bluuebunny/crossref_metadata_2025_split huggingface dataset:
7253 Changes In Bone Density Observed After Transitioning From Denosumab To Alendronate Or Zoledronic Acid
Authors: Khan Aysha , Prakash Ramchandani Bhanvi , Anne Zielinski Rachel , Liu Jiarui , Sardar Mirza Faryal 
Published: October 2024

Abstract
Disclosure: A. Khan: None. B.P. Ramchandani: None. R.A. Zielinski: None. J. Liu: None. F.S. Mirza: None.
Introduction: Discontinuation of denosumab (Dmab) results in rebound increase in bone turnover and increased risk of vertebral fracture. Guidelines recommend that discontinuation of denosumab should be followed by an oral or intravenous bisphosphonate (BP), hormone therapy or selective estrogen receptor modulator (SERM). Hypothesis: We hypothesize that patients who received weekly alendronate (ALEN) after discontinuation of Dmab will have less of a decline in bone mineral density (BMD) compared to patients who received once yearly zoledronic acid (ZA). Methods: We conducted a retrospective chart review to compare the change in BMD and factors affecting BMD loss in patients who received sequential therapy with ZA versus ALEN. IRB approval was obtained. Patients were selected using Epic SlicerDicer if they had taken Dmab therapy from 2018 (year of epic implementation) onwards and had been transitioned to a BP. A total of 251 patients were initially selected. 35 patients met the inclusion criteria of being transitioned off to ALEN or ZA at least 1 year prior to date of data acquisition; 21 transitioned to ZA and 14 to ALEN. The rest of the patients were continuing Dmab and excluded from the analysis. BMD gain after Dmab therapy was evaluated. BMD change after 1 year of receiving sequential therapy was compared between the two groups at the lumbar spine (LS), femoral neck (FN), and total hip (TH). Results: A total of 35 patients were included in data analysis with mean age of 73.7 + 9 years. The mean percentage gain in BMD achieved after Dmab therapy was 9.9 + 8.5%, 4.6 + 10.6%, and 6 + 5.2% at the LS, FN and TH respectively. The mean duration of Dmab therapy was 4.4 + 2.1 years. One year following sequential therapy, mean percentage BMD loss at the LS was 4.5% with ALEN and 3.0% with ZA (p-value: 0.59, 95% CI: -0.04 to 0.08). Following sequential therapy, mean percentage loss at FN was 2.2% with ALEN and 0.2% with ZA (p-value: 0.1895% CI: (-0.01 to 0.04), mean percentage loss at TH was 2.0 % with ALEN and 2.2% with ZA (p-value: 0.78, 95% CI: -0.03 to 0.02). Mean vitamin D level of all patients at time of starting sequential therapy was 45.9 + 12.9 ng/ml. Duration of prior bisphosphonate use before starting Dmab therapy did not have any significant effect on BMD loss after sequential therapy. All patients had vitamin D level in a good range at the beginning and end of the study period. Conclusion: There is invariably some decline in BMD when transitioning from Dmab to BPs. Although our data showed somewhat greater BMD loss at LS and FN with ALEN compared to ZA, this difference was not statistically significant and failed to reject the null hypothesis. These findings need to be evaluated further in larger prospective studies.
Presentation: 6/3/2024
6634 Dual-Mediated PTH And Osteolytic Hypercalcemia In Metastatic Endometrial Carcinoma
Authors: Persaud Christine K , Beckman Darrick J 
Published: October 2024

Abstract
Disclosure: C.K. Persaud: None. D.J. Beckman: None.
Background: Hypercalcemia of malignancy occurs in 20-30% of advanced stage cancer patients. Etiologies include parathyroid hormone-related peptides (PTHrP)-mediated, osteolytic metastases-mediated, overproduction of 1,25-dihydroxycholecalciferol, and rarely parathyroid hormone (PTH)-mediated. PTH-mediated hypercalcemia of malignancy is rare and occurs through ectopic PTH production or primary hyperparathyroidism. We report a rare case of both PTH-mediated and osteolytic-mediated hypercalcemia in the setting of malignancy. Clinical Case: A 57-year-old female with history of endometrial cancer and multiple solid organ metastasis, presented with two weeks of progressive poor oral intake, nausea, emesis, and right flank pain. On hospital admission, she had a serum calcium of &gt;20.1 mg/dL (8.6-10.2), PTH of 203 pg/mL (15.0-65.0), and creatinine of 1.7 mg/dL (0.7-1.2, baseline 1.3). Non-contrasted CT chest/abdomen/pelvis noted increased size of known right adrenal metastasis, new left adrenal metastasis, periaortic lymphadenopathy, and scattered nodules in the subcutaneous tissues of the abdomen and chest, however bone metastasis were not noted. Patient’s hypercalcemia was treated with zoledronic acid, calcitonin, cinacalcet, and eventually denosumab due to difficulty controlling hypercalcemia. Additional labs obtained during evaluation included ionized calcium &gt;2.5 nmol/L (1.12-1.32), PTHrP &lt;2.0 pmol/L (&lt;2.0), 1,25-dihydroxycholecalciferol &lt;10 pg/mL (21-65). Patient’s right adrenal metastasis biopsy one month prior to admission was subsequently stained for PTH and was negative. Technetium-99m sestamibi scan was obtained for localization of parathyroid adenoma or carcinoma. The scan did not localize, however did show numerous new lytic lesions in the skull, spine, sternum, rib cage, and right humerus. Patient’s hospital course was complicated by progressively worsening renal function, anemia, and thrombocytopenia. Patient was discharged to a long-term acute rehab facility off hypercalcemia treatment with a corrected calcium of 10.0 mg/dL. Conclusion: PTH-mediated hypercalcemia is a rare cause of hypercalcemia of malignancy. PTH levels are typically low or low-normal in osteolytic mediated hypercalcemia. Generally, if PTH is elevated in hypercalcemia, an alternate etiology is not evaluated. This case highlights a rare dual-mediated hypercalcemia of malignancy. The patient’s PTH level elevation was discordant with her high degree of hypercalcemia and prolonged treatment course. She was subsequently found to have widespread bone metastases contributing to hypercalcemia. While multiple etiologies of hypercalcemia can be rare, it is important to evaluate for all contributing causes, especially with additional clinical conditions, such as malignancy.
Presentation: 6/3/2024
6976 Early-Onset Paget's Disease- A Unique Presentation In A Young Female With Elevated Alkaline Phosphatase And Low Back Pain
Authors: El Sayed F 
Published: October 2024

Abstract
Disclosure: F. El Sayed: None.
Background Paget disease of bone is an age-related disorder characterized by abnormal growth in certain bones, leading to changes in size and shape. Commonly affecting the skull, spine, pelvis, and long bones, it is more prevalent in men, those over 55, with a family history, and of European ancestry. The prevalence of Paget's disease of bone is approximately 2-3% in individuals over 55 in the United States and Europe, with higher rates in those of European descent. Symptoms, such as pain and deformities, may arise from the condition itself or complications like arthritis. While Paget disease can cause visible abnormalities and fractures in affected bones, most individuals remain asymptomatic. Diagnosis often involves blood tests measuring alkaline phosphatase levels, bone scans, and x-rays. Case Presentation We present the case of a 34-year-old woman who sought evaluation due to persistently elevated alkaline phosphatase (ALP) levels in the thousands. The abnormality was discovered during routine blood work conducted during her pregnancy in 2020, and subsequent investigation revealed a chronic elevation for over three years. The patient reported chronic lower back pain but denied other neurological symptoms. Quantification of ALP Bone showed elevated levels at 629, with normal aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, as well as within-range calcium and gamma-glutamyl transferase (GGT). A whole-body bone scan revealed marked radio tracer uptake in the calvarium, raising concerns for Paget's disease. The patient received a one-time infusion of Zoledronic acid (5 mg), leading to a significant decrease in ALP levels to 182 after three months. Subsequent examination by an Ear, Nose, and Throat (ENT) specialist unveiled bilateral extra bone deposition and mild hearing loss in the right ear, adding a unique dimension to the patient's presentation. This case highlights the importance of a comprehensive approach to diagnose and manage Paget's disease, even in younger individuals with atypical symptoms. Discussion and conclusion Paget's disease presenting in young adults with back pain can be a diagnostic challenge due to its atypical occurrence in this age group. Although back pain is a common symptom, the underlying cause might not immediately be linked to Paget's disease, which typically affects older individuals. However, when encountering persistent back pain in young adults, especially when accompanied by elevated alkaline phosphatase levels, clinicians should consider Paget's disease as a potential differential diagnosis. Further investigation, including imaging studies and bone scans, becomes crucial to confirm the presence of Paget's disease and initiate appropriate management strategies to mitigate its impact on the patient's health and quality of life.
Presentation: 6/2/2024
12609 Navigating The Therapeutic Challenge Of Post-surgical Hypoparathyroidism And Refractory Hypocalcemia
Authors: Fawcett D , Domingo A 
Published: October 2024

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
8387 PTH Analogs in the Management of Osteoporosis in Patients with HIV: An Under-Investigated Treatment Option
Authors: Cappetta K , Erenler F 
Published: October 2024

Abstract
Disclosure: K. Cappetta: None. F. Erenler: None.
Background: Several studies evaluating the fracture risk in individuals with HIV suggest that their fracture burden is elevated compared to the general population due to a multitude of factors.[1] For example, highly active antiretroviral therapy (HAART) is associated with decreased bone mineral density (BMD).[1] Certain agents such as tenofovir disoproxil fumarate (TDF) are particularly associated with reduced BMD, whereas tenofovir alafenamide (TAF) tends to cause fewer deleterious effects.[1] Bisphosphonates are considered first-line options for the treatment of osteoporosis in HIV-infected adults.[1] PTH analogs such as abaloparatide are not well-studied in this population, but case reports with teriparatide have shown promising results.2 To the best of our knowledge, we present the first case in which abaloparatide was initiated in a patient with osteoporosis and HIV with subsequent significant BMD gains. Case: A 64 year-old Indian woman with well-controlled HIV (CD4+ cell count 370 cells/µL; undetectable viral load) on HAART and no history of fractures or hypercalciuria was diagnosed with osteoporosis in 2013 by dual-energy X-ray absorptiometry (DXA) scan. Her most significant risk factors are postmenopausal state, HIV, and HAART, including TDF until 2015; in 2015, she was transitioned to a combination therapy that includes TAF. She was treated with alendronate weekly from 2013-2018. DXA in Sept. 2021 showed T-scores of -2.7 (BMD 0.738 g/cm2) at the spine, -2.3 (0.592 g/cm2) at the femoral neck, and -1.7 (0.732 g/cm2) at the total hip. Given her history of prolonged bisphosphonate exposure, young age, and worst T-score at the spine, the decision was made to start the patient on anabolic therapy with abaloparatide in July 2022. Repeat DXA in Aug. 2023 showed T-scores of -2.4 (0.777 g/cm2) at the spine (a statistically significant 5.3% gain in BMD vs. 2021), -2.4 (0.583 g/cm2) at the femoral neck, and -1.7 (0.733 g/cm2) at the total hip (stable BMD). Discussion: Bone microarchitecture, especially trabecular bone (such as is found at the spine), and the balance of bone resorption and formation is negatively altered by the host immune response and viral proteins in HIV-infected adults, leading to a high prevalence of osteopenia and osteoporosis in this population.[1] Abaloparatide increases BMD—preferentially at the spine—by stimulating osteoblast function.2 Although data on these agents in individuals with HIV are limited, PTH analogs can be efficacious in the treatment of osteoporosis in this population, especially for low BMD at the spine, and warrants further investigation. References: 1.Ahmed M, et al. Bone Health in People Living with HIV/AIDS: An Update of Where We Are and Potential Future Strategies. Microorganisms. 2023; 11(3):789. 2.Wheeler AL, et al. Teriparatide treatment of osteoporosis in an HIV-infected man: a case report and literature review. AIDS. 2015 Jan 14;29(2):245-6.
Presentation: 6/3/2024
6761 PTH-independent Hypercalcemia Secondary to Severe Tophaceous Gout Bone Erosion
Authors: MacLeod R S , Cassetta M A , Majumdar S K 
Published: October 2024

Abstract
Disclosure: R.S. MacLeod: None. M.A. Cassetta: None. S.K. Majumdar: None.
Introduction: Severe hypercalcemia associated with chronic tophaceous gout is extremely rare and usually related to elevated calcitriol secretion by inflammatory granulomatous lesions. Herein is a case where hypercalcemia appears to be mediated by excessive bone erosion in several gout lesions. Case: A 61-year-old man with history of advanced gouty arthropathy presented to the hospital with progressive weakness, lethargy and back pain. For the 3 months prior to presentation, he was noted to have worsening hypercalcemia of unknown etiology. He was not taking calcium or vitamin D supplements and had relatively low dietary calcium intake. He had a recent decrease in mobility and reduced fluid intake due to weakness and back pain in the past 6 months. On presentation, his corrected calcium was 16 mg/dL (8.8-10.2) with suppressed intact PTH of 10.4 pg/mL (16-77) and elevated uric acid at 9.0 mg/dL (2.7-7.3). Further evaluation revealed vitamin D25-OH was 28 ng/mL (30-100), PTH-rp was 21 pg/mL (14-27), and calcitriol was 49 pg/mL (18-72). Due to high normal ranges of PTH-rp and calcitriol, the differential included malignancy and sarcoidosis as possible drivers of hypercalcemia. Serum and urine protein electrophoreses showed no evidence for myeloma, and CT scans of the head, chest, abdomen and pelvis did not reveal malignancy but noted extensive arthropathy with soft tissue masses in the lumbar spine. Skeletal metastatic series showed erosive changes of the axial and appendicular skeleton consistent with inflammatory arthropathy. Two sets of biopsies performed of the L5 right pedicle mass revealed findings consistent with gouty tophus with some granulomas noted at the periphery. Serum CTx measurements were 2403 and 2802 pg/mL (87-345) on consecutive days indicating high bone turnover. Due to reduced renal function at the time, he was given 60 mg denosumab subcutaneously to treat his hypercalcemia. As his gout appeared to be the driver of his hypercalcemia, rheumatology was consulted and recommended uricase infusions for treatment. He had subsequent improvement of his corrected calcium to 10.8 mg/dL on the day of discharge. His calcium and uric acid later normalized and he experienced resolution of his gouty tophi with chronic uricase infusions, later transitioned to maintenance allopurinol. He has yet to receive other anti-resorptive treatments after the single dose of denosumab, now 3 years post treatment. Conclusion: Inappropriately high normal calcitriol in PTH-independent hypercalcemia should raise suspicion for granulomatous lesions or lymphoma facilitating extra-renal vitamin D conversion. In this case hypercalcemia appeared due to severe gouty arthropathy that resolved after treatment with uricase. It is likely that inflammation and granulomatous changes at the tophus-bone interface stimulated osteoclast activity and calcitriol production resulting in hypercalcemia.
Presentation: 6/2/2024
6859 Recurrent Hypercalcemia Due to Prolonged Immobilization After a Profound Vascular Event
Authors: Azocar Villalobos Jorge L , Godasi Bramara , Duro Teodor , Lovato Christina 
Published: October 2024

Abstract
Disclosure: J.L. Azocar Villalobos: None. B. Godasi: None. T. Duro: None. C. Lovato: None.
Background: Hypercalcemia from immobility is rare, typically seen in young men with spinal cord injuries, but it has also been reported in elderly patients with co-morbidities after sustaining a vascular event. The condition is characterized by increased bone resorption after skeletal unloading, which leads to hypercalcemia and decreased levels of parathyroid hormone and 1,25(OH)2 vitamin D. This, in turn, results in decreased bone formation and a significant renal calcium leak. Clinical Case: A 56-year-old woman with a history of cirrhosis due to alcohol abuse and hypertension was admitted after sustaining a left middle cerebral artery infarction, which was complicated by cerebral edema with brain compression and herniation that resulted in profound neurologic deficits. The patient underwent craniotomy, subdural evacuation, and partial temporal lobectomy. During the course of her hospitalization, she developed recurrent episodes of hypercalcemia. The first episode occurred about 6 weeks after her admission. Serum calcium, corrected for albumin, was as high as 16.2 mg/dL (n 8.4-10.4 mg/dL) and PTH &lt;6 pg/mL (n 18-84 pg/mL). The patient was given IV fluids and calcitonin subcutaneously for 48 hours. She also required continuous renal replacement therapy for 3 days due to oliguria. Another episode occurred 2 months later and was managed with IV fluids, calcitonin for 48 hours, and 4 mg IV zoledronic acid. The patient developed hypercalcemia again 4 months later, which required another dose of 4 mg IV zoledronic acid and IV fluids. The patient remained normocalcemic for the following 3 months until she was transferred to a long-term care facility. Additional workup excluded other causes, including hypercalcemia of malignancy with PTHrp &lt;2.0, normal calcitriol, SPEP, UPEP and kappa lambda ratio, and negative CT scans. The diagnosis of hypercalcemia due to immobilization was confirmed by her history. Supporting lab work revealed marked bone resorption with a c-telopeptide 3,277 pg/mL (n 177-1015 pg/mL postmenopausal female). Bone-specific alkaline phosphatase was 22.6 ug/L (7.0-22.4 ug/L postmenopausal female). Clinical Lessons: The diagnosis of hypercalcemia due to immobilization should include patient history, supporting lab work, and must exclude other causes. Skeletal loading is the preferred treatment. However, as this case illustrates, other treatment modalities must be pursued if skeletal loading is not feasible and there is persistent hypercalcemia.
Presentation: 6/2/2024