Gestational Thyrotoxicosis Research Articles

Thyroid Disease I: Hyperthyroidism in Pregnancy

Thyroid physiologic adaptations in pregnancy may be confused with pathologic changes. Human chorionic gonadotropin rises early in pregnancy, stimulating thyrotropin secretion and suppressing thyroid stimulating hormone. These chemical changes are often seen in hyperemesis gravidarum and gestational transient thyrotoxicosis. Therefore, mild thyrotoxicosis may be difficult to differentiate from early pregnancy thyroxine stimulation. However, overt hyperthyroidism usually includes classic symptoms seen outside of pregnancy in addition to suppressed TSH and T4 levels. Treatment includes thionamides propylthiouracil and methimazole. Thyroid ablation is contraindicated in pregnancy. Often, in affected women, the fetus is euthyroid, but neonates can develop hyper or hypothyroidism with or without a goiter. Lastly, thyroid storm, though rare, is life threatening. Often presenting as a hypermetabolic state with cardiomyopathy and pulmonary hypertension, it generally results from decompensation from preeclampsia, anemia, sepsis, or surgery. Treatment requires intensive care level management, with initiation of thionamides, iodine, and beta blockers. This review contains 2 figures, 4 tables and 38 references. Keywords: Thyroid-releasing hormong, thyroid-stimulating hormone, thyromegaly, thyroid-stimulating immunoglobulins, thryotoxicosis, thionamides, thyroid storm

SUN-009 Variable Presentation of Two Patients with Gestational Trophoblastic Disease and Hyperthyroidism

Background: Gestational trophoblastic disease (GTD) represents a group of tumours caused by abnormal proliferation of trophoblastic cells, including molar pregnancy. Elevated β-hCG levels are an established marker for the presence of the disease and useful for monitoring. Due to the shared structural homology of β-hCG and TSH, hyperthyroidism can occur. Clinical Cases: We present two patients with GTD associated with hyperthyroidisim. Case 1, a 20 year old female (G1P0) presented to the emergency department complaining of vaginal bleeding associated with abdominal pain. She was estimated to be 13 weeks. Laboratory evaluation were β-hCG 648 324 IU/L, TSH 0.06 (0.35 - 4.94 mIU/L, free T4 23.2 (9.0 - 19.0 pmol/L, Hb 8.0 (11.6 - 16.4 g/dL). Ultrasound revealed molar pregnancy. She underwent uterine evacuation, thereafter complicated with thyroid storm (Burch Wartofsky score = 45). Post- operative vitals were BP 192/112, pulse rate 120 bpm and temperature 360C. She was managed in high care on labetolol, carbimazole, lugol’s iodine and hydrocortisone.She was subsequently referred to Medical Oncology for further management. Histology sample obtained in theatre confirmed complete molar pregnancy.Her staging CT scan indicated the presence of small lung nodules, suggesting metastatic disease. The patient’s FIGO/WHO score was III: 2. At the time of preparing this study, she had already received 7 weeks of methotrexate intramuscularly and still had detectable β-hCG levels.Case 2 was a 31 year old female presented similarly. This was her second pregnancy (G2P1), 12 weeks by dates. Her vitals were BP 141/74, pulse rate 110 bpm and temperature 36oC. The Ultrasound revealed larger for gestational age uterus with cystic structures in utero. Her quantitative β-hCG was significantly elevated (> 1 500 000 IU/L) she was thyrotoxic [TSH (<0.1 (0.34 - 4.94 mIU/L) free T4 (47.2 (9.0 - 19.0 pmol/L)], however did not develop thyroid storm (Burch Wartofsky score = 20). This patient also underwent uterine evacuation and did well post operatively. She was treated for her thyrotoxicosis with carbimazole, propranolol and thiamine. Further management was by Medical Oncology. Histological examination was in keeping with a partial mole.Her staging CT scan showed no metastasis, and had a FIGO/WHO score of 1: 4 due to her pre-treatment hCG of >1.5 million IU/L. She received 7 cycles of intramuscular methotrexate from which she achieved and maintained suppressed β-hCG levels (<1 IU/L). Conclusions: This study has demonstrated that the β-hCG levels may not always correlate with disease severity and prognosis.When comparing the two patients Case 1 had lower levels of β-hCG and of free T4 than Case 2, however was clinically more unwell, developed thyroid storm and had metastatic disease. Case 2 had hCG levels almost double those of Case 1, wsa stable and her levels decreased much quicker reaching undetectable levels

Fetal and Maternal Outcomes of Gestational Thyrotoxicosis: Single Center Experience, Retrospective Cohort

Objective: Gestational thyrotoxicosis may lead to adverse maternal and fetal events. In this study, the aim was to compare the gestational thyrotoxicosis cases with the control group in terms of their differential diagnoses, clinical observation and gestational follow-up outcomes. Materials and Methods: Pregnant patients with subclinical or overt thyrotoxicosis who were followed up in endocrinology outpatient clinic between December 2009-September 2019 were included in the study. Patients were grouped according to the diagnosis of gestational transient thyrotoxicosis (GTT), Graves’ disease, toxic nodular goiter (TNG), and intra-group comparisons and comparisons with the control group were made in terms of the presence of maternal and fetal pregnancy complications during the gestational period, delivery week, and infant birthweight. Results: A total of 115 patients were divided into GTT group, which had 50 patients, Graves’ group, which had 14 patients, TNG group, which had 1 patient, and control group, which had 50 patients. The prevalence of hyperemesis gravidarum was the highest in GTT group, with 40%. Eclampsia was found in 2 (14.2%) of the pregnant women with Graves’ disease and was not found in other groups (p=0.01). Neonatal death was found in 3 (21.4%) of the pregnant women with Graves’ disease, and 1 (2%) of the pregnant women with GTT (p=0.01). There was a significant positive correlation between delivery week and TSH (p=0.001, r:0.64), and a significant negative correlation withft3(p=0.04 r:-0.3). A significant positive correlation was detected between infant birthweight and TSH and delivery week (p=0.03 r:0.32 and p<0.001 r:0.41, respectively). Conclusion: Gestational transient thyrotoxicosis does not affect infant birthweight and perinatal complications, whereas the prevalence of low infant birthweight and maternal eclampsia is higher in Graves’ disease.

VENTRICULAR FIBRILLATION IN PREGNANCY DUE TO GESTATIONAL HYPERTHYROIDISM AND HYPEREMESIS GRAVIDARUM

Cardiac arrest in pregnancy is rarely reported in the context of gestational hyperthyroidism and hyperemesis gravidarum, conditions that are often comorbid due to thyroid stimulation by hCG. A multidisciplinary approach is critical for prompt evaluation and management. A 31-year-old G2P1 female

Thyrotoxic periodic paralysis: A retrospective, observational study from India.

Background & objectives:Thyrotoxic periodic paralysis (TPP) is an endocrine emergency presenting with acute-onset flaccid paralysis in a patient having thyrotoxicosis accompanied by hypokalaemia. This study was conducted to evaluate the clinical profile of patients with TPP presenting to three centres in India.Methods:This retrospective, observational study was conducted at three tertiary care Armed Forces medical centres, located at Lucknow, Kolkata and Delhi. The history, clinical features, treatment details and outcomes were evaluated.Results:Of the 244 patients with thyrotoxicosis, 15 were diagnosed with TPP and included in the study. These 15 patients (14 male and 1 female) had 32 episodes of TPP which were analyzed. The mean age was 30.2±6.2 yr (range: 21-39), and overt thyrotoxicosis was seen in all patients except one who had subclinical hyperthyroidism. Graves’ disease was the most common cause of thyrotoxicosis (13/15) and the remaining two patients had subacute thyroiditis and gestational thyrotoxicosis. Hypokalaemia (serum potassium <3.5 mmol/l) was seen in 12 patients, and the mean serum potassium was 3.2±0.9 mmol/l (range: 2.1-4.9). All patients had flaccid weakness, predominantly involving the lower limb with no bulbar, respiratory or cranial nerve involvement. The average duration of paralysis was 10.6±5.7 h (range: 3-28 h).Interpretation & conclusions:Our study demonstrated an early age of presentation and presence of clinical and biochemical thyrotoxicosis in majority of patients with TPP. Hypokalaemia may not always be evident in patients with TPP.

Schilddrüse und Schwangerschaft

Pregnancy has a profound impact on the thyroid gland and its function. This has to be considered in the assessment of thyroid function tests on the basis of trimester-specific reference intervals during pregnancy and in the decision making when to start therapy.The adverse impact of overt thyroid disorders in pregnancy is well understood, while the relevance of subclinical thyroid disorders and presence of thyroid antibodies remains a bit controversial. In euthyroid pregnant women with positive thyroid antibodies, levothyroxine (LT4) therapy may be discussed individually in the case of recurrent abortions. Furthermore, the risk of adverse pregnancy outcomes seems to be increased in the presence of both thyroid-stimulating hormone (TSH)-elevation and positive thyroid antibodies. Therefore, in case of subclinical hypothyroidism, taking in consideration the thyroid peroxidase antibody (TPO-Ab)-status individual decision-making and liberal initiation of LT4 therapy is recommended. In contrast, overt hypothyroidism is a strong indication for LT4 administration, aiming at rapid achievement of euthyroidism.The most common cause of hyperthyroidism is transient gestational thyrotoxicosis mediated by human chorionic gonadotropin (hCG), which leads to a reduction or suppression of TSH in the first trimester that does not require antithyroid medication. In other causes of overt hyperthyroidism antithyroid drugs (propylthiouracil or thionamides) need to be considered carefully and require interdisciplinary management.The presented recommendations are based on the current guideline of the American Thyroid Association (ATA) and the European Thyroid Association (ETA) as well as recently published literature.

An abnormal TSH can persist throughout pregnancy following gestational transient thyrotoxicosis and is not associated with increased maternal or foetal risk: a single centre retrospective cohort study

An abnormal TSH can persist throughout pregnancy following gestational transient thyrotoxicosis and is not associated with increased maternal or foetal risk: a single centre retrospective cohort study

SUN-561 Abnormal Gestational Thyrotoxicosis in Twin Pregnancy

Background: Overt hyperthyroidism during pregnancy, though rare (0.1-0.4% of all pregnancies), is alarming as it can lead to many complications such as: preeclampsia, stillbirth, low birth weight, spontaneous abortion, and premature labor. It becomes important to determine the etiology of hyperthyroidism so it can be treated appropriately. The two main etiologies of hyperthyroidism in pregnancy are Graves’ disease, which can be ruled out with TRAb, and hCG-mediated thyrotoxicosis, of which gestational transient thyrotoxicosis (GTT) is a subtype. GTT can present with subclinical hyperthyroidism or a mild overt hyperthyroidism and is more clinically benign than Graves’ disease. It typically resolves by weeks 14-18 of gestation as hCG levels fall. Clinical Case: A 32 year old G1P0 female with subclinical hyperthyroidism presented with a twin pregnancy and abnormal thyroid function tests (TFTs). Prior to pregnancy, she had mildly decreased TSH with normal fT3/fT4 and elevated TPO Ab, but normal thyroglobulin and TRAb. Her thyroid US showed multiple subcentimeter nodules that were too small for biopsy and thyroid parenchyma not consistent with autoimmune thyroid disease or Graves’ disease. The next step was a radioiodine uptake and scan, but it was deferred due to pregnancy. She did not have any symptoms of hyperthyroidism and her physical exam was benign. Her TSH was lower than expected throughout the first month of pregnancy with elevated fT4/fT3, indicating overt hyperthyroidism, which was alarming. Her TRAb was repeated, but was, again, negative, ruling out Graves’ disease. She remained clinically asymptomatic for hyperthyroidism and her TFTs improved during the second trimester and so she was thought likely to have GTT. GTT is a hCG-mediated thyrotoxicosis seen during the end of the first trimester when hCG levels peak. Usually GTT presents with only a mild elevation of fT4/fT3. In this case, the patient presented with a low TSH (even with correction for pregnancy) and higher fT4/fT3 than generally reported for GTT. Graves’ disease was ruled out with negative repeat TRAb, which is important as the management and treatment is very different from GTT. Her abnormal thyroid levels in the setting of GTT were likely related to her multiparity. In twin pregnancies, the placenta produces more hCG for longer period of times and twin pregnancies typically present with lower TSH. Lastly, it was important that her thyroid tests were closely monitored throughout the pregnancy to make sure they downtrended appropriately after the first trimester. Conclusion: GTT in the setting of twin pregnancy may present with thyroid function tests indicating overt hyperthyroidism, but it is important to differentiate it from other etiologies of overt hyperthyroidism in pregnancy so appropriate management can be initiated.

Management of thyroid disorders during and after pregnancy

Сучасний огляд нещодавніх рекомендацій Американської тиреоїдної асоціації та Ендокринного товариства США висвітлює найважливіші питання обстеження та ведення пацієнток із захворюваннями щитоподібної залози на тлі вагітності. Показано, що не тільки вагітність впливає на перебіг тиреоїдної патології, але й функціональні зміни тиреоїдного гормоногенезу становлять серйозну проблему для матері та плода. У вагітних під впливом плацентарного хоріонічного гонадотропіну рівень тиреотропного гормону значно знижується на 0,1–0,4 мкМО/мл для нижньої межі норми та на 1,0 мкМО/мл для верхньої у I триместрі вагітності. У зв’язку зі значним зростанням тироксин-зв’язуючих глобулінів рівні загального тироксину та трийодтироніну суттєво підвищуються з перших тижнів вагітності і можуть збільшуватися у 1,5 раза. Концентрація вільних трийодтироніну і тироксину знижується у другій половині вагітності, під час пологів вона в середньому на 10–15% нижча, ніж у загальній популяції. Часто при вагітності визначаються позитивні рівні антитіл до тиреопероксидази і тиреоглобуліну. Згідно з міжнародними клінічними стандартами не рекомендується здійснювати тотальний скринінг рівня тиреоїдних гормонів у I триместрі вагітності. Визначення тиреотропного гормону проводять лише у групах ризику наявності патології щитоподібної залози. В Україні визначення рівня цього гормону може бути рекомендоване кожній вагітній у I триместрі вагітності або на момент першого звернення. Гіпотиреоз виникає приблизно у 0,5% вагітних, а основною його причиною є аутоімунний тиреоїдит. Препаратом вибору для лікування гіпотиреозу є левотироксин. Інші препарати не мають підґрунтя для використання. Найпоширенішою причиною аутоімунного гіпертиреозу є дифузний токсичний зоб, що виникає у 0,1–1% усіх вагітностей, а серед неаутоімунних причин перше місце посідає гестаційний гіпертиреоз (1–3%). Вважається, що субклінічний гіпертиреоз будь-якого походження не потребує лікування упродовж усієї вагітності. Лікування селеном не рекомендоване жодними клінічними настановами, навіть у жінок із позитивними антитиреоїдними антитілами. Доброякісні вузли щитоподібної залози не потребують лікування впродовж вагітності, а у випадках диференційованого раку щитоподібної залози можна застосовувати помірну супресивну терапію препаратами тироксину.

Management of Thyrotoxicosis: Preconception, Pregnancy, and the Postpartum Period

To review the diagnosis and management of thyrotoxicosis in women who are preconception, pregnant, and in the postpartum period. Literature review of English-language papers published between 1980 and 2018. Overt thyrotoxicosis occurs in 0.2% of pregnancies and subclinical thyrotoxicosis in 2.5%. Hyperthyroidism in women of childbearing age most frequently is caused by Graves disease (GD). Gestational thyrotoxicosis, transient human chorionic gonadotropin (hCG)-mediated hyperthyroidism, may develop in the first trimester. In the first year following delivery, postpartum thyroiditis, which frequently includes a thyrotoxic phase, occurs in 5% of women. Hyperthyroidism from nodular autonomy is uncommon in women of childbearing age. It is essential to understand the underlying etiology for thyrotoxicosis in order to recommend appropriate treatment. Gestational thyrotoxicosis requires supportive care, without antithyroid drug therapy. GD may be treated with antithyroid drugs, radioactive iodine, or thyroidectomy. Pregnancy, plans for pregnancy, and lactation have important implications for the choice of GD treatment. When thyrotoxicosis presents following delivery, postpartum thyroiditis must be differentiated from GD. The diagnosis and management of thyrotoxicosis in the peripregnancy period present specific challenges. In making management decisions, it is essential to weigh the risks and benefits of treatments not just for the mother but also for the fetus and for breastfed infants. A team approach to management is critical, with close collaboration among endocrinologists, maternal-fetal medicine specialists, and neonatologists. GD = Graves disease; hCG = human chorionic gonadotropin; MMI = methimazole; PPT = postpartum thyroiditis; PTU = propylthiouracil; T3 = triiodothyronine; T4 = thyroxine; TBG = thyroxine-binding globulin; TRAb = TSH receptor antibody; TSH = thyroid-stimulating hormone.

Thyroid function and thyroid disorders during pregnancy: a review and care pathway.

To review the literature on thyroid function and thyroid disorders during pregnancy. A detailed literature research on MEDLINE, Cochrane library, EMBASE, NLH, ClinicalTrials.gov, and Google Scholar databases was done up to January 2018 with restriction to English languageabout articles regarding thyroid diseases and pregnancy. Thyroid hormone deficiencies are known to be detrimental for the development of the fetus. In particular, the function of the central nervous system might be impaired, causing low intelligence quotient, and mental retardation. Overt and subclinical dysfunctions of the thyroid disease should be treated appropriately in pregnancy, aiming to maintain euthyroidism. Thyroxine (T4) replacement therapy should reduce thyrotropin (TSH) concentration to the recently suggested fixed upper limits of 2.5mU/l (first and second trimester) and 3.0mU/l (third trimester). Overt hyperthyroidism during pregnancy is relatively uncommon but needs prompt treatment due to the increased risk of preterm delivery, congenital malformations, and fetal death. The use of antithyroid drug (methimazole, propylthiouracil, carbimazole) is the first choice for treating overt hyperthyroidism, although they are not free of side effects. Subclinical hyperthyroidism tends to be asymptomatic and no pharmacological treatment is usually needed. Gestational transient hyperthyroidism is a self-limited non-autoimmune form of hyperthyroidism with negative antibody against TSH receptors, that is related to hCG-induced thyroid hormone secretion. The vast majority of these patients does not require antithyroid therapy, although administration of low doses of β-blocker may by useful in very symptomatic patients. Normal maternal thyroid function is essential in pregnancy to avoid adverse maternal and fetal outcomes.

Hipertiroidismo en el embarazo

La relación hipertiroidismo y embarazo es poco común. Su importancia recae en el pronóstico de la madre y el feto. El reconocimiento de las alteraciones tiroideas durante el embarazo difiere de la población general. En este grupo poblacional es necesario correlacionar las pruebas diagnósticas con los cambios fisiológicos durante este periodo. La principal causa de hipertiroidismo es la enfermedad de Graves, consu componente autoinmune. La tirotoxicosis gestacional transitoria toma relevancia durante el embarazo y es un diagnóstico diferencial importante durante el primer trimestre. El manejo del hipertiroidismo durante el embarazo tiene implicaciones especiales. Las terapias de primera línea convencionales están contraindicadas, y toman relevancia los medicamentos antitiroideos. Ninguna terapia es totalmentesegura durante el embarazo y se deben evaluar los posibles efectos adversos e implicaciones para la madre y el feto. En esta revisión queremos dar a conocer los cambios en la función tiroidea durante la gestación; además, las pautas necesarias para el adecuado reconocimiento, diagnóstico y manejo del hipertiroidismo durante el embarazo, con el fin de disminuir la morbilidad y mortalidad materno-fetal. Se realizó una revisión de la literatura en PubMed y Science Direct utilizando palabras MeSH y conectores. Se incluyeron artículos especiales más relevantes publicados por las sociedades internacionales en los últimos 20 años sobre el diagnóstico y manejo del hipertiroidismo durante el embarazo.

Familial gestational hyperthyroidism caused by Val597ile mutant of TSH receptor gene with human chorionic gonadotropin hypersensitivity

Familial gestational hyperthyroidism caused by Val597ile mutant of TSH receptor gene with human chorionic gonadotropin hypersensitivity

Dysthyroidism in Diabetic Pregnant Women

Introduction: Dysthyroidism is more commonly found in pregnant women, especially diabetic parturients. The purpose of this study was to evaluate the prevalence of thyroid pathologies in diabetic pregnant patients. Patients and methods: A descriptive study that included 204 diabetic parturients (type 1 diabetes, type 2 diabetes and gestational diabetes) who received a systematic TSH and FT4 assay. Results: Mean age of the population = 31.4 ± 4.6 years. Type 1 diabetes = 16.12%; Type 2 diabetes = 38.25% and gestational diabetes = 45.63%. The total prevalence was 28.43%. Subclinical hypothyroidism was present in 16.67% of cases, true hypothyroidism in 5.88%, transient gestational thyrotoxicosis in 4.90% and hyperthyroidism in 0.98%. Conclusions: The most common pathology is mild hypothyroidism and type 1 diabetics are those with the most dysthyroidism. There remains the question of systematic screening among other diabetic parturients.

A Retrospective Analysis of Thyroid Disease in Pregnancy at Chris Hani Baragwanath Academic Hospital, Soweto, South Africa

Background Thyroid diseases in pregnancy are associated with adverse outcomes for mother and fetus. No studies have been reported examining the spectrum and nature of such disorders in the Black population of South Africa. Aims To examine thyroid disorders in pregnancy at Chris Hani Baragwanath Academic Hospital in Soweto, by assessing the causes, management and outcomes. Methods A retrospective review of thyroid disorders was undertaken in 88 patients, attending the Antenatal Endocrine Clinic over a four-year period. All underwent initial and follow-up clinical and biochemical assessments. Maternal delivery records and thyroid function tests of the neonates 48 hours or later following delivery were reviewed. Results Fifty-eight (66%) were hyperthyroid, 23(26%) hypothyroid, and 7(8%) had euthyroid colloid goiters. Forty-eight (83%) hyperthyroid patients had Graves’ disease, whilst had gestational hyperthyroidism. Regarding the hypothyroid patients, more than half followed I 131 ablation for Graves’ disease. Eighty-seven percent of the hyperthyroid and 83% of the hypothyroid patients were euthyroid prior to delivery. One fatal maternal outcome, due to uterine rupture and six intra-partum fetal losses occurred. Amongst neonates, there was one case of a tracheo-esophageal fistula and one of neonatal thyrotoxicosis. Conclusion This is the first report in sub-Saharan Africa detailing thyroid diseases in pregnancy.

Wernicke’s encephalopathy secondary to gestational hyperthyroidism

Wernicke’s encephalopathy is a neurological disorder secondary to the deficiency of vitamin B1 (thiamine). The classic symptoms consist of nystagmus, ophthalmoplegia, ataxia and mental status changes.1 Initially, this was described...

Comparative frequency of four different types of pregnancy-associated thyrotoxicosis in a single thyroid centre

BackgroundPregnancy and delivery markedly influence thyroid function. However, the comparative prevalence of gestational thyrotoxicosis (GT), new onset of Graves’ disease during pregnancy (GD during pregnancy), postpartum destructive thyrotoxicosis (PPT), and postpartum Graves’ thyrotoxicosis (PPGD) has not yet been determined.MethodsWe prospectively registered and performed a review of 4127 consecutive non treated female patients with thyrotoxicosis, seen between August 2008 and December 2013 in our outpatient clinic of Kuma Hospital. 187 out of the 4127 women had new diagnosis of thyrotoxicosis during pregnancy or in the postpartum period. We investigated the prevalence of new diagnosis of GT, GD during pregnancy, PPT and PPGD and compared the characteristics of these types of thyrotoxicosis. The postpartum period is defined as twelve months after delivery.ResultsOut of 187 pregnant or postpartum women, we identified 30 (16.0%) with GT, 13 (7.0%) with GD during pregnancy, 42 (22.5%) with PPT, and 102 (54.5%) with PPGD. The onset time of thyrotoxicosis during pregnancy, i.e., both GT and GD during pregnancy, was delayed by a couple of weeks when hCG peaked at 10 gestational weeks. Seventy-six percent of patients with PPT developed thyrotoxicosis between delivery and 4 months postpartum; on the other hand, 83.3% of patients with PPGD developed thyrotoxicosis at 6 months postpartum or later.ConclusionsWe named gestational thyrotoxicosis, new onset of Graves’ disease during pregnancy, postpartum destructive thyrotoxicosis, and postpartum Graves’ thyrotoxicosis as pregnancy-associated thyrotoxicosis. A clinically significant number of women developed Graves’ disease in the postpartum period in a single thyroid centre.

Severe Mitral Regurgitation by Hyperthyroidism in the Absence of Left Ventricular Dilatation

Introduction Graves’ disease (GD) is an autoimmune disease and the most common cause of thyrotoxicosis,, with multisystem involvement, that mainly affects women between 40 and 60 years of age. It is the most prevalent cause of autoimmune hyperthyroidism in pregnancy,, and it can be distinguished from gestational thyrotoxicosis due to the presence of diffuse goiter and previous history of hyperthyroidism. Clinical hyperthyroidism occurs in 0.2% of pregnant women. Heart failure (HF) is a rare manifestation of decompensated GD and it [...]

Pathogenesis of Hyperthyroidism.

Hyperthyroidism is a form of thyrotoxicosis in which there is excess thyroid hormone synthesis and secretion. Multiple etiologies can lead to a common clinical state of "thyrotoxicosis," which is a consequence of the high thyroid hormone levels and their action on different tissues of the body. The most common cause of thyrotoxicosis is Graves' disease, an autoimmune disorder in which stimulating thyrotropin receptor antibodies bind to thyroid stimulating hormone (TSH) receptors on thyroid cells and cause overproduction of thyroid hormones. Other etiologies include: forms of thyroiditis in which inflammation causes release of preformed hormone, following thyroid gland insult that is autoimmune, infectious, mechanical or medication induced; secretion of human chorionic gonadotropin in the setting of transient gestational thyrotoxicosis and trophoblastic tumors; pituitary thyrotropin release, and exposure to extra-thyroidal sources of thyroid hormone that may be endogenous or exogenous. © 2017 American Physiological Society. Compr Physiol 7:67-79, 2017.

A rare case of gestational thyrotoxicosis as a cause of acute myocardial infarction.

SummaryAngina pectoris in pregnancy is unusual and Prinzmetal’s angina is much rarer. It accounts for 2% of all cases of angina. It is caused by vasospasm, but the mechanism of spasm is unknown but has been linked with hyperthyroidism in some studies. Patients with thyrotoxicosis-induced acute myocardial infarction are unusual and almost all reported cases have been associated with Graves’ disease. Human chorionic gonadotropin hormone-induced hyperthyroidism occurs in about 1.4% of pregnant women, mostly when hCG levels are above 70–80 000 IU/L. Gestational transient thyrotoxicosis is transient and generally resolves spontaneously in the latter half of pregnancy, and specific antithyroid treatment is not required. Treatment with calcium channel blockers or nitrates reduces spasm in most of these patients. Overall, the prognosis for hyperthyroidism-associated coronary vasospasm is good. We describe a very rare case of an acute myocardial infarction in a 27-year-old female, at 9 weeks of gestation due to right coronary artery spasm secondary to gestational hyperthyroidism with free thyroxine of 7.7 ng/dL and TSH <0.07 IU/L.Learning points:AMI and cardiac arrest due to GTT despite optimal medical therapy is extremely rare.Gestational hyperthyroidism should be considered in pregnant patients presenting with ACS-like symptoms especially in the setting of hyperemesis gravidarum.Our case highlights the need for increased awareness of general medical community that GTT can lead to significant cardiac events. Novel methods of controlling GTT as well as medical interventions like ICD need further study.