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Abstract Disclosure: N. Sweis: None. J. Sanchez Perez: None. M. Fariduddin: None. R.M. Sargis: None. D.J. Toft: None. S. Reutrakul: None. Background: Pituitary apoplexy is a potentially fatal condition involving the infarction or hemorrhage of the pituitary gland. Rarely, it can occur in the setting of an ACTH-secreting pituitary adenoma. Clinical Case: A 27-year-old female with a past medical history of obesity, spontaneous miscarriages, and amenorrhea presented to the ER with an acute onset frontal headache of throbbing quality, associated with nausea and vomiting. The headache began two days prior, rapidly intensified, and did not improve with oral acetaminophen. CT of the head revealed an enlarged pituitary gland, while neurovascular imaging showed no abnormalities. Her neurologic examination was normal. She denied visual changes, photophobia, neck rigidity, fevers, chills, or recent infections. Furthermore, she endorsed a weight gain of about 40 pounds over the past year despite no change in dietary habits. This was accompanied by amenorrhea, hair thinning, itchy comedonal acne, hirsutism, and a loss of libido. Her physical examination was remarkable for the presence of cushingoid features including violaceous abdominal striae, facial acne, moon facies, a dorsal fat pad, and acanthosis nigricans around the neck and axillae. Pituitary MRI with and without contrast showed an enlarged sellar and suprasellar macroadenoma measuring approximately 2.1x1.4x1.2 cm abutting the optic chiasm. The visualized lesion contained hemorrhagic products, suggesting pituitary apoplexy. Biochemical testing on admission included a low morning plasma cortisol of 6.5 ug/dL (ref. range: 6.7-22.6 ug/dL), a 24-hour urine free cortisol of 12.0 (<=45.0 ug/24 hour), and an elevated ACTH of 145.0 pg/mL (7.2 - 63.3 pg/mL). A1c was 5.8% (<5.7%). Serum levels of prolactin, IGF1, GH, LH, FSH, TSH, Free T4, estradiol, total and bioavailable testosterone were within normal limits. She was evaluated with an ACTH stimulation test, which showed a morning cortisol level of 1.2 ug/dL at baseline, lower from prior. Cortisol levels were adequately increased at 19.6 ug/dL and 22.6 ug/dL, 30 and 60 minutes after the administration of Cosyntropin 250 mcg, respectively (>=18 ug/dL after 30-60 mins). The level of ACTH at the time was also decreased to 76.6 pg/mL. The patient was therefore started on steroid replacement therapy with hydrocortisone and later underwent transsphenoidal resection of the pituitary mass without complications. Histopathological examination of the resected mass showed pituitary adenoma cells with diffuse weak to moderate ACTH staining, most consistent with a sparsely granulated corticotroph pituitary adenoma. Conclusion: We report an interesting case of Cushing disease that spontaneously resolved after pituitary apoplexy. Our case underlines the importance of close monitoring of such patients who may rapidly undergo a period of adrenal insufficiency after hypercortisolism. Presentation: 6/3/2024

Abstract Disclosure: B.R. Bedell: None. M. Fariduddin: None. J. Sanchez Perez: None. S.C. Kukreja: None. R.M. Sargis: None. Adrenocortical carcinoma is a rare malignancy, with approximately 2,000 cases reported in the United States since 1970.[1] Many secrete excess adrenocortical hormones, adding to morbidity and mortality. Surgery can be curative or prolong survival if diagnosis is made early, but prognosis remains poor due to delayed detection.[2] We present a case of metastatic functional adrenocortical carcinoma that presented with consequences of long-standing uncontrolled hypertension. A 59-year-old male with history of hypertension and CAD presented to the hospital with worsening bilateral pitting edema, dyspnea on exertion, palpitations, headaches, and proximal muscle weakness over for multiple months. His hypertension (HTN) was noted to be uncontrolled despite use of multiple antihypertensives (daily Lasix 20 mg, Lisinopril 40 mg, Metoprolol Succinate 100 mg and Amlodipine 10 mg). Hypokalemia of 3.0 mmol/l (3.5 - 5.2 mmol/l) was noted. Echocardiogram revealed new heart failure with preserved ejection fraction. A subsequent nuclear stress test incidentally revealed a right-sided 15 cm retroperitoneal mass, invading the IVC and the right hepatic lobe. An AM dexamethasone suppression test was notable for a cortisol of 39 ug/dl (<1.8 ug/dl) and an undetectable ACTH level of <1.5 pg/ml (7.2 - 63.3 pg/mL), suggestive of primary hypercortisolism. 24-hour urine cortisol was 930.6 ug/d, (<=60.0 ug/d), DHEA-s 1105 ug/dL (52 - 295 ug/dL), Androstenedione 2.641ng/mL (0.230 - 0.890 ng/mL), and 17-Hydroxyprogesterone 299.87 ng/dL (<=138.00 ng/dL). Plasma metanephrines were normal and aldosterone levels were undetectable, confirming cortisol and its precursor excess as the cause of hypertension. Biopsy of the mass was consistent with adrenocortical carcinoma. Due to disease extent, the patient was not a candidate for surgical debulking, and radiation therapy was commenced. Ketoconazole 200 mg and Spironolactone 150 mg twice daily led to improvement in HTN and hypokalemia. His course was further complicated by bacteremia and acute pulmonary embolism. The patient eventually elected to pursue hospice care. Adrenocortical carcinoma remains challenging to detect at early stages given a paucity of symptoms. This case highlights the need to have a high index of suspicion for hypercortisolism in patients with uncontrolled HTN and hypokalemia, as this may be indicative of a functional adrenal cancer. This could be a potential strategy for earlier diagnosis, thereby increasing survival rates by improving disease amenability to surgical intervention. (1.) Sharma E, Dahal S, Sharma P, et al. The Characteristics and Trends in Adrenocortical Carcinoma: A United States Population Based Study. J Clin Med Res. 2018;10(8):636-640. doi:10.14740/jocmr3503w (2.) Vaidya A, Nehs M, Kilbridge K. Treatment of Adrenocortical Carcinoma. Surg Pathol Clin. 2019;12(4):997-1006. doi:10.1016/j.path.2019.08.010 Presentation: 6/2/2024

Background In 8 females, 1 will be diagnosed with breast cancer in their lifetime. Although medical advances have increased the likelihood of survival, up to 90% of females will gain weight during and after treatment increasing the risk of breast cancer recurrence and obesity-related comorbidities in survivorship. Behavioral lifestyle interventions focused on diet with or without physical activity can provide breast cancer survivors nonpharmacological options to decrease weight gain and cardiometabolic risk. Method A PubMed search was conducted to identify all behavioral lifestyle interventions focused on diet or diet combined with physical activity longer than 4 weeks of duration in breast cancer survivors that included body weight as an outcome. This review aims to summarize the effects on body weight, body composition, and cardiometabolic risk markers. Results The review shows there is high heterogeneity in type and duration of the intervention to affect weight and cardiometabolic risk in survivorship. Calorie restriction with and without physical activity appears to promote weight loss among breast cancer survivors. However, the effects on cardiometabolic factors are less clear. Conclusions Future studies should be powered for body weight and cardiometabolic effects. Researchers should also consider interventions that (1) are less complex, (2) recruit a more racially and ethnically diverse sample, (3) integrate resistance training, (4) implement the intervention in closer proximity to diagnosis, (5) target weight management in this population before it occurs, and (6) analyze body composition in addition to body weight measurements.

Abstract Disclosure: N. Sweis: None. Y. Velis: None. J. Sanchez Perez: None. Introduction: The coexistence of papillary thyroid carcinoma (PTC) and Graves’ disease (GD) presents unique diagnostic and therapeutic challenges. Thyroid nodules in GD patients require careful evaluation, as hyperthyroidism can obscure malignancy risks. This case highlights a patient with GD and PTC, with the diagnosis confirmed after thyroidectomy. Case presentation: A 57-year-old female with a history of GD diagnosed in 2022, characterized by an initial TSH of <0.005 mIU/L (reference range: 0.270-4.200 mIU/L), free T4 of 2.94 ng/dL (reference range: 0.82-1.77 ng/dL), and a positive thyroid-stimulating immunoglobulin (TSI) of 262 (normal <140% baseline), currently managed with methimazole, presented for evaluation of a thyroid nodule. A thyroid ultrasound performed in 2024 revealed multiple nodules, including one in the right thyroid lobe for which fine-needle aspiration (FNA) was recommended. The FNA findings were suspicious for papillary thyroid carcinoma, which was subsequently confirmed on pathology following thyroidectomy. Discussion: While thyroid nodules in hyperthyroid patients are often treated similarly to those in euthyroid individuals, autoimmune inflammation and TSIs may influence nodule development and malignancy risk. The literarture suggests that the malignancy rate for thyroid nodules in patients with GD typically ranges from 2% to 17%, with some studies reporting a rate as high as 45.8%, with the average reported rate being 16.9%.1-2 This is notably higher than the roughly 5% malignancy rate observed in thyroid nodules within the general population. Contrast this with \"hot nodules,\" which are autonomously functioning and have a low risk of cancer; these do not typically require biopsy. However, nodules in the setting of GD should not automatically be assumed benign, underscoring the need for vigilance in their evaluation. In this case, FNA of a suspicious nodule led to the diagnosis of PTC, and thyroidectomy confirmed malignancy while resolving hyperthyroidism. Conclusion: This case highlights the critical role of early detection through ultrasound and FNA, which facilitate timely diagnosis and treatment, as clinical and radiologic assessments can be challenging in hyperthyroid patients. Thyroidectomy continues to be a definitive solution, effectively treating both hyperthyroidism and any concurrent malignancy. References: 1.Keskin C, Sahin M, Hasanov R, et al. Frequency of thyroid nodules and thyroid cancer in thyroidectomized patients with Graves’ disease. Arch Med Sci. 2020;16(2):302-307. doi:10.5114/aoms.2018.81136. 2.Cantalamessa L, Baldini M, Orsatti A, Meroni L, Amodei V, Castagnone D. Thyroid nodules in Graves disease and the risk of thyroid carcinoma. Arch Intern Med. 1999;159(15):1705-1708. doi:10.1001/archinte.159.15.1705. Presentation: Monday, July 14, 2025

Abstract Disclosure: S. Chandran: None. B.R. Bedell: None. J. Sanchez Perez: None. Background: Fewer than 20 case reports have described idiopathic hypercalcemia in patients with advanced cirrhosis (1). In these cases, no other predominant mechanisms for PTH-independent hypercalcemia were identified, representing a rare and poorly understood phenomenon in chronic liver disease. We present a case of idiopathic hypercalcemia in a patient with advanced decompensated cirrhosis and discuss a proposed underlying mechanism. Clinical Case A 52-year-old male with a history of alcohol-associated cirrhosis presented with altered mental status. On physical examination, he exhibited jaundice, significant ascites and asterixis. Labs revealed hypernatremia, elevated bilirubin, acute kidney injury with a creatinine of 2.2 mg/dL (reference range: 0.5-1.5 mg/dL) from a baseline of 1 mg/dL, and hypercalcemia with a calcium of 11.1 mg/dL (8.6-10.6 mg/dL) and an ionized calcium of 6.7 mg/dL (4.2-5.4 mg/dL). Work-up was notable for a parathyroid hormone (PTH) level of 11 pg/mL (12-88 pg/mL), suggesting a PTH-independent process. Further testing for hypercalcemia etiology was also non-revealing: TSH was of 0.73 mciu/mL (0.35-4 mciu/mL), PTHrP was undetectable, 25 OH Vit D was 8 ng/mL (20-80 ng/mL), 1,25-dihydroxy Vit D was 7.0 pg/mL (19.9-79.3 pg/mL), and Vitamin A was 0.08 mg/L (0.3-1.2 mg/L). There was no history of use of thiazides, lithium, or antacids. Imaging did not reveal any focal hepatic lesions. The patient was initially treated with intravenous hydration (normal saline) and calcitonin (4 units/kg BID for five doses), resulting in temporary resolution of hypercalcemia. However, hypercalcemia recurred five days later with an ionized calcium level of 6.5 mg/dL. A dose of Zolendronic Acid (4mg) was administered. Despite this, the patient’s clinical condition deteriorated, and family elected to pursue hospice care. Conclusion: Given the exclusion of typical causes of hypercalcemia, we conclude that the patient’s hypercalcemia may represent idiopathic hypercalcemia of liver cirrhosis. This is a rare phenomenon which adds to the existing literature. The recurrence of hypercalcemia despite treatment raises questions about the underlying pathophysiology and the role of bisphosphonates in this population. Additionally, an elevated C-telopeptide (1275 pm/mL, reference range: 161-737 pm/mL) in our patient suggests that increased bone turnover, potentially driven by cytokine-induced inflammation in acute decompensated cirrhosis (2), may have contributed to the hypercalcemia. References: 1.Zulfikar, Rafia MD; Silodia, Alok MD. Hypercalcemia in Chronic Liver Disease: A Rare Entity: 1207. American Journal of Gastroenterology 108():p S354, October 2013.2.Cadranel, J. F., Cadranel, J., Buffet, C., Ink, O., Pelletier, G., Bismuth, E., & Etienne, J. P. (1989). Hypercalcaemia associated with chronic viral hepatitis. Postgraduate Medical Journal, 65(767), 678-680. Presentation: Sunday, July 13, 2025

Abstract Disclosure: Y. Velis: None. N.S. Sweis: None. J. Sanchez Perez: None. While diabetic hypoglycemia in end-stage renal disease (ESRD) is well-documented, non-diabetic hypoglycemia in this population is less commonly reported. We present a case of non-diabetic hypoglycemia in an ESRD patient, where endogenous hyperinsulinemia was suspected as the underlying cause. A 41-year-old male with history of ESRD on HD, OUD on methadone, PTSD, and hypothyroidism was admitted for suicidal ideations. On admission, he was found to be hyperkalemic and bacteremic, and his clinical course was complicated by symptomatic hypoglycemia. Point-of-care glucose measurements revealed a glucose level of 45 mg/dL (reference range: 65-110 mg/dL), which correlated with a serum glucose level of 39 mg/dL. He endorsed palpitations and diaphoresis, which resolved with the correction of hypoglycemia. Hypoglycemic episodes occurred both before and after treatment with trimethoprim/sulfamethoxazole. There was no history of bariatric surgery. Adrenal insufficiency was ruled out in light of his chronic methadone use with ACTH stimulating testing resulting in cortisol levels of 16.0 UG/DL, 21.4 UG/DL, 29.9 UG/DL at 0, 30 and 60 min, respectively. Additional workup revealed a normal HbA1c of 4.4% (<5.7%), negative insulin antibodies, and elevated biochemical markers of endogenous hyperinsulinemia: C-peptide 6.8 ng/mL (0.8-4.4 ng/mL), proinsulin 7.8 pmol/L (≤7.2 pmol/L), total insulin 13 uIU/mL (3-25 uIU/mL) and beta-hydroxybutyrate (BHB) <0.2 mmol/L (<0.4 mmol/L). Abdominal CT imaging did not reveal a pancreatic mass. The patient also reported a 40-pound weight loss over the past year and had a BMI of 18.8 kg/m². A nutrition consultation was initiated for dietary supplements. Given the concern for endogenous hyperinsulinemia, diazoxide 50 mg qhs was recommended, but the patient declined due to the medication's unpleasant taste. Hypoglycemia in this case was likely multifactorial, occurring in the context of trimethoprim/sulfamethoxazole use, sepsis, decreased endogenous insulin clearance, low glycogen reserves, and impaired gluconeogenesis due to ESRD. Additionally, the patient appears to have hyperinsulinemia, as evidenced by elevated C-peptide, proinsulin, and insulin levels, along with a low beta-hydroxybutyrate (BHB). However, reference ranges for these labs in ESRD patients without diabetes are not well established. While guidelines exist for diagnosing hypoglycemia in patients without ESRD, literature is limited regarding this diagnosis in the ESRD population. This case highlights the challenges of managing hyperinsulinemia and hypoglycemia in ESRD, underscoring the need for further research to define baseline insulin, proinsulin, and C-peptide levels in this population to improve diagnosis and management. Presentation: Sunday, July 13, 2025

Disclosure: J. Sanchez Perez: None. M. Obeid: None. M. Fariduddin: None. D.J. Toft: None. Introduction: Thyroglobulin (TG) measurement is a major means of detecting recurrence of previously treated differentiated thyroid cancers. Human-Anti Mouse Antibodies (HAMA) can interfere with lab measurements of TG levels and affect clinical decisions and treatment for these cancers.Clinical Case: A 65-year-old female was diagnosed with papillary thyroid cancer (PTC). Surgical pathology following total thyroidectomy demonstrated a tumor of 3.5 cm in its greatest dimension, unifocal, without invasion of locoregional tissue classified as Stage I (pT2N0M0) per AJCC 8th edition. Radioiodine whole body scan (WBS) demonstrated iodine uptake in the neck and 126.5 mCi of I-131 was given. In surveillance 5 years later, TSH was found to be 0.17 mcIU/ml (ref range: 0.35 - 4.00) TG 64.7 ng/ml (ref range: 1.3 - 31.8 ng/mL), and anti-Tg antibodies were undetectable. Neck US consistently showed nonspecific findings of stable small nodes with normal morphology in both supraclavicular regions. Given elevated TG levels, 250 mCi of I-131 was given. Follow-up TG levels ranged from 27.8 to 36.4 ng/ml. A repeat WBS did not reveal any uptake, but as TG remained elevated, I-131 (238 mCi) was again given. Subsequent TG throughout the following 15 years ranged from 2.8 - 58.6 ng/ml. Repeat Neck US only showed benign-appearing lymph nodes. WBS did not have any focal activity to suggest recurrent disease and PET/CT did not show any abnormal FDG uptake. The persistently high TG levels without clinical evidence of tumor recurrence raised the suspicion of lab interference. The serum sample was treated with a blocking reagent that contained mouse immunoglobulin after which the TG level decreased to 2.7 ng/ml compared to untreated value of 20.5 ng/ml.Conclusion: HAMA are human antibodies against mouse antibodies which are believed to develop in humans from direct contact with rodents, including mice, and from the recent increase in the use of mouse monoclonal antibodies for diagnostic and therapeutic purposes. These antibodies implicate an unexpected source of interference in immunoassays, as seen in our patient, which can confound laboratory results and create a clinical dilemma. This patient with PTC had a complete radiological response after surgery, but an incomplete biochemical response which caused the patient to be given a total of 614 mCi of I-131. This case highlights the importance of recognizing the possible presence of HAMA when analyzing TG levels, particularly when the TG levels are used for treatment decisions. Presentation Date: Saturday, June 17, 2023

Disclosure: M. Fariduddin: None. J. Sanchez Perez: None. U.N. Syed: None. Y. Eisenberg: None. R.M. Sargis: None. Introduction: Ectopic ACTH-dependent Cushing’s syndrome (CS) is a rare entity accounting for 10-20% of hypercortisolism cases. We present a patient with this syndrome. Case Presentation: A 72-year-old man diagnosed with metastatic prostate cancer to the lumbar spine and pelvis was admitted for persistent hypokalemia. Potassium levels were 2.1 mmol/L (ref. range: 3.5-5.2) despite aggressive potassium supplementation. He reported 30-lb weight gain in the previous 2 months, rounding of his face, increased abdominal girth, and proximal muscle weakness. Facial plethora with puffiness was noted on physical exam. Labs were relevant for impaired glucose tolerance with fasting blood glucose of 110 mg/dL and elevated A1c of 6.3% (<5.7%), compared to 5.0% 1 year earlier. 8 AM cortisol was 59 ug/dL (6.7-22.6) and after dexamethasone, cortisol remained elevated at 65.8 ug/dL (<1.8). ACTH level was 312 pg/mL (7.2 - 63.3) and 24-hr urine cortisol was 3586 ug/dL (<= 60.0). Abdominopelvic CT showed new bilateral adrenal thickening without discrete nodularity or mass. Pituitary MRI showed a 1mm microadenoma, inconsistent with the degree of hypercortisolism observed. Patient’s age, known prostate adenocarcinoma with differentiation into neuroendocrine tumor and rapid onset of development of hypercortisolism were all suggestive of ectopic Cushing’s syndrome. Ketoconazole 200 mg BID, Spironolactone 200 mg BID and Amiloride 5 mg daily were started which resolved the hypokalemia. ACTH staining of the prostate tissue biopsy was negative. Patient later died of respiratory failure from Influenza pneumonia. Conclusion: Ectopic ACTH hypercortisolism is a rare but aggressive form of hypercortisolism. Symptoms like proximal muscle weakness, hyperglycemia, hypokalemia, infections, and blood clots develop rapidly, however, these patients rarely have the clinical stigmata of CS. Neuroendocrine tumors of the lung and small cell lung cancer are the most common tumors associated with ectopic ACTH production, but cases of paraneoplastic prostate cancer have been reported. Published case reports demonstrate positive ACTH staining of these tumor cells, but this was not the case in our patient even though his presentation was consistent with ectopic hypercortisolism. The ACTH staining was done on a sample of prostate tissue taken 2 months prior to presentation, at the time of diagnosis of prostate cancer. Neuroendocrine differentiation could have happened within 2 months after the biopsy. This case impresses upon us that ACTH staining can be negative in ectopic ACTH hypercortisolism and patients can still have CS as tumor cells continue to differentiate throughout the course of the malignancy- and this can be especially rapid in neuroendocrine differentiation of tumors. CS increases mortality by 3 times, therefore making it crucial to recognize it early to institute prompt treatment. Presentation: Thursday, June 15, 2023