Neonatal thyroid storm: the importance of an accurate antenatal history

2021 ◽  
Vol 14 (1) ◽  
pp. e239278
Author(s):  
Sean Tamgumus ◽  
Elisabeth Lauesen ◽  
Michael A Boyle

A near-term infant became unwell immediately after birth with cardiorespiratory compromise—persistent tachycardia, pulmonary hypertension and reduced cardiac function. There had been no concerns during the pregnancy and the obstetrical and maternal medical history was unremarkable apart from hypothyroidism. A thyroid function test on admission revealed a significantly elevated free T4 and a diagnosis of a thyroid storm was made. On questioning it became apparent that she had Graves’ disease after her last pregnancy and was rendered hypothyroid post surgery, she was not aware of the relevance of this at her booking visit. This case highlights the importance of monitoring of women who have a history of a diagnosis of Graves’ disease, regardless of thyroid function status, to allow for appropriate antenatal monitoring, preparedness of the NICU (neonatal intensive care unit) team and correct follow-up of the neonate. It also demonstrates the importance of ensuring a patient is properly educated about their condition.

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Anita Eapen ◽  
Hooman Oktaei

Abstract Introduction: Thyroid conditions are among the most common endocrine disorders. Diagnosis is dependent on interpretation of laboratory tests. The challenge comes when the clinical picture is discordant with laboratory results. Case Report: Patient is a 53-year-old male with history of cardiac transplantation, type 2 diabetes mellitus, history of amiodarone-induced hyperthyroidism. He was noted to have labs indicative of hyperthyroidism, while taking amiodarone, in 2016-2017, which was treated with methimazole. He was then noted to have abnormal thyroid function tests with low TSH to 0.3 IU/L, normal T3 and normal T4 levels. Thyroid stimulating immunoglobulin had been checked multiple times, and was normal, which is inconsistent with Graves’ disease. Prior radioactive iodine uptake scan, while off amiodarone, was noted to be normal. He was also scheduled for thyroidectomy at another hospital, which was cancelled due to normalization of thyroid function tests. Consultation was received for suppressed TSH to 0.323 IU/L, without symptoms of hyperthyroidism. He had been taking biotin during this time, which he subsequently stopped taking. Repeat TSH following discontinuation of biotin, was within normal range, most recent TSH 2.48 IU/L, free T4 1.03 ng/dL, free T3 2.7 pg/mL. Discussion: Thyroid function tests are commonly ordered. Interpretation of these tests relies on the provider’s understanding of thyroid physiology in addition to interferences with medications and other conditions. High doses of biotin, which people take as supplements for multiple sclerosis, or metabolic disorders, or for healthy nails and hair, can cause thyroid function test abnormalities. Streptavidin and biotin are used in some immunoassay platforms to capture antigens (TSH, free T4) or antibodies. High levels of serum biotin can inhibit the formation of T4 antibody complex, which results in a falsely high free T4 result. Conclusion: Thyroid Function tests should be interpreted very cautiously, especially in the setting of discordant clinical findings. Prior to ordering these tests, should attempt to obtain a detailed history of medications including over-the-counter supplements, which are commonly not reported during medication history. References:Elston, Marianne S., et al. “Factitious Graves’ Disease Due to Biotin Immunoassay Interference—A Case and Review of the Literature.” The Journal of Clinical Endocrinology & Metabolism, vol. 101, no. 9, 30 June 2016, pp. 3251-3255., doi:10.1210/jc.2016-1971. Koehler, Viktoria F., et al. “Fake News? Biotin Interference in Thyroid Immunoassays.” Clinica Chimica Acta, vol. 484, 30 May 2018, pp. 320-322., doi:10.1016/j.cca.2018.05.053. Soh, Shui-Boon, and Tar-Choon Aw. “Laboratory Testing in Thyroid Conditions - Pitfalls and Clinical Utility.” Annals of Laboratory Medicine, vol. 39, no. 1, 13 Jan. 2019, pp. 3-14., doi:10.3343/alm.2019.39.1.3.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Diana Colleen Mandocdoc Dimayuga ◽  
Michael Lim Villa

Abstract Hypercalcemia in hyperthyroidism is usually asymptomatic, and related to a concurrent primary hyperparathyroidism. In this report, we describe a case of symptomatic hypercalcemia secondary to Graves’ disease alone. Case Report. A 24-year-old Filipino female presented to the emergency department with generalized weakness, vomiting and abdominal pain. No other symptoms were noted. She was otherwise previously healthy. Family history was unremarkable. During physical exam, she was noted to have a non tender palpable thyroid gland without bruit. Her ECG showed sinus tachycardia. The complete blood count and electrolytes were normal however, ionized calcium was high at 1.6mmol/L (NV 1–1.3). Renal function was normal. Hydration with saline and Furosemide 20mg once daily was started though calcium levels remained elevated. Other causes of hypercalcemia were excluded as PTH was appropriate suppressed (8.8ng/L; NV 14–72), vitamin D was also suppressed (15.29nmol/L; NV >30). CT scan of chest and abdomen and bone scan did not point to any underlying malignancy nor metabolic bone disease. Medication history was also unremarkable. She was hyperthyroid with a suppressed thyroid stimulating hormone level of 0.004pmol/L (NV 0.55–4.78), free T3 of >20pmol/L (NV 2.3–4.2), free T4 of 8.4pmol/L (NV 0.89–1.76). Thyroid receptor antibody levels were raised at 41.07kU/L (NV <1) supporting the diagnosis of Graves’disease. She was started on propylthiouracil 50mg four times daily, along with propranolol 40mg three times daily. She was subsequently seen after two weeks with normal repeat calcium level and thyroid function test. Conclusion. This report aims to highlight that thyroid disease should always be considered as a cause of hypercalcemia. A concomitant primary hyperparathyroidism should also be evaluated. The definitive treatment for the hypercalcemia is correction of thyroid function.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Isabelle Daneault Peloquin ◽  
Matthieu St-Jean

Abstract Clinical vignette ENDOCRINE SOCIETY 2020 Title: A case of T3 thyrotoxicosis induced by a dietary supplement. A 24 yo man consulted for a 2 weeks history of diaphoresis, fatigue, insomnia, palpitations and headache associated with a 20 pounds lost. The patient didn’t have a goiter or any signs of orbitopathy. The results revealed a free T3 level of 45.8 pmol/L upon arrival (normal (N) 3.4- 6.8 pmol/L), free T4 level of 6.4 pmol/L (N 11.0–22.0 pmol/L) and TSH level less than 0.005 mUI/L (N: 0.35 to 3.50 mUI/L). Facing those results, a complete review of the patient medication and natural product consumption was done. The patient revealed that he was using, since a month, a vegetable extracts nutritional supplement that didn’t included iodine. He was asked to stop the nutritional supplement and propranolol 10 mg twice daily was prescribed. Thyroid function tests were done 3 days after. The results demonstrate a fT3 level of 4.6 pmol/L, a fT4 level of 5.6 pmol/L and a TSH that still suppressed. A thyroid scintigraphy was performed 7 days later and showed a homogeneous uptake of 18.5% (N 7.0% – 35.0%). We saw the patient 2 weeks later and we ordered another thyroid function test with TSH receptor antibodies, TPO antibodies and thyroglobulin. The results were the following: fT3 of 5.1 pmol/L, fT4 of 12.1 pmol/L, TSH of 2.31 mUI/L, thyroglobulin of 19.8 ug/L (N: 1.4 – 78) and normal levels of antibodies against TPO and TSH receptors. To confirm the contamination of the nutritional supplement by fT3 we used a plasma pool of normal patients in which we measured thyroid function tests at baseline and after we have added the nutritional supplement powder to reflect the dose suggested by the manufacturer. The results showed that fT3 level increased by 36.5%, fT4 by 11.2% and TSH didn’t changed. The powder was then analyzed by an external laboratory that wasn’t able to demonstrate the presence of fT3 nor fT4. The two diagnostic possibility facing those results were that the powder induced an interference with immunoassay used to measure fT3 and fT4 but not TSH or thyrotoxicosis induced by the nutritional supplement with limitation in the technique that tried to identify fT3 in the powder. Given the presentation of the patient, we are convinced that this case represents a thyrotoxicosis induced by a nutritional supplement. In conclusion, Graves’ disease is responsible for 60–80% of the cases of hyperthyroidism. However, there are few cases reports of thyrotoxicosis induced by nutritional supplement1,2, but some studies demonstrate the presence of thyroid hormone in significant amounts in some commercially available health supplements3. This case highlights the importance of verifying exposition to medications and natural products when confronted to cases of thyrotoxicosis. 1.Regina A et al. MMWR Morb Mortal Wkly Rep. 2016 2. Panikkath R et al. Am J Ther. 2014 3. Kang GY et al. Thyroid. 2013


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A917-A917
Author(s):  
Ahl Jeffrey Caseja ◽  
Samer Nakhle

Abstract Introduction: Hashimotos thyroiditis and Graves disease are two distinct autoimmune disorders of the thyroid. Conversion of hypothyroidism to hyperthyroidism is even more rare. We report a case of an established Hashimotos thyoiditis patient who converted into Graves disease. Case Description: 67-year old female with a past medical history of iron-deficiency anemia, dyslipidemia, and depression presented with a six-month history of fatigue, cold-intolerance, hair loss, and weight gain in September of 2015. Laboratory tests confirmed diagnosis of Hashimotos thyroiditis with an elevated TSH 80.7 (0.40-4.50 mIU/L), FT4 0.2 (0.8-1.8 ng/dL), and positive thyroid antibodies TPO 24 (0.0-8.9 IU/mL). She was started on Levothyroxine 88 mcg daily. Gradually she had a decreased requirement of Levothyroxine; from February 2016 to March 2017 she maintained a normal TSH range while on 50 mcg/day with resolution of her symptoms. The patient was then lost to follow-up until she presented in the clinic in September 2018 with complaints of several weeks of easy fatigability, 10lb-weight loss, and periorbital edema. She was found to have a suppressed TSH 0.01, and elevated FT4 2.3, and FT3 8.4 (2.3-4.2 pg/mL). Her Levothyroxine 50 mcg/day was discontinued for four days and labs were repeated which still showed suppressed TSH and elevated FT4 and FT3. She was found to have a positive TRAB and a positive TSI which are consistent with hyperthyroidism. Thyroid ultrasound was performed which showed a heterogeneous thyroid gland with increased vascularity, confirming the diagnosis of Graves disease. She was started on Methimazole 10 mg daily. Her Methimazole dose was adjusted according to her thyroid function test until she had a total thyroidectomy in October 2019. She was started on levothyroxine post-operatively and as of March 2020 is on Levothyroxine 50 mcg/daily. Conclusion: Despite the rarity of Hashimotos thyroiditis converting to Graves disease, it is possible that those affected can be encountered by primary care providers and hospitalists and could easily be mistaken for over-replacement of levothyroxine. Close monitoring of the patient along with regular thyroid function tests will be required for ongoing follow-up.


2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Manabu Yasuda ◽  
Jun Kumakura ◽  
Kiyonori Oka ◽  
Kazuhito Fukuda

Abstract Background Graves’ disease is characterized by hyperthyroidism and its symptoms often overlap with those of panic disorder, which may make it difficult to distinguish between the two conditions. In this report, we describe how proper diagnosis of thyroid disease in patients with mental illness can lead to appropriate treatment. Case presentation We encountered a 34-year-old woman in whom thyroid crisis from Graves’ disease was misdiagnosed as panic attack. The patient was being managed as a case of panic disorder and bipolar disorder in a psychiatric outpatient setting. About 6 months before presentation she had lost about 16 kg in weight, and a month before presentation she developed several unpleasant symptoms as her condition worsened. Several weeks before she had had severe palpitations, tachycardia, and discomfort in her throat. She became unable to eat solids, ate only yogurt and gelatin, and felt it difficult to take psychiatric drugs. She visited our emergency outpatient department on a Sunday morning, presenting with nausea, severe tachycardia, fever, and restlessness with anxiety. We treated her as panic disorder with fever, but noted proptosis and considered the possibility of Graves’ disease. Thyroid function tests were performed even though data from her clinic was not available because it was a weekend. Because there was no improvement in her condition after her first visit, she returned to our hospital early the next morning. We had misdiagnosed her as having severe panic attacks due to panic disorder, and after a diazepam injection had allowed her to go home. Later that day, the thyroid function test results became available, and her symptoms and the results strongly indicated a thyroid storm. The endocrinology department was consulted immediately, and she was referred for hospitalization the next day. During hospitalization, she was treated with steroid and radioactive iodine therapy and was discharged from hospital in 3 weeks. Conclusion Psychiatrists and doctors engaged in psychosomatic medicine need to consider the possibility of severe hyperthyroidism as a differential diagnosis of panic disorder.


2006 ◽  
Vol 11 (4) ◽  
pp. 245-250
Author(s):  
Peter Gal ◽  
J Laurence Ransom ◽  
Sherri A Davis

A 36-week gestation newborn was admitted to the neonatal intensive care unit for treatment of primary pulmonary hypertension and possible sepsis. The infant developed hyperbilirubinemia on day 4 of life and peaked on day 5 at a total serum bilirubin of 19 mg/dL. Phototherapy was started on day 4 and continued for 5 days. On day 8 of life, ibuprofen was started for fever; a concurrent total serum bilirubin was 15.7 mg/dL. The subsequent hospital course was uneventful, and discharge occurred on day 22 of life. Because the patient failed a hearing screen at discharge, he was referred for a diagnostic audiology workup. He subsequently failed formal audiometric testing on two occasions one week apart, and was given a diagnosis of auditory dys-synchrony and/or auditory neuropathy, consistent with kernicterus. At 5½ months of age, he was reported to be hypotonic and to have frequent arching movements. Since the total serum bilirubin did not exceed 19 mg/dL, concern was raised that ibuprofen may have caused displacement of bilirubin from its albumin binding site, resulting in kernicterus due to excessive unbound bilirubin concentrations. Ibuprofen should be administered with caution in preterm infants at risk for kernicterus.


Author(s):  
Vasim Ismail Patel ◽  
Akshay B. K.

<p class="abstract"><strong>Background:</strong> The thyroid is an<strong> </strong>endocrine gland. It secretes two hormones thyroxine (T<sub>4</sub>), triiodothyronine (T<sub>3</sub>). Hypothyroidism is a common condition encountered by a clinician. Subclinical hypothyroidism (SCH) defined as normal free thyroxine (T4) and elevated thyroid stimulating hormone (TSH), is primarily a biochemical diagnosis with or without clinical symptoms. Studies have observed that TSH levels vary at different times in a day. In practice not much importance is given to the timing of the sample collection (pre-prandial or post-prandial sate). SCH is diagnosed depending on TSH value. So the condition may be under or over diagnosed based on a single value. So we conducted this study to determine whether timing of sample collection had any significant relationship in the determination of levels of thyroid hormones.</p><p class="abstract"><strong>Methods:</strong> The study was carried on 114 patients who visited ENT department, NMCH between July 2018 and June 2019. Group-1 consisted of 38 normal patients. Group-2 consisted of 36 hypothyroidism patients GROUP-3 consisted of 40 subclinical hypothyroidism patients. Thyroid function tests (TSH and free T4) were done in fasting state and 2 hours postprandially.  </p><p class="abstract"><strong>Results:</strong> TSH values were found to be significantly lowered after food in all the three groups. Free T4 values did not show any statistically significant alteration after food.</p><p class="abstract"><strong>Conclusions:</strong> There was a significant decline in TSH values postprandially. This might lead to inappropriate diagnosis and management of patients as cases of hypothyroidism, especially in cases of sub clinical hypothyroidism.</p>


2021 ◽  
Vol 14 (6) ◽  
pp. e243534
Author(s):  
Soban Ahmad ◽  
Amman Yousaf ◽  
Shoaib Muhammad ◽  
Fariha Ghaffar

Simultaneous occurrences of diabetic ketoacidosis (DKA) and thyroid storm have long been known, but only a few cases have been reported to date. Both these endocrine emergencies demand timely diagnosis and management to prevent adverse outcomes. Due to the similarities in their clinical presentation, DKA can mask the diagnosis of thyroid storm and vice versa. This case report describes a patient with Graves’ disease who presented to the emergency department with nausea, vomiting and abdominal pain. He was found to have severe DKA without an explicit history of diabetes mellitus. Further evaluation revealed that the patient also had a concomitant thyroid storm that was the likely cause of his DKA. Early recognition and appropriate management of both conditions resulted in a favourable outcome. This paper emphasises that a simultaneous thyroid storm diagnosis should be considered in patients with DKA, especially those with a known history of thyroid disorders.


2020 ◽  
Vol 13 (3) ◽  
pp. e231337
Author(s):  
Michael S Lundin ◽  
Ahmad Alratroot ◽  
Fawzi Abu Rous ◽  
Saleh Aldasouqi

A 69-year-old woman with a remote history of Graves’ disease treated with radioactive iodine ablation, who was maintained on a stable dose of levothyroxine for 15 years, presented with abnormal and fluctuating thyroid function tests which were confusing. After extensive evaluation, no diagnosis could be made, and it became difficult to optimise the levothyroxine dose, until we became aware of the recently recognised biotin-induced lab interference. It was then noticed that her medication list included biotin 10 mg two times per day. After holding the biotin and repeating the thyroid function tests, the labs made more sense, and the patient was easily made euthyroid with appropriate dose adjustment. We also investigated our own laboratory, and identified the thyroid labs that are performed with biotin-containing assays and developed strategies to increase the awareness about this lab artefact in our clinics.


2012 ◽  
Vol 26 (1) ◽  
pp. 59-61 ◽  
Author(s):  
Livia R. Macedo ◽  
Jehan Marino ◽  
Brady Bradshaw ◽  
Joseph Henry

Graves’ disease is an autoimmune syndrome with symptoms such as tachycardia, atrial fibrillation, and psychiatric symptoms. Limited evidence exists for the treatment of Graves’ hyperthyroidism-induced psychosis with atypical antipsychotics. A 47-year-old female with a psychiatric history of bipolar disorder presented for the first time to the psychiatric hospital. She was agitated and grossly psychotic with delusions. Electrocardiogram showed atrial fibrillation and tachycardia. Drug screen urinalysis was negative. Endocrine workup resulted in a diagnosis of Graves’ disease (thyroid-stimulating hormone [TSH]: 0.005 μIU/mL, triiodothyronine [T3]: 537 ng/dL, thyroxine [T4]: 24 mcg/dL, free T4: 4.5 ng/dL, positive antithyroid peroxidase antibody, and antinuclear antibody). Aripiprazole 10 mg daily was initiated and titrated to 15 mg daily on day 4. On day 16, her suspicious behavior, judgment, and insight improved. Other medications given included aspirin 325 mg daily, metoprolol 25 mg twice daily, titrated to 12.5 mg twice daily, and methimazole 30 mg daily, titrated to 20 mg twice daily, and discontinued on day 29. The patient received radioiodine I-131 treatment 1 week later. We report the first known case on the use of aripriprazole to treat Graves’ hyperthyroidism-induced psychosis. Further studies examining the long-term effects and appropriate dose and duration of aripiprazole in this patient population are needed.


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