSH are not entirely correlated with hCG levels • An increase in acidic forms of hCGhave demonstrated in hyperemesis gravidarum. unusual glycosylation patterns of hCG are common in hydatidiform moles which frequently present as hyperemesis gravidarum

  18. mutation of the TSHR In1998 Cases have been reported about family in which at least two women experienced hyperthyroidism , and hyperemesis gravidarum, during several pregnancies

  19. Cont Hyperthyroidism continued throughout pregnancy.Graves disease was diagnosed based on duration of hyperthyroidism. Surprisingly enough, the `Graves' disease improved in the post-partum period allowing for discontinuationof antithyroid drugs. The following pregnancy was also complicated by hyperemesis and hyperthyroidism, which required treatment with antithyroid drugs, and was followed by recovery of a normal thyroid function post-partum, without any relapse later.

  20. Cont The daughter had a similar story .She had a small diffuse goitre, no Graves‘ ophthalmopathy, no thyroperoxidase or thyroglobulinantibodies,and no TSHR antibodies. The absence of antibodies, occurrence of hyperthyroidism only during gestation and improvement in the post-partum period suggested that Graves' disease was unlikely

  21. Cont • HCG concentration was within the normal range during gestation. • Abnormal hCG, with increased thyrotrophic activity, was hypothesized but ruled out by in vitro tests.

  22. TTG: TSH receptor mutation Rodien et al. Human Reproduction Update,2004, 95-105

  23. Hyperemesisgravidarum and hyperthyroidism

  24. Definition of HG • Hyperemesis gravidarum, defined as severe vomiting in early pregnancy that causes more than 5% weight loss, dehydration, and ketonuria

  25. prevalence • Frequency ranges from 0.15 %to 1% of pregnancies. Variation in frequency is dependent on definition someauthorsdefinehyperemesis gravidarum as severe vomiting requiring hospitalization which leads to a higher frequency (up to 1.5%), • whereas others apply a more stringent definition which includes hydroelectrolytic disorders, ketosis, and weight loss >5% of non-pregnant weight

  26. Prevalence (cont) One puzzling feature of hyperemesisgravidarum is its variable frequency in different ethnic groups occurring at a much higher frequency in the Asian population. This suggests, at least,acommon predisposing genetic background, if not a unique disease

  27. Hyperemesis gravidarum Typically occurs between the 4th and the 10th weekof gestation, with resolution by 20 weeksof gestation. In approximately10% of HG patients, symptoms will persist throughout pregnancy.

  28. During the first trimester, the severity of morning sickness correlates positively with serum free T4 and the concentration of plasma hCG and negatively with the level of serum TSH

  29. Pathophysiology of HG The mechanisms of hyperemesis gravidarum are poorly understood. The syndrome is favored by hypersecretion of hCGalthough normal concentrations of hCG have also been reported, there is no clear threshold, since the normal range of hCG concentration is extremely large.

  30. Prevalence of thyrotoxicosis in hyperemesisgravidarum

  31. Gestational transient thyrotoxicosis has been observed in up to two thirds of women suffering from hyperemesisgravidarum

  32. Distinction between transient thyrotoxicosis of pregnancy (TTP) andGraves' disease

  33. Distinction between TTP and Graves' disease 1.charachteristics of hyperemesis gravidarumare present in former . 2.Goitre is usually but not necessarily absent in the former 3.No past history of thyroid disease is reported by the patient or her family. 4.Ophthalmic examination reveals no abnormality, in contrast to half of patients with graves disease. Graves' disease. 5.Gestational age

  34. Distinction between gestational transient thyrotoxicosis andGraves' (cont) Gestational transient thyrotoxicosis is usually of short duration and spontaneously resolves with the decline of hCG. in these patients freeT4 levels normalized by 15 wk, whereas TSH remained suppressed until 19 wk gestation

  35. Distinction between gestational transient thyrotoxicosis andGraves' disease:TFT • Antithyroid antibodies are usually absent in gestational transient thyrotoxicosis. In particular, TSHR antibodies are absent • Serum free T3 is elevated less frequently in GTT compared with graves disease

  36. Treatment • Clinical symptoms usually are mild • Close observation of the course of the clinical presentation and thyroid hormone abnormalities is indicated. • Beta blockers such as metoprololmay be helpful and may be used with obstetrical agreement De Groot et al. JCEM,2012: 2543–2565

  37. Key massges • Transient thyrotoxicosis of pregnancy should differentiated from hyperthyroidism solely based on clinical judgment • Subjects with TTP should be observed carefully and treated with appropriate beta blockers if have sever symptoms of thyrotoxicosis

  38. Graves disease during pregnancy

  39. Prevalence • Prevalence of hyperthyroidism in pregnancy less than 0.1 • About 85% of cases are Graves’disease De Groot et al. JCEM,2012: 2543–2565

  40. Clinical course of Graves in pregnancy • First trimester • Second and third trimester • Postpartum period

  41. Clinical manifestations • Symptoms are non-specific and may be mimicked by normal pregnancy. • Significance of goiter • TFT must be interpreted in the context of the normal gestational changes of decreased serum TSH and increased T4and T3 levels De Groot et al. JCEM,2012: 2543–2565

  42. Maternal complications of hyperthyroidism in pregnancy Manissto etal.JCEM, 2013, 2725-2733

  43. Fetal complications • Low birth weight • Fetal hypothyroidism (overtreatment of mother) • Fetal central congenital hypothyroidism (undertreatmentof maternal hyperthyroidism) • Fetal thyrotoxicosis placental passage of TSI • Fetal death De Groot et al. JCEM,2012: 2543–2565

  44. Neonatal Graves

  45. Treatment:Goal • Goal of therapy : maintaining free T4 or FTI upper limit of the non pregnant reference range. evidence level :B (1QQEE) De Groot et al. JCEM 2012, 2543–2565,

  46. Treatment:Choosing ATD • PTU is recommended as the first-line drug for treatment of hyperthyroidism during the first trimester of pregnancy • Monitoring liver function is recommended every 3–4 wkand encourage patients to promptly report any new symptoms of hepatitis • MMI may also be prescribed if PTU is not available or if a patient cannot tolerate or has an adverse response to PTU. level: C; evidence, poor (2QEEE) De Groot et al. JCEM 2012, 2543–2565,

  47. Aplasia cutis

  48. Aplasia cutis

  49. Treatment:Choosing ATD • After switching from PTU to MMI, thyroid function should be assessed after 2 wk and then at 2- to 4-wk intervals ( level: B; evidence, fair (1QQEE) . De Groot et al. JCEM 2012, 2543–2565,

  50. Treatment

More Related