History Of Hypertension Research Articles

7944 Elevated Serum Alkaline Phosphatase without other Abnormalities of Liver Associated Enzymes as an early Indicator of Glucose Intolerance: A Case Series

Abstract Disclosure: B.K. Bowens: None. C. Godar: None. D. LaChance: None. T.D. Hoang: None. M.K. Shakir: None. Glucose intolerance (GI) is defined as dysglycemia and includes impaired fasting glucose, impaired glucose tolerance, and prediabetes. Early detection of GI could lead to appropriate treatment and delay the progression to diabetes mellitus. The cases below detail two patients with elevated serum alkaline phosphatase (ALP) without other liver-associated enzyme abnormalities as an early indicator of GI. Case 1: A 54-year-old woman with a history of multinodular goiter status post thyroidectomy (2020), adrenal incidentaloma (2016), and asthma was incidentally found to have an elevated HbA1C (A1C) of 6.3% on screening labs in 2015. At that time, her ALP was 73 IU/L (ref 44−121). Her ALP levels slowly rose from 88 to 152 IU/L by September 2020. Work up did not reveal any etiological factors for the elevated ALP. One month later, HbA1C was found to be 7.6%. Metformin was initiated with improvement in A1C to 6.3% with an ALP of 130 IU/L. However, metformin was discontinued due to intolerance. In April 2023, her A1C was 9.3% with an ALP of 134 IU/L. A1C rose to 12.8% in Jun 2023 at which time she was started on insulin glargine, insulin aspart, sitagliptin, and was restarted on metformin. Her A1C decreased to 8.6% in August 2023 with normalization of ALP to 88 IU/L. Case 2: A 53-year-old woman with a history of hypertension, hyperlipidemia, obstructive sleep apnea, and non-ischemic cardiomyopathy in 2004 was found to have an elevated A1C of 5.8% on her screening labs in Jun 2019. Her ALP was notably in the high-normal range until Oct 2021 when it was found to be 138 IU/L. Her most recent A1C was 5.9% with an ALP of 142 IU/L. The patient was started on semaglutide (WegovyTM) briefly but was unable to tolerate the side effects. She was then started on metformin 500mg BID and dulaglutide with normalized ALP level. Discussion: Emerging evidence has shown that serum ALP activity is modestly increased in cardiometabolic diseases such as type 2 diabetes, dyslipidemia, hypertension, and peripheral arterial disease. These are increasingly being considered as inflammatory disorders and it has been shown that serum ALP level was positively and independently associated with metabolic syndrome both in men and women. It is possible that ALP could be an indicator of non-alcoholic fatty liver disease (NAFLD) which is associated with GI. Typically, NAFLD presents with higher ALT and GGT, however, occasionally isolated enzyme elevations or no elevated enzymes at all may occur. Conclusion: These cases suggest that an isolated elevation in ALP could be indicative of GI. Patients incidentally found to have an elevated ALP should be worked up further for possible evidence of GI. Early detection of GI could delay progression to diabetes and decrease morbidity. Presentation: 6/1/2024

7947 Semaglutide Induced Pancreatitis: A Case Report

Abstract Disclosure: T. Altaweel: None. A. Mathew: None. P. Chalasani: None. L. Lawrence: None. S. Hussain: None. N. Aldaoud: None. Introduction/Background: As semaglutide (GLP1 RA) has become a cornerstone in diabetes and weight management, there have been studies indicating pancreatic inflammation with GLP1 RA use. We report a case of acute necrotizing pancreatitis secondary to semaglutide use.Clinical Case: A 52 year old male with a history of hypertension, morbid obesity with BMI of 40 kg/m2, alcohol induced pancreatitis presented to the hospital complaining of epigastric pain. On presentation, he appeared in distress due to pain but was hemodynamically stable. Physical examination revealed a moderately distended abdomen, tender to palpation over the epigastric area without guarding, and negative Murphy’s sign. The patient reported no alcohol consumption, tobacco usage, or recent abdominal injuries. Laboratory workup revealed elevated WBC 14.6 thous/mcL (4.5-10.5) and lipase 1941 U/L (<60). Abdominal ultrasound showed common bile duct 2 mm without gallstones and CT abdomen revealed acute pancreatitis with suspected necrosis in the pancreatic head and the pancreatic tail. Patient was started on aggressive fluid hydration, pain management and admitted to intensive care. Patient reported that he was started on semaglutide three months ago for weight management by his primary care physician. Patient improved symptomatically with pain control and tolerated oral intake. He was discharged home with recommendations not to resume semaglutide. Conclusion: Semaglutide involves direct stimulation of GLP-1 receptors in pancreatic cells, potentially leading to cell overgrowth, increased pancreatic weight, duct occlusion and inflammation. Despite the SUSTAIN-6 trial indicating no increased risk of acute pancreatitis in diabetic patients using semaglutide, atypical presentations of pancreatitis are noted in patients using the medication for weight management. When all identifiable causes of pancreatitis are eliminated, semaglutide-induced pancreatitis should be a primary consideration in the differential diagnosis. Physicians should exercise caution and give careful consideration when prescribing semaglutide for weight management in patients with conditions that increase risk for pancreatitis. Presentation: 6/2/2024

7112 A Case of Bilateral Adrenal Insufficiency Associated With Borderline Lupus and Antiphospholipid Syndrome

Abstract Disclosure: K.M. Hernandez Mendiola: None. Bilateral adrenal hemorrhage (BAH) is a rare condition leading to acute adrenal insufficiency with a mortality rate of 15%. Known etiologies include abdominal trauma, adrenal vein thrombosis, sepsis, shock, and anticoagulation. Systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) are uncommon conditions associated with BAH. We describe here a 79-year-old woman with a history of hypertension and a 23-year history of borderline SLE treated with hydroxychloroquine (HCQ) who presented at the ED with epigastric pain, diarrhea, and nausea. Six months before, HCQ was discontinued. The exam showed no abnormal findings, and an abdominal CT showed inflammation of the ascending colon. Augmentin was instituted, and the patient was sent home. After a week, the patient returned to the ED due to the persistence of symptoms, complaining of fatigue and right lower quadrant abdominal pain. Upon examination, the abdomen was soft but tender, with the CT suggesting pancolitis, while an MRI showed BAH. Laboratory findings included anemia, thrombocytopenia, elevated PT, low fibrinogen, and 11 mcg/dl cortisol. The patient was then admitted to the hospital, and hydrocortisone (HCT) therapy was initiated. After 12 hours of glucocorticoid initiation, cortisol level was 37 mcg/dl. On day 1, the patient remained hemodynamically stable. On day 2, a positive lupus anticoagulant was detected, with cortisol level dropping to 2 mcg/dl, warranting the continuation of HCT. From day 3 to 6, the patient suffered worsening coagulation and kidney functions. By day 7, an abdominal CT showed an extension of BAH. On day 8, the patient experienced a cerebral intraparenchymal hemorrhage and was transferred to the ICU, where, after two days passed away. The report presented here describes a catastrophic case of BAH associated with borderline SLE and APS in a patient who previously discontinued long-term treatment with HCQ, thereby enhancing the likelihood of a lupus flare-up. The adrenal glands are susceptible to thrombosis and hemorrhage due to their rich vascularity. In stress, the adrenals receive a significant blood volume, causing vascular congestion, potentially exceeding their capacity for venous drainage, and increasing the risk of hemorrhage. Autoimmune conditions, particularly SLE and APS, have been implicated in the etiology of adrenal hemorrhage. Antiphospholipid antibodies may bind to phospholipid-binding plasma proteins, promoting thrombosis in the adrenal vein by disrupting the coagulation fibrinolysis balance and the adrenal blood outflow, ultimately causing bleeding into the adrenal gland parenchyma. Although in this case, no cardiovascular collapse was observed, when unrecognized or undertreated, adrenal insufficiency complicating BAH can evolve into an adrenal crisis. Infections and medications that increase cortisol metabolism can also contribute to this complication. Presentation: 6/3/2024

5074 Licorice Root Supplement As A Cause Of Hypokalemic Hypertension

Abstract Disclosure: G. Gill: None. S.M. Harman: None. L.A. Robles: None. A 67-year-old female Veteran presented to an emergency room with a one-day history of high blood pressure, chest tightness, and exertional dyspnea. Her blood pressure was 162/90 mm Hg, pulse regular at 71 BPM, and pain level 5/10. She had a history of hypertension, stable on hydrochlorothiazide alone, hyperlipidemia, anxiety, and depression. Physical exam was benign. EKG revealed normal sinus rhythm at 60 BPM, normal axis, a prolonged QT interval of 510 ms, and no ST changes. Lab evaluation showed a low potassium of 2.4 mEq/L, sodium 145 mEq/L. Other lab measurements (CBC, liver function tests and cardiac enzymes) were within laboratory reference ranges. Medications included topiramate for migraine and over-the-counter supplements for constipation, “thyroid health,” and a topical “testosterone booster” prescribed by a non-allopathic practitioner. Her hypokalemia was attributed to hydrochlorothiazide and topiramate and both were discontinued. She was started on nifedipine for blood pressure control and 40 mEq/day of potassium for hypokalemia. Within 2 weeks of discharge, she presented again with elevated blood pressure and a plasma potassium of 4.0 mMol/L. Further history revealed that her constipation supplement consisted of licorice root (glycyrrhiza glabra) extract 900 mg per capsule, of which she took 3 to 4 capsules daily. The patient was advised to discontinue all supplements. Thyroid function tests were within normal limits. Due to a suspicion of hyperaldosteronism, the ED physician requested an abdominal CT scan which showed a 1 cm, -17.5 Hounsfield unit, right adrenal nodule. Also consistent with hyperaldosteronism, plasma renin activity (PRA) was suppressed at 0.07 ng/mL/hr. However, a serum aldosterone level was less than 1 ng/dL. Her 24-hour urinary metanephrines were normal and a 24-hour urine free cortisol was 31.6 mcg/dL. Morning plasma cortisol was 5.1 mcg/dL. A tentative diagnosis of licorice-induced hyperaldosteronism was made and the patient was treated with a taper of spironolactone. After discontinuing spironolactone, blood pressure was 116/70mmHg and serum potassium was 4.5 mMol/L with a PRA of 0.66 ng/mL/hr and serum aldosterone of <5.0 ng/dL. The syndrome of factitious hyperaldosteronism due to licorice consumption has been well described. The mechanism, inhibition of renal (type 2) 11-beta-hydroxysteroid dehydrogenase by glycyrrhizic acid, allowing cortisol to exercise its considerable mineralocorticoid action, is well understood. Most prior reports have been in patients habitually consuming licorice candy, usually imported, since conventional licorice sold in the U.S. is artificially flavored. Our report illustrates the importance of obtaining a history of use of over-the-counter supplements and assessing their ingredients and the fact that presence of an adrenal nodule and a low PRA does not always indicate endogenous hyperaldosteronism. Presentation: 6/2/2024

8409 Thyroid Nodules A to V: A Discussion on Thyroid Nodules and a Case Report of a Rare Thyroid Arteriovenous Malformation

Abstract Disclosure: M. Townsend: None. M. Brennan: None. C. Kazmierczak: None. P. Czako: None. Introduction: Thyroid nodules are an increasingly common finding on imaging, and the differential is broad. Arteriovenous malformations (AVMs) are a very rare cause of thyroid lesions, with only 6 reported cases to date. Given their scarcity, there is a lack of information regarding these lesions and how they are diagnosed and managed. Our case aims to address these gaps in information. Case: A 58-yo female with a history of hypertension was found by her PCP to have an enlarged left thyroid lobe with a new left sided bruit and palpable thrill. She had undergone prior thyroid ultrasonography for the enlarged left thyroid lobe which noted dilated and tortuous vascular structures at the posterior aspect of the left thyroid consistent with varices. These were being monitored clinically. Thyroid function tests were all normal. Due to concern for atherosclerotic disease, carotid ultrasound was obtained and showed patent carotid arteries with a large left sided thyroid mass. CTA of the neck revealed the mass to be a large (6.0 x 3.0 x 2.4 cm) AVM centered at the left thyroid gland. She underwent diagnostic angiography that confirmed the size of the mass and showed predominant arterial supply from the left superior thyroidal artery as well as bilateral inferior thyroidal arteries. Since the patient was asymptomatic with no reported neck pain, dysphagia or dyspnea, non-operative management with angioembolization was pursued given the risk of significant blood loss with surgical intervention. Following angioembolization, the results and adequacy of treatment are to be followed with repeat imaging given the high risk of reoccurrence. Discussion: AVMs of the thyroid are a very rare but clinically significant cause of thyroid lesions. Left untreated, they can grow in size and lead to compression of the esophagus or trachea, serious bleeding and high output heart failure. Their presentation is often non-specific and on routine thyroid imaging they can be difficult to differentiate from malignant tumors or varices, as in the case of our patient. Management prioritizes embolization, either alone or in conjunction with surgery, depending on the clinical scenario. Regardless of the treatment modality, reoccurrence rates remain high. Conclusion: Our case aims to add to the available information about thyroid AVMs and discuss the clinical presentation, challenges in diagnosis, imaging findings and treatment modalities available to manage these lesions. Presentation: 6/2/2024

6436 Adrenal Venous Congestion Clinically Mimicking Carcinoma In A Large Degenerated Adrenocortical Adenoma

Abstract Disclosure: K. Ishiwata: None. S. Suzuki: None. S. Watanabe: None. Y. Yamazaki: None. H. Sasano: None. K. Yokote: None. Introduction: A large heterogenous adrenal tumor is often malignant. Only eight reported cases of adrenal adenoma harboring hemorrhage or venous thrombosis have been reported but their details not. We encountered a case of large degenerated adrenocortical adenoma harboring adrenal venous congestion mimicking adrenocortical carcinoma. Case: Adrenal tumor was incidentally detected in a 71-year-old woman with a history of hypertension, dyslipidemia, and osteoporosis in her regular health check-up. Abdominal CT and MRI demonstrated a heterogenous mass measuring 7.6 cm with peripheral enhancement in the left adrenal gland. [1]3[1]I-adosterol scintigraphy revealed accumulation only in the left tumor margins with no accumulation in [1]8F-FDG-PET scan. Results of endocrinologic evaluation were consistent with subclinical Cushing syndrome. The large size and heterogeneous nature of the mass clinically suggested adrenocortical malignancy, and left laparoscopic adrenalectomy was subsequently performed. The resected left adrenal lesion was encapsulated and measured 6.5 x 6.3 x 5.8 cm appearing almost black and partially yellow on the cut surface. Microscopically, the nodule was composed of SF-1 positive, clear cortical cells with abundant hyaline stroma containing numerous dilated veins with CD31/34-positive endothelial cells, and no foci of necrosis or hemorrhage were detected. The tumor cells above were positive for steroidogenic enzymes including CTP17, HSD3β and CYP11B1 but negative for CYP11B2. Ki-67 labeling index was <2% in the tumor. The criteria of Weiss (0 out of 9) revealed that the tumor was cortisol-producing adrenocortical adenoma. Discussion: In this case, clusters of SF1-positive cortisol producing adrenocortical adenoma cells were present in the hyalinized stroma containing many dilated blood vessels. These findings indicated that those histological features were caused by ischemic degeneration due to intratumoral circulatory disturbance, which clinically simulated adrenocortical carcinoma. Conclusion: We have experienced a very rare case of cortisol-producing adrenocortical adenoma with adrenal venous congestion, resulting in marked enlargement of the lesion. Presentation: 6/3/2024

8354 OVARIAN HYPERTHECOSIS: AN UNCOMMON CAUSE OF HYPERANDROGENISM IN A POSTMENOPAUSAL WOMAN

Abstract Disclosure: M.D. Severino: None. F.P. Silva: None. M.V. Lopes: None. C. Nunes: None. M.I. Alexandre: None. M.J. Bugalho: None. Introduction: Severe hirsutism in postmenopausal women demands a careful clinical evaluation to exclude a malignant cause, such as adrenal or ovarian androgen-secreting tumors. Ovarian hyperthecosis is an uncommon and benign cause of hyperandrogenism and, consequently, hirsutism. It is caused by persistent testosterone synthesis due to proliferation of ovarian stromal cells and nests of luteinized theca cells. It occurs more often in postmenopausal women, as aromatization of testosterone to estradiol decreases due to the loss of granulosa cells. It is also frequently associated with obesity and insulin resistance. Clinical case: We present the case of a 61-year-old woman, with a history of hypertension and dyslipidemia, referred to Endocrinology Clinic due to a year long history of hirsutism, most severe on her face, chest, and abdomen. She also mentioned slight clitoromegaly. She had no other virilization symptoms such as acne, male-pattern alopecia, voice deepening or mammary atrophy. Her menarche occurred at the age of 14 and she had regular menses until menopause, at the age of 51. She had a BMI of 32 kg/m2 and an uncharacteristic phenotype. At observation, she had a mild hirsutism (Ferriman-Gallwey score of 9). This contrasted with the biochemical findings of severe androgenism - total testosterone of 366 ng/dL (reference values [RV] for women between 5-48) with free testosterone 7.8 pg/mL and SHBG 74 nmol/L (RV 32-128), resulting in a Free Androgen Index of 17,16 (RV <6.6). DHEAS, androstenedione, 17-hydroxyprogesterone and prolactin were normal, and gonadotropins were in the menopausal range. Blood tests also showed hyperinsulinemia and pre-diabetes with HbA1c 6,2%. She denied exposure to steroids in the form of new medication, supplements, or creams/gels (including second-hand exposure through her partner) and she had no exposure to other drugs with androgenic effect. Abdominal and pelvic CT scan, as well as transvaginal ultrasound, showed no adrenal or ovarian lesions. An ovarian cause was deemed the most likely and laparoscopic diagnostic bilateral salpingo-oophorectomy was performed. Gross pathology revealed ovaries of regular size, while histology showed bilateral ovarian stromal hyperthecosis. Testosterone levels returned to normal one month after surgery (14,2 ng/dL). Conclusion: Benign, ovarian causes of hyperandrogenism are uncommon in postmenopausal women, requiring a high index of suspicion. The diagnosis is difficult, and laparoscopic bilateral salpingo-oophorectomy is essential as both a diagnostic and therapeutic tool. Presentation: 6/2/2024

7659 Iodinated Contrast Induced Thyrotoxicosis Leading to Takotsubu Cardiomyopathy

Abstract Disclosure: A. Jain: None. E. Naous: None. S. Sedrakyan: None. A.T. Sweeney: None. Background: Thyrotoxicosis may cause many cardiovascular manifestations including tachycardia, hypertension, atrial fibrillation and heart failure. Iatrogenic exposure to iodinated contrast media (ICM) precipitating iodine induced thyrotoxicosis (or the Jod-Basedow phenomenon) is often overlooked. Here, we describe a case of iodine induced thyrotoxicosis leading to takotsubu cardiomyopathy, following multiple exposures to ICM. Case Presentation: An 88-year-old male with a history of hypertension, dyslipidemia, chronic obstructive pulmonary disease, and an ED visit one month ago for hemoptysis for which a CT Angiography (CTA) of the chest was obtained (which excluded Pulmonary Embolism(PE)), presented with fever and shortness of breath. On physical examination his temperature was 100.3F, heart rate was 104bpm, blood pressure 130/62mmHg, respiratory rate was 20/min and saturation was 88% (room air). He was frail but his examination was otherwise unremarkable. Electrocardiogram (EKG) revealed sinus tachycardia. Chest CTA excluded PE. Transthoracic echocardiogram (TTE) showed an ejection fraction (EF) of 73% and no wall motion abnormalities. He was admitted to the hospital for a viral upper respiratory infection and was treated conservatively with bronchodilators. Odynophagia prompted a CT with contrast of the neck soft tissue, which was unrevealing. He was planned to be discharged the next day, but overnight developed severe abdominal pain, and atrial fibrillation with a rapid ventricular response (Troponin t was 191 ng/L (normal {nl}: <9 ng/L)). EKG showed new T-wave inversions in the anterolateral leads, raising a suspicion of myocardial ischemia. A repeated TTE revealed a new drop in EF from 73 to 41%, with new apical akinesis, suspicious for takotsubo cardiomyopathy. CT of the abdomen with contrast was unrevealing. Lab results showed a suppressed TSH of <0.01uIU/mL (nl: 0.34-5.60 uIU/mL), elevated FT4 of 13ng/dL (nl: 0.93-1.70 ng/dL), and TSI 4.97 IU/ L (nl: 0-0.55 IU/ L). Endocrinology was consulted. His thyroid examination was normal, and he had no eye findings. Neck ultrasound revealed a homogeneous thyroid gland without any nodules. His clinical course was consistent with the diagnosis of acute thyrotoxicosis precipitating takotsubu cardiomyopathy. He likely developed iodine induced thyrotoxicosis from multiple exposures to ICM, in a background of previously undiagnosed Graves’ disease. Discussion: Screening for thyroid disease is critical in patients with new onset tachyarrhythmias and stress cardiomyopathy. Iodine induced thyrotoxicosis typically presents after patients with underlying thyroid disease are exposed to iodinated contrast. Prior to ordering studies requiring ICM, it is important to thoroughly evaluate patients for possible pre-existing thyroid disease. Presentation: 6/2/2024

12262 Pheochromocytoma Masquerading As An Acute Myocardial Infarction And Takotsubo Cardiomyopathy In A Hispanic Woman: A Case Report

Abstract Disclosure: A. Hoskote: None. J. Seidenberg: None. V. Gupta: None. Pheochromocytoma is a rare neuroendocrine tumor (<1 per 100,000 person-years) that occurs sporadically or due to mutations. While most patients do not have the classic headache, sweating and tachycardia, about 50% have paroxysmal hypertension and 90% have headaches. We present a rare case of pheochromocytoma masquerading as myocardial infarction (MI) and cardiomyopathy. A 67-year-old Hispanic female with history of hypertension and uncontrolled Type 2 DM, presented to the ER for chest pain and diaphoresis. Home medications were metformin, sitagliptin, lisinopril, simvastatin and aspirin. EKG showed non-specific ST elevations in chest leads without STEMI, and labs revealed a dynamic troponin and hemoglobin A1C of 13.6%. CT angiography ruled out pulmonary embolism. A left heart catheterization and echocardiogram revealed non obstructive coronary artery disease (CAD), a left ventricular ejection fraction of 25%, apical ballooning and a laminar thrombus. She was diagnosed with acute myocardial infarction and Takotsubo cardiomyopathy and discharged on metoprolol and apixaban. During our evaluation 7 months later, we noted several ER and hospital admissions for symptomatic hypertensive emergency with a pattern of labile blood pressures and on review of initial CT scan, a sequentially growing left adrenal mass (3.9cm 29HU) was present. A careful history using Spanish interpretation revealed episodic headaches, diaphoresis and palpitations. Subsequently, on two separate occasions, plasma normetanephrine was 2006 pg/mL (ULN<148 pg/mL) and urine normetanephrine was 12516 mcg/g cr (ULN <524 mcg/g cr). Prazosin was prescribed with stabilization of hypertension. An adrenalectomy is now scheduled. Symptoms of pheochromocytoma and paraganglioma (PPGs) are caused by hypersecretion of one or combinations of catecholamines: norepinephrine, epinephrine and dopamine. In one study 27% were discovered due to symptoms while 61% were found incidentally. PPGs occur in up to 1:500 patients with arterial hypertension and can also be a secondary cause of diabetes. MI and acute or chronic cardiomyopathy are rare presenting features of PPGs. Takotsubo cardiomyopathy is the most common phenotype. In one acute MI study, Hispanic women were significantly more likely to receive delayed care as compared to non-Hispanic women, due to misinterpretation of symptoms by patients and providers. A meticulous history with formal interpretation in patients with limited English proficiency can lead to prompt diagnosis of this surgically curable cause of hypertension. Pheochromocytomas rarely present as acute myocardial infarction and stress cardiomyopathy. A high suspicion for PPGs must be maintained in patients with labile hypertension, cardiomyopathy and an incidental adrenal mass. History should be carefully revisited especially in patients with limited English proficiency. Presentation: 6/3/2024

8354 Ovarian Hyperthecosis: an Uncommon Cause of Hyperandrogenism in a Postmenopausal Woman

Abstract Disclosure: M.D. Severino: None. F.P. Silva: None. M.V. Lopes: None. C. Nunes: None. M.I. Alexandre: None. M.J. Bugalho: None. Introduction: Severe hirsutism in postmenopausal women demands a careful clinical evaluation to exclude a malignant cause, such as adrenal or ovarian androgen-secreting tumors. Ovarian hyperthecosis is an uncommon and benign cause of hyperandrogenism and, consequently, hirsutism. It is caused by persistent testosterone synthesis due to proliferation of ovarian stromal cells and nests of luteinized theca cells. It occurs more often in postmenopausal women, as aromatization of testosterone to estradiol decreases due to the loss of granulosa cells. It is also frequently associated with obesity and insulin resistance. Clinical case: We present the case of a 61-year-old woman, with a history of hypertension and dyslipidemia, referred to Endocrinology Clinic due to a year long history of hirsutism, most severe on her face, chest, and abdomen. She also mentioned slight clitoromegaly. She had no other virilization symptoms such as acne, male-pattern alopecia, voice deepening or mammary atrophy. Her menarche occurred at the age of 14 and she had regular menses until menopause, at the age of 51. She had a BMI of 32 kg/m2 and an uncharacteristic phenotype. At observation, she had a mild hirsutism (Ferriman-Gallwey score of 9). This contrasted with the biochemical findings of severe androgenism - total testosterone of 366 ng/dL (reference values [RV] for women between 5-48) with free testosterone 7.8 pg/mL and SHBG 74 nmol/L (RV 32-128), resulting in a Free Androgen Index of 17,16 (RV <6.6). DHEAS, androstenedione, 17-hydroxyprogesterone and prolactin were normal, and gonadotropins were in the menopausal range. Blood tests also showed hyperinsulinemia and pre-diabetes with HbA1c 6,2%. She denied exposure to steroids in the form of new medication, supplements, or creams/gels (including second-hand exposure through her partner) and she had no exposure to other drugs with androgenic effect. Abdominal and pelvic CT scan, as well as transvaginal ultrasound, showed no adrenal or ovarian lesions. An ovarian cause was deemed the most likely and laparoscopic diagnostic bilateral salpingo-oophorectomy was performed. Gross pathology revealed ovaries of regular size, while histology showed bilateral ovarian stromal hyperthecosis. Testosterone levels returned to normal one month after surgery (14,2 ng/dL). Conclusion: Benign, ovarian causes of hyperandrogenism are uncommon in postmenopausal women, requiring a high index of suspicion. The diagnosis is difficult, and laparoscopic bilateral salpingo-oophorectomy is essential as both a diagnostic and therapeutic tool. Presentation: 6/2/2024

7564 Adrenal Pheochromocytoma In A Clinically Inapparent Adrenal Mass

Abstract Disclosure: L. Medina Mora: None. S. Htoo: None. A. Sanchez Ruiz: None. M. Harshan: None. A. Busta: None. Introduction: Pheochromocytomas (PCC) are rare tumors that arise from the adrenal medulla, with an estimated annual incidence of 0.8 per 100,000 person-years. These tumors have been associated with significant morbidity and mortality and are considered among the most life-threatening endocrine diseases, particularly if left undiagnosed. Its symptoms can be related to the tumor's mass effect or catecholamine excess. As a result, they can mimic other conditions, often leading to delayed or incorrect diagnosis. A study conducted on 296 patients with PCC treated from 2005 to 2016 found that 61% were discovered incidentally through cross-sectional imaging (CSI). The widespread use of CSI in recent years has led to the identification of asymptomatic cases that would have otherwise gone undetected. In this case, we present a middle-aged female who was incidentally found to have a PCC. Case Report: A 59-year-old female with a history of hypertension, cerebrovascular accident, pulmonary hypertension, systolic heart failure, mitral valve replacement, and asthma presented to the clinic for evaluation of a right adrenal lesion measuring 4.2 x 3.5 cm found during an emergency room visit during the evaluation of chest pain. She had no known family history of brain or endocrine disorders. Her lab results showed elevated plasma metanephrine and normetanephrine to 578.4 (reference range: 0-88) and 459.9 (reference: 0-244), respectively. Additionally, her 24-hour urine metanephrine was elevated to 984 mcg (normal range: 36-209), and Chromogranin A was 164.3 (reference range: 0-101). The rest of her labs, including cortisol, renin, aldosterone, and DHEA-S were unremarkable. A CT with and without contrast revealed a 3.0 x 3.5 x 5.1 cm solid non-calcified right adrenal mass measuring 39 Hounsfield units (HU). In addition, it measured 53 HU in the venous phase and 61 HU in the 15-minute delayed phase (relative washout of <1%; absolute washout of <7%). The patient was treated with alpha-blockers and underwent a robotic-assisted right adrenalectomy. The pathology was significant for a 5.4 cm well-differentiated PCC. The tumor had extended into but not beyond the adrenal capsule. The postoperative course of the patient was uncomplicated. Discussion: After a PCC is detected, the most effective treatment option is to surgically remove it. This procedure necessitates a combination of alpha and beta-blockade to regulate blood pressure and prevent a hypertensive crisis. Despite the success of surgery, there is still uncertainty about the optimal follow-up after the procedure, which often leads to many patients being lost during the process. Furthermore, even a decade after the initial surgery, there remains a substantial likelihood of illness reoccurrence or metastasis, making the situation even more complex. Therefore, it is crucial to adhere to a lifelong follow-up plan that includes annual biochemical testing. Presentation: 6/2/2024

5142 Pheochromocytoma In The ICU- Hiding In Plain Sight

Abstract Disclosure: N. Chandrashekar: None. B. Arafah: None. Introduction: Pheochromocytomas are catecholamine-secreting tumors that are rare but dangerous and occur in <0.2% of patients with hypertension. Case: A 28 year old female with a 10 year history of hypertension and invasive stage 2b cervical cancer s/p chemoradiation presented to the hospital with circulatory shock from Takutsubo cardiomyopathy requiring intubation, vasopressors, CVVH, and ECMO. The endocrinology service was consulted due to a highly vascular, 3.6 cm, ∼23 Hounsfield units right adrenal mass evidenced on CT abdomen done months prior to admission. There were elevations in plasma normetanephrine to 15 nmol/L (ref <0.90 nmol/L), plasma metanephrine to 1.5 nmol/L (ref <0.50 nmol/L), urinary metanephrine to 565 ug/24-hours (ref 36 - 209 ug/24-hr), and urinary normetanephrine to 2580 ug/24-hr (ref 95 - 449 ug/24-hr). With her acute illness and recent use of vasopressors and quetiapine, these labs could not be accurately interpreted, and outpatient follow up was recommended. She was discharged home on metoprolol and hydralazine for hypertension management by her primary team. She was re-admitted to the CICU 2 days later for hypertensive emergency with flash pulmonary edema. With further questioning, she endorsed longstanding hypertension with episodes of headaches, palpitations, and vomiting. Her cancer therapy related menopause caused frequent nighttime hot flashes while inpatient. These episodes precipitated witnessed symptoms of catecholamine release with severe hypertension and palpitations. It was noted during her hospitalization that her symptoms were controlled during the day with frequent escape during the night despite continuous alpha and subsequent beta blockade every 6 hrs. Estrogen therapy would have been beneficial, however given a recent DVT, this was avoided and instead megestrol acetate and venlafaxine were used. With these additions, her adrenergic spells completely resolved. She then underwent a right adrenalectomy and had no significant fluctuations in her BP intraoperatively with complete resolutions of symptoms postoperatively. The pathology revealed a right 2.7 cm pheochromocytoma with no local invasion or distant metastasis. Conclusion: This is a case of pheochromocytoma crisis with cardiogenic shock followed by subsequent hypertensive emergency in the setting of inappropriate beta-blocker use. Confounders like vasopressors (increases catecholamines), intrinsic stress of critical illness (increases catecholamines), and quetiapine use (can increase normetanephrine levels) make it difficult to analyze labs. In these cases, a thorough history and imaging are key to establishing a diagnosis and initiating life-saving treatment. Another unique feature of this case is the control of the patient’s triggering menopausal hot flashes with megace and venlafaxine to preempt adrenergic spells during her admission. Presentation: 6/2/2024

6637 A Rare Case of a Possible Non-functional (Clinically Silent Biochemically Negative) Adrenal Pheochromocytoma

Abstract Disclosure: V.K. Babu: None. M.T. Corwin: None. S.T. Olatunbosun: None. Introduction: Adrenal pheochromocytomas (pheo) are rare neuroendocrine tumors arising from the chromaffin cells of the adrenal medulla. Their incidence is around 0.8 per 100,000 patient years. They are usually sporadic, with about 40% having a pre-existing familial genetic disease. About 3% of adrenal incidentalomas prove to be pheo. They have a heterogenous presentation and are diagnosed by measuring urinary and plasma fractionated metanephrines (met) and catecholamines (catecho). The diagnosis becomes challenging in patients presenting with small tumors and normal levels of biochemical metabolites, as in our patient. Clinical Case: A 32-year-old male with no significant past medical history was referred to us with a left adrenal incidentaloma of 1.2 cm x 1 cm with 23 Hounsfield units during a non-contrast CT scan performed for abdominal pain. He denied spells of headaches, excessive perspiration, palpitations, history of hypertension, hypokalemia, history of kidney stones, fractures, muscle weakness, easy bruisability, new abdominal striae, change in weight, steroid use, or family history of endocrine tumors. MRI with adrenal protocol 3 months later showed a 1.2 cm x 1.4 cm left adrenal nodule that was markedly hyperintense on T2-weighted and hypointense on T1-weighted images without microscopic fat, suspicious for a pheo. It also demonstrated peripheral enhancement with progressive central filling on the delayed images without washout. Plasma met and catecho were normal: normetanephrines (normet) (45.2 pg/mL), met (36.4 pg/mL), epinephrine (epi) (34 pg/mL), norepinephrine (norepi) (295 pg/mL) and dopamine (<30 pg/mL). Subsequent 24-hour urine testing revealed normal met (155 mcg/day, 154 mcg/day), and normal normet (248 mcg/day, 236 mcg/day) on two separate occasions, and normal epi (9 mcg/L), norepi (36 mcg/day), and dopamine (228 mcg/day). The patient was subsequently referred to Endocrine Surgery for evaluation. Conclusion: Our patient likely has a non-functional pheo. Another possibility is an adrenal hemangioma, which would show discontinuous peripheral nodular enhancement in addition to progressive central filling. Patients with pheo less than 2 cm may present with normal biochemical testing. The size of a pheo is usually proportional to the levels of its biochemical metabolites. This case is unique because patients with a similar sized pheo are expected to have 3 times higher levels of plasma met and catecho, even if still within normal limits. It is important to take tumor size into consideration when interpreting labs to determine its functional status. This may help in determining the need for a pre-operative alpha blockade prior to adrenal surgery. A definitive diagnosis of a pheo’s non-functional status can only be confirmed after histopathological examination of the tumor tissue. Presentation: 6/3/2024

8437 Improved Quality Of Life&Blood Pressure Following Diagnosis And Medical Management Of Primary Aldosteronism (PA) / Georgian Experience

Abstract Disclosure: Q. Gvazava: None. N. Zavrashvili: None. N. Shonia: None. Improved Quality of Life and Blood Pressure Following Diagnosis and Medical Management of Primary Aldosteronism (PA) - Georgian Experience Introduction: PA is the most common cause of secondary hypertension which still remains as an underdiagnosed condition in many countries, including Georgia. The choice of pharmacological or surgical therapy depends on the results of computed tomography scans of the adrenal glands and adrenal venous sampling. In patients with bilateral aldosterone hypersecretion, the optimal is a low-sodium diet and lifelong treatment with a mineralocorticoid receptor antagonist administered at a dosage to reach a high-normal serum potassium concentration. Discussion: 60 y/o male with a 17-year history of hypertension. He was treated with 3 drug-program: valsartan, amlodipine, bisoprolol. BP was not adequately managed with systolic BP >140 mm/Hg. Patient had a history of hypokalaemia and required regular potassium supplements. Patient had never been evaluated for possible PA. We planned case detection test, which came up positive, with increased aldosterone, suppressed renin concentration and increased aldosterone-renin ratio. Abdominal CT performed 1 year ago for another reason revealed “normal” adrenals.After discussing treatment options patient preferred medical management and Eplerenone was started, dose titrated accordingly, K supplements were discontinued which over time resulted in decrease in requirement of his other antihypertensive medications, with BP adequately managed. Patient’s quality of life improved significantly, he has shared his test results and progress on his follow up visits; He is very grateful and feels content with the treatment. We present another case of 49 y/o male patient with a 19 year history of hypertension. Patient was treated with 4 drug-regimen: Valsartan, Hydrochlorothiazide, Amlodipine, nebivolol with average BP findings – 140/90 mm/Hg.Case detection test was positive with increased aldosterone, suppressed renin and increased aldosterone-renin ratio. Patient required confirmatory testing. Salt loading was done which confirmed the diagnosis of PA. On unenhanced CT of the abdomen, bilateral adrenal hyperplasia was found. Patient was started on Eplerenone, on follow up, his BP findings are significantly improved, number of BP meds are also decreased. Conclusion: Diagnosis of PA provides clinicians with unique opportunity to cure or effectively improve hypertension and hypokalaemia, as well as to prevent potential target organ damage and complications. That’s why the importance of increased awareness and having high clinical suspicion cannot be understated. Presentation: 6/3/2024

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

8081 Case report of sympathetic paraganglioma presenting as chronic catecholamine induced cardiomyopathy

Abstract Disclosure: Z. Tan: None. A. Taiwo: None. Background: Sympathetic paragangliomas are rare neuroendocrine tumors (<1/100,000) arising from extra-adrenal autonomic paraganglia, generally in the thorax, abdomen, and pelvis. They secrete catecholamines predominantly norepinephrine, which can cause a rare complication of catecholamine-induced cardiomyopathy. Clinical Case: A 33-year-old male, with history of obesity and borderline hypertension not on medication, presented with dyspnea on exertion, worsening paroxysmal nocturia dyspnea of 1 month duration and sudden onset of severe right flank pain. Work up for his chronic shortness of breath revealed: Troponin negative. EKG showed sinus tachycardia. Echocardiogram revealed enlarged left ventricle, severely decreased LV systolic function of 25-30%. Given the absence of angina symptoms, negative troponin, and EKG findings, his new-onset cardiomyopathy was presumed to be non-ischemic. CT chest, abdomen and pelvis was performed for the new onset right flank pain, which revealed a 4.1 cm x 4.0 cm centrally necrotic aortocaval soft tissue mass. This raise a concern about malignancy. A CT-guided Fine-Needle Aspiration of the retroperitoneal mass suggested paraganglioma. Further investigation showed plasma normetanephrine at 5.56 nmol/L (Reference range: 0-0.89 nmol/L), 24 hour urine normetanephrine at 2411 ug/d (Reference range: 114-865 ug/d), and 24 hour urine norepinephrine at 179 ug/d (Reference range: 14-20 ug/d). Plasma metanephrines and plasma dopamine were within the normal range. A gallium DOTATE PET/CT revealed a necrotic aortocaval mass with peripheral uptake, consistent with the known paraganglioma. He was diagnosed with sympathetic paraganglioma complicated with chronic catecholamine-induced cardiomyopathy and had exploratory laparotomy excision of his paraganglioma. Preoperatively, he was treated with phenoxybenzamine and carvedilol. However, his post-surgical course was complicated by acute on chronic heart failure and pneumonia, and he subsequently passed away from a pulseless electrical activity arrest. Conclusion: Although sympathetic paragangliomas rarely presents as catecholamine-induced cardiomyopathy, this case emphasizes the importance of considering hormonal abnormalities in patients who present with non-ischemic cardiomyopathy without high risk factors. Reference: 1. Alessandra Giavarini, Antoine Chedid et al. Acute catecholamine cardiomyopathy in patients with phaechromocytoma or functional paraganglioma. Heart 2013; 99: 1438-1444. Presentation: 6/2/2024

8800 A Case of Hypopituitarism Due to Sheehan Syndrome

Abstract Disclosure: N. Akabogu: None. S. Dejhansathit: None. F. Marium: None. B. Stanley: None. E.M. Bazuaye: None. L.S. Krusniak: None. L.G. Kurukulasuriya: None. U.Z. Khan: None. Background: Sheehan syndrome, which is also known as postpartum pituitary infarction, refers to the necrosis of the anterior pituitary gland due to postpartum hypovolemia, hemorrhage, shock, resulting in various degrees of hypopituitarism. The pituitary gland enlarges during pregnancy due to estrogen stimulation and becomes hyper-vascular, making it prone to infarction with postpartum hemorrhage. The initial symptoms include hyponatremia, weakness, weight loss, but the most prominent specific symptoms are inability to nurse and postpartum amenorrhea. Depending on the severity of hypopituitarism, symptoms may develop within the first few days to weeks after delivery or may take months to years to develop. Case presentation: 35year-old Caucasian female with a medical history of gestational diabetes, hyperlipidemia, and hypertension, who presented to the hospital with flu-like symptoms, leg pain, abdominal pain, and proximal muscle weakness. The evaluating hospitalist observed that patient appeared sluggish and spoke with a deep coarse voice, which concerned him for hypothyroidism. Thyroid function test revealed undetectable free T4 with inappropriately normal TSH of 1.38 – consistent with secondary hypothyroidism. Additional history from patient uncovered 9 months history of constant fatigue, weight gain, dry skin, hair loss, cold intolerance, and intermittent ankle swelling. There is no history of brain irradiation or head trauma. She has 4 biological children, and her last childbirth 3years ago was complicated by severe bleeding from her incision site, requiring transfusion of 6 units of blood. She has been amenorrheic since and is neither on birth control nor had hysterectomy. Physical exam showed mildly enlarged tongue, diffuse pallor, dry scaly skin on upper arms, scanty eyebrows, and slowed speech. Further work-up for pituitary insufficiency showed secondary adrenal insufficiency, secondary hypogonadism, low prolactin, and growth hormone deficiency. There was no evidence of AVP deficiency. Other lab and clinical findings were hypoglycemia, hyperlipidemia, elevated CK, elevated Cr, pericardial effusion, and diastolic hypertension. Pituitary MRI showed markedly attenuated and flattened pituitary gland with no focal mass. Patient was given stress dose hydrocortisone and thyroid hormone replacement, initially IV then oral. Following hydrocortisone and thyroid hormone replacement, her diastolic BP, hypoglycemia, CK, and Cr improved. Further management plans include initiating estrogen (plus progesterone) for bone health. Conclusion: Although Sheehan syndrome is rare in developed countries, it does occur. This case emphasizes the importance of detailed history taking, to discover the root of patients’ presentation. Even though TSH is the screening test for thyroid disease, when pituitary etiology is suspected, it is important to also check a free T4. Presentation: 6/1/2024

6702 Management And Complications Of Metastatic Adrenocortical Carcinoma Presenting With Severe Cushing Syndrome

Abstract Disclosure: S. Rodrigues: None. A.K. Sumal: None. Background: Metastatic adrenocortical carcinoma (ACC) presenting with Cushing syndrome (CS) is a complicated, aggressive disease that commonly requires multiple adrenal steroidogenesis inhibitors and chemotherapy to achieve hormonal and tumor control. Clinical Case: A 66-year-old man with a history of prostate cancer and hypertension presented with right flank and back pain, worsening type 2 diabetes, profound proximal muscle weakness, and 3+ lower extremity edema to his thighs. CT and PET-CT revealed a 10.9 cm right adrenal mass with pericaval lymphadenopathy and metastatic disease at the L2 vertebral body. Laboratory testing demonstrated evidence of hypercortisolism with elevated 24-hour urinary cortisol excretion (449 mcg/24h; n<45 mcg/24h), and abnormal 1 mg dexamethasone suppression test (cortisol 15 mcg/dL; n< 1.8 mcg/dL) with suppressed ACTH (<6 pg/mL; n=7-63 pg/mL). Surgical resection of the primary tumor was aborted intraoperatively given the discovery of new peritoneal metastases, which were confirmed by biopsy to be metastatic ACC. He was started on mitotane and osilodrostat to manage his severe CS. He was also started on dexamethasone, both to prevent adrenal insufficiency and to avoid influencing serum cortisol measurements used to assess disease control. However, given his significant peripheral edema and weakness, he was functionally unable to receive chemotherapy. Despite rapid uptitration of mitotane and osilodrostat over three weeks, his CS remained uncontrolled, and he was ultimately hospitalized for lower extremity paralysis and septic shock due to pyelonephritis. Repeat imaging revealed severe spinal canal stenosis from an L2 pathologic fracture, as well as worsening hepatic, osseous, peritoneal, and retroperitoneal metastases. After recovery from his septic shock, he was started on chemotherapy with carboplatin and etoposide while hospitalized, but his mitotane was intermittently held due to elevated transaminases. His hospital course was complicated by hypotension requiring pressor support, atrial fibrillation, hemoperitoneum, worsening anasarca, and acute kidney injury requiring continuous renal replacement therapy. Given his worsening condition that precluded him from further chemotherapy or palliative radiation, he elected to pursue comfort care measures and expired shortly thereafter. Conclusion: This case highlights the therapeutic challenges of metastatic ACC presenting with life-threatening CS. Simultaneous use of multiple adrenal steroidogenesis inhibitors is often required for control of hypercortisolism, and chemotherapy is equally necessary to manage tumor burden. However, as in this case, disease-related complications can limit treatment management and result in rapid deterioration. Thus, early diagnosis and prompt treatment of metastatic ACC presenting with CS is critical to prevent morbidity and mortality. Presentation: 6/3/2024

6984 New Onset Diabetes After Transplant: Need for Strict Glucose Monitoring

Abstract Disclosure: T. Chaudhary: None. O. Syed: None. M. Nawaz: None. R. Kaur: None. Introduction: Immunosuppressant use comes at a cost of challenging side effects, which are being discovered more as its use increases. One such example is our case of new-onset diabetes after transplant (NODAT).Patient presentation: A 36-year-old male with a past medical history of end-stage renal disease status post renal transplant (6/2023), hypertension, and hyperlipidemia who presented to the hospital in 10/2023 with fever, chills, and diarrhea. His vitals at that time were as follows: temperature 36.1C, blood pressure 148/84 mmHg, pulse 87 bpm, and a respiratory rate of 22. Lab work was significant for blood glucose 1144, anion gap 22, bicarbonate 13, potassium 7.3, Sodium 135, lipase 427, pH 7.3, urine ketones 80, HbA1C 11.5 %. CT scan of the abdomen revealed loss of peripancreatic fat and inflammatory changes surrounding the pancreas. His medication review included Tacrolimus 12 mg daily, Mycophenolate 500 mg BID, Valtrex 500mg daily, and fluconazole 200mg every other day. He was treated with 2 liters of normal saline bolus and started on maintenance fluid, and insulin drip as per DKA protocol. Calcium gluconate and an albuterol nebulizer were given for hyperkalemia. Tacrolimus and prednisone were held. Endocrinology and Nephrology were consulted. The patient was thought to have diabetes due to steroid use which were discontinued and the patient was discharged on subcutaneous insulin regimen and lower dose of tacrolimus. Despite discontinuation of steroids, patients continued to have raised glucose readings confirming the causative agent as tacrolimus. Conclusion: The current guidelines for post-kidney transplant patients recommend checking fasting blood glucose weekly for the first four weeks, then biweekly for two months, and then monthly thereafter. HbA1C should be checked every 3 months and if it is >6% then home glucose monitoring should be done as well. Although the frequency of these check-ups decreases, it is imperative for physicians to remember that patients can still develop NODAT months post-transplant. It is also essential to reinforce the importance of these glucose checks for the patient as missed diagnosis can lead to dangerous complications such as DKA. Presentation: 6/2/2024

5118 When Thyroid Gland Is Not Made Of Thyroid Cells

Abstract Disclosure: A. Bulut: None. L. Ma: None. J.P. Noordzij: None. S.Y. Lee: None. Introduction: Neurofibroma is a type of peripheral nerve tumor that can arise sporadically or be a part of neurofibromatosis type 1 (NF1), a rare genetic disorder. Neurofibromas within the thyroid gland are extremely rare. Here, we present the fifth reported case of primary neurofibroma of thyroid gland. Case: A 60-year-old woman with history of systemic lupus erythematosus and hypertension presented with enlargement of left thyroid gland. She was diagnosed with Graves’ disease 40 years ago, which was treated with right thyroid lobectomy one year after the initial diagnosis. Five years after the surgery, she had recurrence of her symptoms and received radioactive iodine ablation with subsequent hypothyroidism. On presentation to endocrine clinic, she had thyroid ultrasound (US), which showed surgically absent right thyroid lobe and enlarged heterogenous left thyroid lobe measuring 5.1 cm x 3.8 cm x 3.9 cm with scant blood flow without discrete nodules. In interim, patient developed dysphagia and globus sensation. Repeat thyroid US showed enlargement of left lobe to 5.6 cm x 3.7 cm x 4.7 cm. Patient underwent completion thyroidectomy. Surgical pathology showed neurofibroma (S-100+, CD34+ and MSA-) without any thyroid parenchyma. Whole-body scan revealed no other evidence of tumors. Patient was referred for genetic analysis. Discussion: Neurofibromas are benign peripheral nerve system tumors primarily consist of Schwann cells along with other components of perineurium. They can occur as a sporadic lesion which accounts for 90% of solitary neurofibroma cases or be a part of NF1 on rare occasions. NF1 is an autosomal dominant genetic disorder due to germline mutation in NF1 gene located on chromosome 17q11.2, whose manifestations include café-au-lait macules, Lisch nodules, skeletal abnormalities, neurological deficits, and other benign and malignant tumors. Neurofibromas are the hallmarks of NF1. There are only few cases in the literature reported neurofibromas adjacent to or originating from thyroid gland. To the best of our knowledge, there have been only four other cases reporting primary neurofibroma of thyroid gland, one of which developed from thyroid capsule. Our patient most likely has primary neurofibroma of thyroid gland given the lack of syndromic features, however, genetic testing is needed in order to rule out NF1. In conclusion, clinicians should consider neurofibroma in their differential in cases of enlarging thyroid gland or nodules, especially in the presence of other clinical features. Presentation: 6/1/2024