24-hour Urine Research Articles

6970 Severe Symptomatic Hypophosphatemia After Intravenous Iron Therapy: An Under-recognized Adverse Reaction

Abstract Disclosure: A. Morvant: None. O. Olajide: None. Introduction: Iron deficiency is a common condition that is often treated with intravenous preparations of iron supplementation. It has been documented in the literature that ferric carboxymaltose is the form of intravenous iron supplementation that is associated with the highest incidence of hypophosphatemia, when compared to other formulations of intravenous iron therapy. This case highlights a severe case of hypophosphatemia after ferric carboxymaltose therapy that led to multiple hospitalizations and required several months of oral and intravenous phosphorus repletion. Clinical Case A 36-year-old woman presented to the ED with severe diffuse arthralgias, generalized muscle weakness, and fatigue. Laboratory analysis revealed the following: phosphorus 1.2 mg/dL (2.3-4.7 mg/dL), 25-hydroxyvitamin D 13 ng/mL (25-80 ng/mL), parathyroid hormone 220 pg/mL (16-77 pg/mL), and calcium 8.5 mg/dL (8.4-10.5 mg/dL). She was admitted and started on intravenous and oral phosphorus repletion as well as oral ergocalciferol. She was subsequently discharged home on oral phosphorus and ergocalciferol supplementation, with a phosphorus level of 1.8 mg/dL. She was readmitted one day later with persistent arthralgias, myalgias, and severe fatigue, and found to have a phosphorus level of 1.1 mg/dL. Additional laboratory studies revealed the following: FGF23 41 pg/mL (<59 pg/mL) and 24-hour urine phosphorus 2191 mg/24hr (400-1300 mg/24hr). The patient notably had a history of chronic severe iron deficiency anemia due to menorrhagia and had been treated with intravenous iron sucrose infusions 7 months prior to her presentation. Due to adverse reactions to iron sucrose, this was switched to ferric carboxymaltose, and she had received two doses; one month and two weeks prior to her initial presentation. She was treated again with intravenous and oral phosphorus repletion and ergocalciferol and discharged after two weeks on oral phosphorus and ergocalciferol as well as thrice-weekly intravenous phosphorus infusions in the outpatient setting. She continued intravenous phosphorus infusions for about three months, and this was subsequently discontinued without recurrent hypophosphatemia. She is currently on low doses of oral phosphorus with normophosphatemia. Conclusion: Intravenous ferric carboxymaltose therapy can lead to severe and long-lasting, treatment-resistant hypophosphatemia due to increased urinary phosphate excretion. An increased awareness about this is needed by clinicians in treating patients who receive ferric carboxymaltose and monitoring phosphorous levels is crucial.

8082 Primary Hyperparathyroidism or Familial Hypocalciuric Hypercalcemia? Why Not Both?

Abstract Disclosure: C.A. Zmijewski: None. P.D. Greenberg: None. S.R. Saul: None. Background: Although considered two separate entities, primary hyperparathyroidism (PHPT) and familial hypocalciuric hypercalcemia (FHH) can present concurrently. Case: A 68-year-old male with hypertension was referred to Endocrinology for hypercalcemia and osteoporosis. The patient reported a long-standing history of intermittent hypercalcemia, first diagnosed at age 30 with a strong family history, both his father and son. He denied symptoms of hypercalcemia, history of nephrolithiasis and fractures, and was not taking calcium supplementations. Labs were notable for intermittent elevations in calcium, the highest being 10.9 mg/dL (8.5-10.5 mg/dL), in addition to phosphorus levels as low as 1.7 mg/dL (2.5-4.5 mg/dL). Vitamin D was replete at 50 ng/mL (32-100 ng/mL) and the highest parathyroid hormone (PTH) was 124 pg/mL (10-66 pg/mL). The 24-hour urine for calcium was 117 mg (100-300 mg) with a Ca/Cr 0.01. DEXA scan showed T scores -2.2 at the right femoral neck and -3.4 at the distal radius (Z score -2.3). Due to the significant osteoporosis, a work-up for secondary causes was completed and was unremarkable. The differential diagnosis for the osteoporosis, elevated parathyroid hormone, and intermittent hypercalcemia included PHPT vs FHH or possibly, a combination. Additional imaging included a renal ultrasound which was negative for nephrolithiasis, Sestamibi and 4D-CT which were both negative for a parathyroid adenoma. Genetic testing confirmed a mutation in the CASR gene. Due to the inability to localize a possible lesion, the decision was made to treat the osteoporosis with zoledronic acid. Conclusion: PHPT is a common endocrine disorder; approximately 100,000 people in the United States develop PHPT annually. Conversely, FHH is a rare endocrine disorder with an incidence rate of 1 in 78,000. PHPT occurs due to the over-secretion of PTH by one or more parathyroid glands. FHH is an inherited autosomal dominant disorder, most commonly due to an inactivating mutation in the calcium-sensing receptor (CASR) gene. Distinguishing PHPT from FHH is important because PHPT is cured with surgery while FHH does not require treatment. Hypercalcemia from FHH, as opposed to PHPT, is suggested by the absence of symptoms, a positive family history, normal or high PTH, and hypocalciuria. However, it can be challenging to separate the two especially in atypical presentations (PTH can be normal in PHPT and elevated in FHH, and Ca/Cr can be < 0.01 in PHPT). But what if these two conditions were to co-exist? Case reports have described patients with concurrent PHPT and FHH (parathyroid adenoma confirmed with pathology and CASR gene mutation confirmed with genetic testing). In these cases, parathyroidectomy can still be considered in co-existing PHPT and FHH to alleviate symptoms and prevent complications of hypercalcemia. Though a rare occurrence, PHPT and FHH have been shown to co-exist in prior case reports. Presentation: 6/1/2024

12376 Comparison Of 1 Mg Versus 2 Mg Dexamethasone Suppression In Obesity

Abstract Disclosure: H. Babu: None. A. Nawaz: None. A.J. Spiro: None. T.D. Hoang: None. M.K. Shakir: None. The overnight 1 mg dexamethasone suppression test (DST) is widely used to screen for Cushing’s Syndrome (CS), especially due to its low incidence of false negative results. Serum cortisol concentrations <1.8 µg/dL suggests adequate HPA axis suppression and usually excludes CS. Concentrations >1.8 µg/dL should be verified with a second test. However, the lack of suppression on DST has been documented previously in 1.46% to 15% of obese patients without CS. Previous studies have suggested simultaneous measurements of serum cortisol, ACTH, and dexamethasone levels after DST to ensure adequate suppression. In this retrospective analysis, we compared the plasma levels of ACTH, dexamethasone, and cortisol levels after 1 mg and 2 mg DST in healthy obese (class III) subjects. The study involved 6 subjects (2 males, 4 females, age 37.5 ± 8.79 years, BMI 43.65 ± 3.12 (kg/m2) who were referred for evaluation of abnormal weight gain. Exclusion criteria for these subjects included diabetes mellitus, pregnancy, history of CS, psychiatric disorders, chronic liver disease, chronic renal failure, malabsorption disorders and nephrotic syndrome. The exclusion of CS was done by history and physical examination showing the lack of specific clinical features of CS. Additionally, none of the subjects were taking drugs that interfered with CYP3A4 or oral contraceptives within 3 months preceding the study. None of the participants reported alcohol consumption of more than 30 g per day. Screening tests for CS involved 1 mg, 2 mg DST, LNSC and 24-hour urine cortisol levels. Results: Following 1 mg DST in 5 subjects, the mean serum cortisol levels were 1.35 ± 0.13 mcg/dL and the mean serum dexamethasone levels, and ACTH levels were 282 ± 44 ng/dL and 5.92 ± 1.56 pg/mL, respectively. However, in one subject (BMI 43.5) the post-DST cortisol level was 2.96 mcg/dL with corresponding dexamethasone level of 138 ng/dL and ACTH level of 21 pg/mL. However, following 2 mg DST in all 6 subjects the serum cortisol levels were less than 1.8 mcg/dL (1.21± 0.22 mcg/dL) with ACTH levels (3.87 ± 0.70 pg/mL) and dexamethasone levels of 482 ± 80 ng/dL. The LNSC levels were normal in 4 subjects (0.010 ± 0.005 mcg/dL), whereas in 2 subjects these were minimally elevated. 24-hour urine cortisol levels were normal in 5 subjects (29.4 ± 3.74 mcg) and in one subject this was mildly elevated (67 mcg). Long term follow-up of all subjects confirmed normal cortisol status. Previous studies have demonstrated that routine CS screening of patients affected by severe obesity is not indicated. However, other investigations have shown CS may occur in a small percentage of severe obese patients. In conclusion, 2 mg DST is a preferred test in obese patients suspected to have CS although 1 mg DST generally can be used as an initial screening test. Additionally, serum dexamethasone and ACTH measurements may still be useful in patients who are suspected to have a false-positive DST. Presentation: 6/1/2024

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

7183 Histoplasmosis Of Adrenal In An Immunocompetent Patient From Arizona: A Surprising Biopsy

Abstract Disclosure: R. Habibi: None. S. Penquite: None. N. Ebrahimi: None. R. Cardenas Lara: None. Introduction: Histoplasmosis of adrenal gland in the context of disseminated infection is a rare entity in a non-endemic area. Early diagnosis and treatment can save one’s life. Here we present a case of a patient from Arizona who was referred to us with a large adrenal mass initially resembling malignancy. Presentation: A 58-year-old male with no significant medical history from Bisbee Arizona presented to our clinic with significant weight loss of 120 pounds in 8months, jaundice, fatigue, nausea and vague abdominal pain. He had an abdominal CT scan in a rural area hospital which showed a left adrenal 4.2 x 4.3 x 3.7 cm mass with average HU=40, with interval development from a CT scan 6months prior to that which showed left adrenal 1.5 x 1.3 x 1.3 cm mass. He had the initial CT scan after a mechanical fall. He was experiencing sweating, dizziness and low blood pressure of 90/60 mmhg, but used to have hypertension. Physical examination revealed diffuse jaundice in an ill appearing cachectic individual. Laboratory data were significant for total bilirubin of 4.9, direct bilirubin 0.7. Plasma metanephrines and normetanephrines, 24-hour urine free cortisol, morning cortisol levels and DHEA sulfate were normal. Other findings on the CT scans of head, chest and abdomen were soft tissue thickening between the right posterior 10th and 11th ribs along with hepatosplenomegaly, nodular lung lesions with calcified granuloma, sub centimeter brain lesions within the left putamen/external capsule junction with corresponding mild edema. During the following month after initial visit he developed bilateral tongue masses with dysphagia along with enlarging bilateral adrenal lesions, measuring up to 4.4 cm on the right and 5.2 cm on the left. The patient was admitted to hospital for further extensive work up. He underwent biopsies of left adrenal mass and tongue lesions which demonstrated necrotizing granulomatous inflammation with fungal elements compatible with histoplasmosis. Liposomal amphotericin B was started, which was quickly switched to itraconazole 200mg twice a day once lumbar puncture result was normal. His transient low blood pressures resolved. He was seen in clinic after few weeks with overall improving symptoms. Follow up with imaging of adrenal in few months is planned. He is currently in his third month of treatment for histoplasmosis with itraconazole. Discussion: The presentation of disseminated histoplasmosis can resemble malignancy as illustrated in this case. Southwest of the United States is an unusual geographical area for such infection. Initial unilateral involvement of adrenal as a mass in an immunocompetent individual is also uncommon. Considering dramatic response to antifungal treatment, a clinician should suspect such rare infections when seeing a nonfunctional adrenal mass with rapidly progressive constitutional symptoms. Presentation: 6/3/2024

8790 A Case of Ectopic Cushing’s Syndrome Secondary to Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH)

Abstract Disclosure: T. Goettemoeller: None. R. Lopez Fanas: None. K. Cedeno: None. A. Manavalan: None. Introduction: Ectopic Cushing’s syndrome is a rare disease accounting for <20% of cases of endogenous Cushing’s syndrome. DIPNECH is a poorly understood lung disease characterized by abnormal proliferation of neuroendocrine cells in the bronchial mucosa. It can be a precursor to pulmonary carcinoid tumors and has rarely been associated with ACTH production. Clinical Case: A 70-year-old female with intellectual disability and hypertension presented with diffuse edema and weakness. Examination was notable for hypertension, anasarca, and hirsutism. In addition to hypokalemia and metabolic alkalosis, hypercortisolism was observed: random serum cortisol - 50.1 ug/dL, late-night salivary cortisol - 1.72 mcg/dL (normal < 0.09 mcg/dL) and 24-hour urine free cortisol - 1,845.9 mcg (normal: 4.0 – 50.0 mcg/24h). Cortisol level remained > 25 ug/dL after high-dose dexamethasone suppression test. Ketoconazole was initiated and titrated to achieve normal 24-hour urine free cortisol levels and spironolactone was added to manage hypokalemia. An MRI of the sella and pituitary was unremarkable while an abdomen and chest CT identified a 2.5 cm well-circumscribed right middle lobe pulmonary nodule and mild thickening of the bilateral adrenal glands. A gallium-DOTATATE scan revealed a 2.1 cm right middle lobe pulmonary nodule with mildly increased uptake. A transbronchial biopsy of the right middle lobe nodule confirmed a carcinoid tumor. Immunohistochemistry (IHC) staining was positive for CHR, SYN, CD56, and AE1/3. Ki-67 stain showed a low proliferative index. A right middle lobectomy was performed with pathology revealing two typical carcinoid tumors measuring 2.8 and 0.7 cm each, with multiple carcinoid tumorlets and foci of neuroendocrine cell hyperplasia consistent with DIPNECH. IHC staining for ACTH was positive in the carcinoid tumors and tumorlets. Four days after surgery, AM cortisol was 8.1 ug/dL and potassium levels and blood pressure normalized off ketoconazole and spironolactone. The patient was discharged, but was readmitted a month later for anasarca, lethargy, hypokalemia, and metabolic alkalosis. A recurrence of Cushing’s syndrome was confirmed, and medical therapy was resumed. A chest CT revealed post-surgical changes. Her course was complicated by an aspiration event, septic shock, PEA arrest, resuscitation, and intubation. The patient’s care was ultimately transitioned to hospice. Conclusion: Florid Cushing’s syndrome due to ectopic ACTH production associated with DIPNECH is an exceedingly rare condition. Early recognition and treatment are crucial to prevent the numerous complications that may arise, and close follow-up after tumor removal is critical to ensure continued remission has been achieved. Presentation: 6/1/2024

8165 A Case Of Rhabdomyolysis-Induced Hypocalcemia And Hypercalcemia

Abstract Disclosure: A. Desai: None. A.L. Izzi: None. B. Flores Chang: None. A. Sajan: None. Introduction: Rhabdomyolysis is a syndrome characterized by muscle breakdown and the release of intracellular muscle contents into circulation. It is associated with electrolyte abnormalities and acute renal failure that can lead to prolonged hospitalization. We report a case of persistent hypercalcemia from recovery of acute renal failure and severe rhabdomyolysis. Case Description: A 47-year-old man with past medical history of polysubstance use initially presented with opiate-induced acute encephalopathy and respiratory failure. He developed severe rhabdomyolysis during the hospital course leading to acute renal failure requiring hemodialysis with hypocalcemia. The initial labs showed corrected calcium 6.2 mg/dL [9.2-11.0], ionized calcium 3.48 mg/dL [4.65-5.28], creatinine kinase level was >72,600 U/L [38-174], BUN 110 mg/dL [8-23], creatinine 7.8 mg/dL [0.6-1.2], and GFR 7 ml/min/BSA. His renal function improved over the next several days in the hospital. The serum creatinine improved to 4 mg/dL, BUN 49 mg/dL and GFR 20 ml/min/BSA respectively after couple of intermittent dialysis sessions. Six days after the last hemodialysis session, patient developed severe hypercalcemia with corrected calcium values ranging from 13.5 to 14.7 mg/dL and ionized calcium 7.41 mg/dL. Labs showed PTH 10 pg/mL [15-65], 1,25-dihydroxyvitamin D <10.0 pg/dL [21-65] and 25-OH Vitamin D levels 15.3 ng/ mL [30-96], which is consistent non-PTH medicated hypercalcemia. The 24-hour urine calcium was 696 mg [0-300 mg/24 hrs, 2900 cc]. PTH-related peptide was not collected. He was treated with intermittent doses of calcitonin and a single dose of pamidronate when the calcium levels were >13 mg/dL. Hypercalcemia resolved in eleven days after initially noted to have hypercalcemia. The corrected calcium improved to 10.1 mg/dL on the day of discharge. Discussion:Severe rhabdomyolysis is associated with acute kidney injury. The initial hypocalcemic phase during rhabdomyolysis is due to entry of calcium into damaged myocytes and deposition of calcium salts in damaged muscle. This is seen in the oliguric phase of acute kidney injury. After the recovery of rhabdomyolysis, the polyuric phase persists during renal recovery. During this time, up to one third of patients may have rebound hypercalcemia due to massive muscle calcium release. As per case reports the hypercalcemia phase lasts from 8 days to 3.5 months. In our case, the patient initially developed hypocalcemia in the oliguric phase of acute kidney injury from rhabdomyolysis. He developed hypercalcemia in the polyuric phase of renal recovery. The hypercalcemia resolved with intravenous hydration, calcitonin and pamidronate. Rhabdomyolysis is a rare cause for both hypocalcemia and hypercalcemia. Our case highlights the biphasic calcium response associated with rhabdomyolysis in the setting of renal impairment and recovery. Presentation: 6/1/2024

5165 Cushing’s Disease And Primary Aldosteronism Confounded By A Non-functioning Solitary Adrenal Incidentaloma

Abstract Disclosure: J.G. Friedman: None. W. Huang: None. Background: Adrenal incidentalomas are common, affecting ∼2% of the general population. The presence of adrenal incidentaloma necessitates biochemical testing for hypersecretion, however hypercortisolism and/or hyperaldosteronism may not necessarily originate from the nodule that prompted the initial workup. Clinical Case: A 53-year-old man with a history of obesity and hypertension was referred for workup of a 2.4 x 1.4 cm R adrenal nodule that was incidentally discovered on an abdominal CT to rule out pancreatitis. He was noted on examination to have some Cushingoid features. He was on three antihypertensives (amlodipine 10 mg, carvedilol 50 mg, and spironolactone 50 mg) with adequate blood pressure control and no hypokalemia. He denied spells nor exogenous steroid exposure. Initial testing for hypersecretion showed an elevated cortisol 8.7 ug/dL (<1.8) after 1 mg dexamethasone with adequate dexamethasone level, aldosterone concentration (PAC) 9 ng/dL (3-16), plasma renin activity (PRA) 0.7 ng/mL/h (0.25-5.82), potassium of 3.8 mmol/L (3.5-5.1), and normal plasma metanephrines. Further testing revealed elevated 24-hour urinary free cortisol 81.3 mcg/24h (4-50) and elevated late night salivary cortisol 0.10 and 0.13 mg/dL (<0.09). Baseline 8 AM ACTH was not suppressed 16.3 pg/mL (7.2-63.6). DDAVP stimulation resulted in an increase in cortisol and ACTH suggestive of Cushing’s disease, which was confirmed by inferior petrosal sinus sampling (IPSS). Pituitary MRI showed a 3.6 mm L-sided microadenoma. He underwent transsphenoidal resection with pathology consistent with an ACTH-staining pituitary adenoma. Immediate post-op cortisol nadir was 4.9 ug/dL. A few weeks after surgery, he underwent retesting for primary aldosteronism notable for PAC 14 ng/dL, PRA 0.58 ng/mL/h, and K 4.0 mmol/L. After oral salt loading, 24-hour urine aldosterone was 14.4 mcg/24h (<12) with urine sodium 247 mmol/L/24h (>200). He completed AVS which lateralized to the L adrenal gland despite a R adrenal nodule. He underwent L adrenalectomy with significant improvement in blood pressure which is now well-controlled on carvedilol monotherapy with normalization of PRA to 1.94 ng/ml/h. The R adrenal nodule remains stable in size and appearance on follow up imaging. Conclusion: The presence of an adrenal adenoma with concomitant biochemical evidence of hormonal excess cannot inherently be attributed to nodular autonomous function without further workup. Other hormonal assessment including ACTH level and localization studies are necessary prior to any surgical procedure to avoid missed diagnoses of Cushing’s disease and contralateral primary aldosteronism in the presence of a non-functioning adrenal nodule. Presentation: 6/1/2024

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

7242 Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH) In A Patient With Recurrent Carcinoid

Abstract Disclosure: F. Woron: None. T.L. Anderson: None. P. Madhavan: None. Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) is a rare generalized proliferation of pulmonary neuroendocrine cells. It is considered to be a pre-invasive lesion for pulmonary carcinoid, a rare neuroendocrine tumor (NET). DIPNECH is thought to be underdiagnosed, as patients can be asymptomatic or present with nonspecific cough and dyspnea, though it is also associated with fibrotic lung changes. Long-term annual surveillance imaging is recommended for due to the potential for development and metastasis of carcinoid tumors. We present a patient with recurrent pulmonary carcinoid later diagnosed with probable DIPNECH based on CT findings. The patient is a 72-year-old female with a prior 15 pack-year smoking history, who initially had a left lower lobe typical carcinoid tumor diagnosed and resected in 2018, with no evidence of lymph node metastasis. The patient’s medical history also includes pulmonary sarcoidosis, adrenal adenoma, thyroid nodule, hiatal hernia, and prediabetes. She has no family history of neuroendocrine tumors. Physical exam showed stable vitals with blood pressure of 112/70 mmHg in the right upper arm, heart rate of 84 bpm, and a body mass index of 39. Physical exam was unremarkable except for thyroid nodularity and obesity. Extensive biochemical evaluation for markers including chromogranin A and 24-hour urine 5-HIAA levels were within normal limits. In 2022, surveillance CT imaging showed a new 9 mm nodule in the right lobe within the bronchus, which was shown to be carcinoid on FNA. She complained of dyspnea and wheezing at this time, which has been managed with an albuterol inhaler. In 2023, PET/CT copper 64 dotatate scan showed a focal area of activity related to the nodule in the superior segment, also identified on recent CT scan, with the nodule measuring approximately 2.05 cm x 1.8 cm with a maximal SUV of 4.2. Interestingly, somatostatin receptor scintigraphy did not show any pick-up in the lung in 2018 or 2022. In 2023, the patient underwent right lower lobe superior segmentectomy after the nodule was found to have increased in size. Pathology showed G1, well-differentiated 1.1 cm typical carcinoid tumor with margins negative for invasive carcinoma. All 18 regional lymph nodes were negative for tumor. Immunohistochemical tests show that the tumor cells were positive for INSM1 and chromogranin with a low Ki-67 proliferation index (<2%), supporting the diagnosis. The patient is currently being monitored by yearly CT imaging and followed by both endocrinology and pulmonology. Given this case, we propose that DIPNECH should be considered as a differential in cases of pulmonary carcinoid, especially recurrent ones. Given that DIPNECH is thought to be underdiagnosed and a precursor for carcinoid associated with fibrotic lung changes, it is essential for this disease to be identified in order for patients to receive appropriate long-term monitoring. Presentation: 6/1/2024

12609 Navigating The Therapeutic Challenge Of Post-surgical Hypoparathyroidism And Refractory Hypocalcemia

Abstract Disclosure: D. Fawcett: None. A. Domingo: None. Introduction: Post-surgical hypoparathyroidism poses a challenge due to calcium metabolism disturbances, ranging from mild to life-threatening complications. Despite advancements, vigilant monitoring and tailored interventions are vital for optimizing outcomes. Refractory hypocalcemia, resistant to standard therapies, underscores the need for specialized care to prevent prolonged hospitalization and morbidity. Case description: A 68-year-old woman with a history of Graves' disease and parathyroid carcinoma underwent total thyroidectomy and parathyroidectomy in January 2024. She presented to the emergency department for the second time with a recurrence of bilateral hand and perioral paresthesias, along with numbness, tingling, and weakness throughout her body. Notably, she had a prior hospital admission with similar symptoms and was discharged on calcium carbonate, magnesium, calcitriol, and vitamin D3. Vital signs were not provided. Initial laboratory workup revealed a calcium level of 4.3, with corrected calcium at 5.8, and magnesium levels at 1.8, supplemented with magnesium oxide. A 24-hour urine calcium test, vitamin D, and malabsorptive workup for celiac disease were unremarkable. Immunoglobulin A was low; however, tissue transglutaminase IgA and anti-gliadin antibodies were negative. An electrocardiogram showed a normal sinus rhythm with QT prolongation to 570 ms. Despite resuming her home regimen, her calcium level remained low, prompting initiation of calcium infusion. Consultations with endocrinology and nephrology were made, necessitating close monitoring and uptitration of calcium and vitamin D supplements for achievement and maintenance of low normal calcium levels. High doses of 3g TID of calcium and calcitriol 2mcg PO TID allowed for symptom control and discharge with outpatient follow-up with endocrinology and nephrology. Conclusion: Supplemental therapy with calcium and vitamin D analogues is standard for managing post-surgical hypoparathyroidism. Early identification and adequate management prevent hypocalcemia-related complications, including tetany, seizures, and cardiovascular anomalies such as QTc prolongation, as seen in our patient, which can result in torsade de pointes. Multidisciplinary care alongside nephrology was paramount. Serum calcium should be maintained in the low normal range, and 24-hour urine calcium excretion should also be closely monitored. Daily hydrochlorothiazide can be used to prevent hypercalciuria. In recurrent cases, as in our patient, titration of calcium and vitamin D analogues is imperative. Long-term consequences, including renal dysfunction, osteoporosis, and increased cardiovascular risk, underscore the necessity for timely diagnosis and management. 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

8673 Exploring A Case Study On Navigating Complexities In Endocrine Health And Reproductive Challenges

Abstract Disclosure: S.Y. Rizvi: None. E. Villanueva: None. Introduction: Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting many reproductive-age women, characterized by irregular menstrual cycles, hirsutism, and challenges with fertility. In this case study, we delve into the medical history of a 24-year-old female presenting with PCOS-related symptoms, hirsutism, and infertility, unraveling the multifaceted aspects of her healthcare journey. Case Description: This patient's diagnostic path began when she received an initial diagnosis of PCOS in her home country due to irregular menstrual periods and clinical signs of hirsutism. Her treatment included metformin, but it was interrupted when she relocated to the United States. Upon her arrival in the U.S., her medical course took an unexpected turn as further evaluations revealed elevated salivary cortisol (++), and a 24-hour urine free cortisol recorded 94.2 mcg (normal 4-50 mcg), indicating hypercortisolism. DHEAS: 730 mcg/dl (normal 18-390 mcg/dl), 17-hydroxyprogesterone: 508 (pre-midluteal: 431), free testosterone: 13 pg/ml (normal 0.1-6.4 pg/ml), with normal CBC, TSH, prolactin, and TPO. CT scan showed large 4.8 cm left adrenal mass. These findings indicated adrenal Cushing's syndrome, leading to referral to a tertiary care hospital's endocrine surgeon. Two months post-adrenalectomy, successful removal of the adrenal mass left the patient with relative adrenal insufficiency. Hydrocortisone replacement therapy was initiated, addressing Cushing's syndrome and revealing a potential factor contributing to infertility. Postoperatively, the patient entered the first trimester unexpectedly, complicating her case. Ensuring proper hydrocortisone levels became crucial for her well-being and the fetus, prompting a collaborative approach with obstetricians and maternal-fetal medicine specialists for optimal pregnancy care. Despite ongoing PCOS effects, including hirsutism, treatment options were limited by pregnancy constraints, deferring Aldactone due to its contraindication during pregnancy. Continuous monitoring included hormonal assessments, metabolic panels, and thyroid tests, aiming to balance adrenal insufficiency, PCOS symptoms, and a healthy pregnancy. Conclusion: This case emphasizes challenges in differentiating PCOS from adrenal Cushing's due to overlapping symptoms. Despite classic symptoms, the initial PCOS misdiagnosis highlights the need for vigilance and comprehensive diagnostics. Complex cases underscore the importance of individualized management and interdisciplinary collaboration. Positive outcomes in complex endocrine disorders and pregnancy are attainable through accurate diagnoses and tailored treatments. The case underscores the critical importance of meticulous evaluation for successful outcomes in challenging medical scenarios. Presentation: 6/3/2024

8479 A Challenging Case of Hypercortisolism in an Adult Patient With McCune Albright Syndrome

Abstract Disclosure: P. Kesavan Chary: None. S. Jasim: None. Background: McCune Albright Syndrome (MAS) is a rare genetic disorder that occurs due to a spontaneous post-zygotic missense mutation in the GNAS gene resulting in activating gain of function mutations in G-proteins. MAS classically presents as a triad of café-au-lait skin pigmentation, fibrous dysplasia of bone, and precocious puberty. However, continuous autonomous stimulation of endocrine glands can also result in various other endocrinopathies. We present a rare case of hypercortisolism due to bilateral multinodular adrenal hyperplasia (BMAH) in an adult patient with MAS. Case Report: A 38 year old female had MAS, clinically manifested by precocious puberty, renal phosphate wasting with rickets and osteomalacia, fibrous dysplasia of bone with history of multiple fractures, growth hormone excess, and multinodular thyroid status-post total thyroidectomy. A surveillance CT abdomen showed bilateral (right 3.8 x 1.3 cm and left 1.0 x 0.9 cm) adrenal adenomas with low intrinsic attenuation and washout. On diagnosis, the patient had an AM cortisol of 32.5 ug/dL (6.2-19.4 ug/dL) after a low-dose dexamethasone suppression test (DST), and an AM cortisol of 27.3 ug/dL after a high-dose DST. Late night salivary cortisol was 0.518 ug/dL (<0.010-0.090 ug/dL), 24-hour urine cortisol was 78 ug/24hrs (6-42 ug/24hrs), and ACTH was <1.5 pg/mL (7.2-63.3 pg/mL). The patient was initially asymptomatic and monitored for a few months, but subsequently developed easy bruising, recurrent skin infections, and irritability. The patient declined surgical intervention and was initiated on Osilodrostat. Shortly after medication initiation, she was hospitalized for perforated diverticulitis, hypokalemia, and hypomagnesemia. During hospitalization, AM Cortisol was 49 mcg/dL (4.8-19.5 mcg/dL) and 24-hour urine cortisol was 1023 mcg/24hrs (normal range 3.5-45 mcg/24hrs; the patient’s level prior to admission was 170-190 mcg/24hrs). Osilodrostat was held and the patient was initiated on Etomidate infusion. Once plasma cortisol levels normalized, she resumed Osilodrostat prior to discharge. The patient subsequently tried multiple medical therapy options before undergoing a bilateral adrenalectomy as a definitive treatment choice. Conclusion: The gain of function mutations in MAS result in autonomous endocrine gland function that can manifest clinically as various endocrinopathies. While the most common endocrinopathies in MAS are precocious puberty, hyperthyroidism, and pituitary dysfunction, active surveillance is critical to monitor for less common presentations such as hypercortisolism. This is the first report of adrenal Cushing’s in an adult patient with MAS. Presentation: 6/3/2024

6630 Crooke Cell Pituitary Adenoma Without a Cushingoid Appearance

Abstract Disclosure: J. Hodge: None. S. Idriss: None. I. Jamal: None. R. Panta: None. Background: Crooke cell pituitary adenomas are corticotroph adenomas with Crooke’s cell changes, which are cytoplasmic accumulation of cytokeratin filaments in response to glucocorticoid excess. They are aggressive, invasive tumors, typically macroadenomas, with a high rate of Cushing’s disease and post -treatment (surgery and/or radiotherapy) recurrence. We present a case of Crooke cell pituitary adenoma without a Cushingoid appearance. Clinical Case: A 66-year-old Hispanic male with a 16-year history type II diabetes mellitus with retinopathy, presented with a pituitary macroadenoma at age 60. This was found incidentally when he had a brain CT for evaluation of vertigo. Subsequent brain MRI demonstrated a large 2.4 x 2.0 x 1.7 cm pituitary macroadenoma with extension into the suprasellar cistern and the left cavernous sinus. He was asymptomatic, without Cushingoid features. Hormonal evaluation revealed central hypogonadism and hypothyroidism, mildly elevated prolactin of 39.3 (4-15.2 ng/mL) and morning cortisol level of 12.7 (6-18.4 ug/dL). A 24-hour urine cortisol was normal. He was started on testosterone and thyroid hormone replacement therapy. His diabetes mellitus became progressively difficult to control with a peak HbA1C of 10.1%, about 7 years prior the macroadenoma finding. His HbA1C remained persistently elevated in the 8.1-9.5% range despite being on 6 anti-hyperglycemic agents, including basal insulin. A morning ACTH level 4 years after the initial visit, was 115 (6-50 pg/mL) with a cortisol level of 13.7 (6-18.4 ug/dL). Repeat morning ACTH and cortisol levels 7 months later were very similar. 5 years after the macroadenoma finding, he was noted to have worsening glaucoma, which was believed to be due to optic nerve compression. Therefore, he underwent endoscopic transphenoidal resection for tumor debulking. Pathology supported the diagnosis of Crooke cell corticotroph pituitary adenoma. Repeat brain MRI 3-months post-surgery demonstrated residual tumor, but normal optic chiasm and optic tracts. He had an abnormal dexamethasone suppression test prior to surgery (cortisol 6.4 ug/dL) and continued to do so post-operatively (cortisol 3.7 ug/dL with persistently elevated ACTH). Just prior to his surgery, testosterone replacement therapy was held. Total testosterone level after surgery was normal 309.6 (280-800 ng/dL) and free testosterone 7 (5-21 ng/dL); he remained off replacement therapy. Conclusion: Crooke cell pituitary adenomas are rare with limited data on prognosis and guidance for clinical management. Some patients may have subtle features of hypercortisolism, such as difficult to control diabetes mellitus, without an overt Cushingoid appearance. Presentation: 6/1/2024

6853 A Curious Case of MACS

Abstract Disclosure: M. Dillon: None. A. Syeda: None. V. Kantorovich: None. Introduction: Mild autonomous cortisol secretion (MACS) is characterized by biochemical evidence of mild hypercortisolemia inducing metabolic comorbidities without any obvious phenotypic stigmata of Cushing’s syndrome (CS). This case highlights the challenges faced in the diagnosis and management of MACS. Case: A 76-year-old female with past medical history of class II obesity (BMI 31.83 kg/m2), type 2 diabetes mellitus, hypertension, hyperlipidemia, osteoporosis and chronic kidney disease stage IIIb was diagnosed with MACS after an overnight 1 mg dexamethasone suppression test (DST) showed unsuppressed 8 AM cortisol of 2.4 mcg/dL (<1.8 mcg/dL). Dexamethasone level was appropriate at 355 ng/dL (180-550 ng/dL), ACTH was <5 pg/mL (6-50 pg/mL) and DHEA-S was normal. Late night salivary cortisol (LNSC) levels were elevated to 0.12 mcg/dL (< 0.09 mcg/dL). The 24-hour urine cortisol level was normal. Baseline 8 AM cortisol level was 17 mcg/dL and ACTH was 19 pg/mL. Abdominal CT scan showed a 1 cm left adrenal nodule of 25 HU density and a normal right adrenal with no atrophy. Phaeochromocytoma and primary hyperaldosteronism work up was negative. She started on Mifepristone 300 mg daily and titrated up to 600 mg daily. She presented to our institution one month later with 1 week of nausea, vomiting and muscle weakness. Laboratory studies revealed acute kidney injury with creatinine of 6.69 mg/dL (baseline Cr 1.5 mg/dL) and rhabdomyolysis with creatinine kinase level of 12,819 U/L (24-173 U/L) and urine myoglobin level of 888 ng/mL (0-13 ng/mL). It was evident that her catastrophic presentation was from development of adrenal insufficiency in the setting of Mifepristone glucocorticoid receptor blockade. The drug was discontinued immediately. She was treated with intravenous hydration and intermittent diuretics. Over 10 days, her clinical status gradually improved and creatinine decreased to baseline levels. Discussion: MACS is a challenging diagnosis as cortisol levels are affected by several variables including obesity, drugs, and poorly controlled diabetes. Hence, a meticulous evaluation is mandated before confirming the diagnosis. Our patient’s baseline cortisol and ACTH levels were normal, and her DST and LNSC levels were mildly elevated. Unilateral cortisol producing adenoma causes contralateral gland atrophy due to suppressed ACTH. This was not evident in our patient, thus making the diagnosis questionable. Adrenalectomy is the treatment of choice in MACS with adrenal adenoma. Off label medical management with Mifepristone, a glucocorticoid receptor antagonist, is being pursued in select cases and was trialed due to our patient's age and surgical risk. Mifepristone is approved for the treatment of hyperglycemia due to CS. The data supporting its use in MACS is sparse. Therefore, it is important to be aware of associated risks of Mifepristone when advising patients. Presentation: 6/3/2024

7576 A Rare and Atypical Presentation of Bladder Paraganglioma in a Patient on Long-Term Left Ventricular Assist Device

Abstract Disclosure: S.D. Leungsuwan: None. S.J. Lee: None. S.D. Lim: None. L. Loh: None. Background: Paragangliomas (PGLs) are rare neuroendocrine tumors arising from chromaffin cells. Capable of producing catecholamines, functional PGLs often cause a myriad of autonomic symptoms and complications, including cardiomyopathy. We report a case of bladder PGL in a patient on Left Ventricular Assist Device (LVAD). Clinical Case: A 64-year-old Chinese Female with a history of non-ischaemic cardiomyopathy on long-term continuous LVAD and Cardiac Resynchronisation Therapy Defibrillator (CRT-D) was admitted for recurrent low LVAD flow <2 Litres per minute and labile mean arterial pressure (MAP) 57-151mmHg. She has been on long-term Nebivolol, Entresto, Hydralazine, and Sildenafil without recent dose adjustment. Workup for acute illnesses was non-contributory. 24-hour urine metanephrine and normetanephrine (NM) were 939nmol/d [normal 400-1500nmol/d] and 33883nmol/d [normal 600-1900nmol/d] respectively. Plasma free metanephrine and NM were 0.37nmol/L [normal <0.33nmol/L] and >10.00nmol/L [normal <0.99nmol/L] accordingly. A review of previous ultrasonography and Computed Tomography (CT) imaging revealed a right adnexal mass indenting the bladder which the patient formerly declined further assessment; adrenal glands were normal. FDG-PET CT was done and showed an isolated focus of increased tracer uptake corresponding with the right pelvic mass. An impression of likely bladder PGL was made. A multidisciplinary team including Cardiology, Anaesthesiology, Interventional Radiology (IR), Urology, Gynaecology, and Endocrinology was convened; the patient was recommended surgical resection of the tumor. Preoperatively, she was started on phenoxybenzamine 10mg BD and advised judicious fluid and salt intake. Nebivolol was continued while hydralazine was stopped. This achieved targets of i) MAP 70-80mmHg, ii) approximately 10mmHg MAP postural fluctuation, iii) sitting and standing heart rates 60-70 beats-per-minute (BPM) and 70-80BPM, and iv) no more than 1 PVC every 5 minutes. Two weeks later, she underwent IR-guided angioembolisation and tumor resection uneventfully. Intraoperatively, the patient had haemodynamic fluctuations requiring dynamic administrations of phentolamine, norepinephrine, epinephrine, vasopressin, glyceryl trinitrate, and sodium nitroprusside. Histopathology was consistent with PGL with intact SDH-A and SDH-B expression. Postoperatively, phenoxybenzamine was discontinued and no recurrent LVAD low flow was noted. Subsequent plans for repeat plasma metanephrines and genetic studies were made. Discussion: This case is the first to report an atypical presentation of PGL with LVAD low flow and labile blood pressure. The significant elevations of urine NM (17.8x upper normal limit) and plasma NM (>10.1x upper normal limit) also underline the concept of fold-elevations and post-test probability of PGL. Presentation: 6/3/2024

8233 Cushing Disease Presenting As Severe Persistent Hypokalemia

Abstract Disclosure: G. Palaguachi: None. A. Randhawa: None. M. Sattar: None. G. Mahajan: None. J. Karam: None. Introduction: The clinical presentation of Cushing Disease represents a wide spectrum of clinical and laboratory findings, including electrolyte derangements such as hypokalemia. In this case report, we describe a patient in whom the admission for severe persistent hypokalemia prompted the diagnosis of Cushing Disease. Clinical Case: A 35-year-old woman with history of type 2 diabetes, hypertension, and hyperlipidemia, presented to the Emergency Department with worsening bilateral lower extremities swelling, impairing her ability to walk, found to have severe hypokalemia with K level of 2.8 (3.4-4.8 mmol/L), in additional to right pubic rami fracture, left breast abscess, oral thrush, and severe hyperglycemia with HbA1C of 15.4%. Additional history was relevant for hirsutism, scalp hair thinning, weight gain, and amenorrhea of few months duration. Physical examination was significant for round face, thin scalp hair, oral thrush, facial hirsutism, central obesity, wide abdominal striae, onychomycosis, thin skin with multiple ecchymoses, bilateral lower extremity edema, and thin extremities. Her hypokalemia was resistant to therapy and K level remained in 3.2-3.5 mmol/L range on the third week of admission despite oral and intravenous potassium replacements and spironolactone high dose therapy at 100mg twice a day. Additional laboratory testing showed Cortisol 25.0 (6.70 - 27.60 ug/dL) and normal Aldosterone and renin levels. Given absence of otherwise clear etiology of hypokalemia, and presence of multiple features of Cushing’s syndrome, further inpatient evaluation included 24-hour Urine Free Cortisol level that came back at 2754 (3.5 - 45.0 mcg/24hour), 1 mg Dexamethasone Suppression Test Cortisol of 24.9 (6.70 - 27.60 ug/dL), ACTH of 151.0 (7.2 - 63.3 pg/mL), and 8 mg Dexamethasone Suppression Test Cortisol of 14.2 (6.70 - 27.60 ug/dL). MRI Pituitary showed a pituitary adenoma (0.7 x 0.3 cm) with cavernous sinus involvement. A diagnosis of Cushing disease was made and the patient underwent transsphenoidal surgery on the fourth week of hospital stay with diffuse ACTH staining of the tumor. Postoperatively, cortisol levels were not suppressed suggesting persistent disease, but hypokalemia resolved while on Spironolactone. Conclusion: This patient had several classical features of hypercortisolemia with associated hyperglycemia, recurrent infections, and bone fractures, however the finding that connected the dots and prompted establishing her diagnosis was her severe refractory hypokalemia. Although not a defining feature of Cushing Disease, and usually more pronounced with ectopic ACTH secretion, severe and/or persistent hypokalemia can be part of the presenting symptoms. This case demonstrates the importance of including Cushing Disease as part of the differential diagnosis of persistent hypokalemia in correlation with other clinical signs and diagnostics. Presentation: 6/2/2024

12434 History Of Surgical Menopause Is Associated With An Accelerated “Adrenal Aging” In Menopausal Women

Abstract Disclosure: J. Saini: None. R. Nathani: None. J. Larson: None. V. Fell: None. I. Bancos: None. Background: Surgical menopause due to bilateral salpingo-oophorectomy (BSO) at a younger age is associated with an increased risk of cardiovascular disease, cognitive decline, and increased mortality. Aging is associated with abnormalities in steroid metabolome, most notably an increased glucocorticoid to androgen ratio (“adrenal aging”). We hypothesized that in postmenopausal women of the same age, the duration of menopause is associated with adrenal aging. Objective: To determine the differences in the adrenal steroid metabolome of women with a history of BSO as compared to age-matched women following natural menopause. Methods: We conducted a single-center cross-sectional study in postmenopausal women with or without a history of BSO, between December 2020 to December 2022 Each participant collected 24-hour urine, which was analyzed for steroid profiling by liquid chromatography-tandem mass spectrometry (25 steroids). Exclusion criteria were inability to collect a 24h urine sample, exogenous glucocorticoid use, advanced malignancy, and chronic opioid use. Primary endpoints were glucocorticoid/androgen ratio, 11β-hydroxysteroid dehydrogenase type 2 activity (cortisol/cortisone, Tetrahydrocortisol (THF) + 5 α-tetrahydrocortisol (5 α-THF)/ Tetrahydrocortisone, THE) and 5 α-reductase type activity (Tetrahydrocortisol (THF)/5 α-tetrahydrocortisol (5 α-THF) and Etiocholanolone/Androsterone, Et/An). Results: A total of 245 women were enrolled: 124 women (median age of 66 years, IQR 63-72) with a history of BSO and 121 women (median age of 68 years, IQR 64-71) who underwent natural menopause (P=0.214). Median age at menopause was 44 years (IQR 41-46) in the BSO group, and 50 years (IQR 48-53) in the natural menopause group. History of hormone replacement therapy with estrogen was reported in 161 (66%) women, more frequently (92% vs 39%, P<0.001) and for a longer duration (median 12 years (IQR 6-16) vs 6 years (IQR 3-9), P<0.001) in in the BSO group, as compared to the natural menopause group. Although both groups had similar levels of urinary androgens (median 1387 vs 1686 mcg/24h, P=0.063) and total glucocorticoids (median 10877 vs 10277 mcg/24h, P=0.354), women with a history of BSO demonstrated a higher glucocorticoid/androgen ratio (median 7.9 (IQR 5.0-11.1) vs 6.7 (4.3-9.9), P=0.014), and a lower Et/An ratio (median 1.4 vs 1.6, P=0.045), but not THF/5aTHF ratio (median 1.7 vs 1.8, P=0.380) in comparison to women with natural menopause. No differences were found in other ratios. Conclusion: Women with a history of BSO demonstrated a higher glucocorticoid/androgen ratio in comparison to women undergoing natural menopause, suggestive of BSO-induced accelerated “adrenal aging”. Future studies need to examine associations between the abnormal steroid metabolome and increased cardiovascular morbidity, frailty, and mortality reported following BSO. Presentation: 6/3/2024

Effect of educational intervention based on the theory of planned behavior (TPB) on amount of salt intake in pregnant women with PreHypertension

BackgroundPrehypertension is one of the common disorders during pregnancy. Reducing salt intake is among the best cost-effective interventions to reduce the risk of hypertension. The present study aimed to explore the effect of an educational intervention based on the Theory of Planned Behavior (TPB) on amount of salt consumed by prehypertensive pregnant women.MethodsThe present quasi-experimental study was conducted in 2022 on 61 prehypertensive pregnant women visiting the Comprehensive Health Services Centers in Birjand, Iran. Pregnant women were selected through a convenience sampling method and randomly assigned to intervention and control groups. A blood pressure test and a 24-hour urine test were taken in 3 stages (before, immediately after, and one month after the intervention). A reliable and valid questionnaire based on the TPB was used to measure the cognitive variables. The intervention program included three training sessions based on the TPB held on an online platform (WhatsApp social network). Data were analyzed using repeated measures ANOVA and longitudinal marginal model with the GEE approach in SPSS19. The significance level for all statistical tests was set at p < 0 0.05.ResultsAfter intervention, the mean score of perceived behavioral control (p = 0.02), intention (p = 0.004), and salt consumption behavior (p = 0.03) increased significantly in the intervention group, and the mean score of systolic blood pressure (p < 0.001) and diastolic blood pressure (P < 0.01) decreased significantly in this group. In the control group, a statistically significant difference was observed in the systolic and diastolic blood pressure of the subjects (p < 0.01). However, the score of attitude, subjective norms, perceived behavioral control, intention, salt consumption behavior and the daily salt intake did not show a statistically significant difference over time (P < 0.05).ConclusionThe present findings showed that the perceived behavioral control, intention, behavior, systolic and diastolic blood pressure can be modifiable variables to improve the amount of salt consumed by pre-hypertensive pregnant women. Therefore, we recommend that the present model be used to develop interventions to improve health indicators in pregnant women as a highly susceptible group in society.