Free T4 Research Articles

8471 A Rare Case of Graves' Disease in a Three-Year-Old

Abstract Disclosure: A. Rajesh: None. A. Ravari: None. L.E. Kimball-Ravari: None. H. Roan: None. Graves’ Disease (GD) is an autoimmune disease that causes hyperfunctioning of the thyroid gland which may be triggered by environmental factors such as infection or stress. Though the leading cause of hyperthyroidism in both adult and pediatric populations is GD, it is extremely rare in children under the age of four years old. Some studies show the incidence to be 1 per 1,000,000 cases[1],2. Detecting GD in children early is very important as untreated GD poses a risk for failure to thrive. There have also been cases of young children suffering from psychomotor delays, craniosynostosis, and language delays because their suspected diagnosis of GD had not been detected for one to two years. In this article, we report the case of a previously healthy three-year-old Caucasian female who presented to the pediatric endocrinologist after collapsing from an episode of hypoglycemia; plasma glucose 47 mg/dL (71-180) . The patient was diagnosed with Graves’ Disease due to her significantly elevated free T3 and T4, decreased TSH, positive thyroid peroxidase (TPO) antibodies, and elevated TSIg. She was started on methimazole treatment; however, she did not respond after six months of ATD and underwent total thyroidectomy. Her hypoglycemia was attributed to abnormal proinsulin processing and glucose metabolism, which has been associated with hyperthyroidism; thyroid hormones can produce increased GLUT2 transporters3. This case report demonstrates the importance of recognizing the signs and symptoms of GD early, as well as discuss the importance of increasing the recognition of autoimmune diseases in the pediatric population.

8124 Prevalence and Characteristics of Patients with Hypothyroidism in the Danish Blood Donor Study

Abstract Disclosure: N.L. Frisk: None. J.R. Shorter: None. O.B. Pedersen: None. L.T. Dalgaard: None. Introduction: While impaired thyroid function leading to subclinical hypothyroidism and overt hypothyroidism is common in Denmark, the knowledge about the paths by which patients’ progress to impaired thyroid function is limited. Undiagnosed hypothyroidism as well as subclinical hypothyroidism constitute serious risk factors for development of cardio metabolic disease. The Danish Blood Donor Study (DBDS) is a large longitudinal cohort and biobank containing information and samples dating more than 10 years back. Blood donors donate blood every 3-6 months and each time provide a sample for research. Research question: The aim of the study was to obtain up-to-date information about prevalence and characteristics of patients with hypothyroidism in a Danish longitudinal cohort of blood donors. Methodology: The study employed a cross-sectional design. Hypothyroidism was defined based on at least two prescriptions of levothyroxine (LT4) and used for calculations of prevalence. Case numbers were compared to all controls that were currently not being prescribed LT4 nor anti-thyroid drugs (carbimazole, propylthiouracil, thiamazole). We compared cases of hypothyroidism to two different control (ctrl) groups: 1) All the participants of the DBDS having TSH levels in the normal range, and 2) Normothyroid participants matched to hypothyroid cases based on age and sex. Incidence was determined based on DBDS participants developing hypothyroidism after being enrolled into the DBDS during a 10-year follow-up. Men and women were compared separately among cases and controls. Students’ t-test was used to compare cases and controls, and corrected using Bonferroni. Major results: There were 3397 cases of hypothyroidism and 153791 ctrl subjects in the DBDS, giving a prevalence of 2.2%. 85% of cases were female, while among ctrl 50% were female. Average age of cases was 52±13 years (mean±SD) for women and 58±13 for men, while ctrls were 45±13 and 48±14 years, respectively (both P<0.001). BMI among cases were: 25.8±4.7 for women and 26.8±3.9 kg/m2, while cases were 25.1±4.4 and 26.0±3.6, respectively (both P<0.001). TSH levels were, for female cases: 4.6±4.0 iu/mL and 5.7±4.9 for men, while ctrls were 1.8±1.1 and 1.7±1.1, respectively (both P<0.001). Free (F) T4 levels were, for female cases: 14.4±6.4pmol/L and male: 14.0±4.6, while ctrls were: 14.8±4.5 and 15.0±3.9 respectively (P<0.003 for females, P<0.0001 for males), while FT3 levels were for cases: 4.3±1.7 and 4.3±1.4 pmol/L and 4.5±2.0 and 4.7±1.5 for ctrls (both P<0.0001). Conclusion: Hypothyroidism is less prevalent among blood donors than reported in the general Danish population, which is accordance with ‘the healthy donor’ bias. Hypothyroid donors were on average older and with higher BMI than normothyroid controls. Donors with hypothyroidism were generally well regulated, but despite that FT4 and FT3 levels were lower than ctrls. Presentation: 6/1/2024

12265 Isolated Adrenocorticotropic Hormone Deficiency In The Setting Of Anti-PD1 Immunotherapy

Abstract Disclosure: J. Poncelet: None. Q. Wang: None. A.J. Montero: Advisory Board Member; Self; AstraZeneca, Gilead. Other; Self; Medical Advisor for Paragon Infusion Services. L. Tranchito: None. Isolated Adrenocorticotropic Hormone Deficiency in the Setting of Anti-PD1 Immunotherapy Introduction: Immune checkpoint inhibitors have been associated with endocrine immune-related adverse events, such as secondary adrenal insufficiency with isolated ACTH deficiency in rare instances. Case Presentations: We present two different cases of isolated ACTH deficiency (IAD) while on anti-PD1 therapy with pembrolizumab. Patient A is a 66-year-old woman with history of tobacco use, hypertension, and COPD diagnosed with stage IV lung adenocarcinoma. After completing 15 cycles of pembrolizumab, she reported symptoms of fatigue, weakness, lightheadedness, and was subsequently admitted to the hospital for symptomatic hyponatremia. Lab workup revealed a morning cortisol level of 0.6 ug/dL (n2.5-20 ug/dL) and ACTH <1.5 pg/mL (n7.2-63.3 pg/mL), both of which had previously been normal. Her TSH was mildly elevated with a normal free T4. Her FSH, LH, prolactin, and IGF levels were normal as was MRI of the pituitary. She therefore was diagnosed with IAD and started physiologic steroid replacement therapy with hydrocortisone with subsequent symptomatic improvement and normalization of her serum sodium. Patient B is a 60-year-old woman with a history of osteoporosis, aortic stenosis, and stage II triple negative breast cancer treated with neoadjuvant chemotherapy and pembrolizumab. Two months after starting immunotherapy, she presented to her oncology office with symptoms of fatigue, poor appetite, body aches, and dizziness. Her labs revealed mild hyponatremia, cortisol of 0.9 ug/dL (n2.5-20 ug/dL) and ACTH <1.5 pg/mL (n7.2-63.3 pg/mL). TSH, LH, FSH, and prolactin levels were normal. She started physiologic steroid replacement therapy with hydrocortisone for IAD, which led to improvement in her symptoms. Both patients continue pembrolizumab. Conclusions: Immune-related adverse events affecting endocrine pathways have been reported with immune checkpoint inhibitors. There is no method to predict which patients may be affected, and no guidelines exist on when or how often to monitor hormone levels in these patients. Importantly, patients can continue immune checkpoint inhibitors despite IAD if controlled by hormone replacement, though ACTH recovery should not be expected[1]. Recognition of symptoms can prompt earlier evaluation for secondary adrenal insufficiency and provide greater benefit to patients. 1.Schneider BJ, Naidoo J, Santomasso BD, et al. Management of Immune-Related Adverse Events in Patients Treated With Immune Checkpoint Inhibitor Therapy: ASCO Guideline Update [published correction appears in J Clin Oncol. 2022 Jan 20;40(3):315]. J Clin Oncol. 2021;39(36):4073-4126. doi:10.1200/JCO.21.01440 Presentation: 6/1/2024

8264 An Interesting Case of Hypophysitis in a Young Woman

Abstract Disclosure: A. Garcia: None. R. Sharma: None. C.M. Knight: None. Background Hypophysitis is an uncommon disorder and presents with clinical signs and symptoms along with biochemical abnormalities. Herein, we present a case of hypophysitis that responded well to high dose steroids. Case An 18 y.o black, adopted woman presented to hospital with complaints of headache and vision disturbances. Endocrinology was consulted for pituitary macroadenoma. Symptoms started a month prior. She had extensive work-up at an outside hospital including brain imaging, CSF analysis, and bloodwork. No definitive diagnosis was made and she was sent home on topiramate. Her symptoms continued to worsen prompting her to seek another opinion. No family history as she is adopted. She has a history of depression controlled with medication. MRI Brain showed 1.8x1.1x1.6 cm T2-enhancing mass with suprasellar extension deforming the midline optic chiasm. Initially, a diagnosis of macroadenoma was made and Endocrinology and Neurosurgery services consulted. Patient denied galactorrhea, menstrual abnormality, polyuria, polydipsia, cold intolerance, orthostasis, or weight gain. Bloodwork was significant for low TSH (0.045 uIU/ml; normal 0.35-4.94), low free T4 (0.58 ng/dl; normal 0.76-1.79). Thyroid functions were normal approximately one year prior. Cortisol was very low at 1.8 mcg/dL and ACTH inappropriately low-normal at 12 pg/ml (normal 6-50). LH and estradiol were low, while FSH was low normal. Prolactin, GH, IGF-1, sodium, glucose and creatinine were normal. Endocrine reviewed the previous MRI brain done four weeks ago that was reported as normal. Discussion with previous outside hospital radiologist suggested that pituitary was indeed not normal but was fuller with convexity towards chiasm although no definitive adenoma was found. Since it is unlikely that such adenoma would develop over 4 weeks, Endocrinology reached out to our radiologist who assessed this as pituitary enlargement due to likely hypophysitis, especially when compared to imaging 4 weeks ago. Further work up showed mildly-elevated ESR, and normal ACE, dsDNA, ANA, and Sjogren’s antibody levels. Tests for pregnancy, Lyme disease, tuberculosis, EBV and syphilis were negative. SARS-CoV-2 was negative for COVID. IgG4 levels were normal. CSF analysis was normal. She was started on levothyroxine and high-dose corticosteroids with improvement in her symptoms. Repeat imaging after 5 days of corticosteroids showed about 30% decrease in pituitary size. A diagnosis of likely lymphocytic hypophysitis was made and pituitary surgery averted for time being. Conclusion We present a case of possible lymphocytic hypophysitis in a young woman who avoided pituitary surgery due to diligent history and examination, in addition to a multidisciplinary team approach. It is very important to have prompt multidisciplinary approach if there is any doubt about a diagnosis as in this case. Presentation: 6/3/2024

7039 Isolated Gonadotropin Deficiency Transmitted From Mother to Daughter Conceived Through Assisted Reproduction Due Newly Identified, Autosomal Dominant Mutation Within the SOX10 Gene

Abstract Disclosure: S. Bakjaji: None. R.P. Hoffman: None. Title: Isolated gonadotropin deficiency transmitted from mother to daughter conceived through assisted reproduction due newly identified, autosomal dominant mutation within the SOX10 gene. Objectives: We report a case of genetic isolated gonadotropin deficiency occurring in a mother and in her daughter conceived through assisted reproductive technology using mother’s ovum. Methods Case report Results: The daughter was initially seen at 12 years 0 months for evaluation of short stature and concerns she had not grown in the last year. She was otherwise in good health and reported normal sense of smell. At the time of assessment, her height was 132.6 cm (0.61 percentile; Z=-2.5). The mother had been diagnosed with Kallmann’s syndrome and achieved pregnancy through ovarian stimulation. Her height was 152.4 cm, while the father's height was 177.8 cm. Two male siblings were born at the same time and were in normal health. Physical examination of the daughter was unremarkable. She had Tanner stage 1 pubic hair and Tanner stage 1 breasts. The growth chart displayed a notable deceleration in growth Laboratory results showed normal free T4 of (0.9 ng/dL) with slightly elevated TSH (8.348 uIU/mL), positive thyroid antibodies, normal IGFI at 164 ng/mL (normal range for Tanner I: 54 - 301) and IGFBP-3 at 5.8 ug/mL (2.4 - 8.4 ug/mL). The karyotype was 46 XX. Her peak growth hormone using glucagon-arginine stimulation was 12.8 ng/ml. When no pubertal development was seen over the next 6 months, GnRH stimulation testing revealed baseline LH of 0.04 mIU/ml and a peak of 1.78 and baseline FSH of 0.41 mIU/ml with a peak of 2.83. Bone age was 8 years 4 months.Over the next year her growth velocity was 4.8 cm/year and she remained prepubertal. Genetic testing done identified a new heterozygous sequence variant (c.226G>A) in the SOX10 gene which would lead to replacement of valine by isoleucine at position 76 and was thought to be damaging in silico. This variant was subsequently found to be shared with her mother but not her father. Conclusions: Most Kallmann’s syndrome or genetic isolated gonadotropin deficiency cases are due to autosomal dominant but spontaneous new mutations since infertility is usually present in those with the syndrome. This case emphasizes the importance of genetic counselling regarding inheritance risk when assisted reproduction technology using maternal ovum is used. Presentation: 6/2/2024

6601 A Case of Recurrent Painless Thyroiditis and Discussion of Management

Abstract Disclosure: M.C. Slack: None. S. Grock: None. Introduction: Painless (silent) thyroiditis is characterized as a subacute and generally self-limited disease process in which patients develop transient thyrotoxicosis, which is often followed by a hypothyroid phase before entering the recovery euthyroid phase. Given high frequency of positive thyroid antibodies, it may be autoimmune-mediated; recurrence is rare. Here we present a case of recurrent painless thyroiditis and discuss management options. Clinical Case: A Korean woman was followed by endocrinology from age 38 to 60 and experienced at least seven episodes of painless thyroiditis over this time. The episodes occurred without an identifiable trigger and were not preceded by viral illness. During episodes she developed palpitations, hair loss, and dyspnea on exertion and biochemical evidence of thyrotoxicosis with TSH suppressed to <0.2 mIU/mL (normal 0.3-4.7) and elevated free T4 levels as high as 5.4 ng/dL (normal 0.8-1.7). TSI, TPO, and TSH receptor antibodies were checked during multiple episodes and resulted negative, though thyroglobulin antibody was significantly elevated. A radioactive iodine uptake scan was obtained during an active episode of thyroiditis and revealed diffusely low uptake. The patient’s episodes lasted approximately two to three months before normalization of her TSH and FT4. She had at least one instance of transient hypothyroidism after thyrotoxicosis with a TSH of 13.2 and FT4 of 0.6 which subsequently normalized 6 weeks later. The patient did not have known cardiovascular disease and DXA scans revealed mild osteopenia with the lowest T-score -1.3. RAI was considered for the patient based on the total number and increasing frequency of her episodes. She ultimately declined treatment with RAI and continues to follow with endocrinology. Clinical Lessons: While the deleterious effects of prolonged hyperthyroidism (e.g. osteoporosis, arrhythmia, cardiovascular disease) are well known, it is unclear what risk recurrent painless thyroiditis episodes pose. As there are no guidelines regarding treatment, clinical gestalt incorporating frequency and duration of episodes, as well as symptoms, is often used to determine if definitive management is indicated. There are case reports in the literature of treatment of recurrent thyroiditis with RAI ablation performed during a euthyroid state, which eliminated recurrence of episodes but did lead to permanent hypothyroidism necessitating hormone replacement. Surgical thyroidectomy may also be considered in select patients. This case highlights the challenges in treating rare cases of recurrent painless thyroiditis given the lack of research or established guidelines. It is reasonable to consider the frequency, severity, and total number of episodes, as well as patient risk factors, symptoms, and preferences when making recommendations regarding management. Presentation: 6/1/2024

8278 Myxedema Coma With COVID-19 Infection

Abstract Disclosure: R. Kalas: None. V. Manohar: None. N.S. Bapat: None. Y. Kim: None. Myxedema coma is a rare medical emergency that occurs in severe hypothyroidism with a mortality rate reaching 60%. The hallmarks include depressed mental status and hypothermia, but hypotension, hyponatremia, bradycardia, and hypoventilation can also occur. This complication can occur in patients with a longstanding history of severe hypothyroidism especially when precipitated by an acute event such as infection, myocardial infarction, or surgery. Prompt recognition and treatment of the condition is important to prevent fatal outcomes. We present a case of myxedema coma in the setting of COVID-19 infection and nonadherence to medication. A 91-year-old woman with history of hypothyroidism, hypertension, coronary artery disease, cardiomyopathy, and chronic obstructive pulmonary disease presented with dyspnea. Her home medications included levothyroxine 75 mcg daily, which she reported not taking for at least 3 weeks. Vital signs revealed a normal heart rate and blood pressure of 84 beats/min and 137/78 mmHg, but the patient was hypothermic to 35.7 °C. On exam, she was somnolent. Labs were notable for markedly elevated TSH level of 111 (0.380 - 4.700 uIU/mL), low free T4 level of 0.57 (0.93 - 1.70 ng/dL), random cortisol level of 25.5 (6.2-18.4 ug/dL), and positive SARS-COV-2 PCR test. Chest x-ray revealed bilateral lower lung parenchymal consolidations and arterial blood gas revealed a pH of 7.29 and pCO2 of 52.5 (35-45 mm Hg), indicating hypercapnia. She was treated for COVID pneumonia and given concern for COVID induced myxedema coma she was given IV levothyroxine 100 mcg for 2 days, after which the patient’s hypothermia and somnolence improved, with an improved repeat free T4 level 0.87 ng/dL. She was subsequently transitioned to oral levothyroxine 112 mcg daily and discharged after improvement of her COVID symptoms. Myxedema coma is a rare complication of decompensated hypothyroidism, frequently triggered by an infection. Thyroid hormone plays an important role in regulating both the innate and adaptive immune systems. As a result, individuals with hypothyroidism are at increased risk of acquiring infections, which can further lead to myxedema coma. COVID-19 infection has been associated with thyrotoxicosis, thyroiditis and hypothyroidism. Given the associated high mortality rate, regardless of the underlying precipitant, prompt diagnosis and early administration of thyroid hormone replacement therapy is crucial to improve outcomes. Presentation: 6/3/2024

8747 A Rare Receptor Resistance with Paradoxical Outcomes!

Abstract Disclosure: I. Patoli: None. S. Batool: None. A.S. Gill: None. A. Makdissi: None. Introduction: Resistance to thyroid hormone receptor is an uncommon cause of abnormal TFTs. (1) We present an interesting case of THRB resistance with cardiac arrhythmia (CA). Clinical Case: 46-year-old man with history of atrial fibrillation (Afib) was referred to endocrinology for evaluation of abnormal TFTs and thyroid nodule. He had a recent hospital admission for Afib with rapid ventricular response; 3 years ago, he was treated with amiodarone for 2 months. TFTs revealed normal TSH of 1.375, elevated FT4 of 2.76 (normal ranges 0.55-4.78 and 0.89-1.76, respectively). Neck CT scan showed large peripherally enhancing centrally necrotic mass with calcification encompassing nearly the entirety of left thyroid lobe measuring 2.2 x 3.6 x 4.6 cm. A 0.8 cm hypodensity within right thyroid lobe also visualized. Thyroid ultrasound showed nodules bilaterally with the largest one in the lower pole of left lobe. FNA biopsy showed Bethesda category- II benign, benign appearing follicular cells and abundant colloid. Repeat labs showed similar results with persistently elevated free T4 (2.56) with equilibrium dialysis, normal alpha subunit, normal TSH (2.14) with human anti-mouse antibody (HAMA) antibody was negative. Alpha subunit:TSH ratio was <1. He remained clinically euthyroid over the course of 1.5 year but repeat labs at that time indicated that TSH had increased to 17 with elevated free T4 (2.6) . MRI brain ruled out TSH secreting adenoma. He reported thyroid abnormalities in son and brother but was unable to provide details. He was referred for genetic screening which showed THRB with pathogenic variant: c.9628> G (p.Y321C). Conclusion: THRB resistance is an uncommonly diagnosed modality in endocrinology. The genes encoding thyroid hormone receptors are THRα gene and THRβ gene (2). Patients with inherited THRB pathogenic variants present with resistance to thyroid hormone and often enlarged thyroid gland. Interestingly, despite having receptor resistance, patients may manifest with CA. This is hypothesized to be due to elevated T4 and T3 concentration in the heart which primarily has higher expression of THRA (3). The diagnosis of thyroid hormone resistance is important to avoid treating asymptomatic patients where treatment is not warranted.

8230 Adrenal Crisis, Unrevealing the Impact of Immigration on Central Adrenal Insufficiency

Abstract Disclosure: D.H. Sacoto: None. K. Madani: None. D. Patel: None. A. De Rosairo: None. G. Rai: None. R. Belokovskaya: None. A.A. Franco-Akel: None. Introduction: Even though patients with secondary adrenal insufficiency (AI) may go through life without an episode of adrenal crisis, there is a 50% chance of developing it. Around 90% have a known precipitating, with infections and surgery being frequent causes. However, emotional stress is unrecognized. With the recent increase in worldwide immigration, it is important to recognize these as potential triggers in those with AI. Here, we present a case of adrenal crisis triggered by immigration. Case presentation: A 41-year-old female diagnosed eighteen years ago with Sheehan syndrome, with unknown replacement therapy status, is brought to ED for altered mental status. One week before, she crossed the Mexican-US border as an illegal immigrant and was hospitalized in Arizona after developing mutism and mood lability. She was initiated and discharged on hormone replacement therapy. She arrived in New York confused with flat affect and impaired recent memory. She was hypotensive (BP: 92/64 mmHg), hyponatremic (Na: 133 mEq/L), and anemic (Hb: 10.6 g/dL). She had an inappropriate normal ACTH of 25 pg/mL (7.2-63.3 pg/mL). MRI findings confirmed empty sella, suggestive of central AI. Additional studies revealed central hypothyroidism (low normal TSH (1.36 uIU/mL), low-normal Free T4 (1.4 ng/dL), gonadotroph dysfunction with low FSH (2.7 IU/L), and low estrogen levels (20 pg/mL) for her age, and low normal prolactin (4.6 ng/mL). After initiating a stress dose of IV hydrocortisone and IV levothyroxine, her affect, memory, mental status, and vital signs (BP: 128/80 mmHg) improved. She was educated regarding the need for maintenance doses as an outpatient. At the one-month follow-up, she continued with a positive response. Discussion: Patients with chronic AI are unable to produce sufficient cortisol and are at risk of acute adrenal crisis when under stress. Stressful situations, including accidents, job interviews, or death in the family, have been described. However, with almost doubling the number of people entering the US without prior authorization between 2022 and 2023, immigration, which poses physical and emotional stress, certainty will become a matter of importance for those with AI. Guidelines to manage cortisol replacement in times of fever, infections, trauma, surgery, or severe pain are available. However, it is more difficult to define how emotional and psychological challenges affect the stress response, mainly because each challenge is unique. Therefore, it is important to advocate for policies to provide medical alert bracelets to immigrants with known AI in addition to providing education about emergency injection kits in cases of impending crisis. Presentation: 6/3/2024

12452 Unraveling An Intriguing Clinical Sequence: Thyrotoxicosis Antecedent To Stiff Person Syndrome

Abstract Disclosure: A. Jain: None. M.N. Rayan: None. Title: Unraveling an Intriguing Clinical Sequence: Thyrotoxicosis Antecedent to Stiff Person Syndrome Background: Stiff Person Syndrome (SPS) is an autoimmune phenomenon resulting in the progressive rigidity of limbs and trunk muscles. It is associated with GAD-positive antibodies in the CSF and serum and is linked to Type 1 Diabetes, Celiac disease, and other autoimmune diseases. Clinical Case: A 34-year-old female with no past medical history was brought into the ED by family for paranoia, suicidal ideations, and visual and auditory hallucinations. She was found to be tachycardic and altered in the ED. Endocrinology was initially consulted for concerns of hyperthyroid pathology due to lab work showing a TSH of <0.008 uIU/mL and free T4 of 4 pg/mL. Thyroid ultrasound revealed heterogeneous, hypervascular thyroid tissue. Further investigation revealed TRAB 4.05 IU/L (n 0-0.9 IU/L) and TSI 3 IU/L (n < 0.577 IU/L). A diagnosis of Graves’ disease was made, and she was started on methimazole 20mg daily and metoprolol 25mg daily. Due to a lack of response to methimazole, other organic causes were investigated including psychiatric and neurological etiology. The patient's symptoms continued to worsen, with new tremors of the upper and lower extremities. Thyroid labs showed improvement, and hence thyrotoxicosis was not thought to be the underlying etiology of her encephalopathy. Neurology was consulted, and EEG and MRI Brain were performed which were unrevealing. Lumbar puncture revealed elevated oligoclonal bands and GAD-65 antibodies, suggesting autoinflammatory encephalitis. High-dose steroids were started, with no improvement. Due to the failure of steroids to treat her symptoms, she was given 5 days of plasmapheresis and a dose of rituximab. Slowly, the patient began to improve and could follow commands and communicate with staff. A formal diagnosis of SPS was made at this time. Upon seeing her in follow-up 1 month after discharge, her TRAB and TSI antibodies were negative, and she was able to be titrated off of methimazole. Conclusion: SPS is strongly associated with autoimmune diseases, with up to 30-40% having T1DM. The association between hyperthyroidism and SPS, however, is exceedingly rare and the etiology remains unclear. Presentation: 6/1/2024

SAT-520 Massive Thyroid Enlargement due to Langerhans Cell Histiocytosis

Abstract M. Barbera: None. M. Fasen: None. H.M. Lawler: None. M.T. McDermott: None. A.M. Elsheikh: None. Massive Thyroid Enlargement due to Langerhans Cell Histiocytosis Introduction: Langerhans cell histiocytosis (LCH) is a multisystem disease with diabetes insipidus (DI) being the most common initial manifestation. However, this case demonstrates a rare presentation of a massive goiter from LCH involvement of the thyroid gland causing respiratory distress which rapidly improved following treatment with trametinib. Clinical Case: A 27-year-old male presented with large central neck mass, stridor, dysphagia, night sweats, and dysphonia. Initial laboratory evaluation showed TSH 4.94 uIU/ML, with a free T4 of 0.64 ng/dL. Neck CT revealed diffuse enlargement of the thyroid gland with mass effect and lymphadenopathy. PET showed hypermetabolic thyroid gland which extended to the superior mediastinum and low level associated FDG uptake of bibasilar lung nodules. Biopsy of the thyroid mass resulted with lesional histiocytes with elongated, grooved nuclei, with intermixed eosinophils, CD207 (langerin) and CD1a-positive histiocytes in lesional tissues by immunohistochemistry consistent with LCH. Genetic testing was positive for BRAF mutation, exon 12, N486_P490 deletion. He was readmitted due to airway compromise and hypophysitis resulting in diabetes insipidus (DI), adrenal insufficiency (AI), hypogonadism, and hypothyroidism. He was initially treated with 10 mg of IV dexamethasone with minimal improvement, then transitioned to trametinib 2 mg daily resulting in rapid improvement of symptoms and thyroid size. Trametinib treatment was complicated by hyponatremia, skin lesions, and GI bleed for which treatment was held then decreased to 0.5 mg every other day. Repeat CT neck five months after treatment initiation showed complete resolution of thyroid enlargement and lymphadenopathy. Clinical lessons: Rarely, LCH presents with direct involvement of the thyroid gland making diagnosis difficult. This is further complicated by pathologic features that can be mistaken for papillary thyroid cancer and cooccurrence of other thyroid disorders. Given these challenges, it is necessary to consider LCH as a cause of thyroid goiter especially if the patient presents with DI and AI to prevent delay in diagnosis. This is particularly important when targeted therapy can be offered as in this case where trametinib resulted in rapid improvement of airway compromise. Reference:(1) Makras, P, Alexandraki, K, Chrousos, G, Grossman, A, and Kaltsas, G. Endocrine Manifestations in Langerhans cell histiocytosis. Trends in endocrinology and Metabolism. Vol 18 No. 6 (2) Mi, B, Wu, B, Fan, Y, Ka Seng Thong, B, Chen, Y, Wang, X, and Wang, C. Thyroid Langerhans cellhistiocytosis concurrent with papillary thyroid carcinoma: A case report and literature review. Frontiers in Medicine. DOI 10.3389/fmed.2022.1105152 Saturday, June 1, 2024

MON-567 Clinical Significance of Thyroid-stimulating Hormone Receptor Mutation on Fine Needle Aspiration

Abstract E. Skutnik: None. W. Kamran: None. S. Koshy: None. S. Shaik: None. Introduction: Patients with primary toxic goiters have decreased TSH levels and are less likely to foster malignancy in the thyroid due to inhibition of related oncogenes. Therefore, hyperfunctioning thyroid disorders were thought to be protective against thyroid malignancy. However, recent data has shown an increased incidence of thyroid malignancy in toxic goiter patients, 12-18%2. Thyroid-stimulating hormone receptor (TSHR) is a G protein coupled receptor that is expressed primarily in follicular cells. This receptor plays a critical role in thyroid cell proliferation and function. Mutations of the TSHR gene are seen in hyperfunctioning nodules, hyperfunctioning follicular thyroid cancers (FTC), and papillary thyroid cancers (PTC). High allelic frequency of the TSHR gene is associated with a higher risk of cancer even when hyperfunctioning. In contrast, benign nodules are strongly associated with low allelic frequency of the TSHR gene3. Case: A 28-year-old female with mosaic turner syndrome and obesity presented with difficulty losing weight; thyroid lab work revealed TSH of 1.92 uIU/mL (0.45-5.33), free T4 of 0.82 ng/dL (0.61-1.12), and free T3 of 4.33 pg/mL (2.5-3.9). Thyroid ultrasound showed an enlarged mildly heterogeneous thyroid gland with multiple bilateral nodules, including a right lower hypoechoic solid nodule measuring 1.4 x 0.8 x 1.1 cm. She underwent fine needle aspiration (FNA) of this right lower nodule which resulted as Atypia of undetermined significance (AUS) . Afirma Xpression Atlas testing showed mutations of the TSHR p.M453T c.1358T>C (p.Met453Thr) genes with risk of malignancy estimated at 25%. No other mutations were identified. Nuclear medicine thyroid uptake scan showed a right lower lobe hyperfunctioning nodule without suppression of the rest of the thyroid gland. As the risk of malignancy in the hyperfunctioning nodule is low, the decision was made to monitor with thyroid labs and ultrasound without surgery. Discussion: TSHR mutations occur in about 5% of thyroid nodules that have intermediate cytology. Isolated TSHR mutations are rarely found in thyroid cancer. Twenty-two different TSHR mutations were identified and the most common one is M453T1. The inability to determine if a thyroid nodule is benign or malignant by cytology remains an obstacle in 20-30% of cases. Molecular markers have been developed to improve diagnostic yield and for prediction of thyroid cancer3. Although the clinical and diagnostic significance of TSHR mutation testing in FNA specimens remains unclear, in our patient finding a mutation with TSHR p.M453T on Afirma Xpression Atlas helped us determine further management. Monday, June 3, 2024

8791 A Case of Hyperfunctioning Thyroid Nodules Evaluated for Thyroid Metastasis in the Setting of Oropharyngeal Squamous Cell Carcinoma

Abstract Disclosure: M. Alashoor: None. J. Gogineni: None. A. Bakar: None. Introduction: Identifying and evaluating hyperfunctioning thyroid nodules in the setting of metastatic head and neck cancers represents a diagnostic challenge that may result in inaccurate identification of perithyroidal lymph node metastasis as malignant or metastatic thyroid nodules with standard workup. Case presentation: A 72-year-old male with a history of stage IV metastatic oropharyngeal squamous cell carcinoma, metastasized to the lymph nodes, lungs, mediastinum, and bilateral iliac bones. He was diagnosed two years ago and received chemotherapy, maintenance immunotherapy with pembrolizumab, and targeted palliative radiation therapy, with good clinical response. Restaging PET-CT two years later revealed local progression. During his workup, he was noted to have persistently abnormal thyroid function test with low TSH (0.03​​µIU/mL, n 0.3-5.33), normal free T4 (0.97ng/dL, n 0.60 - 1.40), mildly elevated free T3 (3.91pg/mL, n 2.5-3.9), negative thyrotropin receptor antibodies levels, negative TSI, negative TPO antibody, noted evidence of subclinical hyperthyroidism consistent over the past year. Radioactive iodine uptake demonstrated multinodular gland, mildly elevated 24-hour uptake of 28% consistent with hyperthyroidism, with decreased activity in the left lobe. Thyroid ultrasound revealed multiple probable malignant thyroid nodules, a 1.8 cm TI-RADS 5 lesion of the deep margin of the lower pole of the right lobe, and a 1.6 cm TI-RADS 5 lesion of the upper pole on the right lobe. He was treated with methimazole 5 mg. Further workup with fine needle aspiration demonstrated the right upper lobe nodule sample was positive for squamous cell carcinoma, findings suspicious for metastasis. He subsequently proceeded with radical tonsillectomy, right neck dissection, and right hemithyroidectomy. Surgical pathology results noted, right neck metastatic HPV-associated squamous cell carcinoma involving the lymph nodes with extranodal extension, right oropharyngeal HPV-mediated squamous cell carcinoma. The thyroid gland biopsy was significant for incidental papillary microcarcinoma 2mm, thyroid follicular nodular disease, without evidence of squamous cell carcinoma or metastatic infiltration. Post-hemithyroidectomy, his thyroid function normalized, and methimazole was discontinued. Conclusion: Thyroid metastasis from head and neck cancers represent a rare entity. In patients with a history of malignancy, evaluation of new thyroid masses remains crucial. While FNA is a sensitive method for detecting thyroid metastases, inaccuracies may occur, impacting the identification of thyroid nodules in the presence of local metastatic lymphadenopathy. Identifying squamous cell carcinoma in the thyroid can significantly influence the treatment plan of patients with metastatic carcinomas, therefore careful consideration must be undertaken on evaluation. Presentation: 6/1/2024

12238 A Case Of Drug-induced Vasculitis

Abstract Disclosure: C. Javier: None. M.H. Horani: None. Title: A Case of Drug-Induced VasculitisChristian Javier, DOMohamad Horani, MD Introduction: Graves’ disease is commonly managed with thionamides. These have rare but serious complications of drug-induced lupus-like syndrome and vasculitis. In patients who present with rheumatologic and inflammatory findings, it is important to consider the possibility of these complications . Case Presentation: We present a 30-year-old female with Graves disease, asthma, and hypertension with concerns for cough, body aches, fatigue, bilateral flank pain, erythema, itching and burning of the hands, in the setting of recent spontaneous miscarriage. She was diagnosed with Graves’ nearly 2 years ago and was started on methimazole, but discontinued due to adverse effects of the medication. She was then started on PTU. The patient had a seizure, and head CT revealed a left-sided 4 cm brain mass in the left frontal lobe. The patient was admitted to the ICU, intubated, and started on IV Decadron. Further imaging showed multiple enlarged lymph nodes in the axilla, mediastinum, and hilum. Her brain mass was biopsied showing acute inflammation with early acute necrosis and multifocal fibrinous vascular necrosis, which has been reported in ANCA vasculitis. She had undetectable TSH (0.35-5.0) and free T4 of 1.54 (4.87-11.72). She was also found to have proteinuria and AKI. At this point, PTU-induced vasculitis and drug-induced lupus were suspected and PTU was discontinued. She was found to have low complement levels (C3 40, C4 6.1), elevated p-ANCA (>1:1280), ANA (1:640), anti-histone IgG (2.3) dsDNA (1:160), SSB La antibodies (70), anti-Smith antibodies (319), anti-RNP antibodies (146). Renal biopsy is pending. After discontinuation of PTU and administration of IV steroids, her symptoms largely resolved and she was extubated and stable for discharge. Conclusion: In patients being treated for Graves’ disease with PTU, there are rare but life-threatening complications associated with this medication including lupus-like state or vasculitis with elevated ANCA antibodies. Common presenting symptoms of drug-induced vasculitis include fever, joint pains, myalgias, skin lesions, glomerulonephritis, cerebral angiitis, and pulmonary hemorrhage. The onset of vasculitis can occur at any time after starting medication, with one study showing an average onset of 36 months after initiation of therapy. Other case reports have demonstrated positive serologies for ANA and anti DS-DNA antibodies in those with PTU-induced lupus. Drug induced lupus can also occur in patients taking PTU, with kidney and CNS involvement being more uncommon. In those with p-ANCA associated vasculitis secondary to PTU, anti-GBM, antiphospholipid, and antinuclear antibodies can also be present. Presentation: 6/1/2024

6983 Pembrolizimab Induced Hypophysitis: Uncommon Side Effect Leading To Late Diagnosis

Abstract Disclosure: T. Chaudhary: None. O. Syed: None. A. Shridar: None. R. Kaur: None. O. Chaudhary: None. M.S. Zubair: None. Background: Pembrolizumab, an immune checkpoint inhibitor, has shown efficacy inducing remission in various malignancies. Associated immune-related adverse effects (irAEs) have been recorded but cases of concomitant hypophysitis and thyroiditis are rare. Clinical case: The patient is a 41-year-old male with a past medical history significant for metastatic melanoma of the left calf, status post sentinel lymph node biopsy and left inguinal lymph node dissection, treated with pembrolizumab for one year. He initially presented with a severe headache that was preceded by two months of fatigue and impaired concentration. CT and MRI head were both unremarkable while lab work was significant for cortisol 0.2 ug/dL and adrenocorticotropic hormone (ACTH) 1.1 pmol/L. A full hormone panel was ordered which showed normal insulin-like growth factor-1 (IGF-1), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Free testosterone was at the lower end of normal. Prolactin was elevated at 27.3 ng/mL. The thyroid function tests showed primary hypothyroidism with elevated thyroid stimulating hormone (TSH) at 109 uIU/mL, low T4 at 1.5 ug/dL, and low free T4 at 0.4 ng/dL. There were no signs or symptoms of posterior pituitary dysfunction. The patient was diagnosed with hypophysitis and started on hydrocortisone 20 mg once daily along with levothyroxine 175 mcg once daily. DEXA scan showed normal bone mineral density. Subsequently, the patient presented to our care and reported symptom improvement after taking the prescribed medication however he continued to develop fatigue by the end of the day. Therefore, hydrocortisone prescription was switched to 15 mg in the morning and 10 mg at noon. A repeat thyroid function panel, sex hormone binding globulin, and LH were ordered, to be followed up at the patient's next visit. The patient was also advised to wear a medical alert bracelet at all times moving forward. Conclusion: Due to non-specific symptoms at onset, hypophysitis can be undiagnosed or misdiagnosed therefore it is important to have a high clinical suspicion with patients on PD-1 inhibitors presenting with such symptoms. It is also imperative to order a full set of hormones as this patient had concomitant primary hypothyroidism. Presentation: 6/1/2024

7078 Diagnostic Obstacles in Thyroid-Stimulating Hormone-Secreting Pituitary Adenoma (TSH-oma): A Case Report

Abstract Disclosure: V.A. Mendpara: None. P.P. Rao: None. M.D. Lundholm: None. Background: Thyroid-stimulating hormone-secreting pituitary adenoma (TSH-oma) is a rare cause of hyperthyroidism, forming 0.5-3% of all functioning pituitary tumors and <1% of hyperthyroid cases. Here, TSH secretion is autonomous and unresponsive to the normal negative feedback of thyroid hormones, leading to inappropriate TSH, T4 and T3 elevation. In the absence of clinical symptoms it can be difficult to distinguish between thyroid hormone resistance (THR) and lab errors. Clinical Case: A 44-year-old Swahili-speaking female with a history of type 2 diabetes was admitted for hypoglycemia requiring insulin adjustment. In her workup, thyroid function tests were obtained, revealing normal or low TSH (0.28 mIU/L) and high free T4 levels (2.7 ng/dL). At outpatient follow-up, repeat labs showed elevated TSH, T3 and FT4 (5.22 mIU/L, 377 ng/dL and 4.7 ng/dL, respectively). She reported weight loss, occasional palpitations, and chronic insomnia but denied other symptoms. Graves' antibodies (TSI, TSHR Ab) were negative. On exam, she had a 30-40 gm, smooth, non-tender thyroid without adenopathy, and a BMI of 23 kg/m2. The initial differential diagnosis included TFT lab error, THR or TSH-oma. A FT4 by equilibrium dialysis was high at 7.8 ng/dL (1.1-2.4 ng/dL). N-telopeptide (NTX) and sex hormone-binding globulin (SHBG) were elevated, consistent with a true hyperthyroid state. Genetic testing for THR posed time and cost barriers. Elevated alpha-subunit levels (87 ng/mL, normal ≤1.8 ng/mL) with normal levels of other pituitary hormones prompted a pituitary MRI, unveiling a 4.7 cm suprasellar bilobed pituitary mass abutting the optic chiasm and invading the cavernous and sphenoidal sinuses. She denied peripheral vision loss or headaches. Hyperthyroidism was managed with methimazole until surgical intervention for the TSH-oma. A transsphenoidal resection was performed with histopathological confirmation of a TSH-staining pituitary adenoma. She was started on levothyroxine for central hypothyroidism thereafter. Discussion: It is challenging to find the cause of abnormal TFTs when patients are asymptomatic and the differential includes THR, lab errors or TSH-oma. Inaccurate diagnosis can lead to delays in care or unnecessary thyroid ablation or pituitary surgery. Conversely, early identification and appropriate treatment of TSH-omas can prevent neurological and endocrinological complications, such as optic chiasm compression, visual disturbances, headache and hypopituitarism. Despite a lack of convincing symptoms of hyperthyroidism, we used confirmatory labs (NTX, SHBG) to rule in biochemical hyperthyroidism along with alpha-subunit testing and pituitary MRI to solidify the TSH-oma diagnosis, leading to surgical intervention. This case highlights the vital steps in the diagnosis of a TSH-oma, emphasizing the need for logical evaluation and differentiation of this rare condition. Presentation: 6/1/2024

8534 Comorbid Autoimmune Thyroid Disease in a Parent-Child Pair with Resistance to Thyroid Hormone Beta

Abstract Disclosure: A.H. Smith: None. E. Grethen: None. Resistance to Thyroid Hormone Beta (RTHβ) is an inherited disorder caused by mutations in the gene encoding the thyroid hormone receptor beta protein, resulting in decreased binding affinity to triiodothyronine in certain tissues. An asymptomatic individual with RTHβ may demonstrate abnormalities in serologic evaluation of thyroid hormone markers. When other thyroid pathologies present with RTHβ, however, the diagnosis and management can quickly become complex. Below we discuss two cases, a parent-child pair, with different presentations of presumably the same RTHβ gene. Patient 1 is a 61-year-old male with a history of autoimmune thyroiditis several years ago, presenting for continuation of care; he has had levothyroxine doses gradually uptitrated to over 3 mcg/kg to normalize TSH despite persistently high free T4 levels. He also has a family history notable for six out of seven siblings with autoimmune thyroid disease. Patient 2 is a 44-year-old male who was evaluated for hypothyroidism and difficulty with levothyroxine titration. Prior to consultation, he underwent radioactive iodine ablation for presumed Grave’s disease, followed by total thyroidectomy due to persistent symptoms. Post-operatively, he required high doses of levothyroxine to maintain normal TSH levels; however T4 and T3 levels remained high. Both patients confirmed proper levothyroxine supplementation. Further analysis of both patients demonstrated mildly elevated TBG and normal alpha subunit. Patient 2 pursued genetic testing while patient 1 declined, revealing a heterozygous R320S mutation in the TR-beta protein. Further testing and genetic counseling were offered to other family members. Propranolol and levothyroxine supplementation were titrated accordingly; triiodothyronine administration was attempted but did not alleviate symptoms. These two cases demonstrate the increased risk of autoimmune thyroid disorders in patients with RTHβ and the unique challenges they pose in accurate diagnosis. Autoimmune thyroiditis in RTHβ, with goiter, elevated T4 and elevated T3 levels, can be easily confused with Grave’s disease, especially when TSH is suppressed during active thyroiditis. Timely diagnosis can aid in targeted management of sequelae, prevent ineffective treatments for comorbid conditions which may mimic other diseases, and provide anticipatory/preventive guidance for family members to help with screening. Presentation: 6/1/2024

8227 Complex Case of Myxedema Coma Complicated by Cardiac Arrest in a Geriatric Patient with Multiple Comorbidities

Abstract Disclosure: M. Parvez: None. L. Makahleh: None. S. Nagpal: None. A. Kavarthapu: None. V. Vedantam: None. Introduction: This case report details a rare instance of cardiac arrest in a patient with myxedema coma, a severe form of hypothyroidism. It highlights the diagnostic and therapeutic challenges in managing such complex endocrine emergencies. Case Presentation: A 70-year-old female with a history of hypothyroidism, type 2 diabetes, atrial fibrillation, pacemaker implantation, and COPD presented with a 3 day history of progressive lethargy and weakness. EMS found her with critically low blood glucose level of 20. History and Examination revealed non-compliance with thyroid medication and myxedematous features including moon-like facies, periorbital edema, generalized edema, elevated JVP, and cold extremities with sluggish capillary refill. In the ER, she was hypotensive, labs showed a significantly elevated TSH level of 30.55 (0.45-4.5), free T3 level of 1.2 (2.3-4.2), free T4 level of 1.12 (0.93-1.70), high lactate, metabolic acidosis, renal impairment, and liver enzyme elevation. These findings, coupled with the clinical presentation, led to the diagnosis of myxedema coma. The patient's critical state was further complicated by distributive shock, shock liver and oliguric AKI. Management included sodium bicarbonate infusion for severe acidosis, IV hydrocortisone, IV levothyroxine, and broad-spectrum antibiotics. Amiodarone was discontinued due to its potential contribution to acute liver injury and hypothyroidism. Despite interventions, she developed acute respiratory failure, requiring intubation and norepinephrine for low mean arterial pressure. Her renal function improved with pressor support, and her lactic acidosis resolved. She recovered quickly and was subsequently extubated. After stabilization, she was switched to oral levothyroxine and discharged. Shortly after discharge, she returned again with generalized weakness, confusion, and dysuria. ER evaluation revealed lethargy, hypotension, hypoglycemia, severe metabolic acidosis, and a UTI. She tested positive for Influenza. While in the ER, she had cardiac arrest, presenting with agonal breathing and PEA. CPR was initiated, achieving ROSC after two rounds and one dose of epinephrine. She was treated again with IV levothyroxine, and IV antibiotics. She recovered well and was discharged to rehab facility with re-education on compliance. Conclusion: This case exemplifies the complexity and challenges in managing a geriatric patient with multiple comorbidities, particularly in the context of myxedema coma. The intricate interplay of endocrine, cardiovascular, respiratory, and infectious complications necessitated a multifaceted and dynamic therapeutic approach. This case underscores the importance of compliance, vigilant monitoring, prompt recognition of complicating factors, and the need for a coordinated multidisciplinary approach in managing similar cases. Presentation: 6/2/2024

MON-536 Exogenous Cushing Syndrome Resulting from Undisclosed Dexamethasone in an Over-the-Counter Arthritis Supplement

Abstract S. Wagle: None. D. Abraham: None. Introduction: Exogenous Cushing syndrome is prevalent due to prolonged exposure to glucocorticoid-containing medications, often found in over-the-counter (OTC) products imported from overseas. We report a patient who developed Cushing’s Syndrome after self-medicating with an agent from Mexico called Artri King. Case Description: A 39-year-old female with a history of non-alcoholic fatty liver disease and arthralgia presented to the emergency department with epigastric pain, melena, 60 lbs weight gain, and bilateral lower leg swelling for 4 months. Her medications included Artri King for arthralgia (2 tablets twice daily for the last four months) and Spironolactone, for leg swelling. Vital signs revealed an elevated blood pressure of 141/108 mmHg and a BMI of 31.28 kg/m². Clinical examination revealed purplish wide striae, bruising, proximal muscle weakness, and peripheral edema. Laboratory testing showed a white blood cell count of 26.73 k/μL, a blood glucose level of 132 mg/dL, HgbA1C 5.9%, a cortisol level of 0.3 µg/dL, and an ACTH level of < 1.5 pg/mL. Her TSH was 3.07 mU/L with a free T4 of 0.6 ng/dL. Imaging studies, including computed tomography and magnetic resonance imaging, revealed a normal adrenal gland. Gastroscopy was unremarkable. An exogenous source for corticosteroids was suspected with suppressed ACTH levels and normal adrenal glands on imaging. Therefore, mass spec testing for corticosteroids was performed. Her serum dexamethasone level of 1076 ng/dL confirmed the diagnosis. Upon inquiry, the patient recalled that her symptoms began after starting the Artri King supplement. Discontinuation of Arti King for two days resulted in a cortisol level of 6.8 µg/dL suggesting rapid recovery of adrenal function. Discussion: Artri King, an OTC supplement marketed for joint pain in Mexico, recommends a dosage of two tablets three times daily. On April 20, 2022, the FDA issued public warnings against its use, as laboratory testing detected undisclosed amounts of dexamethasone and diclofenac, which were not listed on the product label. The presence of surreptitious steroids in supplements should be suspected in patients presenting with exogenous Cushing syndrome. Physicians should review self-administered supplements closely and counsel patients on the risks. Monday, June 3, 2024

8539 Curcumin a Double Edged Sword: A Case of Curcumin Induced Pituitary Macroadenoma Apoplexy

Abstract Disclosure: P. Balozian: None. D. Alfakara: None. M. Linz: None. <Curcumin, the active component of turmeric, exerts numerous beneficial anti-inflammatory, antiplatelet, and anticoagulant effects. Recent literature has shown however that curcumin inhibits proliferation and induces apoptosis of pituitary cells. Despite these findings, there are limited clinical cases reporting an association between curcumin and pituitary adenoma apoplexy.We report the case of a 39-year old G9P6A3 female with Hashimoto’s disease and class II obesity who presented with a constant bifrontal excruciating headache, blurry vision, photophobia, and nausea. She also had fatigue and amenorrhea for two years. Her exam showed normal vitals, decreased visual acuity, diplopia, and bitemporal hemianopsia. Data showed a serum prolactin of 69 ug/L , plasma IGF-1 of 133 ng/ml (Z score -0.4), TSH of 2.58 with a free T4 of 0.47 ng/dl [0.61-1.12 ng/dL], a random cortisol of 12.7 mcg/dl despite her stress and pain, ACTH of 27 pg/ml, DHEA-S of 46 mcg/dl, an LH of 0.5 IU/L, and an FSH of 4mIU/ml with an estradiol of 25 pg/ml. MRI of the pituitary revealed a 1.8 cm macroadenoma with a mass effect on the overlying optic chiasm and a T1 intrinsic hyperintense signal indicative of a hemorrhagic component. She was given IV dexamethasone for 24 hours then underwent transsphenoidal resection of the hemorrhagic tumor that resulted in rapid resolution of headaches and visual symptoms. She was not given any glucocorticoids during or after surgery. Labs immediately after surgery revealed a prolactin of <1ug/L and a cortisol of 26.7 mcg/dl. Pathology showed corticotroph tumor with hemosiderin deposition with a 4.2% Ki67 and negative ACTH immunostaining. On medication review, patient had been taking large doses of curcumin. In the absence of other recent precipitating factors, it was highly likely that she had curcumin-triggered apoplexy of a pituitary macroadenoma. Most recent bloodwork, about 20 months from presentation, revealed a serum prolactin of 5.0 ug/L, IGF-1 of 123ng/mL (Z score -0.6), TSH of 0.97 mIU/L with a free T4 of 0.85 ng/dL, a random cortisol of 5.3 ug/dL, ACTH of 18.2 pg/mL, DHEA-S of 94 ug/dL, LH of 2.5 IU/L, FSH of 4.3 IU/L, and an estradiol of 45 pg/mL. Regular menstrual cycles had resumed. Headaches, nausea, and vision abnormalities completely resolved.The case illustrates the need to identify any herbal remedies and supplements a patient is taking, particularly turmeric, as supplements may contribute to increased bleeding tendency of an already existing adenoma. The case also emphasizes the potential rapid recovery of pituitary function after surgical resection of an apoplectic pituitary tumor.> Presentation: 6/3/2024