Gestational Thyrotoxicosis Research Articles

5125 Severe Gestational Thyrotoxicosis Leading to Unwarranted Treatment

Abstract Disclosure: C. Bell: None. L.A. Barbour: None. Introduction: Gestational transient thyrotoxicosis (GTT) is the most common cause of thyrotoxicosis in pregnancy yet is often confused with Graves’. Although usually mild, we present a severe case leading to the unsupported use of anti-thyroid drugs (ATDs), which could have resulted in fetal hypothyroidism if continued. Case: A 30-year-old female G1P0 at 10 wks with a single gestation presented with 4 wks of vomiting, palpitations, and weight loss. She had no history of thyroid disease. She was diaphoretic and ill-appearing and had a non-tender, smooth normal-sized thyroid, a stare without exophthalmos, and a fine tremor. TSH was < 0.01, FT4 5.57 ng/dL (0.89-1.76), and TT3 201 ng/dL (60-181). TPO Ab 51 (< 60). TRAb, TSI Ab, and TgAb were negative. β-hCG level was 334,106 mIU/mL. She was diagnosed with GTT and briefly hospitalized for dehydration but was re-hospitalized 2 wks later with worsening symptoms and 25 lb weight loss. Unexpectedly, her FT4 and TT3 rose to 6.24 ng/dL and 339, respectively. A thyroid ultrasound showed mildly increased vascularity. PTU was started for seronegative Graves’ at 50 mg tid with metoprolol. After 3 days, her FT4 improved to 3.59 ng/dL and TT3 was 176. Further consultation recommended stopping PTU. She was sent home with metoprolol. Her symptoms and FT4 levels improved. FT4 was normal and hCG levels dropped to 54,821 by 18 wks. Discussion: GTT is caused by a transient elevation in T4 due to direct hCG stimulation of the TSH receptor. It is more common with multiple or molar gestations and hyperemesis gravidarum, also mediated by hCG. It typically results in mild thyrotoxicosis, highlighting the uniqueness of this case. Only a couple of case reports exist where GTT presented as severe thyrotoxicosis or thyroid storm and persisted this long. It is critical to distinguish GTT from Graves’ given their different outcomes and treatment. GTT is commonly misdiagnosed as Graves’ as both result in thyrotoxic labs and symptoms and can present in 1st trimester. GTT typically presents at 8-10 wks and lasts until 14-16 wks when hCG levels fall, but Graves’ may also improve by 2nd trimester due to the immune suppression of pregnancy. It is also possible for both to co-exist. hCG levels >100,000 are associated with GTT but due to the variable sialylation of hCG, which changes its affinity to the TSH receptor and half-life, they are unreliable diagnostically. Key clues supporting GTT include no goiter, exophthalmos, or symptoms pre-pregnancy, negative TRAb and TSI, and, notably, a lower T3/T4 ratio compared to Graves’, as seen in this case. To conclude, GTT is often mistaken for Graves’ but inappropriate use of ATDs can result in fetal hypothyroidism and does not improve outcomes. Although the severity of our case is unusual, accurate distinction from Graves’ by endocrinologists is crucial to ensure optimal maternal-fetal outcomes. Presentation: 6/1/2024

7527 Subacute Thyroiditis in First Trimester of Pregnancy: Rare Cause of Thyrotoxicosis

Abstract Disclosure: K. Wilcher: None. A. Gupta: None. Background: Subacute thyroiditis (SAT) is extremely rare in pregnancy with only 8 prior cases reported in the literature. SAT can result in maternal and fetal complications. In this case report, we describe a case of subacute thyroiditis presenting in the first trimester of pregnancy. Case Presentation: A 38-year-old female with past medical history of stillbirth presented with thyrotoxicosis in gestational week 10 of her pregnancy. The patient has a history of stillbirth in gestational week 38 of her first pregnancy requiring cesarean section one year prior to presentation. She was in the process of getting in vitro fertilization (IVF) and had an egg retrieval. During the process, she started on thyroxine 50 mcg daily for blood thyroid-stimulating hormone (TSH) 3.77 mcIU/mL. She became pregnant without the help of IVF and stopped thyroxine. One month later, labs showed low TSH 0.022 mcIU/mL (reference range: 0.4-4.5 mcIU/mL) and high blood free thyroxine (FT4) 1.87 ng/dL (reference range: 0.7-1.8 ng/dL). Repeat labs two weeks later showed low blood TSH 0.012 mcIU/mL, high FT4 2.08 ng/dL, and high blood free triiodothyronine (FT3) 5.2 pg/mL (reference range: 2.3-4.2 pg/mL). She was referred to endocrinology for evaluation. She reported mild intermittent right sided neck pain since diagnosis of pregnancy. She denied any history of viral infection, cough, or fever. She reported symptoms of severe nausea, mild constipation, and mild anxiety. She denied diarrhea, tremors, changes in voice, palpitations, or weight loss. Her family history is significant for hypothyroidism in her father. Physical exam demonstrated a non-tender, symmetric thyroid without enlargement or nodules. Ultrasound showed heterogenous thyroid with an ill-defined heterogenous area in the right lobe appearing pseudo-nodule, and increased vascularity. At this time, the patient was diagnosed with mild gestational hyperthyroidism with a plan to monitor thyroid hormone levels. Repeat labs two weeks later showed low blood TSH 0.005 mcIU/mL, high FT4 2.35 ng/dL, and high FT3 6.4 pg/mL. TSH-receptor antibodies, thyroid stimulating immunoglobulin, and thyroid peroxidase antibodies were normal on testing. In gestational week 16, labs showed normal TSH 2.76 mcIU/mL, low FT4 0.56 ng/dL, and low FT3 2.1 pg/mL. At that time, she started on levothyroxine 75 mcg daily and was diagnosed with subacute thyroiditis. Follow up labs in gestational weeks 18, 20, and 24 showed improvement in TSH and FT4 on thyroid hormone supplementation. Conclusion: This case report discusses the findings of SAT in first trimester pregnancy. Currently, she is in gestational week 28 and still requiring thyroid hormone supplementation. SAT in pregnancy is very rare. This case report significantly contributes to the literature and current knowledge of the prevalence, presentation, and disease process of subacute thyroiditis in first trimester pregnancy. Presentation: 6/2/2024

Hyperthyroidism and Pregnancy

Introduction: Hyperthyroidism in pregnancy is defined by low TSH, below the specific reference values of each trimester with high levels of free T3, free T4 or both. Source of serious complications for both the mother and the fetus. The aim of our study is to determine the clinical, paraclinical, etiological and therapeutic aspects. Material and Methods: We have collected in this work the cases of hyperthyroidism duringpregnancy encountered in the endocrinology, maternal intensive care and gynecology departments of the Marrakech University Hospital. Results: we have collected 32 cases of hyperthyroidism during pregnancy. The average age was 29 years old. Functional signs were dominated by uncontrollable vomiting and weight loss. As for the thyroid assessment, the average TSH level was 0.017 with an average T4 level of 53.30 and T3 of 15.74. The etiologies were dominated by transient gestational hyperthyroidism (TGH) and Graves' disease. The management was essentially based on hydro-electrolyte rebalancing, then the etiological treatment in a second step. Discussion: Hyperthyroidism is considered to be the second endocrinopathy in pregnant women, after gestational diabetes. It would be present in 1 to 3% of pregnant women, the most common causes are Graves' disease and TGH. Conclusion: Pregnancy hyperthyroidism is a frequently encountered situation. The identification of the cause of hyperthyroidism must be established because it guides the follow-up andpregnancy care.

Thyroid Dysfunction in Pregnancy: A Literature Review

Due to structural similarities between HCG and thyroid-stimulating hormone, thyroid stimulation during pregnancy starts in the first trimester (TSH). The volume of thyroid hormone distribution increases along with placental metabolism, maternal thyroxine transport, and estrogen-mediated changes in thyroxine-binding globulin (TBG), all of which cause a 20–40% rise in early pregnancy thyroid hormone demand. Due to the human chorionic gonadotropin alpha subunit's cross-reactivity with the TSH receptor, the reference range of laboratory values for TSH is lower. High serum protein levels may alter estimates rather than direct measurements of free thyroxine (FT4), leading to reported results that are inaccurate. The clinical range of thyroid dysfunction during pregnancy can include both hyperthyroidism (Graves' disease and transitory gestational thyrotoxicosis) and hypothyroidism (overt hypothyroidism, subclinical hypothyroidism, and autoimmune thyroid disease). The risk of preterm and infant respiratory distress syndrome is increased by this malfunction.

Gestational thyrotoxicosis due to molar pregnancy complicated by pre-eclampsia

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Abstract #1404976: Severe Gestational Thyrotoxicosis Complicated by Thyroid Storm in a Primigravid Patient with Hyperemesis Gravidarum in a Multiple Pregnancy

Gestational transient thyrotoxicosis (GTT) is seen in 3% of pregnancies and occurs in 30-60% of patients with hyperemesis gravidarum (HG). The incidence of thyroid storm in this setting has not yet been reported. The severity of GTT and HG is positively related to serum hCG levels. Treatment in GTT with antithyroid drugs is not routinely indicated since GTT usually is described as a disorder of spontaneous resolution without unfavorable maternal and fetal outcomes. We describe a case of severe GTT complicated by thyroid storm in a primigravid 20-year-old patient with twin gestation and HG. A 20-year-old female primigravida with twin gestation and HG presented with nausea, vomiting, altered sensorium, and weakness for four days at 14 weeks’ gestation. At 9 weeks’ gestation during inpatient management for HG, TSH < 0.01 was found. Outpatient FT4 3.1 was obtained. On current presentation, tachycardia HR 169 bpm, mild abdominal tenderness, disorientation, a repeated TSH < 0.01 resulting in Burch-Wartofsky point scale of 45 warranted MICU admission for thyroid storm management. FT4 3.3, T3 239, and hCG level 99,080 were found. Transvaginal US and positive MSSA blood cultures confirmed spontaneous septic abortion. Antibiotics were given, and dilation and evacuation were performed. FT4 and T3 improved to 2.1 and 114, respectively. TSH receptor antibody (TRAb) was found negative and thyroid US did not reveal hypervascularity or nodules. Post admission TSH 0.544 and FT4 1.02 were found. The association between HG and thyrotoxicosis was made in 1980 by Valentine et al. Estrogen and hCG levels are significantly higher in women with HG, leading to increased thyroid hormone secretion and lower TSH levels. GTT resulting from inappropriate hCG secretion is a common form of hyperthyroidism in HG. GTT usually is described as an entity with spontaneous resolution as thyroid hormones normalize by the second trimester. Treatment for GTT with antithyroid drugs is not routinely indicated and they are reserved for a minority of patients with extremely severe GTT. Fasting, hydration, and evaluation of thyroid function are recommended as the most appropriate management for GTT in HG. Genetic mutations changing lysine into an asparagine leading to an increased sensitivity of TSH receptor to hCG ultimately causing severe and prolonged GTT have been found. TRAb is recommended as a more sensitive and specific diagnostic tool to differentiate GTT and Graves’ disease. However, physiological immunosuppression tends to suppress the TRAb levels during pregnancy. Comparative follow-up studies are required to establish a final diagnosis.

Pregnancy Risk Factors for Gestational Diabetes and Hyperthyroidism

The significant frequency of thyroid dysfunction in women with pre-gestational DM calls for evaluation of thyroid function in these people during pregnancy. Thyroid dysfunction was present in both pregnant women with GDM and healthy pregnant women, but in 27% of them, TPO Ab titers were positive, indicating the need for additional testing for postpartum thyroiditis and dysfunction. Therefore, it can be concluded from the findings that women with gestational diabetes mellitus were more likely than healthy pregnant women to have thyroid dysfunction, which is manifested as hypothyroidism with high anti-TPO levels.

Tiroid Disfonksiyonu Olan Gebelerin Demografik Özelliklerinin Araştırılması- Ege Üniversitesi Örneklemi

Aim: Thyroid diseases can cause maternal and fetal adversities, and proper diagnosis, follow-up and&#x0D; treatment during pregnancy requires special attention. In the evaluation of thyroid functions during&#x0D; pregnancy, free thyroxine (FT4) is used primarily with thyroid-stimulating hormone (TSH). Our aim is to&#x0D; investigate the prevalence and the effects of thyroid dysfunction during pregnancy.&#x0D; Material and Methods: Our study is a prospective study including 960 pregnant women and spanning&#x0D; from November 2017 to May 2019 in Ege University Endocrinology outpatient clinic.100 pregnant&#x0D; women with thyroid dysfunction out of 960 pregnant women were included in the study. Maternal&#x0D; age, gestational trimester, family history of the thyroid disorder, TSH, FT4, free triiodothyronine (FT3),&#x0D; anti-thyroid peroxidase antibody (Anti-TPO), anti-thyroglobulin antibody (Anti-TG), thyrotropin (TSH)&#x0D; receptor antibody (TRAb) were collected. The correlations between TSH, FT3 and FT4 were examined.&#x0D; Results: In the study, the mean age of pregnant patients was 29.33 ± 5.97. Anti-TPO was positive %18 and&#x0D; Anti-TG was positive (5%). 24 of 100 (24%) patients had nodules. 1 (8.3%) patient with hyperthyroidism&#x0D; was positive for TRAb. Age differences in patients with or without nodule were not statistically significant.&#x0D; 1 (1%) of the patient had Graves disease, 81 (81%) had subclinical hypothyroidism, 7 (7%) had clinical&#x0D; hypothyroidism, 11 (11%) had gestational thyrotoxicosis. The frequency of prematurity was determined&#x0D; in 7 patients (15.6%) by the data of 45 pregnant women who gave birth.&#x0D; Conclusion: TSH levels in pregnant patients with positivity for anti-TPO and anti-TG were significantly&#x0D; higher than pregnant patients with negativity for anti-TPO and anti-TG. In addition, the relationship&#x0D; between thyroid diseases and nodule frequency, autoimmunity, premature birth in pregnant women&#x0D; were not detected. More comprehensive study series are needed.

ODP453 A Lady Changes from Hypothyroid to Hyperthyroid State during Pregnancy

Abstract A 34-year-old lady presented to the Endocrine Clinic in 2021 initially for hypothyroidism complicated pregnancy. She volunteered history of Graves’ disease at age 11 and went into remission after taking anti-thyroid medication for 1-2 years. She did not have family history of thyroid disease. She was found to have hypothyroidism during pre-pregnancy check-up in 2017 and started thyroxine (LT4) replacement. The anti-thyroid peroxidase antibody was elevated to 358 (&amp;lt; 35) kIU/l. She had first pregnancy in early 2018 and LT4 was increased to 128 microgram daily which was reduced to 50 microgram daily after delivery. Before the second pregnancy, her TSH was decreasing. The family doctor reduced LT4 to 25 microgram 5 days per week. The TFT just before the patient became pregnant showed TSH 0. 08 (0.35-3.8)mIU/l, fT4 15 (9.5-18.1) pmol/l. At 8th week of pregnancy, her TSH became undetectable, while fT4 was 20.8 (11.8-25.7)pmol/l. At 17th week, her fT4 further increased to 19.9 (10.1-19.4) pmol/l and fT3 was 7.3 (3.25-5.2)pmol/l. TSH remained undetectable. Clinically, she complained of palpitation. She had goiter but no thyroid bruit. Her pulse rate was 118 bpm. LT4 was stopped. She was suspected to have relapse of thyrotoxicosis. Anti-TSH receptor antibody was raised to 3.3 (&amp;lt;1. 0) IU/l. The thyroid stimulating immunoglobulin (TSI) was raised to 155% above baseline activity (nl&amp;lt;140%). At 22th week, her fT4 remained elevated at fT4 19.1 (9.2-17.44), fT3 7.6 (3. 03-4.75) pmol/l. Carbimazole was started at 5mg daily for 2 weeks then 5mg alternate day. At 28th week, her fT4 was still elevated fT4 17.7 (9.2-17.4), fT3 6.9 (3. 03-4.75) pmol/l. She was also noted to have poor maternal weight gain from 61kg pre-pregnancy to 62.4kg at 22th week. She had nausea and vomited once per week. She had iron deficiency anaemia requiring iron supplement. Carbimazole was increased again to 5mg daily for 3 weeks then tailed down to 5mg alternate day. At 33th week, her anti-TSH receptor antibody level reduced to 1.9. At 36th week of gestation, her fT4 level came down to mid normal range 14.1 (9.2-17.4)pmol/l. She delivered at 40th week uneventfully. There are a number of clinical challenges. Usually, the dose of thyroxine is increased by 30% in early pregnancy with TSH aim of 0.5-2. 0mIU/l. But in this patient, the TSH was already low before pregnancy and then became undetectable so LT4 was not increased. Gestational thyrotoxicosis is a differential diagnosis but seldom persisted towards second trimester and TSI is expected to be normal in such case. Graves’ disease usually becomes quiescent during pregnancy due to immunosuppression or haemodilution of autoimmune antibodies. Changing from hypothyroidism to hyperthyroidism is a rare phenomenon. It is related to the concentration and the affinity of anti-thyroid stimulating antibodies and blocking antibodies. The outcome depends on which antibodies predominate. Presentation: No date and time listed

ODP390 Metastatic Gestational Trophoblastic Neoplasia Masquerading as Thyroid Storm in a Girl with Molar Pregnancy and Hyperthyroidism

Abstract The Case Patient is a 16-year-old female with molar pregnancy, admitted for D&amp;C, referred for hyperthyroidism, concern for thyroid storm. A month prior, she presented with heavy vaginal bleeding, morning sickness. Ultrasound showed blighted ovum. HCG was significantly elevated, 668,123 mIU/mL. TSH was low at 0. 01 mIU/L, Free T4 elevated 2.3 ng/dL. No family history of thyroid dysfunction. She was for was noted to have respiratory distress, hypoxia, and tachycardia in the 120s post-operatively. LFTs normal, no fever, jaundice or CNS manifestations. Chest CT showed bilateral lower lobe localized pulmonary edema concerning for trophoblastic fluid embolism vs thyroid storm. BWPS = 40. She was placed on PTU, beta blockade, Lugol's iodine, and hydrocortisone. Repeat chest CT showed diffuse pulmonary nodules consistent with gestational trophoblastic neoplasm (GTN). No other metastasis on further imaging (chest, abdomen, pelvis, brain). Clinical status improved, FT4 normalized 5 days after starting treatment. TRAbs negative. She was discharged on Methimazole and Atenolol, which were eventually discontinued. HCG levels significantly decreased after D&amp;C but remained detectable on follow-up. Endocervix/uterine curettage showed intraplacental choriocarcinoma arising within a complete hydatidiform mole. She is followed by Oncology and currently undergoing chemotherapy. Discussion HCG-mediated hyperthyroidism include gestational transient thyrotoxicosis, hyperemesis gravidarum, and trophoblastic hyperthyroidism (TH). Due to significant homology between TSH and the beta-subunit of HCG, HCG can cause hyperthyroidism. 2-60% of women with trophoblastic disease may have symptomatic hyperthyroidism at time of diagnosis which can be severe. Patients with GTN (choriocarcinoma in our case) have a higher likelihood of TH, as HCG exceeds 100,000 mIU/mL. Choriocarcinoma is the most aggressive type of GTN characterized by vascular invasion and widespread metastases, of which the most common sites are vagina and lungs. Patients with pulmonary metastasis my present with respiratory distress, chest pain, cough or hemoptysis. Our patient was initially thought to have impending thyroid storm mainly from findings of pulmonary edema, respiratory distress, tachycardia, and precipitant history (D&amp;C), and was managed as such while further workup was being undertaken. Realization that the initial chest CT findings of pulmonary edema were actually related to multiple pulmonary nodules and GTN made thyroid storm less likely. Hyperthyroidism typically resolves with decreasing HCG levels in TH. Indeed, our patient no longer needed ATD once her HCG levels subsided s/p D&amp;C. Conclusion One of the most common sites of metastasis in GTN is the lungs. An acute presentation of respiratory distress and pulmonary findings on chest imaging upon simultaneous discovery of TH may complicate management as thyroid storm needs to be considered. Although a higher index of suspicion for metastatic GTN should be made in this situation, a conservative management approach of treating for possible impending thyroid storm until definitive diagnosis has been established is prudent. Presentation: No date and time listed

Thyrotropin Receptor Antibodies in Early Pregnancy.

Thyrotropin (TSH) receptor antibodies (TRAb) are important when distinguishing between Graves' and gestational hyperthyroidism, but sparse evidence exists on the recommended cutoff during pregnancy. This work aimed to establish a method- and pregnancy-specific cutoff for TRAb, to describe the frequency of TRAb positivity in early pregnancy, and to follow up the women in the years after pregnancy. This cohort study used the North Denmark Region Pregnancy Cohort and Danish nationwide registers of women in the North Denmark Region who had a blood sample drawn in early pregnancy, 2011 to 2015, that was stored in a biobank for assessment of thyroid function and thyroid autoantibodies. A cutoff value for TRAb was established in a reference cohort (n = 524) and used to identify TRAb-positive and TRAb-negative hyperthyroidism in early pregnancy for evaluation of frequency and follow-up. The method- and cohort-specific cutoff for TRAb in early pregnancy was 0.98 IU/L (95% CI, 0.96-0.99 IU/L). Among women with low TSH in early pregnancy and no known thyroid disease (n = 414), 21 women (5.1%) were TRAb positive and 393 (94.9%) were TRAb negative. Follow-up in the years following the pregnancy (median 8.1 years) revealed that 52.4% of women with TRAb-positive hyperthyroidism and 8.4% of the women with TRAb-negative hyperthyroidism were diagnosed with hyperthyroidism. This is the first study to measure TRAb in a large group of women in early pregnancy and to establish a pregnancy-specific cutoff. Results reveal that TRAb-negative hyperthyroidism is predominant in early pregnancy and rarely associated with later development of hyperthyroidism.

Thyroid Disease in Pregnancy: A Descriptive Review of Guidelines.

Thyroid disorders represent one of the most frequent complications of pregnancy associated with adverse obstetric, fetal, and neonatal outcomes, especially in case of delayed diagnosis and suboptimal management. The aim of this study was to review and compare the recommendations of the most recently published guidelines on the diagnosis and management of these common conditions. A descriptive review of guidelines from the Endocrine Society, the European Thyroid Association, the Royal Australian and New Zealand College of Obstetricians and Gynecologists, the American Thyroid Association, and the American College of Obstetricians and Gynecologists on thyroid disease in pregnancy was carried out. There is an overall consensus regarding the diagnosis of overt and subclinical hypothyroidism and hyperthyroidism in pregnancy using the pregnancy-specific reference ranges and the definition of postpartum thyroiditis. The reviewed guidelines unanimously discourage universal screening for thyroid function abnormalities before and during pregnancy and support targeted screening of high-risk patients by measuring serum thyroid-stimulating hormone levels. Moreover, they all highlight the need of treating overt hypothyroidism and hyperthyroidism, not only during pregnancy, but also before conception, suggesting similar management policies and treatment targets. There is also agreement regarding the management of gestational transient hyperthyroidism with hyperemesis gravidarum, suspected fetal thyrotoxicosis, postpartum thyroiditis, and thyroid malignancy. Scanning or treating with radioactive iodine is contraindicated during pregnancy and breastfeeding. On the other hand, there is controversy on the management of subclinical thyroid disease, thyroid function surveillance protocols, and iodine nutrition recommendations. Of note, the American College of Obstetricians and Gynecologists makes some specific recommendations on the treatment of thyroid storm and thyrotoxic heart failure in pregnant women, whereas the American Thyroid Association makes a special reference to the management of women with thyroid cancer. As the disorders of the thyroid gland affect a significant proportion of pregnant women, it is of paramount importance to develop uniform international evidence-based protocols for their accurate diagnosis and optimal management, in order to safely guide clinical practice and eventually improve perinatal outcomes.

Hyperemesis Gravidarum Presenting as Severe Hypokalemic Periodic Paralysis and Type II Respiratory Failure: A Different Form of Thyroid Storm?

Hyperthyroidism in pregnancy is a condition that results from an excess of beta-human chorionic gonadotropin hormone resulting in gestational thyrotoxicosis. This thyrotoxicosis of pregnancy might be linked with hyperemesis gravidarum and is usually a self-limiting disease. Hyperthyroidism can cause hypokalemic periodic paralysis, which presents as pure motor areflexic flaccid paralysis. In severe cases, it may involve respiratory muscles and cause hypercapnic respiratory failure requiring invasive ventilation. A positive feed-forward cycle of hypokalemia could be triggered by the loss of function of inward rectifier potassium channel 18 (Kir2.6) along with the increased activity of sodium, potassium-adenosine triphosphatase (Na⁺/K⁺-ATPase). Hyperthyroid periodic paralysis is characterized by biochemical hyperthyroidism, normal urine potassium excretion, and electrocardiography abnormalities.We report a case of a 23-year-old female (G2P0L0A1) who had severe hyperemesis gravidarum and later on developed flaccid quadriplegia. Her thyroid profile revealed hyperthyroidism. She later developed hypercapnic respiratory failure and was managed by potassium replacement and invasive ventilation.

Management and Outcomes of Pregnancy with Gestational Hypertension and Hyperthyroidism: A Case Report

Introduction: Hyperthyroidism associated increases in thyroid hormone concentrations have to be differentiated from physiological adjustments in thyroid hormone economic system that rise up all through being pregnant, especially in the first trimester. For one thousand births, one or two instances of gestational hyperthyroidism exist. It's critical to stumble on hyperthyroidism in a pregnant female due to the fact it is able to have harmful outcomes for each the mom and the infant.&#x0D; Presenting Complaint and Investigations: Patient’s chief complaints were vomiting, discomfort since 2 days. After physical examination and investigations, doctor diagnosed this as case of G2A1 with 35 weeks gestational age. This was a known case of gestational hypertension with hyperthyroidism. Investigations included Blood test, urine test, thyroid Profile, USG.&#x0D; Obstetric History: Patient had bad obstetric history. 2.5 months spontaneous abortion was reported.&#x0D; The Main Diagnoses, Therapeutic Interventions, and Outcomes: Gestational Hypertension with Known case of Hyperthyroidism. The patient had undergone various investigations like blood tests, USG, Physical examination. After physical examination and investigation doctor took a decision of emergency Lower segmental Caesarean section. Under spinal anaesthesia Lower segmental Caesarean section was done and outcome is good.&#x0D; Nursing Perspectives: Administered fluid replacement i.e. DNS and RL, Fetal monitoring, monitored all vital signs and observed the outcomes of treatment.&#x0D; Conclusion: Treatment and control of hypertension and hyperthyroidism in pregnancy at the right time increases the pregnancy's outcome.

Hyperthyroidism management during pregnancy and lactation (Review).

Thyroid dysfunction is a significant public health issue, affecting 5-10 more women compared to men. The estimated incidence is up to 12% and only for women the treatment rises up to 4.3 billion dollars annually. Thyroid pathology can have a major impact on female fertility and it can only be detected when preconception tests are performed. Untreated or poorly treated hyperthyroidism in a mother can affect the fetal development and pregnancy outcome. Between 0.1 and 0.4% of the pregnancies are affected by clinical hyperthyroidism. Thyroid dysfunction is associated with higher rates of pregnancy loss. Hyperthyroidism can complicate fetal health problems intrauterinely and in the neonatal period. The TSH receptor is stimulated by TSH and HCG which has a similar structure. This can lead to gestational thyrotoxicosis. Hyperthyroidism can be treated with propylthiouracil or methimazole and in selected cases, surgical treatment or radioactive iodine can be chosen. In pregnancy, the most used treatment is represented by propylthiouracil which can be used from the first trimester. The aim of this review is to assess the current data regarding the impact of thyroid dysfunction on pregnancy and to synthesize the treatment options during pregnancy and lactation.

Triploid pregnancy-Clinical implications.

Triploidy is a life-limiting genetic aberration resulting from an extra haploid set of chromosomes of paternal (diandric triploidy) or maternal origin (digynic triploidy). Triploidy affects around 1%-2% of all conceptions. The majority of cases is miscarried at early developmental stages. In consequence of genomic imprinting, parental origin affects the phenotype of triploid pregnancies as well as the prevalence and spectrum of related maternal complications. Distinctive ultrasound features of both triploid phenotypes as well as characteristic patterns of biochemical markers may be useful in diagnosis. Molecular confirmation of the parental origin allows to predict the risk of complications, such as gestational trophoblastic neoplasia, hyperthyroidism, hypertension, or preeclampsia associated with the paternal origin of triploidy. Diagnosis of partial hydatidiform mole associated with diandric triploidy is challenging especially in the first trimester pregnancy loss due to the limitations of both histopathology and ultrasound. We present important clinical aspects of triploid pregnancies and indicate unresolved issues demanding further studies.

Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum

Untreated or inadequately treated overt hyperthyroidism in pregnancy can have devastating consequences for both mother and fetus. At the same time antithyroid drugs (ATDs) are known for their teratogenic effect and should be avoid when possible; once the diagnosis of hyperthyroidism is made in a pregnant woman, attention should be focused on determining the etiology of the disorder and whether it warrants treatment. Here, we report a case of hyperemesis gravidarum patient presenting with significant elevation of thyroid hormones and a review on diagnosis and management of gestational transient thyrotoxicosis. A 33-year-old female, G4P3 at 8 weeks pregnant admitted for nausea and vomiting. Thyroid labs showed TSH < 0.01 (Reference: 0.4-4.0mU/L) and free T4 is 3.53 (Reference: 0.76-1.46ng/dl). Patient was discharged on antiemetics with a diagnosis of hyperemesis gravidarum. She was re-admitted at 9 weeks pregnant with ongoing nausea and vomiting. She had palpitations, fatigue and reported 15 pound weight loss in 2 weeks. Past medical history included thyroid hormone abnormality noted during pregnancies of 2011 and 2017. Physical exam was significant for tachycardia and diffusely enlarged thyroid gland. Repeat labs showed TSH <0.01, free T4 5.81, total T3 of 317 (Reference: 60-181ng/dl). Thyroid ultrasound showed multiple nodules. Considering significant elevation in free T4 and total T3; empiric therapy with propylthiouracil was recommended. Patient declined anti-thyroid therapy. TSI and TRH antibodies came back later as negative. Patient was treated with enteral feeding for hyperemesis gravidarum. Thyroid labs 3 weeks later improved; FT4 down to 1.63 and TT3 down to 250. Patient delivered healthy baby at 40 weeks of gestation. Although the differential diagnosis of thyrotoxicosis in pregnancy includes any cause that can be seen in a nonpregnant patient, the most likely causes for hyperthyroidism in pregnancy are gestational thyrotoxicosis (GTT) with or without hyperemesis gravidarum or Graves’ disease. GTT is described as an hCG-mediated hyperthyroidism that occurs in the first trimester of pregnancy; it is generally asymptomatic with mild biochemical hyperthyroidism. Distinguishing true overt hyperthyroidism from GTT in a setting of hyperemesis gravidarum is challenging. The absence of clinical signs of hyperthyroidism and negative thyroid antibodies supports the diagnosis of GTT. T3 tends to be disproportionately elevated more than T4 in patients with overt hyperthyroidism. HCG level has not been found to be useful in distinguishing between GTT and GD. Overt hyperthyroidism is treated using anti-thyroid drugs (ATD) whereas supportive therapy without ATD is the accepted standard of treatment of patients with hyperemesis gravidarum and GTT. More studies addressing the best management of these group of patients is needed.

A Million Reasons for Hyperthyroidism. Reporting a Case of Thyrotoxicosis in a Setting of Metastatic Choriocarcinoma

Background: Human chorionic gonadotropin (hCG) induced transient hyperthyroidism is often seen during pregnancy. Other rare causes of beta hCG induced hyperthyroidism include trophoblastic tumors (hydatidiform mole and choriocarcinoma) and in men, germ cell tumors. The mechanism for hCG induced thyrotoxicosis lies in the structural similarity between TSH and hCG molecules leading to the direct stimulation of the TSH receptors. In regard to treatment, while gestational thyrotoxicosis is usually mild, self-limited and does not need medications, the hyperthyroidism of trophoblastic tumors may require antithyroid medications in addition to treating the underlying tumor. Thionamide use is reserved for moderate to severe cases of hyperthyroidism and for presurgical optimization. In our case report, we present a 22-year-old African American female with choriocarcinoma induced thyrotoxicosis requiring thionamide therapy. Clinical Case: A 22-year-old African American female presented to our emergency room after a witnessed generalized tonic-clonic seizure. Her brain CT scan showed a 4 CM mass concerning for AVM malformation with a subsequent brain MRI confirming parenchymal hematoma with surrounding vasogenic edema. Past medical history was significant for molar pregnancy managed with dilation and curettage followed by laparotomy to remove the pelvic mass. Given her history of molar pregnancy, pelvic ultrasound was performed which showed complex heterologous structure of uterine origin concerning for malignancy. Additional imaging studies of the lung, brain, abdomen and pelvis were performed, which showed possible metastasis to the lung, adnexa, and to the brain. Her clinical exam showed heart rate of 130 beats/min with a normal rhythm, fine tremors, aphasia, and a decrease grip strength in her right upper extremity. Her thyroid gland was slightly enlarged with no tenderness. Laboratory tests showed hCG of >1,000,000 mIU/mL, TSH of < 0.01mcU/mL, free T4 of 5.1ng/dL. Her TPO and TSI were negative. With a diagnosis of hyperthyroidism due to trophoblastic disease, she was treated with methimazole and propranolol resulting in rapid clinical and biochemical improvement. Later, left frontal craniotomy and hematoma evacuation was performed with histology confirming the diagnosis of metastatic choriocarcinoma. She was later transferred to a specialized center where she received chemotherapy. Her hCG subsequently dropped down to 699 mIU/mL. Conclusion: We report a rare case of metastatic choriocarcinoma causing symptomatic hyperthyroidism. The diagnosis is made by excluding other common causes of hyperthyroidism and it should be considered in females of childbearing age. Methimazole is an effective agent to control the hyperthyroidism while waiting for treatment of the underlying cancer.

Comparison of ATA and Updated ACOG Guidelines for Thyroid Disease in Pregnancy. Russian translation

Thyroid dysfunction is relatively common in pregnancy. The American Thyroid Association (ATA) published its most recent guidelines regarding the management of thyroid disorders in pregnancy in 2017. The American College of Obstetricians and Gynecologists (ACOG) has recently published an updated practice bulletin for thyroid disease in pregnancy that supersedes its previous guidance published in 2015. A comparison of the similarities and differences between the clinical guidelines from the ATA and ACOG can serve to highlight areas of uncertainty where additional studies are needed and may also demonstrate areas where endocrinologists and obstetricians may elect differing approaches to clinical care. The ACOG and ATA guidelines recommend similar approaches to the interpretation of thyroid function testing during gestation and to the management of thyroid cancer, thyroid nodules, gestational thyrotoxicosis, and postpartum thyroiditis Both strongly recommend levothyroxine (L-T4) treatment for overtly hypothyroid pregnant women, and both recommend against the use of T3-containing thyroid hormone preparations when treating hypothyroidism in pregnancy.

Сравнение рекомендаций Американской тиреоидной ассоциации (АТА) и Американского колледжа ­акушеров-гинекологов (АКАГ) по заболеваниям щитовидной железы при беременности. Русский перевод

Thyroid dysfunction is relatively common in pregnancy. The American Thyroid Association (ATA) published its most recent guidelines regarding the management of thyroid disorders in pregnancy in 2017. The American College of Obstetricians and Gynecologists (ACOG) has recently published an updated practice bulletin for thyroid disease in pregnancy that supersedes its previous guidance published in 2015. A comparison of the similarities and differences between the clinical guidelines from the ATA and ACOG can serve to highlight areas of uncertainty where additional studies are needed and may also demonstrate areas where endocrinologists and obstetricians may elect differing approaches to clinical care. The ACOG and ATA guidelines recommend similar approaches to the interpretation of thyroid function testing during gestation and to the management of thyroid cancer, thyroid nodules, gestational thyrotoxicosis, and postpartum thyroiditis Both strongly recommend levothyroxine (L-T 4 ) treatment for overtly hypothyroid pregnant women, and both recommend against the use of T 3 -containing thyroid hormone preparations when treating hypothyroidism in pregnancy.