Elevated Free T4 Research Articles

Biotin induced biochemical hyperthyroidism: a case report and review of the literature

BackgroundBiotin is a commonly used supplement for hair, nail, and skin. Recent literature suggests that high-dose biotin therapy for neurological diseases like Multiple sclerosis can interfere with lab results that use biotin/streptavidin immunoassay, called biotin interference. Biotin interference can affect thyroid lab results, giving biochemical hyperthyroidism.Case presentationOur patient, a 64-year-old white man with a known history of multiple sclerosis, presented with elevated free T3, free T4, and low TSH that resembled hyperthyroidism. He had no symptoms of hyperthyroidism except some fatigue and tachycardia on the first encounter. He was started on anti-thyroid medications. He was then re-evaluated since his lab results remained the same after two months of anti-thyroid medications. It was found that he was on biotin, 10000mcg/day, for his multiple sclerosis. Biotin was discontinued, and five days later his lab results returned to normal values.ConclusionThe lack of knowledge of biotin use by patients can lead to misdiagnosis of patients’ thyroid lab results and improper management. Awareness about biotin interference and abnormal thyroid lab values should be a priority among clinicians and the public. If the biotin is discontinued on time, such misdiagnosis can be avoided.

Code Pseudo Stroke - A Case of Hypokalaemic Periodic Paralysis Mimicking Stroke.

Hypokalaemic periodic paralysis is an acute flaccid paralysis secondary to hypokalaemia, triggered by hyperthyroidism, environmental elements such as a high carbohydrate intake or rest after intense exercise, and an underlying genetic component with mutations in the muscle ion channels.The pursuit of code stroke protocol in the in-patient setting must bear in mind reversible but potentially fatal and disabling alternative diagnoses such as stroke mimics including hypokalaemic periodic paralysis.Stroke mimics defined as acute onset neurological deficits that are not related to vascular cause are a true challenge, multiple scales have been created to distinguish them from an actual stroke, such as the Recognition of Stroke in the Emergency Room (ROSIER) scale.

Abstract #1406483: Thyroid Hormone Resistance Diagnostic and Therapeutic Challenges

Resistance to thyroid hormone (RTH) is a clinical syndrome defined by impaired sensitivity to thyroid hormone (TH). We present the challenges in diagnosing and treating a 24-year-old male who presented with a mixed picture of hypothyroidism and hyperthyroidism with elevated TSH, upper normal free T4, and elevated free T3 and was found to have a mutation in the THRβ gene. A 24-year-old male was referred for a second opinion of post-ablative hypothyroidism with elevated TSH, elevated free T3, and suspicion of pituitary microadenoma. He complained of fatigue, weight gain, tremors heat cold intolerance. Family history is Graves’ disease in his mother's status post partial thyroidectomy due to a salivary tumor. Initially, in 2020, he was diagnosed with negative antibody Grave’s disease. Labs were TSH 0.86 mIU/L, free T4 1.99 ng/dl (0.89-1.76), and free T3 4.66 pg/ml (2.3-4.2). A thyroid ultrasound showed mild thyromegaly. A thyroid uptake scan showed 24-hour thyroid uptake of 36.7%. Thyroid antibodies including thyroglobulin, TPO, thyroid receptor, and thyroid stimulating immunoglobulin were negative. He was treated with radioactive iodine ablation (I-131). Afterward, His TSH increased gradually along with free T3. Free T4 was normal. The patient remained symptomatic, and he was not on any thyroid replacement therapy. A repeat thyroid uptake scan showed an increase uptake of 36% at 24 hrs. During our evaluation, a repeat TSH 54.05 mIU/l, free T4 1.3 ng/dl, free T3 4.3 pg/ml, and T3 by equilibrium dialysis 4.0. A repeat magnetic resonance imaging of the head showed no definitive focal enhancing lesion. Pituitary axis hormones were normal, and the alpha subunit was 0.73 (high); however, the alpha-glycoprotein subunit /TSH molar ratio 0.135 sex hormone binding globulin 5.8 nmol/l (low), macro TSH was not detected. These findings raised suspicion for THRB mutation; hence genetic studies were obtained. PCR amplification of THRB gene exons 10, 9, and 8, followed by gene sequencing, showed a heterozygous missense mutation C >G located at exon 10. The mutation caused a change in thyroid hormone receptor beta protein amino acid 453 proline to an alanine, P453A Initially, he was started on levothyroxine 25 mg PO daily but soon after, it was stopped due to palpitations; a beta blocker was started along with liothyronine 5 mg every other day and levothyroxine 50 mg every other day. The patient tolerated the regimen with significant improvement in his symptoms. RTH is rather uncommon; it is important to be able to recognize the syndrome to avoid unnecessary invasive treatment. There is no specific therapy currently available to fully correct the TRβ defect. The goal of treatment is based on the patient's symptoms and clinical picture instead of aiming to normalize thyroid hormone levels. Thyroidectomy and radioactive iodine ablation result in lifelong levothyroxine replacement therapy and RTHβ persistently high serum TSH. Levothyroxine therapy is challenging, and supraphysiologic doses are often needed to maintain serum TSH in the lowest tolerable level.

Abstract #1411935: A Radiographic Diagnosis: IgG4-Related Hypophysitis Presenting with Hypopituitarism and Central Diabetes Insipidus

Hypophysitis is defined as inflammation of the pituitary gland. IgG4-related hypophysitis is a rare form and isolated IgG4-related hypophysitis is even more rare. Here, we discuss an interesting patient who presented with symptoms of diabetes insipidus and was found to have panhypopituitarism with suspicious MRI findings of a suprasellar mass and a thickened pituitary stalk, suggestive of IgG4-related hypophysitis. A 69-year-old male with past medical history of lung adenocarcinoma status-post right pneumonectomy, chronic obstructive pulmonary disease, orthostatic hypotension, and poor oral intake due to esophageal compression presented with acute encephalopathy and sepsis secondary to pneumonia. CT head scan done for encephalopathy showed a 1.2 cm suprasellar mass. On consultation, the patient was found to be hypernatremic. Upon further questioning, the patient reported experiencing polydipsia, nocturia, chronic cold intolerance, fatigue, and impotence for several weeks to months. He denied any vision changes, breast tenderness, or galactorrhea. Laboratory testing revealed a sodium level of 157 mmol/L (n.135-145 mmol/L) with plasma osmolality elevated at 332 mOsm/kg (n.275-295 mosm/kg). Urine sodium was low at < 20 mmol/L. Desmopressin (DDAVP) 0.1mg nightly was started given concern for diabetes insipidus. Peak cortisol after performed Cosyntropin stimulation test resulted at 13.5mcg/dL with an ACTH 6 pg/mL (n.6-50 pg/mL). TSH was < 0.01 mU/L, free T4 1.79 ng/dL, and free T3 4.9 nmol/L. The elevated free T3 was felt to be from heparin displacement. Total testosterone was 84 ng/dL with suppressed FSH and LH. Elevated prolactin of 39 ng/mL was thought to be from stalk-effect. MRI of the pituitary gland revealed a 1.3cm enhancing suprasellar mass in the region of the optic chiasm and a smaller 9mm intra-sellar mass, with a thickened pituitary stalk. Given these radiologic findings and the patient's age and gender, the possibility of IgG4 hypophysitis was suspected. CT chest, abdomen, and pelvis were unremarkable. In addition to the DDAVP, he was started on high-dose hydrocortisone, thyroxine replacement, and testosterone replacement. Serum IgG4 level was 23.6 mg/dL (n. 4-86 mg/dL). A six week repeat pituitary MRI is pending; however, the patient is clinically improving and doing well. Specific radiologic findings, such as thickened pituitary stalk and pituitary enlargement with suprasellar mass, led us to strongly consider IgG4-related hypophysitis in our differential for this patient. Clinical presentation of panhypopituitarism, along with patient age and gender, also supported the diagnosis of IgG4-related hypophysitis. Although this patient does not meet all Leporati diagnostic criteria for IgG4-related hypophysitis, the high degree of suspicion led to prompt treatment with high dose steroids. High dose steroids have been shown to revert symptoms and prevent irreversible fibrosis. This case highlights the need for radiologists and endocrinologists to work together in the early recognition of the diagnosis and treatment of IgG4-related hypophysitis.

Abstract #1402838: Thyroid Stimulating Hormone-Secreting Adenoma: A Rare Case of Hyperthyroidism

TSH-secreting adenomas account for only 0.5 to 3 % of all functioning pituitary tumors. We present this case report to highlight the importance of early diagnosis and prevention of severe complications. A 48-year-old postmenopausal female with a history of hypothyroidism was referred to our clinic for a second opinion. The patient had been stable on levothyroxine for over 10 years. Routine blood work was significant for elevated TSH and free T4. Despite adjustments to her levothyroxine, TSH and free T4 remained elevated. Her prior endocrinologist discontinued the levothyroxine and ordered an MRI brain, which showed an 8mm pituitary adenoma. The patient was referred to a neurosurgeon for evaluation, which then prompted the second endocrinology evaluation. Patient denied any palpitations, weight loss, heat intolerance, headaches, vision changes, or galactorrhea. Lab work repeated off of thyroid supplementation showed persistent elevated TSH at 6.5 mIU/L and free T4 at 2.1 ng/dL. Differential diagnosis included thyroid hormone resistance versus interference to thyroid assays versus TSHoma. The patient tested negative for the thyroid hormone resistance beta mutation, deeming thyroid hormone resistance unlikely. She tested negative for the human anti-mouse antibody, making interference to thyroid assays unlikely. Her alpha subunit level was normal, after which TSHoma was not a certainty. Since the diagnosis was unclear, patient was advised to follow up closely. Repeat MRI showed the tumor was now 1.2cm. Due to the increase in size, she was advised to proceed with trans-sphenoidal surgery (TSS). Pathology stained for TSH, confirming it was a TSH-secreting adenoma. After TSS, TSH normalized and free T4 was low, requiring the patient to be restarted on levothyroxine. TSH-secreting adenomas are quite rare, accounting for less than 1% of all cases of hyperthyroidism. Common clinical features include goiter, visual field defects, headache, menstrual disturbances, and galactorrhea. The presence of high free T4 and T3 and measurable serum TSH in the presence of a macroadenoma on MRI present strong evidence of a TSHoma. Definitive therapy includes transsphenoidal resection. Long-acting somatostatin analogs or dopamine agonists are used to restore euthyroidism prior to surgery. Long-term antithyroid drug therapy or thyroid ablation is not recommended because prolonged decreases in thyroid hormone secretion can stimulate TSH secretion and tumor growth. If TSHomas are left untreated, they can grow aggressively and impinge on nearby structures. Complications include visual field defects due to optic nerve compression, galactorrhea due to pituitary stalk compression, hypopituitarism leading to blood pressure dysregulation and decreased sexual function, and cardiac arrythmias leading to blood clots, stroke, and heart failure. Therefore, when hyperthyroxinemia is present with an elevated TSH, TSHoma should be considered. Even when alpha subunit levels are low or normal, TSHoma is still a possibility. Further investigation and close monitoring should be done to confirm diagnosis and prevent negative outcomes.

A Curious Case of Cocaine-Induced Hypokalemic Periodic Paralysis Mimicking Guillain-Barre Syndrome (P10-5.003)

<h3>Objective:</h3> To describe a rare cause of progressive ascending paralysis resembling Guillain-Barre Syndrome (GBS). <h3>Background:</h3> Cocaine inhibits the reuptake of monoamines at the synaptic cleft to prolong sympathetic output. This adrenergic hyperresponsiveness mimics thyrotoxicosis as it replicates sodium/potassium ATPase hyperactivity, causing a cellular influx of potassium (hypokalemia), hyperpolarization, and sodium channel inactivation that presents as sudden, painless muscle weakness and paralysis. <h3>Design/Methods:</h3> Consent obtained from patient. <h3>Results:</h3> A 30-year-old female with no past medical history was evaluated in the ED for acute lower extremity weakness that ascended to the upper extremities within &lt; 12 hours. Labs were significant for hypokalemia at 1.6, elevated inflammatory markers, elevated Free T4 at 2.58, and low TSH at &lt; 0.015. Urine drug screen was positive for cannabis and cocaine. Serum toxicology was negative. MRI of the T-spine and L-spine were unremarkable. Lumbar puncture was unremarkable. Cranial nerves were intact. Strength was 1/5 throughout, including at the neck. Flaccid tone. Lower extremity reflexes were 2+. Negative Babinski. Positive Hoffman bilaterally. Preserved sensation. The patient was admitted to the ICU, intubated for impending respiratory distress, and treated with IVIg. MRI of the C-spine was unremarkable. Further labs demonstrated elevated Free T3 at 7.13 and positive anti-TPO antibodies, significant for Grave’s disease. Urine labs were substantial for distal RTA. Anti-SSA and SSB antibodies were positive, indicating likely Sjogren’s syndrome (SS). Ganglioside panel was negative. Potassium was aggressively repleted. By day 1, the patient was moving all four extremities, and IVIg was discontinued. By day 2, she was successfully extubated. She was ambulating without difficulty on discharge. <h3>Conclusions:</h3> Secondary hypokalemic periodic paralysis may mimic Guillain Barre syndrome (GBS), a life-threatening demyelinating neuropathy that presents as rapidly progressive, symmetric, ascending paralysis or paresthesia with loss of reflexes. In our case, cocaine was the most plausible trigger for hypokalemia. <b>Disclosure:</b> Dr. Baumann has nothing to disclose. Dr. Rizvi has nothing to disclose. Ms. Alayon has nothing to disclose. Mr. Kendall has nothing to disclose. Dr. Shaffer has nothing to disclose. Dr. Mouhanna has nothing to disclose. Dr. Kenniff has nothing to disclose.

Identifying elevated plasma free triiodothyronine levels: age-adapted reference intervals for pediatrics.

Elevated free T3 (FT3) is an important feature for the early diagnosis of several diseases among which Grave's disease or Allan-Hernon-Dudley syndrome. However, there is a lack of age-adapted reference intervals for plasma thyroid hormones in children. We conducted a study to define reference values of peripheral FT3 in children using a commonly used automated immunoassay. All thyroid function test (TFT) results from our lab collected during 9 months were extracted anonymously, and reference intervals establishment followed recommendations validated by International Federation of Clinical Chemistry (IFCC). We defined five reference intervals covering the whole pediatric period. Overall, 26.1% of peripheral FT3 measured in children with normal TSH are out of the adult reference range, and 22.2% are upper it leading to misinterpretation. In a 9-month old patient with severe neurodevelopmental disorders, a pathological elevated FT3 has been securely interpreted using the newly established interval. The study highlights the poor relevance of adult intervals in pediatric cares, as it confirms that plasmatic FT3 is higher during the whole pediatric period. This work reports useful age-adapted reference intervals for free T3 in pediatrics using a widely used electrochemiluminescent Immunoassay (ECLIA) kit.

LBODP100 A Rare Case Of Pembrolizumab Induced Graves’ Disease

Abstract Cancer immunotherapies have recently changed the therapeutic armamentarium of anti-cancer treatments, particularly for melanoma and cancers of the kidneys, lungs, and colon. Immune checkpoint inhibitors (ICPis) act on various immune checkpoints. Of them, anti-PD-1 antibodies (such as pembrolizumab) are monoclonal antibodies that act against programmed cell death 1 protein. However, by counteracting the regulators of adaptive immunity, this class of drugs may cause immune-related adverse events that involve multiple organs and endocrine glands, such as the thyroid gland. The symptoms of thyroid dysfunction usually present during the first weeks of ICPis therapy. In the current report, we present a case of a 50-year-old male who presented to the emergency department complaining of fever, chills, nausea, and vomiting for one week. The patient had a history of colon cancer with lymph node metastasis status post tumor resection and colostomy. He began Keytruda® (pembrolizumab) treatment after tumor resection, and the presenting symptoms appeared after receiving the first immunotherapy infusion. His medical history was significant for psoriasis and rheumatoid arthritis. The patient's history was unremarkable for thyroid diseases, and he did not receive thyroid medications with no previous exposure to intravenous contrast media, over-the-counter iodine preparations, or biotin. At the emergency department, the patient had a temperature of 101.4°F, a heart rate of 110 bpm, and blood pressure of 130/70 mm Hg. On examination, tenderness was indicated upon palpating the anterior part of the neck. The patient was treated with intravenous fluids, steroids, beta-blockers, and broad-spectrum antibiotics. A workup for sepsis was requested, and it revealed negative blood culture and urine culture results. His laboratory indices demonstrated a suppressed level of TSH (0. 01 mIU/mL) and elevated Free T4 (3.16 ng/dl). Still, his TSH level reported at the Oncology clinic before Keytruda administration was (0.9 mIU/mL), and Free T4 was (1.7 ng/dl). Thyroid ultrasound revealed a heterogeneous thyroid gland consistent with thyroiditis. Antibody testing showed positive thyroid antithyroglobulin antibodies and elevated thyroid-stimulating antibodies (TSI). A radioactive iodine uptake test was ordered, revealing increased contrast uptake. These findings suggested that the cause of thyroid dysfunction was Graves’ disease. The patient was started on Methimazole 20mg per day and discharged home after scheduling an outpatient follow-up appointment with the endocrinologist. This case is one of the rare cases of thyrotoxicosis attributable to Graves’ disease related to pembrolizumab therapy. To the best of our knowledge, two studies in the literature reported three cases of ICPi-induced thyrotoxicosis with thyroid antibody positivity following anti-PD-1 antibody therapy. Presentation: No date and time listed

ODP635 A rare case of metastatic papillary thyroid carcinoma on NTRK inhibitor with thyrotoxicosis

Abstract We present a case of 26-year-old Hispanic female with neck enlargement and worsening dyspnea. She was noted to have enlarged thyroid nodules; biopsy revealed papillary thyroid carcinoma (PTC) with ETV6-NTRK fusion by next-generation sequencing (NGS). Further work up revealed extensive bilateral milliary pulmonary metastases and Graves’ disease with elevated thyrotropin receptor antibodies and thyroid-stimulating immunoglobulin titers. Tuberculosis work up was negative and bronchoalveolar lavage revealed metastatic PTC. The patient was initiated on larotrectinib (100mg administered twice daily) as well as block-and-replace regimen with levothyroxine and methimazole. Her dyspnea improved and she successfully underwent total thyroidectomy as well as bilateral neck dissections; methimazole and thyroid hormones were discontinued thereafter. Interestingly, patient developed thyrotoxicosis post-surgery even without being on levothyroxine with elevated free T3 at 18 pg/mL (normal range 2.3–4.2), compared to 5.8 pg/mL prior to surgery. Despite discontinuation of levothyroxine, patient continued to be biochemically and clinically hyperthyroid. She was treated with methimazole for 4 months after surgery, and subsequently underwent radioactive iodine (RAI) ablation with 30 mCi of I-131 of sodium iodide. After RAI, thyroid function started to improve, prompting re-initiation of very low dose levothyroxine about 5 months after surgery. Since then, she has remained clinically stable. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

PSAT346 Persistent Fluctuation Between Hypothyroidism and Hyperthyroidism in a Patient with Both Hashimoto's Thyroiditis and Graves’ Disease: Challenges in Diagnosis and Treatment Approach

Abstract Introduction The two most common autoimmune disorders affecting the thyroid gland, namely Graves’ disease and Hashimoto's thyroiditis, represent opposite ends of the same spectrum. They can rarely co-exist in the same patient (1) leading to an unpredictable clinical course and pose a therapeutic challenge, necessitating close monitoring. We present a unique case of a female who switched multiple times between a hypothyroid and hyperthyroid state due to the co-existence of both Hashimoto's thyroiditis and Graves’ disease. Case Description A 78-year-old Caucasian female was diagnosed with hypothyroidism in 2011 by her primary care physician and was started on levothyroxine 50 mcg daily. The TSH level prior to initiation of levothyroxine therapy is unknown, but the first documented TSH level while on therapy in June 2012 was 0.347 uIU/ml (0.45-4.50), free T4 1.1 ng/dl (0.8-1.8) and free T3 3.4 pg/ml (2.3-4.2). Levothyroxine was lowered to 25 mcg daily but repeat TSH was 0.01 uIU/ml in February 2013 and the levothyroxine was discontinued. The TSH level rose to 7.35 uIU/ml in December 2014 and levothyroxine was restarted. However, subsequent dose reduction was required followed by discontinuation due to persistently suppressed TSH levels and the TSI antibody during that time was elevated at 24.10 IU/L (0.00-0.55). Patient established care at our endocrinology clinic in 2019. Initial laboratory findings showed suppressed TSH &amp;lt;0.005 uIU/ml (0.30-4.00), elevated free T3 4.72 pg/ml (2.00-4.40), normal free T4 1.70 ng/dl (0.80-1.80) and elevated TSI antibody 15.50 IU/L. Radioactive iodine uptake scan showed high normal 24 hour uptake at 32% (10-35%) with mild heterogeneous distribution of the radiotracer throughout both lobes of the gland with diminished uptake in the right lower lobe, which corresponded to a 1.3 cm nodule that was biopsied and reported to be Bethesda category II. Patient was initiated on methimazole 5 mg daily. In June 2019, labs showed elevated TSH 6.91 uIU/ml, low free T4 0.74 ng/dl and free T3 2.01 pg/ml. Methimazole was held, and labs repeated after a few weeks, did not change significantly. In September 2020, levothyroxine 25 mcg daily, was initiated due to fatigue symptoms and an elevated TSH 10.61 uIU/ml with low FT4 0.8 ng/dl. Patient did not follow up for a while after that. In December 2021, levothyroxine was increased to 50 mcg daily in response to an elevated TSH 12.91 uIU/ml. The TPO and TSI antibodies remain elevated at 210 IU/ml (0-34) and 9.08 IU/L respectively. Conclusion Our case highlights the diagnostic and therapeutic challenges encountered when both Hashimoto's thyroiditis and Graves’ disease co-exist in the same patient. Reference (1) Alvin Mathew A, Papaly R et al. Elevated Graves’ Disease-Specific Thyroid-Stimulating Immunoglobulin and Thyroid Stimulating Hormone Receptor Antibody in a Patient With Subacute Thyroiditis. Cureus 13(11): e19448. doi: 10.7759/cureus.19448 Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

LBSAT314 Diagnosis And Management Of A Rare Case Of Marine-Lenhart Syndrome

Abstract Introduction Marine-Lenhart syndrome is defined as Graves’ disease with co-existing toxic thyroid nodules. Approximately 25% to 30% of patients with Graves’ disease have accompanying nodules. More than 95% of these nodules are hypoactive, and thus, only a tiny percentage are hyperactive. In these patients, Graves’ disease and toxic nodules both contribute to thyrotoxicosis11. Here we present a case that details this syndrome's diagnosis, management, and treatment complication. Clinical Case A 68-year-old female presented to the primary care physician's office with complaints of anxiety and heat intolerance. Three years before this visit, the patient was diagnosed with Graves’ disease. She had achieved remission after one year of methimazole therapy. During the office visit, the patient was in sinus tachycardia at 112 BPM. There were no signs of exophthalmos on examination, and the thyroid was not palpable. Further testing revealed thyrotoxicosis with suppressed TSH of &amp;lt;0. 01 mcIU/mL (0.36-3.74) and elevated free T4 of 2.49 ng/dL (0.76-1.46). Thyrotropin receptor antibody (TRAb) was positive at 2.60 IU/L (0. 00-1.75). The patient was started on atenolol. Although TRAb was positive, thyroid ultrasound and radioactive iodine uptake scan (RAIU) were ordered to look for alternative diagnoses. The thyroid ultrasound showed four nodules in the left lobe, the largest of which was 1.8×1.5×1.3 cm. RAIU showed increased 24-hour uptake of 45% and three areas of increased focal uptake in the left thyroid lobe consistent with toxic nodules. Definitive treatment was needed due to both toxic nodules and Graves’ disease. The patient agreed to radioiodine ablation therapy (RAI) and received a dose of 21 uCi. One month after receiving RAI, the patient complained of worsening anxiety and heat intolerance. On repeat testing, TSH was &amp;lt;0. 01mcIU/mL, and free T4 was 4.78 ng/dL. The patient developed radiation thyroiditis and was given methimazole 10mg daily for two weeks. Three weeks after the course of methimazole, the patient became hypothyroid and was managed with 88 mcg of levothyroxine daily with no symptoms. Conclusion Common causes of hyperthyroidism are Graves’ disease or autonomous functioning thyroid nodules per the American Thyroid Association12. However, in hyperthyroid patients, Marine-Lenhart syndrome should be considered, especially those with thyrotoxicosis recurrence. This diagnosis steers management away from antithyroid drugs and toward RAI or thyroidectomy. For patients treated with RAI, antithyroid medications should be included as an adjunct therapy to reduce post-radiation thyroiditis. References 1 Cakir, Mehtap. "Marine-Lenhart Syndrome.," Journal of the National Medical Association 97, no. 7 (July 2005): 1036-38.12 Ross, Burch, et al., Thyroid. Oct 2016, 26(10): 1343-1421. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

PSUN36 Subacute Thyroiditis Following mRNA Vaccine for COVID-19 in a 40-Year-Old Male Patient

Abstract Background Subacute thyroiditis typically occurs a few weeks after a viral infection and is the most common cause of painful thyrotoxicosis. Cases of subacute thyroiditis have been reported following both inactivated and live-attenuated vaccines, such as the influenza vaccine. We describe a case of subacute thyroiditis in the setting of the Pfizer-BioNTech mRNA COVID-19 vaccination. Clinical Case A 40-year-old man with no significant medical history presented with signs and symptoms of thyrotoxicosis after receiving the Pfizer COVID-19 vaccine. Symptoms began 3 days after receiving the second vaccine dose and included 9 kg unintentional weight loss, arthralgia in both knees, palpitations, fatigue, bilateral thigh weakness, and diffuse neck swelling, pain, and tenderness. Initial treatment with antibiotics for presumed upper respiratory infection did not improve symptoms, and PCR testing for COVID-19 infection was negative. Thyroid ultrasound obtained 15 days after symptoms onset revealed a 4 cm nodule in the left lobe of the thyroid gland. Testing 30 days after onset of symptoms demonstrated TSH&amp;lt;0.005 uIU/mL (ref: 0.45-4.50 uIU/mL), elevated free T4 of 2.53 ng/dL (ref: 0.82-1.77 ng/dL), and elevated erythrocyte sedimentation rate of 42 mm/hr (ref: 0-15 mm/hr). Repeat labs and imaging 9 days later demonstrated improvement with a TSH of 0.071 uIU/mL and free T4 of 1.04 ng/dL as well as decreased nodule size (2.5 cm). At this time, the patient reported resolution of all symptoms and return to baseline weight. Thyroid ultrasound obtained 3 months after symptoms onset demonstrated normal thyroid without detectable nodules or enlargement, and complete normalization of TSH and free T4 levels to 4.250 uIU/mL and 1.22 ng/dL, respectively. Conclusion This is the second documented case of subacute thyroiditis following the Pfizer-BioNTech vaccine for COVID-19 in a male patient. A literature review demonstrates 12 other cases of subacute thyroiditis following the Pfizer-BioNTech mRNA COVID-19 vaccine, 3 cases following the Moderna mRNA COVID-19 vaccine, 8 cases following the AstraZeneca recombinant COVID-19 vaccine (one male patient), 4 cases following the CoronaVac inactivated SARS-CoV-2 COVID-19 vaccine, 1 case following the Covaxin inactivated SARS-CoV-2 COVID-19 vaccine, and 3 cases following the Janssen viral vector SARS-CoV-2 COVID-19 vaccine. Albeit uncommon, providers should be aware that transient thyrotoxicosis following COVID-19 vaccination may occur. Similar to subacute thyroiditis due to viral infection, the clinical course is generally self-limited with patients returning to a euthyroid state within a few months. Usual management of subacute thyroiditis with symptomatic management and watchful waiting is appropriate. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

PSUN39 A rare presentation of autoimmune thyroid diseases and myasthenia gravis: A clinical case report

Abstract We report a case of a 37-years-old female that presented with a three-week history of diplopia, ptosis, muscle weakness, difficulty chewing, tachycardia, and fatigue; these clinical symptoms were concerning for acute myasthenia gravis crisis. The diagnosis of Myasthenia gravis was further confirmed by a positive immunology workup. Chest CT imaging during her assessment showed anterior mediastinal mass/enlarged thymus indicative of thymic hyperplasia. Medical therapy with intravenous immune globulin, pyridostigmine and further treatment with high-dose steroid. She had a positive response to treatment but still reported persistent symptoms of fatigue, tachycardia, and intermittent diplopia, raising suspicions for underlying Graves’ thyrotoxicosis. Thyroid function testing was performed which showed a very suppressed thyroid-stimulating hormone (TSH) and elevated Free t4 levels. Further workup for Graves thyroid autoimmune antibodies indicative of extremely elevated thyroid stimulating hormone receptor autoantibodies consistent with Graves’ disease. We initiated medical therapy for Graves’ disease with a beta-blocker and thioamide (methimazole). She endorsed progressive improvement in her symptoms following treatment for Grave's disease. She was discharged with high dose steroids, pyridostigmine, and appropriate therapy for Graves’ disease. She did well after her discharge from the hospital and six months afterwards she returned to the hospital for a robot-assisted right thymectomy. Final pathology report indicative of non-thymomatous myasthenia gravis. She continued to follow up with us in the endocrinology outpatient clinic. Her steroid therapy was tapered off and medical therapy for Graves’ disease was continued accordingly. She demonstrated a positive response to medical therapy with remarkable improvement in the remaining of her symptoms, especially her neurological and ocular symptoms after initiation of treatment for Graves’ disease. Conclusion we report two rare concomitant autoimmune diseases, myasthenia gravis, and Graves’ disease. Both conditions have similar overlapping clinical features making diagnosis and treatment challenging in clinical practice. It is well reported in clinical literature and studies that hyperthyroidism may worsen symptoms of MG and management of hyperthyroidism in the setting of MG may lead to worsening of myasthenia symptoms; hence, certain precautions should be taken to avoid worsening symptoms of myasthenia gravis. Therefore, we call for more case-control, case series and clinical trials to explore more clinical knowledge about the association between the two conditions and formulate better management strategies. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

ODP570 Immunotherapy and its Implications for the Future of Endocrinology: A Case Discussion of Pembrolizumab Induced Myxedema Coma

Abstract Introduction Immunotherapy is a relatively new type of cancer treatment that has been successful in prolonging survival time and improving quality of life for patients with a wide variety of cancers.1 While these therapies do not usually have the same systemic toxicities seen in traditional chemotherapies, they can lead to significant autoimmune disorders due to their method of action.2 We present a case of pembrolizumab induced Hashimoto's thyroiditis leading to myxedema coma. Case A 67-year-old male presented to the hospital ED via EMS after being found unconscious in his car by his neighbor. On arrival, he was confused, lethargic, unable to answer questions, and had a Glasgow Coma Scale of 12. He was hypotensive 87/55 mmHg, bradycardic 55 bpm, respirations 12 breaths/min, SpO2 99% on room air, temperature 37 °C. Past medical history included type 2 diabetes mellitus on insulin and non-small cell lung cancer metastatic to bone and brain treated with pembrolizumab, denosumab, steroids, and radiation therapy. Initial labs revealed elevated TSH of 47. 01 with undetectable T3 and T4, glucose 514 mg/dL and elevated beta hydroxybutyrate 1.61, WBCs 3.9, hemoglobin 11.7, platelets 105. TPO antibodies were elevated 44.5IU/ml. Patient was treated with IV levothyroxine, hydrocortisone, insulin, and fluids and his condition improved rapidly. Patient was transitioned to oral levothyroxine with plans for outpatient endocrinology follow upon discharge. Thyroid tests done during a prior hospitalization following the initiation of pembrolizumab six months earlier demonstrated a low TSH of &amp;lt;0. 003 and an elevated free T4 of 2. 09. The diagnosis of autoimmune thyroiditis induced by immunotherapy was made. Discussion Pembrolizumab is one of several immune-checkpoint inhibitors (ICIs) used to treat cancer by blocking the programmed-death (PD-1) receptor, allowing T-cells to detect malignant cells and mount an immune response. ICIs are part of a larger therapeutic class known as immunotherapy which acts to enhance the body's own detection and elimination of cancerous cells.1 As a result, approximately 10% of patients treated with immunotherapy develop autoimmune reactions.2 In this case, the patient had positive thyroid autoantibodies for Hashimoto's thyroiditis, that eventually lead to his profound hypothyroid state and myxedema coma. As these therapies become more widely utilized, the incidence and prevalence of autoimmune induced endocrine disorders will naturally increase. Awareness of the mechanisms and implications of immunotherapy in patients presenting with endocrine disorders will led to early recognition, treatment and improved patient outcomes. Waldman AD, et al Nat Rev Immunol. 2020;20(11): 651-668. Barroso-Sousa R, et al. . JAMA Oncol. 2018;4(2): 173-182. Presentation: No date and time listed

ODP519 Thyroid Cyst Grows E. coli

Abstract Background Thyroid abscesses are extremely rare, representing less than 1% of all thyroiddiseases. The thyroid gland is very robust against infections due to its vastlymphatic drainage, dual blood supply, encapsulation, and iodine concentration. Immunocompromised patients are at greater risk of developing thyroid abscesses. 1 Case: A 51-year-old female presented to her primary care provider with acute onset ofpainful right neck mass with associated cough, hoarseness, fever, and fatigue. She was seen by an Otolaryngologist who aspirated 6 cc of brown purulentmaterial from a suspected thyroid mass. The thyroid fluid was sent for culture,and she was empirically started on Augmentin. CT neck demonstrated a cysticlesion of the right thyroid gland, retropharyngeal edema, and mass effect withleftward deviation of the larynx and trachea without airway obstruction. Due tothese findings, the patient was admitted to the hospital where initial two setsof blood cultures were negative but repeat blood cultures revealed 2 of 2positive for E. coli. Thyroid cyst fluid also grew E. coli. Urine culture hadno growth. She was found to have a suppressed TSH of 0.24 uIU/mL, elevated free T4 of 1.80 ng/dL, and suppressed total T3 of 0.52 ng/mL. Previous TSH was within normal limits, 0.82 uIU/mL. The suppressed TSH and suppressed T3 were thought to be secondary to euthyroid sick syndrome. She was maintained onCeftriaxone while admitted and discharged on Ciprofloxacin. Pathology from theright thyroid cyst revealed acute inflammatory cells only consistent with anabscess, negative for malignancy. The patient elected to undergo a righthemithyroidectomy with isthmusectomy. Discussion Thyroiditis is defined as inflammation of the thyroid gland and has a variety ofetiologies. Suppurative thyroiditis, which includes thyroid abscess as in thiscase we have described, is an infrequent cause of thyroiditis. It is usuallycaused by hematogenous spread or direct inoculation of a pathogen. Treatmentincludes systemic antibiotics targeting the causative organism; although thegold standard remains surgical drainage. Surgical management is the mainstay ofmanaging patients with thyroid abscesses. 2

PSAT321 Post-partum Thyroiditis Precipitated by SARS CoV-2 Infection-a Case Report

Abstract Introduction Postpartum thyroiditis is a form of destructive thyroiditis. It is thought to originate from an autoimmune mechanism that develops within one year of parturition. The condition results in inflammation of the thyroid resulting in damage to the thyroid follicles and release of previously stored thyroid hormone. There are only a handful of documented cases of postpartum thyroiditis associated with SARS CoV-2. Since the onset of COVID-19 a multitude of thyroid abnormalities have been associated with the virus. Case Summary A 33-year-old female, 5 months post-partum with a medical history significant for hypertension presents to the clinic for evaluation of hyperthyroidism. She tested positive for SARS-CoV-2 eleven days prior to delivering her child. Her pregnancy was only complicated by chronic hypertension. COVID-19 infection was symptomatic for mild respiratory symptoms. She had no history of hypo or hyperthyroidism prior to or during her pregnancy. At presentation, patient was largely asymptomatic with a physical exam significant only for sinus tachycardia. Laboratory tests done two weeks before her visit, were significant for a suppressed TSH &amp;lt;0.001 uIU/mL (reference range: 0.450- 4.50) and a mildly elevated Free T4: 1.84 NG/dL (reference range: 0.82-1.77) and T3: 139 NG/dL (reference range: 71-180). We repeated the tests and noted a recovering TSH of 0.110 uIU/mL; a low Free T4: 0.77 NG/dL and T3: 66 NG/dL. Thyroglobulin level was found to be elevated at 742.6 IU/mL (reference range 0.0-0.9). Thyroid Stimulating Immunoglobulin level was &amp;lt;0.10 IU/L (Normal- 0.00-0.55) and serum thyrotropin receptor Ab &amp;lt;1.10 IU/L (Normal- 0.00-1.75). Radioactive iodine uptake &amp; scan was deferred as patient was breast-feeding at the time. As our patient was asymptomatic, she was prescribed only propranolol for her tachycardia. Discussion Documented cases of post-partum thyroiditis associated with SARS-CoV-2 infection are far and few. Post-partum thyroiditis is characterized by an initial thyrotoxic phase followed by hypothyroid phase and then a recovery period. Most patients are only mildly symptomatic during the initial hyperthyroid phase. At the time of referral to our clinic, the patient was already entering a hypothyroid state. She was asymptomatic at the time and therefore treated with expectant management only. COVID-19 has been identified as a cause of subacute post-infectious thyroiditis. It is known to be associated with a hyperinflammatory state characterized by a cytokine storm. Elevation of these cytokines can contribute to thyroid dysfunction. Conclusion It is hard to say whether our patient's acute thyroiditis was secondary to postpartum thyroiditis, subacute thyroiditis secondary to COVID-19 infection, or a combination of both factors. However, regardless of etiology it is important to note a possible correlation of post-partum thyroiditis in the setting of a SARS-CoV-2 infection. It is necessary to identify all cases of COVID-19 infection that can be associated with thyroid dysfunction. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

ODP526 Thyrotoxic Periodic Paralysis in Graves’ Disease: A rare presentation in an African American male

Abstract INTRODUCTION: Thyrotoxic Periodic Paralysis is a rare but life-threatening manifestation of hyperthyroidism characterized by hypokalemia, acute flaccid paralysis, and signs of hyperthyroidism. Despite being commonly seen in East Asian males, TPP has been increasingly reported in other parts of the world including western countries. Early recognition and prompt treatment of TPP is essential in preventing its grave and potentially life-threatening consequences. CASE PRESENTATIONA 21-year-old African American male patient with past medical history significant for hypertension and untreated hyperthyroidism presented to the emergency department with sudden onset bilateral lower extremity weakness and difficulty walking for one day. Upon arrival to the emergency department, vitals were unremarkable. On examination, patient had a decreased muscle tone in bilateral lower extremities with depressed deep tendon reflexes. The thyroid gland was diffusely enlarged. The remainder of physical exam was normal. Electrolyte abnormalities were also present with decreased serum potassium level of 1.2 mEq/L (3.6-5.1 mEq/L) and magnesium of 1.7 mg/dL (1.8-2.5 mg/dL). A low TSH level of &amp;lt;0. 010 mIU/mL (0.350-4.940 mIU/mL) with elevated free T4 levels of 4.30 ng/dL (0.70-1.48 ng/dL) were noted. CT Head/ Brain without contrast and Chest X ray were unremarkable. Potassium replacement was initiated with oral and intravenous potassium chloride. He was also started on oral atenolol (25 mg daily) and methimazole (10 mg daily). The patient's symptoms resolved in few hours after the treatment was started. An ultrasound of the thyroid gland showed diffuse heterogeneity of the gland most consistent with thyroiditis or similar abnormality. No definite focal abnormalities were noted. TSH receptor antibodies were also elevated with levels at 10.70 IU/L (≤1.75 IU/L) making Graves’ disease the most likely diagnosis. The patient's condition significantly improved along his hospitalization with complete resolution of symptoms and electrolyte abnormalities. He was subsequently discharged on atenolol and methimazole with outpatient follow up at the endocrinology clinic. DISCUSSION TPP is an underreported yet possibly fatal medical complication of hyperthyroidism. Prevalence is higher in Asia, however, incidence in Western countries has been increasing. While the underlying pathophysiology is poorly understood, h ypokalemia in TPP results from an intracellular shift of potassium induced by an increased adrenergic sensitization of Na + /K + –ATPase pump. Genetic and environmental factors may possibly play a role. Treatment of TPP entails beta-blockade to prevent intracellular shift of potassium, replenishing potassium stores, as well as correcting the underlying hyperthyroid state. Immediate diagnosis and initiation of treatment prevents serious cardiopulmonary complications and increases the probability of full recovery of muscle weakness. Presentation: No date and time listed

ODP515 Severe thyrotoxicosis caused by subacute thyroiditis

Abstract Background Subacute thyroiditis, also named giant cell thyroiditis, painful thyroiditis, and de Quervain's thyroiditis, usually presents with neck pain or discomfort, a tender diffuse goiter and mild or moderate elevation of serum free T4 and T3 levels. Here we report a case of subacute thyroiditis patient presenting with severe thyrotoxicosis. Clinical case: A 27-year-old woman with no significant past medical history presents to the emergency room with palpitations and abnormal EKG with heart rate at 160 beats per minute. She developed a sore throat 3 days prior to the presentation, but she did not have neck pain or fever. She reports a 3-month history of hair loss, headaches and weight gain. Labs showed significantly elevated free T4 greater than 7.7 ng/dl (0.8-1.7) and free T3 level at 20.7 pg/ml (2. 0-4.8), and suppressed TSH less than 0. 01 uIU/ml (0.45-4.5) and normal ESR at 15 mm/hour. Her TPO antibody was greater than 1300 u/ml. Thyroid stimulating immunoglobulin (TSI) and TSH receptor antibody (TRab) were obtained but results were pending when she was discharged from the hospital. She has no typical clinical features of subacute thyroiditis with normal ESR and her free T3 and free T4 levels were significantly elevated. She was discharged on Methimazole and Propranolol and to do neck ultrasound as outpatient and follow-up TSI and TRab results and repeat free T4 and T3 in 1 week. Her neck ultrasound revealed mild hypervascularity but no Graves’ features. Her TSI and TRab were negative and free T4 level had no improvement even on significant dose of Methimazole. All the findings argue against Graves’ disease, but support subacute thyroiditis. Then Methimazole was discontinued and Prednisone was started at 20 mg daily and quickly taper to 5 mg daily in 2 weeks then stopped. After on Prednisone for 3 weeks, her free T4 was close to normal at 2. 0 ng/dl, T3 normal at 120 ng/dl, although TSH is suppressed. After stopped Prednisone for 2 weeks, her free T4, T3 and TSH were all back to normal. She is currently euthyroid without any medication at 5 months after her initial presentation. Conclusion Treatment of patients with subacute thyroiditis is pain relief with NSAID or Prednisone when NSAID is not effective. Anti-thyroid medications are rarely effective even in subacute thyroiditis patient with thyroid storm. Our case illustrated the role of corticosteroids in the treatment of subacute thyroiditis patient with severe thyrotoxicosis. Neck ultrasound and thyroid antibodies including TSI and TRab are critical to make a correct diagnosis in subacute thyroiditis patient with severe thyrotoxicosis. Presentation: No date and time listed

RF23 | PSAT301 Plasmapheresis and Extracorporeal Membrane Oxygenation (ECMO) for Treatment of Thyroid Storm with Multiorgan Failure

Abstract Introduction Thyroid storm is a life-threatening condition with a high morbidity and mortality rate. It can lead to severe end organ damage including liver injury, which can preclude the use of thionamides. Therapeutic plasma exchange can be a lifesaving option for treatment of thyroid storm in such cases. Multiorgan failure can also necessitate the use of extracorporeal membrane oxygenation (ECMO) and continuous renal replacement therapy (CRRT). Case Presentation A 34-year-old woman with a history of Graves’ disease, untreated for several years, presented to the emergency department with fatigue, palpitations, dyspnea, and edema which developed over 1 month. Labs showed suppressed thyroid stimulating hormone (TSH) with significantly elevated free T4 of 10.8 ng/dL (normal 0.89-1.76 ng/dL). She had evidence of atrial fibrillation and heart failure. She was started on treatment with propylthiouracil, propranolol, and hydrocortisone and then Lugol's iodine was added. However, she quickly deteriorated with worsening mentation, dyspnea, and hypotension. She progressed to multiorgan failure including significant liver injury likely due to ischemic hepatitis. Thus, thianomides could not be used any further. She was started on cholestyramine; hydrocortisone and Lugol's iodine were continued.An echocardiogram revealed global hypokinesis with a left ventricular ejection fraction of 20%. Beta blockers were discontinued due to hypotension. The cardiogenic shock worsened despite aggressive medical therapy requiring initiation of veno-arterial (V-A) ECMO. She also required CRRT due to renal failure.Plasmapheresis was initiated for treatment of thyroid storm and she received 4 treatments with normalization of free T4: 1.48 ng/dL and T3 levels: 3.4 ng/dL (normal 2.3-4.2 ng/dL). Her condition subsequently improved and she was decannulated from the ECMO device after 5 days. She was then able to receive definitive treatment with thyroidectomy 11 days following admission. The patient was discharged in improved condition after a 10-week hospital course. Discussion Thyroid storm is a rare complication of thyrotoxicosis with a mortality rate of 10-30%. Treatment classically involves inhibiting the synthesis, release, and peripheral conversion of thyroid hormone as well as supportive management. Major causes of mortality in thyroid storm, present in our patient, include cardiogenic shock, arrhythmia, and multiorgan failure. Cardiac and hepatic failure can preclude the use of beta blockers and thionamides, which may necessitate the use of extracorporeal treatments, such as plasmapheresis for clearance of high burden of circulating thyroid hormone; V-A ECMO and CRRT for end organ damage. These therapeutic measures were used in our patient and led to a favorable outcome. This case highlights the successful use of these extracorporeal treatments as a bridge to thyroidectomy when standard medical treatment is contraindicated or unsuccessful. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m., Sunday, June 12, 2022 12:42 p.m. - 12:47 p.m.

ODP501 New-Onset Graves’ Disease in a Patient with Recent Diagnosis of Covid-19 Infection

Abstract Background Thyroid disorders have been described in patients with Covid-19 infection. Although thyrotoxicosis secondary to thyroiditis is mostly reported in several publications worldwide in patients infected with Covid-19, new-onset Graves’ disease is rarely reported. Clinical Case A 41-year-old female without significant past medical history presented to emergency room with nausea, vomiting, palpitations and syncope. She was diagnosed with COVID-19 infection five days prior to her presentation. On admission, patient was normotensive, tachycardic with heart rate of 135 beats/min, and oxygen saturation &amp;gt;90% on room air. Thyroid exam was unremarkable. Initial labs showed suppressed TSH, elevated free T4 of 2.58 ng/dL (0.76–1.70 ng/dL) and elevated total T3 of 210 ng/dL (80–175 ng/dL). The computed tomography pulmonary angiogram (CTPE) was negative for pulmonary embolism. Transthoracic echocardiogram (TTE) showed moderate cardiac effusion without tamponade. Patient had no prior history of thyroid disease, but her mother had hypothyroidism. With Burch-Wartofsky score of 50, treatment for thyroid storm was initiated: Hydrocortisone, propranolol, and propylthiouracil (PTU), followed by cholestyramine, and super saturated potassium iodide (SSKI). Shortly after, patient developed hypotension requiring norepinephrine infusion and transfer to intensive care unit. Repeat TTE showed ejection fraction of 50%, moderate pericardial effusion without tamponade, and global hypokinesis suggestive of myocarditis. Propranolol was held. Although patient's blood pressure improved overnight, patient developed shock liver with AST elevated at 4,095 IU/L (8-30 IU/L), ALT at 2,837 IU/L (&amp;lt;35 IU/L), and total bilirubin at 1.6 mg/dl (0.2-1.2 mg/dl) compared to normal values on admission. PTU was discontinued after two doses due to elevated liver enzymes. Thyroid scan showed diffuse mildly increased radiotracer uptake suggestive of autoimmune thyroid disease. Thyroid stimulating immunoglobulin (TSI) was elevated at 6.5 IU/L (&amp;lt;0.55IU/L) with thyrotropin receptor antibody (TRAb) of 8.39 IU/L (0. 00 - 1.75 IU/L) suggestive of Graves’ disease. On discharge, patient was asymptomatic. At outpatient follow up, patient had improvement in liver enzymes and mild hyperthyroidism, methimazole was started with the plan for close monitoring of liver enzymes and thyroid function tests. Conclusion New-onset Graves’ disease can occur in the setting of Covid-19 infection. It is crucial to report this type of cases to gain more insights in the exact relationship between thyroid disease and Covid-19 infection. Physicians should be aware of the possibility of Graves’ disease in addition to thyroiditis in the setting of thyrotoxicosis and Covid-19 infection. Making the right diagnosis is essential as treatment and course of disease are very different. Presentation: No date and time listed