bluuebunny/crossref_metadata_2025_split huggingface dataset:
9288 National Trends in Fragility Hip Fractures Among Community Dwelling Women With Low Femoral Neck Bone Mineral Density
Authors: Atri Avica , Anastasopoulou Catherine 
Published: October 2024

Abstract
Disclosure: A. Atri: None. C. Anastasopoulou: None.
Introduction: Fragility hip fractures are a major public health burden and are considered a good measure of the quality of healthcare. However, contemporary trends in fragility hip fractures in women with low femoral neck bone mineral density (BMD) in the United States are not known. Methods: We used data from the National Health and Nutrition Examination Survey (NHANES) for the years 2009-10, 2013–14 and 2017–18 to include U.S. women aged ≥ 60 years with bone mineral density (BMD) T score ≤ -1 at the femur neck, which was measured by dual energy x-ray absorptiometry (DEXA) on Hologic Discovery Model A Densitometers (Hologic, Inc., Bedford, Massachusetts). Fragility fracture at the hip was defined as self-reported hip fracture resulting from a fall from standing height or less. Participants with missing BMD and fracture data were excluded. ANOVA was used for comparing means. The Cochran-Armitage test was utilized for trend analysis. Results: Overall, in women aged ≥ 60 years with femoral neck T score ≤ -1, the average age of women of low BMD decreased from 71(±7.2) years to 69.6 (±6.7) years, whereas the mean T-score modestly worsened from – 1.96 (±0.62) to -2.04 (±0.77) from 2009-10 to 2017-18. Similarly, the prevalence of women with T score ≤ -2.5 increased from 18.1% to 21.3%. We also found no significant change in proportion of women who reported treatment for osteoporosis (2009-10: 19.8%, 2013-14: 18.5%, 2017-18: 19.7%; p trend = 0.052). However, proportion of women who experienced fragility hip fractures decreased significantly (2009-10: 2.4%, 2013-14: 1.5%, 2017-18: 1.2%; p trend = 0.001). The mean age of index fragility hip fracture was 70.6 years in 2009-10, 68.3 years in 2013-14 and 71.7 years in 2017-18 (p = 0.001). Age stratified analysis showed a decreasing trend in proportion of women ≥ 80 years who experienced their index fragility hip fracture (2009-10: 25.9%, 2013-14: 14.7%, 2017-18: 15%; p trend = 0.001) and 70-79 years (2009-10: 40.9%, 2013-14: 21.1%, 2017-18: 35.8%; p trend = 0.001), while an increasing trend was seen in women 60–69 years (2009-10: 33.2%, 2013-14: 64.2%, 2017-18: 49.2%; p trend = 0.001). Discussion In this nationally representative cohort of community-dwelling US women with a low femoral neck BMD, we found a 50% decrease in burden of fragility hip fractures over a 10-year period from 2009-10 to 2017-18. This trend was observed despite worsening mean femoral neck T-scores, T score ≤ -2.5, and similar rates of osteoporosis treatment. Interestingly, the proportion of women who experienced their index fragility hip fracture showed a declining trend among the 70-79 years and ≥ 80 years age-groups. This change may be due to increasing awareness and utilization of measures to decrease falls such as exercise, nutrition, health education and environment modifications targeted towards the elderly population.
Presentation: 6/2/2024
7660 Navigating Hypercalcemia: MAC Treatment Hurdles and the Unforeseen Impact of Vitamin D Supplementation
Authors: Noguchi Sumire , Lai Sunny , Rajpal Aman 
Published: October 2024

Abstract
Disclosure: S. Noguchi: None. S. Lai: None. A. Rajpal: None.
Introduction: Hypercalcemia is a recognized complication in granulomatous disorders such as sarcoidosis and tuberculosis, resulting from increased 1 alpha-hydroxylase activity in macrophages leading to excessive conversion to 1,25(OH)2 vitamin D (calcitriol). Mycobacterium avium complex (MAC) is an infectious granulomatous disease often suspected in immunocompromised individuals, including those with human immunodeficiency virus (HIV). Additionally, vitamin D deficiency is prevalent in the general population, prompting supplementation. We hereby present a patient with advanced HIV and disseminated MAC who developed severe calcitriol-induced hypercalcemia in the setting of high dose vitamin D supplementation. Case description: A 48-year-old male with advanced HIV (CD4 count &lt;20 cells/mm^3) presented for evaluation of abdominal pain and constipation, and was found to have severe hypercalcemia of 14.8 mg/dL. Five months prior, he had restarted anti-retroviral therapy (ART) after having been out of care for over a year and was diagnosed with disseminated MAC for which he was on azithromycin and ethambutol. Cultures drawn during this admission were negative for MAC. Hypercalcemia was possibly due to paradoxical immune reconstitution inflammatory syndrome (IRIS) and with appropriate management his calcium level rapidly normalized to 9.7 mg/dL and remained stable until the recent admission. He represented one year later with a calcium level of 13.8 mg/dL with suppressed parathyroid hormone levels, which was refractory to bisphosphonate therapy, therefore was empirically initiated on dexamethasone. By day 4, his calcium levels improved significantly and was discharged on a taper regimen. Cultures collected this admission later revealed ongoing MAC infection, which raised concern for treatment failure and calcitriol-induced hypercalcemia. Calcitriol levels were elevated at 105 pg/mL, which further supported this hypothesis. Additionally, prior to admission he had been prescribed ergocalciferol 50,000 units weekly for 8 weeks, after which he was transitioned to 2,000 units daily. This likely exacerbated the calcitriol-induced hypercalcemia by providing sudden availability of substrate, 25-OH vitamin D, for the activated macrophages. Conclusion: ART has reduced the incidence of opportunistic infections such as MAC, however mortality remains high. Vigilant monitoring for complications, particularly life-threatening calcitriol-induced hypercalcemia and timely use of corticosteroids, is crucial. This case also highlights the need for careful oversight in high-dose vitamin D supplementation for individuals with granulomatous disease and vitamin D dysregulation.
Presentation: 6/2/2024
8651 Parathyroiditis- An Unusual Autoimmune Mediated-Process Presenting as Primary Hyperparathyroidism
Authors: Abdel-Malek M , Alexiadou K , Chander N , Damji S , Mukhopadhyay S , Palazzo F , Tan T 
Published: October 2024

Abstract
Disclosure: M. Abdel-Malek: None. K. Alexiadou: None. N. Chander: None. S. Damji: None. S. Mukhopadhyay: None. F. Palazzo: None. T. Tan: None.
Background: Inflammatory processes of the parathyroid gland are rare, not widely reported in the literature nor fully understood.Clinical case: A 67-year-old female was referred to the Endocrine team with a diagnosis of primary hyperparathyroidism in the context of severe symptoms related to hypercalcaemia and a background of osteoporosis. There was no known family history of endocrinopathies or autoimmune disease. Despite Cinacalcet treatment, she had a significant hypercalcaemia with an adjusted Calcium level of 2.99 mmol/L (RR 2.20 to 2.60) and a high Parathyroid Hormone (PTH) level of up to 46.1 pmol/L (RR 1.6 to 7.2). Localisation studies in the form of a Sestamibi and ultrasound scan failed to locate a parathyroid adenoma.During a four-gland exploration procedure, she had two pathological glands in the right inferior and left superior positions. She therefore underwent a bilateral inferior parathyroidectomy with no intra or immediate post-operative complications. On removal of the two abnormal parathyroid glands, her PTH level dropped from its peak of 48.1pmol/L to 12.2 pmol/L. However, most remarkably, the outcome of her histology revealed morphological appearances of a chronic parathyroiditis.On post-surgery follow-up, her symptomology of fatigue, nausea, abdominal pain and bowel symptoms resolved in addition to reported improvement in energy level. Her adjusted Calcium remained in the range 1.88mmol/L to 2.32mmol/L with a normalised and appropriately reactive PTH level.Over a year later, she developed sudden onset alopecia as well as oncholysis. Her autoimmune serology was negative with no other endocrine biochemical disturbance observed suggestive of an autoimmune-mediated polyendocrine process.She later developed hypocalcaemia despite high-dose Adcal D3, replete Vitamin D status and detectable PTH level (3.7 to 5.0 pmol/L), requiring admission for intravenous Calcium infusion. She was diagnosed with a functional hypoparathyroidism and subsequently commenced on regular Alfacalcidol with good symptomatic response. Conclusion: This case illustrates how a chronic parathyroiditis can mimic a primary hyperparathyroidism, and the even more unusual late presentation of a functional hypoparathyroidism in this context.
Presentation: 6/2/2024
8031 Pelvic Fracture Related to Brown Tumor in Severe Secondary Hyperparathyroidism
Authors: Bodenstab M , Lieberman-Ulm M , Lagari-Libhaber V S 
Published: October 2024

Abstract
Disclosure: M. Bodenstab: None. M. Lieberman-Ulm: None. V.S. Lagari-Libhaber: None.
Background: Severe hyperparathyroidism can result in end-organ damage to the skeleton, known as osteitis fibrosa cystica (OFC). Histologically, OFC manifests as “Brown tumors”, which are so named due to the hemosiderin deposition that occurs from recurring microtraumas with subsequent hemorrhage. Typical sites of presentation include the mandible, clavicle, ribs, or pelvis, but can occur anywhere in the body. Patients can present with diffuse bone pain, pathological fracture, or bone deformities, though some may be asymptomatic and diagnosed incidentally. While these tumors do not have malignant potential, they can become debilitating in their burden and mimic malignant disease. Treatment focuses on treating the underlying cause of the hyperparathyroidism. Clinical Case: A 52-year-old female with ESRD on thrice weekly hemodialysis secondary to T2DM and HTN presented with right thigh pain and difficulty bearing weight, which began one week after a mechanical fall from standing. X-ray on admission revealed acute nondisplaced pathologic fracture of the right superior pubic ramus related to an underlying 4.7 x 2.2 cm expansile osteolytic lesion. Calcium level corrected for albumin on admission was 9.3 mg/dL, phosphorous 5.6 mg/dL, and PTH 563 pg/mL. Review of our institution’s electronic medical record revealed a maximum PTH level of 1,808 pg/mL three months prior. On CT pelvis, the patient was found to have multiple osteolytic lesions also involving the sacrum, multiple vertebral bodies, and the left pubic ramus, concerning for metastatic disease. Patient underwent pelvic rami bone biopsy resulting as osteoclast type giant cells, hemosiderin deposition and fibrosis in keeping with "brown tumor" of hyperparathyroidism. The patient was started on Cinacalcet 30 mg daily, with plans to titrate as outpatient to target PTH levels. She was also instructed to continue calcium, vitamin D and calcitriol to treat the underlying condition of metabolic bone disease from CKD. Referrals were given for both orthopedic spine and orthopedic oncology for surgical evaluation of her lesions. Discussion: Osteitis fibrosa cystica has become exceedingly rare in the United States and occurs in about 2% of patients with hyperparathyroidism. Due to their low prevalence and radiologic similarity to neoplasm, “Brown tumors” may be mistaken for metastatic disease and can lead to delay in diagnosis. Histology reveals collections of osteoclasts due to excess activity intermixed with fibrous tissue and poorly mineralized woven bone, which will differentiate brown tumor from malignancy. However, further correlation with hypercalcemia and hyperparathyroidism is imperative as brown tumors and other giant cell-containing lesions may be difficult to differentiate histologically. We present this case due to its rarity in clinical practice.
Presentation: 6/2/2024
8312 Predictors of Mortality in Primary Hyperparathyroidism: Long-Term Follow Up
Authors: Gibb F W , Seckl J R , Reid L , Lyall M J 
Published: October 2024

Abstract
Disclosure: F.W. Gibb: None. J.R. Seckl: None. L. Reid: None. M.J. Lyall: None.
Background: Primary hyperparathyroidism has been associated with an increased risk of death and cardiovascular disease in observational studies. We have previously published associations between PTH concentration (and other potential explanatory variables) and mortality risk and now present results based on longer follow up duration. Methods: Retrospective cohort study of individuals (n = 611) presenting with PHPT between 2006 and 2014 to a University teaching hospital. Predictors of mortality were assessed by the Cox proportional hazard model. Results: Median age was 68 years (IQR 58 – 77) and 503/611 (82%) were female. Parathyroid surgery was performed in 274 (45%). Median duration of follow up was 12 years over which time 38% of the cohort died (n = 230). Results are subsequently presented for the total cohort and the subgroup (n = 337, 55%) who did not have parathyroid surgery. Total cohort Higher age at diagnosis (HR 1.09 per year, p &lt;0.001), lower BMI (HR 0.97 per kg/m2, p = 0.037), greater socioeconomic deprivation (HR 0.6 for least deprived quintile, p = 0.01), higher serum creatinine (HR 1.01 per μM, p &lt;0.001) and vitamin D deficiency (HR 1.58, p = 0.005) were all associated with mortality in univariate analysis. Adjusted calcium (HR 1.5 per mM, p = 0.101) and PTH at diagnosis (HR 1.002 per pM, p = 0.415) were not significantly associated with subsequent mortality. However, in a multivariate model, adjusted calcium was independently associated with mortality (HR 9.0 per mM, p &lt; 0.001) whilst higher PTH was associated with a lower risk of death (HR 0.98 per pM, p = 0.012). No surgery cohort Adjusted calcium (HR 13.3 per mM, p &lt; 0.001), PTH (HR 1.04 per pM, p &lt;0.001), higher age at diagnosis (HR 1.07 per year, p &lt;0.001), lower BMI (HR 0.96 per kg/m2, p = 0.012) and vitamin D deficiency (HR 1.4, p = 0.047) were all associated with mortality in univariate analysis. Socioeconomic deprivation (p = 0.218) and creatinine (p = 0.105) were not associated with mortality in the non-surgical subgroup. In multivariate analysis, higher age (p &lt;0.001), higher adjusted calcium (p &lt;0.001), lower BMI (p = 0.025) and socioeconomic deprivation (p = 0.049) were all independently associated with mortality but PTH was not (p = 0.745). Conclusions PTH concentration does not appear to be independently associated with mortality risk in people with PHPT. Plasma calcium concentration appears to be a more important association but can be affected by many factors which are independent of PHPT (e.g. concomitant medications, hydration status, delay in seeking medical attention etc.)
Presentation: 6/2/2024
8298 PrimaryHyperparathyroidism after Initiation of Burosumab in a Patient with X-linked Hypophosphatemic Rickets
Authors: Melhim Abdullah , Samarasinghe Shanika , Camacho Pauline 
Published: October 2024

Abstract
Disclosure: A. Melhim: None. S. Samarasinghe, MD: None. P. Camacho, MD: None.
Title: Primary Hyperparathyroidism after Initiation of Burosumab in a Patient with X-linked Hypophosphatemic Rickets Abdullah Melhim, MD; Shanika P Samarasinghe, MD; Pauline M. Camacho, MD FACE Introduction: X-linked hypophosphatemic rickets is an autosomal dominant disease that is characterized by high phosphate wasting at the proximal tubule resulting in slow growth, rickets and osteomalacia. It is usually associated with low serum phosphate, normal calcium, and either normal or modestly elevated levels of parathyroid hormone (PTH). We present a case of a male patient who developed primary hyperparathyroidism after initiation of Burosumab, a new monoclonal antibody directed against fibroblast growth factor 23 (FGF23). Clinical Case A 47-year-old man with a history of juvenile X-linked hypophosphatemic rickets and confirmed PHEX mutation presented to our clinic. He previously had normal to low-normal PTH levels, normal calcium and vitamin D levels with persistently low phosphorus, despite being on calcitriol and phosphate supplements. Patient was started on Burosumab on 7/2021 and 2 months later was noted to have rising PTH levels up to 104 pg/ml (14 – 67) with high normal calcium of 10.3 mg/dL (8.9 - 10.3), albumin of 4.5 gm/dL, vitamin D, 25- Hydroxy of 34 ng/ml (30 – 80) and low phosphorus of 1.9 mg/dL (2.5 - 4.7) consistent with primary hyperparathyroidism. Initially the patient was normocalcemic with high PTH but eventually developed frank hypercalcemia. After further discussion, the patient reported urinary frequency, constipation, and worsening fatigue, but denied any history of nephrolithiasis. Sestamibi scan completed on 8/2023 revealed increased uptake in a right inferior nodule suggestive of a parathyroid adenoma. He subsequently underwent subtotal parathyroidectomy on 11/2023 confirming enlarged hypercellular right superior and inferior and left inferior parathyroid glands. Few reports have described increasing PTH levels after prolonged anti-FGF23 treatment, however our patient started developing primary hyperparathyroidism only a few months after starting treatment. Some recent studies suggest that FGF23 and PTH could have an interdependent phosphaturic effect, this can explain the development of primary hyperparathyroidism in the setting of suppressed FGF23 levels with Burosumab. Conclusion: Burosumab is a new monoclonal antibody directed against FGF23 recently approved for patients with X-linked Hypophosphatemia (XLH). Burosumab use can result in primary hyperparathyroidism through a poorly understood mechanism, more studies are needed to better understand this relationship. Reference: Erik A Imel, et al. Burosumab versus conventional therapy in children with X-linked hypophosphataemia: a randomised, active-controlled, open-label, phase 3 trial. Lancet 2019 Jun 15;393(10189):2416-2427.
Presentation: 6/1/2024
8690 Severe Hypocalcemia Following Treatment with Venetoclax for AML
Authors: Ruddiman Kathleen , Price Catherine 
Published: October 2024

Abstract
Disclosure: K. Ruddiman: None. C. Price: None.
Background: Venetoclax is a chemotherapeutic agent which has known side effects of tumor lysis syndrome, but few reports of isolated hypocalcemia. Clinical case: A 73 year old male with medical history pertinent for myeloproliferative and myelodysplastic disease was admitted for evaluation of failure to thrive. Workup revealed progression to acute myeloid leukemia. Following treatment with decitabine 34mg/day for 5 doses and initiation of venetoclax 100mg daily, he developed progressive, severe, symptomatic hypocalcemia with positive Trousseau and Chvostek sign. The patient was normocalcemic prior to admission with serum calcium ranging between 8.6-9.7mg/dL. Corrected calcium at admission was 8.8mg/dL. Serum calcium decreased steadily following venetoclax, requiring repletion with 3 doses of calcium chloride and gluconate 1gm IV and initiation of oral calcium carbonate 1900mg TID. At its nadir, corrected calcium was 6.1mg/dL on day 19 of treatment with venetoclax despite oral and IV repletion. Further workup showed undetectable 25 hydroxy vitamin D, PTH 62pg/mL, normal range uric acid, low phosphorus (lowest 2.2mg/dL), mild hypokalemia (lowest 3.2mg/dL), and mild hypomagnesemia of 1.8mg/dL. GFR was &gt;90mL/min. Hypocalcemia improved after 3 infusions of calcium gluconate 10gm IV in 1 L normal saline to 7.2mg/dL. Oral repletion with calcium carbonate was transitioned to calcium citrate due to concomitant PPI use. PO calcium citrate titrated to 2850 mg TID to target corrected calcium 7.5 - 8.5 and limit further need for diuresis following calcium gluconate infusions. Ergocalciferol 50,000 IU was given thrice weekly in addition to daily cholecalciferol 5,000 IU with improvement in 25 hydroxy vitamin D to 17ng/mL. This patient was suspected to have multifactorial etiology for hypocalcemia, secondary to undetectable 25 hydroxy vitamin D as well as diuresis with furosemide during the admission, but the most strongly attributed factor was initiation of venetoclax prior to development of progressive hypocalcemia. FDA prescribing information reports hypocalcemia as a side effect of venetoclax when used in treatment for CML, but in phase 2 and 3 studies of venetoclax used alone and in combination with low dose cytarabine to treat AML, no significant episodes of hypocalcemia were reported. Tumor lysis syndrome (TLS) is a known adverse effect of venetoclax in which hypocalcemia is an expected feature, however, this patient did not have laboratory to support this diagnosis. His other electrolyte deficiencies were mild and transient. Conclusion: While electrolyte abnormalities associated with TLS are an expected side effect of venetoclax, isolated severe hypocalcemia is a rarely reported side effect. Calcium should be closely monitored during treatment.
Presentation: 6/1/2024
7073 Treasure or Terror: Dilemmas in the Management of a Giant Parathyroid Adenoma
Authors: Galia A d , De Guzman R , Suib - Salvilla S 
Published: October 2024

Abstract
Disclosure: A.D. Galia: None. R. De Guzman: None. S. Suib - Salvilla: None.
Background: Primary hyperparathyroidism is a common endocrine disorder with an incidence of 25 per 100,000 people in the general population. More commonly caused by parathyroid adenomas in 80-85%, giant parathyroid adenomas weighing more than 3.5 g or measuring more than 2 cm may rarely occur. There have been no reported prevalence data of parathyroid adenoma among ASEAN countries, especially in the Philippines. Clinical Case: A 43-year-old, female, Filipino, initially asymptomatic with anterior neck mass for 8 years then presented with generalized body malaise, easy fatigability, lower extremities pain and numbness. Six years ago, neck ultrasound showed left thyroid nodule; abdominal sonogram showed bilateral medullary nephrocalcinosis, with hypercalcemia, elevated intact PTH, and elevated creatinine. She was unable to undergo further workup and management until she presented a few months ago because of generalized body malaise, abdominal pain, nausea, and vomiting because of hypercalcemia and non-oliguric renal failure. Serum ionized calcium was 1.90 mmol/L (NV 1.15 - 1.30), intact PTH 2000 pg/mL, and serum creatinine 6.08 mg/dL. With unavailability of calcitonin and pamidronate, medical management of hypercalcemia included cautious hydration followed by diuresis, zoledronic acid, and cinacalcet. Sestamibi scan showed a large parathyroid adenoma. Bone densitometry showed osteoporosis (T score = below -2.5). After medical evaluation, she underwent parathyroidectomy under general anesthesia. Intact PTH level perioperatively were as follows: pre-op = 2,078.2 pg/mL; 30 mins = 477.1 pg/mL; 1 hour = 335.7 pg/mL, 1 day = 67.2 pg/mL. The resected mass was 4.2 x 2.4 x 1.6 cm and weighed 4 g; histopathology report was consistent with Parathyroid Adenoma. Post-operatively, patient did not develop hungry bone syndrome. Conclusion: Giant parathyroid adenoma is a rare condition that is usually asymptomatic but can lead to serious complications. In the Philippines, limited availability of laboratory techniques (PTH and sestamibi scan) and availability of medications for hypercalcemia may contribute to underdiagnosis and management. Early detection and treatment can help prevent further complications and improve the overall quality of life.
Presentation: 6/3/2024