bluuebunny/crossref_metadata_2025_split huggingface dataset:
6487 Hypercalcemia In Pregnancy Due To An Ectopic Parathyroid Adenoma: A Diagnostic Dilemma
Authors: Patel S S , Sharma M B 
Published: October 2024

Abstract
Disclosure: S.S. Patel: None. M.B. Sharma: None.
Introduction: Hypercalcemia is a rare complication of pregnancy, with the most common cause being primary hyperparathyroidism due to a parathyroid adenoma. Ultrasound is the primary modality used for localization, as sestamibi and computed tomography (CT) carry the risk of potential harm to the fetus. We present the case of hypercalcemia in a pregnant female that failed to resolve after two gland parathyroidectomy, necessitating a sestamibi parathyroid scan to localize an ectopic parathyroid adenoma. Case: A 40-year-old pregnant woman at 12 weeks of gestation presented with hypercalcemia, with a corrected calcium level of 12.5 mg/dL (8.7-10.4 mg/dL). She complained of nausea and vomiting but denied any personal or family history of hypercalcemia. Further evaluation revealed primary hyperparathyroidism as the etiology, with Intact PTH of 429.2 pg/mL (18.5-88.0 pg/mL), ionized calcium of 1.45 mmol/L (1.12-1.32 mmol/L), 25-OH vitamin D of 16.4 ng/mL (30-100 ng/mL), phosphorus of 1.3 mg/dL (2.4-5.1 mg/dL), and creatinine of 0.71 mg/dL (0.5-0.8 mg/dL). Notably, her calcium level had been 19.2 mg/dL two weeks earlier during an episode of hyperemesis gravidarum. Hypercalcemia proved relatively resistant to treatment with intravenous hydration and subcutaneous calcitonin. Ultrasound of the neck failed to reveal a parathyroid adenoma. The patient then underwent surgical neck exploration, during which two parathyroid glands were removed, resulting in an intraoperative PTH drop from 440 to 340 pg/mL. Postoperative calcium levels remained elevated at 12.9 mg/dL, prompting the resumption of treatment. Oral sodium and potassium phosphate was added to bind dietary calcium. After an extensive multidisciplinary discussion, a 99mTc-sestamibi parathyroid scan with a lower dose of sestamibi and without CT was recommended. This revealed an ectopic parathyroid adenoma in the anterior mediastinum. Surgical removal of the ectopic parathyroid adenoma in the second trimester finally led to a significant intraoperative PTH drop from 315 to 28 pg/mL. The postoperative course was complicated by hypocalcemia and hypomagnesemia, requiring calcium, vitamin D, and magnesium supplements. These complications resolved over the following days. The patient remained normocalcemic for the remaining pregnancy and delivered a healthy male infant at 34 weeks. Conclusion: Hypercalcemia in pregnancy is associated with fetal and maternal complications, warranting adequate management and close follow-up. The use of 99mTc-sestamibi parathyroid scan is typically not recommended in pregnancy due to concern for fetal harm; however, there are a few studies showing no association with increased birth defects or adverse pregnancy outcomes at low radiotracer doses. Hence, a sestamibi parathyroid scan can be considered during pregnancy to localize an adenoma after a careful review of the benefits versus risks.
Presentation: 6/2/2024
6734 Hypercalcemia Of Immobilization (HCOM) Responding To COVID Treatment: A Mere Coincidence Or More?
Authors: Shafiq Ramsha , Javed Ammad , Haider Adnan 
Published: October 2024

Abstract
Disclosure: R. Shafiq: None. A. Javed: None. A. Haider: None.
A paraplegic patient who developed HCOM and subsequently received steroids for COVID-19 pneumonia with improvement in calcium levels. After completing steroid treatment his hypercalcemia relapsed and received IV bisphosphonates with normalization of calcium levels. Case: A 58-year-old male who became paraplegic after a fall in August, of 2022. In October 2022, during admission for sepsis related to an Indwelling foley catheter, his corrected calcium was 12 mg/dl. Despite IV hydration calcium remained elevated. In December 2022, the patient was readmitted for COVID-19 pneumonia & received Decadron 6 mg daily. On admission calcium was 13.2mg/dl with pertinent labs of PTH 4 (8.5-77 pg/ml), Vitamin D 1,25 was 31 (18-72 pg/ml), and PTHrp was normal. C- telopeptide was 1068 (87-345 pg/ml) which improved to 877 pg/ml after completing Decadron for COVID pneumonia. Also, Calcium transiently improved from 13.2mg/dl on admission to 9.8 mg/dl. Calcium levels were noted to be elevated again up to 14 mg/dl a month after discharge. February 2023, after IV bisphosphonate infusion corrected calcium normalized. In June 2023 calcium was high again at 14.4 mg/dl. IV hydration with a brief 3-day course of dexamethasone before receiving the second dose of zoledronic normalized corrected calcium. Discussion: Dysregulation in bone formation & resorption is due to the absence of mechanical stress in prolonged bed rest which is essential for bone remodeling. Lack of mechanical stress results in increased secretion of Sclerostin, a protein secreted by mature osteocytes that inhibits the Wnt signaling pathway resulting in increased bone resorption & decreased bone formation. Steroids reduce sclerostin production causing an improvement in calcium levels due to reduced bone resorption. His C telopeptide level was 1068 pg/ml) which improved to 877 pg/ml after steroids also supported Sclerostin-mediated bone resorption as a cause of hypercalcemia. Antiresorptive agents like IV bisphosphonates and Denosumab especially in patients with renal failure are the first-line treatments for HCOM. He did require an additional dose of IV zoledronic acid 4 months after the initial dose to maintain normocalcemia. Conclusion: HCOM is managed by physical therapy, IV hydration, and IV bisphosphonates. Since hypercalcemia of immobilization is a sclerostin-mediated bone resorption process, a short course of steroids or the use of anti-sclerostin monoclonal antibody Romosozumab can be a reasonable treatment consideration however more research is needed for that.
Presentation: 6/2/2024
8732 Hypercalcemia: When It’s Not PTH, Why Not Blame Your Neighbor?
Authors: Misra Daniel , Roger Brennan Michael , Misra Lynda 
Published: October 2024

Abstract
Disclosure: D. Misra: None. M.R. Brennan: None. L. Misra: None.
A 60-year-old female with a history of recently diagnosed hyperthyroidism, hypertension, and seizure disorder presents with a four-month history of neck swelling and pain. The patient was diagnosed with hyperthyroidism four months prior to admission and was started on methimazole 10 mg three times a day for two months, then instructed to decreased to 10 mg daily. In addition to the four months of neck swelling and pain, the patient also endorsed difficulty swallowing, palpitations, constipation, and bilateral ankle edema. Vital signs were stable other than a heart rate in the low 100s. Physical exam revealed a fixed painful L sided neck mass with no signs of airway compromise and bilateral exophthalmos. Labs revealed TSH &lt;0.01 uIU/mL, Free T4 2.1 ng/dL, TSI was elevated (&gt;40) IU/L. potassium 3.2 mmol/L, hypomagnesemia 1.3 mg/dL, troponin of 55 ng/l and hemoglobin 9.3 g/dL. The patient had a calcium of 10.6 mg/dL and an ionized calcium of 5.73 mg/dL with a normal PTH (34 pg/mL) and a low Vitamin D (22 ng/mL). A CT of the neck was performed showing marked thyromegaly with innumerable subcentimeter hypodense nodules in both lobes and a dominant 1.1 nodule in right lobe. Initial therapy involved correction of the electrolytes, telemetry monitoring, and a consultation to the endocrine service. The endocrine team started the patient on methimazole 10mg/daily and ordered a thyroid scan. Scintigraphy was performed and was consistent with Graves’ disease. On Day #2 the patient’s vital signs had normalized and the patient was able to swallow and tolerate a regular diet, The scan showed an enlarged thyroid with diffuse nodular character and moderate hyperemia consistent with diffuse thyroiditis. The scan also described a multinodular goiter with the largest nodule measuring 2.2 cm. She was discharged on Day #3 on methimazole 10mg daily and asked to follow up with endocrinology. Graves’ disease is a common cause of hyperthyroidism and is caused by autoantibodies that increase the production of thyroid hormone. Along with classic symptoms of hyperthyroidism, our patient had hypercalcemia. This was non-PTH mediated and in the absence of other signs or symptoms of a malignancy or granulomatous process, the hypercalcemia is likely due to her hyperthyroid state. Hyperthyroidism-associated hypercalcemia is a rare complication in hyperthyroid patients but should not be forgotten when evaluating non-PTH mediated hypercalcemia as it can be corrected easily with appropriate medications or in this case with the correction of the hyperthyroidism. Consideration of this etiology may also reduce the number of extraneous labs and imaging when no other common etiology is found.
Presentation: 6/2/2024
8541 Hypocalcemia In Setting Of Hypoparathyroidism And Gastric Bypass
Authors: Abrahimi Nora , Abrahimi Aryan 
Published: October 2024

Abstract
Disclosure: N. Abrahimi: None. A. Abrahimi: None.
Background: Hypocalcemia secondary to hypoparathyroidism is a known complication for patients who undergo thyroidectomy. (1) Additionally, patients who undergo bariatric surgery are similarly at risk for developing hypocalcemia. (2) Clinical Case: 52-year-old female with past medical history of thyroid carcinoma status post total thyroidectomy complicated by post operative hypoparathyroidism and history of gastric bypass presented to the hospital with paresthesia and fatigue. On presentation, calcium measured at 6.9 mg/dL, EKG showed Qtc prolongation at 503. Physical exam was positive for Chvostek sign and Trousseau sign. The patient received 1 g of intravenous calcium gluconate and was admitted to medicine for management of symptomatic hypocalcemia. Calcium initially improved to 8.2 mg/dL with a subsequent drop to 7.5 mg/dL. An additional 1 g of intravenous calcium gluconate was administered, calcium then corrected to 8.0 mg/dL, symptoms and Qtc prolongation resolved. The patient endorsed compliance with daily calcium supplementation of oral calcitriol prior to presentation. Prior to discharge, calcitriol dosage was increased, and patient was instructed to follow up calcium levels in one week outpatient with endocrinologist. Conclusion: Bariatric surgery, specifically gastric bypass or Roux-en-Y bypass reduces absorption of vitamin D and calcium as the primary sites for absorption are bypassed. (3) Although not commonly studied, severe hypocalcemia is linked to an increased risk for development of serious cardiac arrhythmias. (4) This emphasizes the importance of close calcium monitoring in patient with history of bariatric surgery and hypoparathyroidism.
References:
1. Lee YS, Nam KH, Chung WY, Chang HS, Park CS . Postoperative complications of thyroid cancer in a single center experience. J Korean Med Sci. 2010;25(4):541. Epub 2010 Mar 19.
2. Slater GH, Ren CJ, Siegel N, Williams T, Barr D, Wolfe B, Dolan K, Fielding GA. Serum fat-soluble vitamin deficiency and abnormal calcium metabolism after malabsorptive bariatric surgery. J Gastrointest Surg. 2004;8:48-55. doi: 10.1016/j.gassur.2003.09.020
3. Panazzolo DG, Braga TG, Bergamim A, Pires B, Almeida H, Kraemer-Aguiar LG. J Med Case Rep. 2014; 8: 357. Epub 2014 Oct 28. doi: 10.1186/1752-1947-8-357
4. Khalid S, Albaba I, Neu K. Hypocalcemia: A Little Known Cause of Supraventricular Tachyarrhythmia. Cureus. 2023;15(5):e38456. Published 2023 May 2. doi:10.7759/cureus.38456
Presentation: 6/1/2024
8025 Hypocalcemia Secondary To Relative Hypoparathyroidism After Parathyroidectomy For Tertiary Hyperparathyroidism
Authors: Solanki Naisargee N , Bahrou Mohamad A , Taha Wael 
Published: October 2024

Abstract
Disclosure: N.N. Solanki: None. M.A. Bahrou: None. W. Taha: None.
Parathyroidectomy is one of the treatment options for patients with tertiary hyperparathyroidism. Hypocalcemia following parathyroidectomy is a well-known occurrence due to a sudden drop in parathyroid levels, commonly to normal levels. We describe a case of hypocalcemia following subtotal parathyroidectomy for tertiary hyperparathyroidism with elevated parathyroid hormone (PTH) levels but relatively low compared to baseline. A 56-year-old female with a history of end-stage renal disease status post renal graft rejection presents for elective parathyroidectomy for tertiary hyperparathyroidism. Pre-operative investigations showed serum calcium levels of 11.6 mg/dL, normal value (NV): 9-10.5 mg/dL, serum phosphorus levels of 5.6 mg/dL, NV: 2.7-4.5 mg/dL, very high levels of serum intact PTH of 1257 pg/mL, NV: 10-65pg/mL and high level of alkaline phosphatase of 376 U/L, NV: 40-150 U/L. The patient underwent right and left inferior parathyroidectomy. Postoperatively, the patient's intact PTH levels remained elevated [895 pg/mL]; however, they decreased compared to baseline, but she developed hypocalcemia requiring intravenous and oral calcium supplementation. On postoperative day seven, she was discharged on oral calcitriol and calcium carbonate. Hypocalcemia following parathyroidectomy is well-described in cases where the PTH levels drop to the normal range. This case highlights that hypocalcemia can also occur when there is a relatively lower PTH level while the absolute value remains elevated.
Presentation: 6/1/2024
5071 Impact of Estrogen Replacement Therapy on Bone Health in a Novel Non-human Primate Model of Postmenopausal Women Living with HIV
Authors: Sauter K , Takahashi D L , Webb G , Hofmeister H , Varlamov O , Sacha J , Kievit P 
Published: October 2024

Abstract
Disclosure: K. Sauter: None. D.L. Takahashi: None. G. Webb: None. H. Hofmeister: None. O. Varlamov: None. J. Sacha: None. P. Kievit: None.
Current antiretroviral therapy (ART) regimens have rendered HIV a manageable chronic condition rather than a fatal disease, with people who initiate ART soon after infection achieving nearly normal life expectancy. As a consequence of increased survival, more women living with HIV (WLWH) will now undergo menopause and be subject to a disease burden that reflects age along with adverse skeletal consequences of postmenopausal estrogen deficiency. In addition to known bone loss and increased fracture risk in postmenopausal women, ART also causes decreased bone mineral density. Therefore ART-suppressed WLWH may have a compounded detrimental effect on bone due to long-term ART treatment combined with menopause that may be attenuated with estrogen replacement. Eleven rhesus macaques were infected intravenously with SIVmac239M and received ART two weeks post-infection (PI). All animals were ovariectomized (OVX) at 35 weeks PI and received estrogen implants (n=6) or cholesterol implants (n=5). Weekly blood samples were collected and animals were monitored longitudinally for body composition including bone mineral content (BMC) via dual x-ray absorptiometry (DEXA). Infection with SIV caused a significant decrease, -8.2%, in pelvis BMC after 14 days of peak viremia with SIV. These changes were not observed in the BMC of spine or extremities. BMC remained suppressed by ∼7% for an additional 25 weeks PI during ART treatment. Measurement of circulating bone turnover markers (BTMs), osteocalcin and C-terminal telopeptide of type 1 collagen (CTX), decreased post infection without significant improvement after ART suppression. Induction of menopause via OVX and loss of estrogen induced a drastic increase in BTMs with a much larger increase in CTX, indicating potential global bone loss due to OVX. Post-implant, the control animals’ pelvis BMC continued to decrease to -20.9% and pelvis BMD to -9.3% indicating that OVX further exacerbated the effect of SIV and ART. However, animals that received estrogen implants demonstrated marked improvement in both measures to greater than baseline. SIV and subsequent long-term ART negatively impact pelvic BMC and BMD and this effect is compounded by menopause in our model of post-menopausal WLWH. However, estrogen replacement post-menopause may attenuate these detrimental bone effects despite long-term ART treatment.
Presentation: 6/1/2024
8810 Improvement in bone mineral density in tertiary hyperparathyroidism after renal transplant treated with parathyroidectomy
Authors: Zakher Mariam , Barnett Braden G 
Published: October 2024

Abstract
Disclosure: M. Zakher: None.
55 year old man with past medical history of end-stage renal disease (ESRD) and alcoholic cirrhosis who underwent simultaneous liver-kidney transplant (SLKT) seven months prior to presentation to endocrinology who was referred for management of hypophosphatemia as low as 1.0 mg/dl. Prior to the transplant, he had hyperphosphatemia and hyperparathyroidism with phosphate and parathyroid hormone (PTH) levels as high as 8.2 mg/dL and 682 pg/mL, respectively. PTH remained elevated at 244 pg/mL and vitamin D was 35 ng/mL the week of the initial endocrinology visit. Initial DXA scan six months after SLKT showed osteoporosis of the lumbar spine, total left proximal femur, and left femoral neck with T-scores of -3.4, -4.9, -5.6, respectively. Alendronate was started three weeks prior to the initial visit. Urine studies confirmed phosphate wasting with urinary phosphate excretion significantly higher than 100 mg/24h, FEPO4 greater than 70%, and TmP/GFR less than 2 mg/dL. Increased urinary excretion of phosphate was consistent with hyperparathyroidism. The extremely low urinary calcium in the setting of normocalcemia and the history of renal transplant suggested a tertiary hyperparathyroidism. Alendronate was discontinued eight months after the initial visit to reduce the risk of post-parathyroidectomy hypocalcemia and post-parathyroidectomy bone remodeling inhibition.One year after the initial visit, the patient had a bilateral neck exploration with total parathyroidectomy and auto transplantation of the parathyroid. Pathology showed hypercellular parathyroid tissue. He was hospitalized one week after surgery for symptomatic hypolcalcemia (calcium 5.8 mg/dL). He was taking one tablet of calcium carbonate three times daily at home instead of three tablets three times daily as prescribed. He was discharged on calcitriol 0.5 mcg once daily, magnesium oxide 800 mg twice daily, calcium carbonate 1 g three times daily, and cholecalciferol 5000 units once daily. He remained on these for eleven months as well as calcitriol for fifteen months with dose adjustments during visits. Calcitriol was discontinued when calcium was found to be 8.9 mg/dL and the patient was asymptomatic. Repeat DXA scan two years after the baseline DXA showed osteoporosis of the left femoral neck with a T score of -2.5. There was a tremendous improvement from the baseline DXA scan from +20% in the total lumbar spine to +170% in the left femoral neck. DXA scan four years after the baseline DXA scan showed osteopenia of the lumbar spine, total left proximal femur, and left femoral neck with T-scores of -1.7, -2.4, -1.9.This is a 55 year old man who underwent SLKT seven months prior to presentation to endocrinology who was referred for management of hypophosphatemia as low as 1.0 mg/dL found with tertiary hyperparathyroidism who underwent a parathyroidectomy that resulted in significant improvement in bone mineral density test.
Presentation: 6/2/2024
7630 Incidental Calvarial Brown Tumor in an ESRD patient with seizures
Authors: Nikita Pereira Kristal , mehta vidhi , Sekaran Sruthi , Renzu Mahvish 
Published: October 2024

Abstract
Disclosure: K.N. Pereira: None. V. mehta: None. S. Sekaran: None. M. Renzu: None.
Brown Tumor [BT], also known as Osteitis fibrosa cystica [OFC], is a rare tertiary manifestation of hyperparathyroidism [HPTH]. BT commonly affects the maxilla/mandible, long bones and spine and presents as lytic bone lesions on imaging. Among the crania-facial bones, the maxilla, palate, temporal bone, nasal cavity, orbital bone and paranasal sinuses are affected. We describe a case of a 37 year old African-American female with extensive medical history including ESRD on hemodialysis who initially presented to the hospital with hypertensive emergency in the setting of 1 week of missed dialysis. During her presentation, she had an unexplained seizure which led to further workup with imaging. CT head revealed findings suspicious of renal osteodystrophy as well as a discrete lucency at the calvarial vertex suggestive of a brown tumor. Endocrinological studies were noted to have very high PTH levels with hypercalcemia, hyperphosphatemia and vitamin D deficiency indicative of tertiary hyperparathyroidism. Based on her clinical presentation, labs and imaging, her bone disease including BT and pathologic fractures, was deemed to be due to tertiary hyperparathyroidism in the setting of ESRD, which were not amenable to surgical intervention. Extensive literature review did not reveal any reported BTs in the calvarial vertex. This case emphasizes on the holistic approach to diagnosis of BTs and underlines that fact that BT can occur in any cortical bone including unusual presentation sites like the calvarial vertex.
Presentation: 6/3/2024
8519 Investigating the Role of Protein Inhibitor of Activated STAT1 (Pias1) in Growth Plate Chondrocyte Maturation
Authors: Baronas John , Ahmed Usman , Hirschhorn Joel N , Renthal Nora E 
Published: October 2024

Abstract
Disclosure: J. Baronas: None. U. Ahmed: None. J.N. Hirschhorn: None. N.E. Renthal: None.
Development of growth plate chondrocytes is a complex process that involves a wide array of regulatory elements. Recently our laboratory conducted a genome wide CRISPR knockout (KO) screen of growth plate chondrocyte maturation to discover novel genes and gene networks in the proliferation and maturation of chondrocytes. Among targets uncovered is Protein Inhibitor of Activated STAT 1 (Pias1), an E3 SUMO ligase that plays a multi-faceted role in genetic regulation, driving post-translational modifications, directly binding to transcription factors, and functioning as a DNA-binding protein. While Pias1 has been shown to be involved in the regulation of many cellular processes across multiple tissues, its function in growth plate development and chondrocyte maturation has been previously unstudied. In our genome-wide screen, our laboratory identified that loss of Pias1 led to early maturation of chondrocytes. This project seeks to investigate the role of Pias1 in chondrocyte maturation and differentiation. We first developed a Pias1-KO chondrocyte cell line, observing upregulation of hypertrophic markers Cd200 and Col10a1 in KOs relative to control via qPCR, in addition to proliferative regulators IHH and Pth1R. Through Bulk-RNAseq of the same cell line, we identified additional chondrocyte markers as upregulated in KO, as well as osteoblast marker Sp7. Members of the HoxD family, regulators of limb development, were downregulated. Cell culture data suggests that loss of Pias1 leads to increased cell proliferation and increased matrix production, indicating dysregulation of multiple chondrocyte processes. Immunohistochemistry of micromass culture sections also suggests morphological differences between KO and control, with KO cells significantly larger in diameter. Early SUMO-1 profiling yields limited evidence of decreased global SUMOylation in KO cells, one possible mechanistic explanation for the observed dysregulation. Ongoing studies are focused on identifying specific SUMOylation targets of Pias1 in chondrocytes, analyzing proteomic differences in KO and control, seeking putative DNA-binding sites of Pias1, and observing in vivo murine Pias1-KO growth plates. Our findings suggest that PIAS1 plays a crucial role in the growth plate by prolonging growth and delaying terminal hypertrophy. Our study aims to provide a better understanding of the regulatory pathways involved in growth plate development and related phenotypes such as height, and contribute to the development of novel therapies for growth-related disorders, such as achondroplasia and hypochondroplasia.
Presentation: 6/1/2024