bluuebunny/crossref_metadata_2025_split huggingface dataset:
6402 Unsuspected Bladder Mass Turns Out To Be A Paraganglioma
Authors: Lamichhane Shristi , Flowers Ashley , Price David T , Kaur Arshpreet 
Published: October 2024

Abstract
Disclosure: S. Lamichhane: None. A. Flowers: None. D.T. Price: None. A. Kaur: None.
Background: Urinary bladder (UB) paragangliomas are extremely rare tumors comprising of less than 0.05% of all bladder neoplasms and 10% of all paragangliomas. The diagnosis is usually suspected based on clinical features of painless hematuria, episodic headaches, hypertension, palpitations associated with micturition or bladder and confirmed biochemically by elevated urinary and/or plasma fractionated metanephrines (MN). Here, we present a case of a UB mass that was initially diagnosed on biopsy and subsequent biochemical workup revealed elevated MN. Case Report: A 64-year-old man with type 2 diabetes and hypertension, admitted for revision surgery of subdural hematoma was incidentally found to have a 3.3 x 3.4 x 3.9 cm polypoid heterogenous hyper enhancing UB mass attached to the anterior wall on CT abdomen done for abdominal pain. Cystoscopy and TURBT were complicated by hypertensive urgency. Pathology turned out to be paraganglioma. Detailed history at this time revealed a long-standing history of frequency, urgency, nocturia 4 times nightly, recurrent urinary tract infections, an episode of gross hematuria 1-2 years ago, and difficulty controlling blood pressure on 4 anti-hypertensives. Subsequently, labs showed plasma free MN of 97 pg/ml (ref range &lt;=57), free normetanephrine (NMN) of 2392 pg/ml (ref range &lt;=148), and total MN of 2489 pg/ml (ref range &lt;=205). Genetic panel was negative for SDHA, SHD, AF2, SDHB, SHDC, SDHD, VHL, RET, TMEM127. He received 6 doses of Lantreotide due to suspicion of metastasis based on abdominal, pelvic, and inguinal lymphadenopathy seen on DOTATATE scan. After preparation with alpha and beta blockers, he underwent uneventful robot-assisted cystectomy with lymph node resection that resulted in a well-differentiated paraganglioma negative for margins, lymph node involvement, and extra bladder extension. A week later, MN reduced, plasma free MN 37 pg/ml, free NMN 178 pg/ml, and total plasma MN 215 pg/ml. His BP improved, and micturition-induced palpitations resolved. Conclusion: Due to the rarity of UB paraganglioma, the diagnosis can be missed and delayed. This has a serious implication due to the risk of hypertensive crisis during the surgery and increased risk of cardiovascular complications. This case highlights the need for awareness among physicians of the clinical presentation associated with UB paraganglioma, its early recognition and management.
Presentation: 6/2/2024
12315 Unveiling A Paraganglioma: Catecholamine-Induced Hyperglycemia Masquerading As Type 2 Diabetes Mellitus
Authors: Salman Shiza , Hussine Mohamed , Tibaldi Joseph 
Published: October 2024

Abstract
Disclosure: S. Salman: None. M. Hussine: None. J. Tibaldi: None.
Background: Excessive catecholamines have been demonstrated to exert adverse effects on insulin homeostasis and carbohydrate metabolism, potentially resulting in the onset of secondary DM. We present a case of a patient who had been previously misdiagnosed with T2DM for an extended period. Clinical Case: A 34-year-old woman with history of T2DM, HTN, and chronic tachycardia on beta blockers, presented with complaints of palpitations, headaches, and abdominal pain for two weeks. Upon admission, she was found to be in DKA, necessitating transient administration of insulin drip. Furthermore, she exhibited persistent tachycardia and intermittent episodes of hypertensive urgency. Notably, thyroid levels revealed euthyroidism. Although DKA resolved, her fasting blood sugar levels remained elevated and refractory to escalating insulin therapy. CT abdomen with contrast revealed a large enhancing mass in the RUQ. MRI abdomen confirmed an 8.1 cm heterogeneously enhancing T2 hyperintense mass located in the RUQ, abutting the right hepatic lobe, right adrenal gland, extrahepatic biliary ducts, and adjacent vessels. Given suspicions of a neuroendocrine tumor, she was transferred to the surgical service for tumor excision. Hormonal analysis revealed elevations in plasma metanephrines (620 pg/mL, n 0-88 pg/mL), plasma normetanephrines (9954 pg/mL, n 0-210.1 pg/mL), 24-hr urine normetanephrines (10,952 μg/24hr, n 110-720 μg/24hr) and 24-hr urine metanephrines (1406 μg/24hr, n 35-278 μg/24hr). Additionally, she exhibited elevated 24-hr urine epinephrine fraction (218 μg/g Cr, 0-20 μg/g Cr) and 24-hr urine norepinephrine fraction (2775 μg/g Cr, 0-45 μg/g Cr). Preoperatively, appropriate alpha and beta blockade were administered, followed by successful retroperitoneal tumor resection. Postoperatively, her glucose levels normalized without the need for further insulin therapy, and no episodes of hypoglycemia were reported. Histopathological examination of the excised mass revealed an 11 cm sympathetic paraganglioma with retention of SDHB staining. Genetic testing for SDHB, SDHD, VHL, and RET mutations is pending. Conclusion: This case underscores the potential oversight of pheochromocytomas and paragangliomas due to their nonspecific symptomatology, often mimicking more prevalent conditions, thereby presenting diagnostic challenges. The catecholamines secreted by these tumors can lead to both impaired insulin secretion and increased insulin resistance, resulting in clinically significant manifestations. The exact mechanism underlying the glycemic dysregulation remains controversial, necessitating further investigation through large-scale multicenter prospective studies to enhance understanding and inform diagnostic and therapeutic strategies for these tumors, which can manifest with severe and potentially fatal glycemic disturbances.
Presentation: 6/1/2024
7686 A Case Of A 66-Year-Old Male With Systemic Macrocytosis Complicated By Osteoporosis
Authors: Michelle Gri Jacqueline , Hillhouse Melodie , Madhavan Parvathy 
Published: October 2024

Abstract
Disclosure: J.M. Gri: None. M. Hillhouse: None. P. madhavan: None.
Background: Osteoporosis in men is underestimated and warrants investigation for secondary causes of osteoporosis. Systemic mastocytosis is a rare secondary cause of osteoporosis. Clinical Case: This is a 66-year-old male with a past medical history of severe persistent asthma, eczema, hypertension, GERD with esophagitis, basal cell carcinoma, and systemic mastocytosis (diagnosed in 2010). Family history was significant for lung cancer in both of his parents. Patient was first noted to have hyperpigmented skin lesions on his legs, trunk and upper extremities in the early 1990s. The spots were biopsied and he was diagnosed with urticaria pigmentosa in 1998. Due to persistent symptoms of facial flushing and soft stool, he was referred to Hematology and was started on antihistamines. He later underwent a bone marrow biopsy in 2010 which showed multifocal mast cell aggregates but normal trilineage hematopoiesis. He endorsed back pain shortly after his diagnosis and a DXA scan was completed. The DXA scan showed osteopenia of the spine T score of -1.8, BMD 0.999 mg/mm3 and normal bone density in bilateral hips. He had no history of fractures. He was started on alendronate and remained on the medication from 2012 to 2015. It was stopped due to intolerable symptoms of acid reflux and he required proton pump inhibitors. DXA scan in 2017 showed normal bone density of the hips and osteopenia of the lumbar spine (T score -1.2). DXA scan in 2022 showed a decrease in spine BMD by 6% (T score -1.8) from 2017 to 2022 but unchanged from 2010. Hip bone mineral density was normal but decreased by 10% since 2010 and by 6% since 2017. Labs obtained in May 2022 showed normal serum electrophoresis, normal urine calcium and creatinine ratio, calcium and vitamin D level and urine NTX of 41 nM BCE/mM (21-83) and bone specific alkaline phosphatase level of 31.5 U/L (15-41.3). After discussion with the patient, conservative management with calcium, vitamin D and exercise has been implemented along with close follow up. Should the patient’s bone turnover markers increase or fracture risk increase, additional antiresorptive therapy will be initiated. Conclusion: This case study highlights the importance of screening for osteoporosis in patients with systemic macrocytosis. As this patient was diagnosed with osteopenia at age 53, this case also emphasizes the importance of early screening in both women and men with this rare condition.
Presentation: 6/3/2024
8165 A Case Of Rhabdomyolysis-Induced Hypocalcemia And Hypercalcemia
Authors: Desai Aneree , Lucia Izzi Ana , Flores Chang Bessy Suyin , Sajan Alen 
Published: October 2024

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 &gt;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 &lt;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 &gt;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
8586 A Case Of Vitamin D Toxicity: From Michigan To Hawaii, Vitamin D Is Very High
Authors: Abu Limon Ahmad , Aldasouqi Saleh A , Patel Kunjal , Akanbi Folake , Khan Shaza , Kachhadia Palak 
Published: October 2024

Abstract
Disclosure: A. Abu Limon: None. S.A. Aldasouqi: None. K. Patel: None. F. Akanbi: None. S. Khan: None. P. Kachhadia: None.
We report a patient case who is a 46-year-old male, managed for Type 2 diabetes and Vitamin D deficiency (Defined by 25-hydroxy vitamin D levels less than 20ng/ml) at Michigan State University Endocrinology specialty clinic.He started taking 5000 IU daily Vitamin D supplements and on subsequent follow up his levels corrected to 88 ng/ml. His supplements were held.On a routine repeat lab check, his 25-hydroxy vitamin D level is reported to be higher than 200 ng/ml. Which meets the biochemical diagnosis of Vitamin D toxicity. His Calcium level was 9.7 mg/dL (N 8.7-10.3 mg/dL) and PTH-intact level was 38.3 pg/mL (N 14.0-72.0 pg/mL).On questioning the patient, he assured us he is still not on any Vitamin D supplements and that he just got back from a two-weeks long trip from Hawaii and spent hours daily on the beach without using sunblock.He is sure he didn't get tanning, sunburns, or any burns during that period.He was feeling fine without any symptoms or complications.While in Michigan during the winter, with limited number of sunny days, His 25-hydroxy vitamin D levels trended down slowly over the following few months, while Vitamin D supplements kept on hold.The most common cause of Vitamin D toxicity is excessive supplemental Vitamin D use. Other reasons can be related to excessive tanning or burns, that our patient didn't have. Excessive sun exposure or dietary intake is not a known reason to raise Vitamin D levels to a toxic range.Our patient lives in Mid-Michigan, an area known for low number of sunny days (150-180 sunny/ partly sunny days per year ), Which is a reason for high prevalence of vitamin D deficiency in the population. This is Compared to mostly sunny days on the Hawaiian Islands.Coming Back home for the winter season did help his Vitamin D levels to continue trending down back to a safe, non-toxic range.
Presentation: 6/2/2024
8184 A Case With Primary Hyperparathyroidism Caries A New Variant Of Uncertain Significance (VUS) Of The Multiple Endocrine Neoplasia Type 1 (MEN1) Gene
Authors: Guzelce E Caliskan , Fieg E , Pallias C 
Published: October 2024

Abstract
Disclosure: E. Caliskan Guzelce: None. E. Fieg: None. C. Pallias: None.
Background: Multiple endocrine neoplasia type 1 (MEN1) is a rare, autosomal dominant disorder caused by mutations in the MEN1 tumor suppressor gene. MEN1 syndrome is classically characterized by a predisposition to tumors of the parathyroid glands, anterior pituitary, and pancreatic islet cells. However, the clinical spectrum of this disorder has been expanded: carcinoid tumors,adrenal adenomas and lipomas are more common than in the general population.We report a case whose personal and family history is highly suggestive of and consistent with a monogenic disorder such as MEN1, also found to be a carrier of a new variant of uncertain significance (VUS) of the MEN1 gene. A study performed with the French Universal Mutation Database (UMD) for the MEN1 gene showed that one-third of the missense MEN1 variants were VUSs, mainly due to the lack of clinical and segregation data. Therefore, it is very important to identify and report the subjects with VUS of the MEN1 gene. Case report: 68-year-old female with a past medical history significant for hypertension, type 2 diabetes mellitus, hyperlipidemia, CKD stage 4, and nephrolithiasis, GERD who presented with chief complaints of nausea and upper abdominal/epigastric pain and dark stools and found to have moderate hypercalcemia c/w primary hyperparathyroidism, several pancreatic cystic lesions most likely branch duct intraductal papillary mucinous neoplasms, and multinodular goiter and adrenal adenoma. Family history significant for recurrent hyperparathyroidism and nephrolithiasis; her daughter and brother had nephrolithiasis; her daughter has undergone parathyroidectomy twice. The patient's mother died at a young age because of gastric ulcer-related complications. Hyperparathyroidism-related genes were analyzed; AP2S1, CASR, CDC73, CDKN1B, GNA11, RET, MEN1, and only a Variant of Uncertain Significance, c.247_249dup (p.Leu83dup), was identified in MEN1 gene. The patient’s daughter and granddaughter are found to have the same mutation. Conclusion: This variant, c.247_249dup, results in the insertion of 1 amino acid(s) of the MEN1 protein (p. Leu83dup), but otherwise preserves the integrity of the reading frame. This variant is not present in population databases (gnomAD no frequency). The literature has not reported this variant in individuals affected with MEN1-related conditions.
Presentation: 6/3/2024
8472 A Little Too Much Of Tums: A Unique Presentation Of Milk Alkali Syndrome
Authors: Al-Hiti Zena , Misbah Afrah 
Published: October 2024

Abstract
Disclosure: Z. Al-Hiti: None. A. Misbah: None.
Milk-Alkali Syndrome is characterized by a triad of hypercalcemia, metabolic alkalosis, and renal dysfunction. Historically associated with the excessive consumption of milk and alkali-containing antacids, it has re-emerged in recent years due to the widespread use of calcium and vitamin D supplements. It primarily results from an imbalance between calcium intake and renal excretion, leading to elevated calcium levels in the bloodstream. We present a case of milk-alkali syndrome with persistent renal dysfunction after normalizing calcium levels. We present the case of a 65-year-old male who presented to the emergency department with generalized weakness, poor oral intake, and confusion for 3 days. He was noted to have been more adherent with taking his prescribed medications over the last 2 weeks, which include calcitriol 0.5 mcg BID, calcium acetate 667 mg TID, and calcium carbonate 800 mg TID. On admission, he was afebrile and hemodynamically stable. . On examination, he had dry mucous membranes. He had no focal neurological deficits but he was confused and lethargic, and was only oriented to self. Other examination was noncontributory. Complete blood count and urinalysis were largely unremarkable. Chemistry demonstrated an elevated calcium level of 16.0 (8.3-10.6 mg/dL), ionized calcium of 7.3 (4.6-5.3 mg/dL), sodium of 134 (135-145 mmol/L), potassium of 5.4 (3.5-5.1 mmol/L), high phosphorus of 5.3 (2.4-5.1 mg/dL), and bicarbonate of 36 (20-31 mEq/L). Creatinine was elevated at 2.9 (0.6-1.1 mg/dL) from baseline of 1.3 to 1.4 mg/dL, and he had a BUN of 40(9-23 mg/dL). Venous blood gas showed a pH of 7.54( 7.32-7.42), pCO2 of 56 (40-52 mm Hg), and bicarbonate of 38 (23-28 mEq/L), indicating metabolic alkalosis. TSH was elevated at 36.15 (0.55- 4.78 uIU/mL) with a level of 140 two weeks back. Chest X-ray, renal ultrasound and CT head all showed no acute disease. Further work-up revealed a low PTH level of 6.3 (18.4-80 pg/mL), normal PTHrP level and 25-OH Vitamin D. There was no monoclonal gammopathy. Management included aggressive IV fluid resuscitation and IV calcitonin. However, no zoledronic acid was given due to a history of parathyroidectomy and risk of hypocalcemia. His serum calcium improved and eventually normalized. His confusion resolved. However, his creatinine and BUN increased to 3.4 mg/dL and 77, respectively, and did not improve to his baseline. This case highlights the importance of recognizing Milk-Alkali Syndrome as a potential consequence of over-the-counter calcium supplementation and highlights the potential for acute kidney injury which could be irreversible. Healthcare providers should be vigilant in identifying patients at risk, which includes older patients and patients with chronic kidney disease. Early recognition and appropriate management are crucial to prevent further renal deterioration and improve outcomes in individuals with Milk-Alkali Syndrome.
Presentation: 6/2/2024
12478 A Pilot Evaluation Of Automated Morphometry Performance On Vertebral Fracture Assessment (vfa) And Its Impact On Interpretation
Authors: Syed S , Binkley N 
Published: October 2024

Abstract
Disclosure: S. Syed: None. N. Binkley: None.
Introduction: Prevalent vertebral fractures convey increased fracture risk but are often clinically silent; thus, imaging is required for their detection. Vertebral fracture assessment (VFA) can be performed at the time of DXA. We hypothesized that VFA automated morphometry does not accurately identify the number of vertebrae visualized nor the number of fractures present and sought to begin exploring if morphometry impacted the formal interpretation. Methods: Patients seen by an Orthopedic bone health provider were studied. Their VFA images were independently assessed by two physicians, after which a consensus “gold standard” (GS) reading was reached. The number of vertebral bodies able to be assessed and the number of fractures identified by morphometry (M), the formal interpretation (I) and the GS result were compared by one way ANOVA. Results: The study cohort included 100 patients with mean (SD) age 77.6 (8.6) years, 81% female with BMI 26.7 (5.0) kg/m2, 91 of whom had prior clinical fracture. M reported visualizing more vertebral bodies than I and GS; 1243, 1168 and 1063 respectively. I identified numerically more (13) fractures than did M (150 vs. 137) but was lower than GS (167). The automated and formal reports were identical in 52 patients; in this subgroup, 8 patients (15%) had vertebral fractures that were not identified on the formal interpretation. In this same group of 52 patients, an additional 7 (13%) with vertebral fractures had 9 vertebral fractures missed. Conclusion: In this pilot study assessing VFA, automated vertebral morphometry reports identifying more vertebrae than are actually able to be evaluated while missing almost 18% of vertebral fractures that were actually present. That the formal interpretation is identical to that of morphometry in over 50% of patients, while missing vertebral fractures over 12% of the time, implies that morphometry is adversely impacting the formal interpretation and thereby potentially patient care. Further study with larger datasets is indicated.
Presentation: 6/3/2024