bluuebunny/crossref_metadata_2025_split huggingface dataset:
5144 Lessons Learned: Evaluation of a Fracture Liaison Service Quality Improvement Efforts
Authors: Sara Rothman Micol , Fixen Danielle R , Schilling Lisa M , Mahmoud Elsheikh Arwa , Marcus Alexandra M , Billups Sarah J 
Published: October 2024

Abstract
Disclosure: M.S. Rothman: None. D.R. Fixen: None. L.M. Schilling: None. A.M. Elsheikh: None. A.M. Marcus: None. S.J. Billups: None.
Background: The Fracture Liaison Service (FLS) care model, a care coordination program for patients experiencing a fragility fracture, is proven to improve management of patients with an osteoporotic fracture, but treatment initiation gaps persist. We describe the evolution of a centralized FLS within a university-based healthcare system, including impact of adding clinical pharmacist consultation and describe circumstances surrounding continued care gaps. Design: Cohort analysis of osteoporosis medication initiation before FLS, after initial implementation, and after addition of pharmacist consultation. Patients: Individuals aged 65 and older experiencing any fragility fracture between 7/1/16 - 3/31/22. Intervention: A centralized team outreached eligible patients, ordered dual x-ray absorptiometry and laboratory tests as needed, and scheduled an osteoporosis-focused primary care appointment. Three years after FLS implementation, clinical pharmacist consultative review was added prior to the primary care visit. Main Measures: Initiation of osteoporosis pharmacologic therapy, completion of DXA, primary care follow-up rate, and description of circumstances where therapy was not initiated. Key Results: Of 1204 new fractures between 7/1/16-3/31/22, 315 patients were enrolled in one of two FLS phases, and 89 eligible historical controls were identified. Medication initiation rates went from 22/89 (25%) pre-FLS to 201/428 (47%) after-FLS phase 1 [POST1], (p&lt;0.001) and to 106/187 (57%) after FLS phase 2 (POST2), when clinical pharmacist consultation was added (p=0.03 versus POST1). DXA was completed in 56/89 (67%) of pre-FLS patients, 364/428 (85%) POST1 patients (p&lt;0.001 versus pre), and 163/187 (87%) POST2 (p&lt; 0.001 versus PRE, p=0.59 versus POST1). Of 375 patients who did not initiate osteoporosis medication, more in the combined post-FLS cohorts attended a follow-up primary care appointment (233/308, 76% attended, versus pre-FLS 41/67, 61% , p=0.016). Conclusion: An FLS including centralized outreach and care coordination significantly improved patient follow-up, DXA, and medication initiation. Addition of de-centralized pharmacist consultation further improved medication initiation rates.
Presentation: 6/3/2024
8410 Lipid modification enhances the calcemic and bone building effects of injected PTH(1-14) and PTH(1-11) fragment peptides in mice
Authors: Höppner Jakob , Noda Hiroshi , Khatri Ashok , Jüppner Harald , James Gardella Thomas 
Published: October 2024

Abstract
Disclosure: J. Höppner: None. H. Noda: None. A. Khatri: None. H. Jüppner: None. T.J. Gardella: None.
PTH analogs with improved actions in vivo are of interest as potential treatment options for bone and mineral ion diseases such as hypoparathyroidism and osteoporosis. The efficacies in vivo of conventional PTH peptides are generally limited by rapid rates of clearance from the circulation (t1/2 = ∼ 5-30 minutes) and relatively short-dwell times on the receptor (PTH1R). This is especially true for small fragment analogs, such as M (modified)-PTH(1-14), and M-PTH(1-11), which have only been shown to be active in vitro. We explored whether PTH fragment peptide efficacy in vivo could be enhanced by addition of a lipid chain (e.g., a C15 palmitoyl chain (palm)) to either the peptide C-terminus or to the side chain of the amino acid residue at position 11 or 13. The C-tail lipid modifications were specifically designed to promote binding to serum albumin, and hence extend circulation half-life, while the lipid chains at sidechains of residue positions 11 and 13 were designed, based on structural models, to anchor the ligand to the receptor in situ -- i.e. by projection of the acyl chain between two adjacent transmembrane helices and into the surrounding plasma membrane -- to thereby extend receptor dwell time. Assessment of cAMP signaling potencies in HEK293/hPTH1R/glosensor cells revealed that both types of lipid modifications can preserve agonist potency, and that the lipid extensions at position 11 or 13 can indeed prolong receptor dwell times, as shown by extended durations of cAMP signaling after initial binding of Palm 11 or 13-modified M-PTH(1-14) and M-PTH(1-11) peptide fragment. Single subcutaneous injection of either Palm-13-M-PTH(1-14) or Palm-11-M-PTH(1-11) into mice resulted in prolonged increases in blood serum calcium levels, while 14 days of daily injection resulted in profound increases in bone mass, as measured by uCT, and marked increases in blood levels of the bone turnover markers CTX1 and P1NP, whereas non-lipidated M-PTH(1-14) control peptides were inactive in vivo. Peptide lipidation thus holds promise as a strategy to employ in the design of new PTH analogs with improved efficacies in vivo.
Presentation: 6/1/2024
6578 National Trends in Vitamin D Deficiency and Racial-Ethnic Differences Among US Women With Low Bone Mineral Density
Authors: Atri Avica , Anastasopoulou Catherine 
Published: October 2024

Abstract
Disclosure: A. Atri: None. C. Anastasopoulou: None.
Introduction: Vitamin D (Vit D) plays a critical role in maintaining bone mineralization and its deficiency adversely impacts bone health. Contemporary trends of Vit D deficiency (VDD) and racial-ethnic differences in these trends among US women with low bone mineral density (BMD) are not well elucidated. 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 ≥ 50 years with femoral neck T score ≤ -1. Osteoporosis was defined by a T-score ≤ -2.5. BMD assessment in NHANES was not completed in 2011–12 and 2015–16, and therefore not included in the analysis. Femoral neck BMD was measured by dual energy x-ray absorptiometry (DEXA) on Hologic Discovery Model A Densitometers (Hologic, Inc., Bedford, Massachusetts). VDD was defined as serum 25(OH)D &lt;30 nmol/L. Participants with missing data on race-ethnicity, BMD and Vit D data were excluded. Independent samples median test was used for comparing medians. The Cochran-Armitage test was utilized for trend analysis. Results: Overall, in women with low BMD, from 2009-10 to 2017-18, prevalence of osteoporosis increased from 13.7% to 16.9% while VDD decreased significantly from 5.6% to 2.3% (p trend = 0.001). When stratified by race-ethnicity, the prevalence of osteoporosis increased in Whites (14.1% to 17.6%, p trend = 0.001), Hispanics (12.6% to 13.7%, p trend = 0.001) and Other race-ethnicity (Asian/Mixed) (14.1% to 21.4%, p trend = 0.001), but a modest decrease was noted among the Black population (7.3% to 6.8%, p trend = 0.001). VDD was disproportionately high among Blacks (In 2009-10: 28.1% vs 4.2% in Whites, 5.4% in Hispanics and 10.7% among Others). However, significantly improving trends in VDD were observed among all the groups, regardless of race/ethnicity, to 12.5% prevalence among Blacks, 1.3% in Whites, 4.9% in Hispanics and 1.1% in the Other race ethnicity group (p trend = 0.001). Discussion In this contemporary analysis, rates of VDD have decreased from nearly 1 in 20 to 1 in 50 women with low BMD in the US. Highest prevalence of VDD was noted among Blacks, seen in nearly 1 in 3 Black women in 2009-10, with improvement to 1 in 8, in 2017-18. Similar favorable trends of decline in VDD were observed across all other racial-ethnic groups as well. Despite the overall improvement in VDD, prevalence of osteoporosis declined only among Black women, suggesting the potential role of other protective factors against osteoporosis among them. Nevertheless, VDD continues to remain prevalent in this high-risk group, emphasizing the need for public health interventions to bridge this gap.
Presentation: 6/2/2024
7633 Novel CASR Gene Mutation in a patient with Familial Hypocalciuric Hypercalcemia and Papillary Thyroid Cancer
Authors: Parihar A , Nylen E S , Gandhi S M 
Published: October 2024

Abstract
Disclosure: A. Parihar: None. E.S. Nylen: None. S.M. Gandhi: None.
Familial Hypocalciuric Hypercalcemia (FHH) is predominantly caused by loss-of-function mutations in the calcium-sensing receptor (CaSR) characterized by a benign elevation in calcium and PTH which can be mistaken for primary hyperparathyroidism (PHPT). Missense mutations in the CaSR gene causing FHH have been documented but not much is known regarding their clinical significance. We describe a patient with FHH found to have a novel variant mutation. A 37-year-old male with hypogonadism and fatty liver was incidentally found to have hypercalcemia suggestive of PHPT with elevated PTH (102-114 pg/ml), normal vitamin D, and Fractional Excretion of Calcium (FECa) of 0.014. His father also had hypercalcemia and had undergone parathyroid surgery. The patient denied kidney stones and had a normal bone density. Subsequent Sestamibi and 4D CT scan suggested parathyroid adenoma on the left mid-lower pole of the thyroid. Neck ultrasound also showed a left 1.2 x 1 x 1 cm thyroid nodule as well as a left neck mass with calcifications. Fine needle aspiration was positive for metastatic Papillary thyroid cancer(PTC) in the left neck mass and patient underwent total thyroidectomy along with subtotal parathyroidectomy and lateral neck dissection. Thyroid pathology confirmed multifocal PTC with lymph node involvement that were BRAF V600 positive. Parathyroid pathology was benign hyperplasia. The PTH level decreased appropriately intraoperatively (69%), but postoperatively a rise was noted with levels remaining 70-90 pg/ml with normal calcium levels. Repeat FECa was 0.007, supporting the diagnosis of FHH. Given patient’s father also had hypercalcemia, genetic testing was pursued. This revealed CaSR gene missense mutation (c.1382T&gt;C p.Leu461Pro, heterozygous). This variation is not present in population databases and has been classified as a variant of uncertain significance. It can be difficult to distinguish PHPT from FHH based on FECa as in this case. The patient also had PTC which is not known to be associated with FHH. Due to uncertain significance of this novel CaSR missense mutation, long term follow-up and further familial genetic testing will help better understand clinical implications.
Presentation: 6/2/2024
12375 Rhabdomyolysis As A Cause Of PTH-independent Hypocalcemia In A Child With Acute Influenza Infection
Authors: Bhattarai Samhita , Halpin Kelsee 
Published: October 2024

Abstract
Disclosure: S. Bhattarai: None. K. Halpin: None.
Introduction: Hypocalcemia is characterized by low blood calcium level. Normal range for calcium for ages 12- 19-year is 8.5-10.6 mg/dli . Severe hypocalcemia is considered as serum calcium level of &lt;7 mg/dl. Hypoparathyroidism, pseudohypoparathyroidism and Vitamin D deficiency are some of the most common causes encountered by pediatrician endocrinologists. Rhabdomyolysis with hypocalcemia and elevated PTH is a rare presentation that should be considered, particularly for children presenting with acute viral illness. We present a rare case of rhabdomyolysis associated with hypocalcemia not related to hypoparathyroidism. Case: A 12-year-old female presented to the ED with body ache, poor oral intake and vomiting. She was found to be influenza positive. Labs showed hypocalcemia (4.8 mg/dl). She had an undetectable 25-OH vitamin D level (&lt;5 ng/ml) and elevated iPTH level (609 pg/ml). We discussed the possibility of her etiology of hypocalcemia as Vitamin D deficiency although her presentation was atypical at an older age with negative imaging for rickets, hyperphosphatemia (6.0 mg/dl), and normal ALP (334 unit/L). She did not have any phenotypic features of Albright’s hereditary osteodystrophy with normal renal function. She had elevated CK (4829 U/L) supporting rhabdomyolysis secondary to acute influenza as a cause of her hypocalcemia. Rhabdomyolysis, a known complication of influenza infection, causes cell membrane destruction which impairs the normal function of Na-K-ATPase channel leading to increase in intracellular sodium activating Na/Ca exchanger. This in turn causes influx of calcium intracellularly causing hypocalcemia. Additionally, any injury leads to high phosphorus release from cells due to its lysis. High phosphorus is also caused by reduced oxidative metabolism in muscles impairing phosphate use. This excess of phosphate then combines with calcium and causes calcium-phosphate complex in soft tissues. Hyperphosphatemia additionally inhibits 1 alpha hydroxylase limiting formation of calcitriol leading to hypocalcemia. iiConclusion: Our patient had severe hypocalcemia due to influenza-related rhabdomyolysis. Rhabdomyolysis is an important cause of hypocalcemia in children, especially with acute viral illness. Accordingly, it is also important to obtain serum electrolytes in patients presenting with rhabdomyolysis as hypocalcemia may lead to complications like seizures and cardiac arrhythmia. Endnotes:i Roizen, Jeffrey & Shah, Vipul & Levine, Michael & Carlow, Dean. (2013). Determination of Reference Intervals for Serum Total Calcium in the Vitamin D-Replete Pediatric Population. The Journal of clinical endocrinology and metabolism. 98. 10.1210/jc.2013-3105.ii Ding LN, Wang Y, Tian J, Ye LF, Chen S, Wu SM, Shang WB. Primary hypoparathyroidism accompanied by rhabdomyolysis induced by infection: A case report. World J Clin Cases. 2019 Oct 6;7(19)
Presentation: 6/2/2024
6858 Robot-Assisted Surgery of Mediastinal Intrathymic Parathyroid Adenoma: A Case Report
Authors: Jovanovic Filip , Jovanovic Visnja , Attaullah Khan Mohammed , Fletcher Stephen 
Published: October 2024

Abstract
Disclosure: F. Jovanovic: None. V. Jovanovic: None. M. Khan: None. S. Fletcher: None.
Background: Ectopic foci of parathyroid tissue pose a diagnostic challenge and lead to a delay in patient care. We present a case report of intrathymic parathyroid adenoma with successful removal using robot-assisted surgery. Case Report: A 33-year-old female with past medical history of gastroesophageal reflux disease, depression, and chronic anemia was found to have hypertension during her third trimester prenatal visit. The patient was complaining of fatigue, abdominal discomfort, and constipation. Laboratory results showed elevated serum calcium 11.3 mg/dL (7.9–10.6), albumin 2.7 gm/dL (3.4–5.0), corrected calcium 12.3 mg/dL (7.6–10.6), and parathyroid hormone (PTH) 122 pg/mL (14–72). A year after childbirth, she continued to experience these symptoms with persistent hypercalcemia and no etiology identified. As part of diagnostic workup, the patient underwent computed tomography (CT) with and without (WWO) contrast of the neck and sestamibi parathyroid scan, both of which were unremarkable. The patient was then referred to a tertiary hospital for a technetium 99m sestamibi followed by single-photon emission computed tomography (SPECT) imaging of neck and chest, which showed scintigraphic findings suspicious of ectopic parathyroid adenoma in the upper mediastinum. Over the next few months, the patient underwent SPECT imaging and 4D helical CT WWO contrast of the neck and thorax that showed 1cm ectopic parathyroid adenoma within the left thymic lobe, at the level of the top of the pulmonary artery arch and upper ascending aorta proximal to the arch. Upon patient’s admission to a quaternary medical center, her lab work showed serum calcium 11 mg/dL and PTH 237 pg/dL. The decision was made to proceed with surgical resection of intrathoracic parathyroid adenoma using robot-assisted (da Vinci® Surgical System) thymectomy. Histopathology analyses of surgery specimens were consistent with parathyroid adenoma and benign thymic tissue. The patient’s lab work on the following day showed significant improvement with serum calcium 8.5 mg/dL and PTH 30.9 pg/mL. While literature review acknowledges intrathymic location of ectopic thyroid[1], research on minimally invasive surgical approach involving this pathology is scarce. Upon surgery, the patient reported full resolution of her symptoms. Conclusion: Persistent hypercalcemia in the setting of unrevealing parathyroid adenoma should prompt suspicion for ectopic parathyroid location. Robot-assisted thymectomy poses a minimally invasive surgical approach in diagnosing and treating mediastinal intrathymic parathyroid adenoma. References:1.Abraham BM Jr, Sharkey E, Kwatampora L, Ranzinger M, von Holzen U. Mediastinal Intrathymic Parathyroid Adenoma: A Case Report and Review of the Literature. Cureus. 2023 Jul 22;15(7):e42306.
Presentation: 6/2/2024
6795 Romosozumab improves bone mineral density and markers of bone resorption in a patient with osteogenesis imperfecta
Authors: Shakir Mohamed K M , Godar Cassandra M , Piech Ricard , Duc Hoang Thanh 
Published: October 2024

Abstract
Disclosure: M.K. Shakir: None. C.M. Godar: None. R. Piech: None. T.D. Hoang: None.
The efficacy of romosozumab for improving osteoporosis and preventing skeletal fractures is uncertain in patients with osteogenesis imperfecta (OI). In this case report we describe the beneficial effect of romosozumab on markers of bone turnover and bone density in a patient with OI. A 64-year-old man with OI was referred to endocrinology for evaluation of repeated fractures. The patient had a few fractures as a child (2 collar bones and wrist, oldest at age 14); and he recovered well. He reports that he has had a short stature and blue sclera but was otherwise asymptomatic. His son was also diagnosed with OI based on bone biopsy showing abnormalities suggestive of OI type II or IV. This son has had multiple fractures, 10 shoulder dislocations, and 2 hip replacements. He has another son with a history of multiple fractures but no formal diagnosis of OI. His third son has no findings. The patient’s brother has been diagnosed clinically with OI type 4, and had genetic testing showing a COL1A1 pathogenic variant (c. 976G&gt;C, p.Gly326Arg) . Genetic testing in our patient revealed a COL1A1 pathogenic variant (c. 976G&gt;C, p.Gly326Arg) confirming the diagnosis of OI type 4. 8 years ago, he was treated with alendronate for 12 months, which did not prevent recurrent fractures, and all therapies were discontinued. However, recently, the frequency of fractures involving multiple sites had increased. At presentation, his lumbar and bilateral total hip bone mineral density (BMD) values were severely decreased to 0.725 and 0.566 g/cm2, (T scores -3.3 and -3.1) respectively. Because of severe osteoporosis, he was treated with romosozumab 210 mg every month. After 12 months of treatment, his lumbar and total hip BMD increased by 28.3% and 7.2 % respectively. Additionally, bone formation markers increased, and bone resorption markers decreased at 12 months of therapy. He did not develop any fractures after treatment with romosumab. No severe adverse drug effects were observed. At the end of 12 months he received 5 mg zoledronic acid IV. This case revealed good responses of BMD and bone turnover markers to romosozumab treatment, which can be considered as an effective treatment option for osteoporotic OI patients. Studies involving large number of patients are required.
Presentation: 6/2/2024
5122 Severe Hypercalcemia as a Manifestation of Immune Reconstitution Inflammatory Syndrome in a Patient with AIDS and Disseminated MAC Infection
Authors: Vahidi Rad Mona , Ahmed Samir , Kumar Aditi 
Published: October 2024

Abstract
Disclosure: M. Vahidi Rad: None. S. Ahmed: None. A. Kumar: None.
Introduction: Granulomatous disease can cause hypercalcemia due to increased production of 1,25 dihydroxyvitamin-D. Mycobacterium avium complex (MAC) infection is an AIDS (acquired immunodeficiency syndrome)-defining illness and a granulomatous disease that can lead to hypercalcemia. We report a case of severe hypercalcemia from Immune Reconstitution Inflammatory Syndrome (IRIS) in a patient with AIDS and disseminated MAC which developed several months after initiation of appropriate antibiotic and antiviral therapy. Clinical Case: A 30-year-old female with HIV on anti-retroviral therapy and disseminated MAC infection on antibiotics developed PTH independent mild hypercalcemia in the 10.9-11.5 mg/dL range about 4 months after initiation of antiviral and antibiotic therapy. 1,25 dihydroxyvitamin D level was normal at 50 pg/mL (reference range 18-78 pg/mL). The hypercalcemia worsened and about 8 months after initiation of antimicrobial therapy, she had a hospitalization for severe hypercalcemia with corrected calcium of 15.2 mg/dL and acute kidney injury. PTH was suppressed at 6.9 pg/mL and repeat 1,25 dihydroxyvitamin D level was elevated at 129 pg/mL (reference range 18-78 pg/mL). Other testing for PTH independent hypercalcemia including PTH- Related Peptide, serum protein electrophoresis (SPEP) and TSH were normal. She was diagnosed with hypercalcemia from increased calcitriol production in the setting of IRIS secondary to disseminated MAC. Hypercalcemia secondary to increased production of calcitriol in patients with MAC and HIV infection might happen or worsen months after starting the antimicrobial treatments and has been reported as a potential manifestation of immune reconstitution. MAC-associated IRIS has been reported to be associated with a T-helper cell response with increased number of interferon-gamma-producing T-cells and Th1-cytokines that can potentially cause a granulomatous reaction. These granulomas will have increased macrophage 1-alpha-hydroxylase activity that can further result in more production of 1,25 dihydroxyvitamin D3 and cause more hypercalcemia. Prednisone was started with resultant improvement in hypercalcemia. Conclusion: Severe hypercalcemia due to worsening of subclinical granulomatous infections such as MAC can be a manifestation of IRIS in patients with HIV infection or AIDS who are on antiretroviral treatments. This responds to glucocorticoids.
Presentation: 6/2/2024