Symptomatic Hypercalcemia Research Articles

Oral Versus Injectable Vitamin D Therapy for Treating Nutritional Rickets in Indian Children: A Comparative Study.

Rickets is a common metabolic bone disease in children, primarily caused by vitamin D deficiency. This study aimed to compare the efficacy of oral weekly vitamin D supplementation and injectable stoss therapy in treating nutritional rickets in Indian children. This prospective, randomized, controlled trial was conducted over 18months at a tertiary care center. Forty children aged 6months to 16years with clinical, biochemical, and radiological evidence of nutritional rickets were enrolled and randomly assigned to receive either oral vitamin D3 (60,000IU weekly for 10weeks) or a single intramuscular injection of vitamin D3 (600,000IU). Clinical, biochemical, and radiological assessments were conducted at baseline and at 3weeks, 6weeks, 3months, and 6months post-treatment. Both treatment regimens significantly improved vitamin D, calcium, phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) levels, with no significant differences between the groups. Radiological healing, assessed by Thacher's score, was achieved in both groups by 6months. While both treatments were effective, injectable stoss therapy resulted in a more sustained increase in vitamin D levels and may offer better compliance due to its single-dose administration. No cases of local skin complications or vitamin D toxicity or symptomatic hypercalcemia were observed. Oral weekly and injectable stoss therapies are both effective and safe for treating nutritional rickets. Injectable stoss therapy may be more suitable for the Indian population due to its cost-effectiveness and lower compliance demands. Serum parathyroid hormone (PTH) levels emerged as a useful early marker of rickets severity as well as treatment response. Early diagnosis and treatment are crucial to prevent long-term skeletal deformities.

Unveiling a Diagnostic Enigma: A Rare Case Report of Abdominal Sarcoidosis

Sarcoidosis is an idiopathic inflammatory granulomatous disorder that primarily affects the lungs. Abdominal manifestations without pulmonary involvement are infrequent. We present an atypical case of sarcoidosis in an elderly lady who presented with symptomatic hypercalcemia with computed tomography (CT) revealing multiple hepatosplenic hypodense granulomatous lesions with raised angiotensin-converting enzyme (ACE) levels. She had a good response to immunosuppressants. There is a rare possibility of isolated organ involvement without any pulmonary manifestation. Hence, ruling out other differentials and starting appropriate immunosuppressive treatment is necessary.

Chapter 12: PREPARATION FOR PARATHYROID SURGERY.

Preoperative treatment of PHPT aims to 1) manage severe and/or symptomatic hypercalcemia and 2) prevent postoperative hypocalcemia. Severe hypercalcemia, defined as a blood calcium level ≥ 3.5 mmol/L, requires admission to hospital in a conventional or critical care unit, depending on clinical symptoms and comorbidities. Decision to admit a patient in a critical care unit relies on the existence of one or more clinical manifestations (impaired alertness, dehydration with acute renal failure, severe acute pancreatitis) or threatening electrocardiographic signs, or one or more significant comorbidities, notably cardiovascular. Oral rehydration and/or intravenous volume expansion, adapted to cardiac and renal function, form the basis of treatment to lower blood calcium level. If insufficient, intravenous bisphosphonates (zoledronate or pamidronate) are recommended to achieve a reduction in blood calcium levels sufficiently long to allow surgery to be organized. All bisphosphonate injections must be preceded by a minimum etiological work-up of hypercalcemia, including PTH, phosphate and 25-hydroxy vitamin D levels, as well as calciuria and creatininuria. Since bisphosphonates take 24-36 hours to take effect, calcitonin can initially be combined with them, as it has a rapid onset of action of a few hours. Denosumab is recommended in second line where bisphosphonates cannot be used, notably because of impaired renal function. Hemodialysis is proposed for patients with an identified vital risk, especially if volume expansion is not possible due to cardiac or renal insufficiency. Correction of vitamin D deficiency is recommended before parathyroid surgery if blood calcium levels are < 3.5 mmol/L, to prevent or attenuate severe postoperative hypocalcemia due to massive calcium transfer to the bone.

Particularités de l'hypercalcémie des patients du CHU de Cocody- Côte d’Ivoire

describe the epidemiological, clinical, etiological and therapeutic aspects of hypercalcemia seen in the rheumatology department of Cocody University Hospital. Descriptive cross-sectional study carried out in the rheumatology department of Cocody University Hospital from January 2013 to July 2022 and covering the files of patients with hypercalcemia. The hospital frequency of hypercalcemia was 0.88%, or 60 cases out of 6771 hospitalizations during the study period. The workforce included 35 men and 25 women (M/F ratio=0.14), aged on average 56±11.52 years (range 25 and 80 years). The main reason for consultation related to the underlying disease was osteoarticular pain syndrome. The signs related to symptomatic hypercalcemia were digestive (23.33%), neurological (8.33%) and cardiovascular (5%). The main extra-articular signs were asthenia (90%) and weight loss (78.33%). On the biological level, there was a clear predominance of mild hypercalcemia (76.67%), followed by moderate hypercalcemia (10%) and severe hypercalcemia (13.33%). The etiologies were dominated by multiple myeloma (45%), followed by bone metastases (40%), granulomatosis (13.33%) and secondary hyperparathyroidism (1.67%). The molecules used for the treatment of hypercalcemia were corticosteroids and biophosphonates. The outcome was favorable in 18.33% of patients, and unspecified in 66.67% of cases due to the patient's transfer to another department. There were 9 deaths, or 15% of cases. Hypercalcemia is rare and most often asymptomatic in rheumatological hospitalizations in Abidjan. Multiple myeloma is the main etiology.

8592 Parathyroid Carcinoma: A Rare Cause of Primary Hyperparathyroidism

Abstract Disclosure: S.E. Koshy: None. C.F. Mulcahy: None. P.S. Kothari: None. E.M. Jacobi: None. T.D. Cubb: None. Introduction: Parathyroid carcinoma (PC) is a rare malignancy that accounts for &amp;lt;1% of cases of primary hyperparathyroidism (PHPT). Patients often present with symptoms of hypercalcemia, serum calcium (Ca) &amp;gt;14 mg/dL, large tumor size, and a very high parathyroid hormone (PTH) level. We report a case of an asymptomatic patient with incidentally found hypercalcemia consistent with PHPT who was ultimately diagnosed with PC. Clinical Case: A 31yo male was found to have elevated serum Ca of 12.7 mg/dL (8.6-10.3 mg/dL) on labs obtained during routine physical exam. He had no known significant medical or family history and notably had no laboratory evaluation within the prior 10 years. He denied constipation, polyuria, confusion, depression, bone pain, and history of fractures or nephrolithiasis. Workup showed an inappropriately elevated PTH of 505 pg/mL (16-77 pg/mL). Neck ultrasound demonstrated a left inferior 3.9 cm complex thyroid nodule. Sestamibi scan confirmed increased uptake in the inferior left thyroid. Left neck exploration was performed. Intraoperatively, a 3.7 cm left parathyroid mass weighing 13.0 grams was encountered and excised in an en bloc fashion. The left superior parathyroid gland was evaluated and found to be normal. Intraoperative PTH level decreased from 529 pg/mL to 48 pg/mL 10 minutes after excision. Left hemithyroidectomy was not performed. Surgical pathology revealed PC with lymphovascular invasion, suspected capsular invasion, and negative margins. Immunohistochemical staining showed a Ki67 proliferation index up to 5% and complete loss of nuclear staining for parafibromin. Next generation sequencing demonstrated a somatic CDC73 p.L8fs mutation, tumor mutational burden 4.7m/MB, and stable microsatellite instability. Germline testing was negative for a CDC73 mutation. Postoperative staging did not demonstrate evidence of metastatic disease in the neck or chest. Serum Ca remained within normal limits. After multidisciplinary discussion, no further surgical intervention was recommended and plan was for ongoing biochemical and imaging surveillance. Conclusion: Though rare, PC should be considered as a cause of PHPT. The primary treatment is complete surgical resection. Unfortunately, there is a high rate of recurrence, &amp;gt;50%, with most occurring 2-5 years after initial surgery with a median overall survival of 14 years. Thus, long-term surveillance is of utmost importance. Treatment of recurrent disease is surgical resection when feasible as well as medical management of hypercalcemia. Further research is needed to better understand the role of targeted systemic therapy in addition to immunotherapy. PC is most commonly sporadic but can be hereditary, thus genetic evaluation is recommended. Given its rarity and complexity, PC is best managed in a multidisciplinary setting. Presentation: 6/1/2024

8592 Parathyroid Carcinoma: A Rare Cause of Primary Hyperparathyroidism

Abstract Disclosure: S.E. Koshy: None. C.F. Mulcahy: None. P.S. Kothari: None. E.M. Jacobi: None. T.D. Cubb: None. Introduction: Parathyroid carcinoma (PC) is a rare malignancy that accounts for &amp;lt;1% of cases of primary hyperparathyroidism (PHPT). Patients often present with symptoms of hypercalcemia, serum calcium (Ca) &amp;gt;14 mg/dL, large tumor size, and a very high parathyroid hormone (PTH) level. We report a case of an asymptomatic patient with incidentally found hypercalcemia consistent with PHPT who was ultimately diagnosed with PC. Clinical Case: A 31yo male was found to have elevated serum Ca of 12.7 mg/dL (8.6-10.3 mg/dL) on labs obtained during routine physical exam. He had no known significant medical or family history and notably had no laboratory evaluation within the prior 10 years. He denied constipation, polyuria, confusion, depression, bone pain, and history of fractures or nephrolithiasis. Workup showed an inappropriately elevated PTH of 505 pg/mL (16-77 pg/mL). Neck ultrasound demonstrated a left inferior 3.9 cm complex thyroid nodule. Sestamibi scan confirmed increased uptake in the inferior left thyroid. Left neck exploration was performed. Intraoperatively, a 3.7 cm left parathyroid mass weighing 13.0 grams was encountered and excised in an en bloc fashion. The left superior parathyroid gland was evaluated and found to be normal. Intraoperative PTH level decreased from 529 pg/mL to 48 pg/mL 10 minutes after excision. Left hemithyroidectomy was not performed. Surgical pathology revealed PC with lymphovascular invasion, suspected capsular invasion, and negative margins. Immunohistochemical staining showed a Ki67 proliferation index up to 5% and complete loss of nuclear staining for parafibromin. Next generation sequencing demonstrated a somatic CDC73 p.L8fs mutation, tumor mutational burden 4.7m/MB, and stable microsatellite instability. Germline testing was negative for a CDC73 mutation. Postoperative staging did not demonstrate evidence of metastatic disease in the neck or chest. Serum Ca remained within normal limits. After multidisciplinary discussion, no further surgical intervention was recommended and plan was for ongoing biochemical and imaging surveillance. Conclusion: Though rare, PC should be considered as a cause of PHPT. The primary treatment is complete surgical resection. Unfortunately, there is a high rate of recurrence, &amp;gt;50%, with most occurring 2-5 years after initial surgery with a median overall survival of 14 years. Thus, long-term surveillance is of utmost importance. Treatment of recurrent disease is surgical resection when feasible as well as medical management of hypercalcemia. Further research is needed to better understand the role of targeted systemic therapy in addition to immunotherapy. PC is most commonly sporadic but can be hereditary, thus genetic evaluation is recommended. Given its rarity and complexity, PC is best managed in a multidisciplinary setting. Presentation: 6/1/2024

7759 Undetectable PTHrP and Elevated Il-6 in a 517759 Year Old Male With Clear Cell Renal Carcinoma, Complicated by Paraneoplastic Hypercalcemia

Abstract Disclosure: E. Cedeno: None. T. Patel: None. C. Zacharia: None. Title Undetectable PTHrP and elevated IL-6 in a 51-year-old male with clear cell renal carcinoma, complicated by paraneoplastic hypercalcemia. Introduction: Malignant hypercalcemia as a paraneoplastic syndrome is very common in lung and kidney cancers. Traditionally, humoral hypercalcemia of malignancy (HHM) is linked to excess PTHrP production, but other possible contributors, such as interleukin-6 (IL-6), have been identified. We present a case of HHM with undetectable PTHrP and elevated levels of IL-6. Case A 51-year-old male with RCC presented with symptomatic hypercalcemia (polyuria and polydipsia), found during a pre-op visit. Initial tests were consistent with non parathyroid-mediated hypercalcemia: adjusted Ca 13.2 (9.1-11.2 mg/dL), iCal 1.69 (0.95-1.32 mmol/L), iPTH &amp;lt;4.0 (8.0-85.0 pg/mL), 25-OH-Vit D 41(30-80 ng/mL), 1,25-OH D 64.7 (24.8- 81.5pg/mL), PTHrP undetectable (&amp;lt;2.0 pmol/L), SPEP and UPEP without abnormalities. A CT showed a large 15x12x14 cm partially necrotic mass arising from the right kidney, consistent with malignancy. The patient was treated with isotonic IV fluids and underwent a right nephrectomy on day 6 of hospitalization with subsequent complete resolution of hypercalcemia 24 hours post-surgery. Adjusted Ca and iCal normalized. iPTH from initial 4 improved to 30.1 (8.0-85.0 pg/mL), and IL-6 was found to be high to 62.5 (0.0-13.0 pg/mL). Final pathology was consistent with clear cell RCC. The patient was discharged, with normal laboratory values on follow-up. Conclusion: Hypercalcemia is the most common paraneoplastic complication of RCC, and approximately 17% of all patients with RCC will develop hypercalcemia. Although usually mediated by PTHrP, evidence points towards other possible contributors. IL-6 has been hypothesized to be a possible mediator of malignant hypercalcemia in paraneoplastic syndromes¹. This is evidenced by our case, where our patient had undetectable levels of PTHrP in the setting of RCC, and was later found to have elevated IL-6, pointing to the latter as a possible culprit. In conclusion, our case supports IL-6 as a possible contributor to the pathogenesis of malignant hypercalcemia in RCC patients, literature is sparse on PTHrP-independent HHM and rare case reports demonstrated this phenomenon not just in RCC but also in other malignancies like ALL. There are some hypotheses implicating IL-6 influencing tumor growth as well as bone metastasis. Our case adds a valuable contribution to this limited database. Further studies are warranted to understand the role of IL-6 in HHM as well as anti-IL6 agents as a potential therapeutic option for treatment-resistant hypercalcemia. Reference: Max G. Weissglas, The Role of Interleukin-6 in the Induction of Hypercalcemia in RCC Transplanted into Nude Mice, Endocrinology, Volume 138, Issue 5, May 1997, Pages 1879-1885. Presentation: 6/2/2024

7254 An Unusual Case Of Hypercalcemia

Abstract Disclosure: S. Shushtarian: None. M. Balogun: None. T. Kaur: None. Hypercalcemia varies depending on severity. Higher serum calcium levels and more severe symptoms may indicate primary hyperparathyroidism or a malignant cancer. This is a case of a 32 year old female who presented with recurrent history of nephrolithiasis, found to have hypercalcemia of 13.4 mg/dL and parathyroid hormone of 1928.9 pg/mL, with phosphorus of 1.5 mg/dL. Ultrasound of her thyroid revealed a complex nodule arising from the right parathyroid gland measuring 2.2 X 2.0 cm. CT chest revealed diffuse osseous sclerosis secondary to metabolic disorder. Sestamibi scan did not localize any parathyroid adenoma. MRI of the thoracic and lumbar spine showed multiple small enhancing lesions throughout the pelvis and in the left rib, likely brown tumors related to hyperparathyroidism. X-ray of bony prominence on the patient’s left knee revealed a large lytic lesion of the proximal tibial diaphysis measuring 5.1 X 1.9 cm, concerning for aggressive neoplasm. Subsequent left tibial bone biopsy revealed giant cell rich lesions consistent with brown tumor of hyperparathyroidism. Due to our patient’s high calcium levels and large nodule size, she was referred to a tertiary center as the concern for parathyroid carcinoma and post-op hungry bone syndrome was high. Pre-op PTH level was 1408 pg/mL and post-op PTH was 96 pg/mL. The tumor removed was 2.1 cm. Post surgical pathology was consistent with atypical parathyroid adenoma. Patient was referred for genetic testing. An atypical parathyroid adenoma (APA) only accounts for 1.2 to 1.3% of cases of primary hyperparathyroidism. 80-85% of primary hyperparathyroidism is due to typical adenoma, and 10 to 15% of cases are due to hyperplasia or multiple gland disease. APA can often be confused with parathyroid carcinoma (PC), as they both have a 1:1 male to female ratio, high serum calcium levels, symptomatic hypercalcemia, high PTH levels, and fragility fractures. There are studies showing that both APA and PC have loss of nuclear parafibromin immunoreactivity. In addition, neither APA nor PC have any correlation with menopause, hormones, or gene deletions, unlike typical adenomas. Biopsy is necessary for diagnosis as the histological and immunohistochemical differences can differentiate APA vs PC. Histological features include pseudo-capsular invasion, bands of fibrosis, pronounced trabecular growth, nuclear atypia, and prominent nucleoli. Also, APA has a strong membranous staining pattern of E-cadherin, whereas PC has a loss of membranous staining. These differences are essential as although APA and PC clinically present similarly, APA lacks the invasive growth and possibility for metastatic disease that PC has. The likelihood for relapse of APA is low. Presence of malignancy criteria are indicative that a mass is actually PC and not APA. Despite this, APA is still considered a tumor of uncertain malignant potential and requires follow up. Presentation: 6/3/2024

7027 A Rare And Multifactorial Etiology Of Severe Parathyroid Hormone Independent Hypercalcemia In An Adult Female With Rett Syndrome

Abstract Disclosure: M.I. Foo: None. M. Thompson: None. Background: Symptomatic hypercalcemia is a rare, but potentially life-threatening disorder. Although dehydration is an unusual cause of severe hypercalcemia, in the appropriate clinical setting dehydration may amplify underlying mild or moderate hypercalcemia to dangerous levels.Case: A 46-year-old non-verbal, non-mobile Caucasian female with Rett Syndrome (RS) with Stage III Chronic Kidney Disease (CKD3) who is dependent on percutaneous endoscopic gastrostomy (PEG) tube for nutrition and known PTH independent hypercalcemia of unknown etiology presented to the hospital with intractable vomiting and constipation, an outpatient serum calcium level of 16.0 mg/dL, and serum creatinine 4.03 mg/dL (baseline 1.2 mg/dL). Initial laboratory assessment revealed elevated corrected serum calcium levels (15.7 mg/dL), with appropriately suppressed PTH levels (12.5 pg/mL) and hypernatremia (146 mmol/L). Thyroid function tests, both Vitamin D 1,25(OH)2D and D 25(OH)D levels and PTH-RP were normal. Computed tomography of the abdomen and pelvis revealed bilateral nephrolithiasis and moderate stool burden, but no evidence of malignancy or granulomatous disease. Skeletal scintigraphy was also without evidence of osseous metastatic disease or Paget’s disease of bone. An in-depth interview with the patient’s caregiver uncovered that the patient had a relative intolerance to enteral hydration and had been receiving minimal water flushes prior to admission, contributing to severe dehydration. Hypercalcemia was ultimately ascribed to prolonged immobilization due to RS compounded by inadequate fluid intake and auto-diuresis secondary to hypercalciuria in the setting of CKD (prior baseline eGFR 45 mL/min/1.73m2).Outcome: The patient's hypercalcemia improved after a multidisciplinary and multi-directed approach involving intravenous and enteral fluid resuscitation, calcitonin, furosemide, and ultimately zoledronic acid following improvement in creatinine with fluid resuscitation. The dietary service employed a strategy of 24-hour enteral feeding, increasing both the frequency and amount of enteral water, which the patient tolerated well, and provided her with a new pump for home use. Education on monitoring tube feed tolerance and providing adequate enteral hydration was provided to both the caregiver and group home. On discharge, eGFR stabilized at 33 mL/min/1.73m2 and corrected calcium stabilized at 10.0–10.4 mg/dl. She was provided with an endocrinology follow-up to continue bisphosphonate therapy.Discussion: Hypercalcemia of immobility should remain a differential diagnosis in severe hypercalcemia, especially PEG tube dependent patients with underlying kidney disease. This case highlights the importance of thorough history taking and a multidisciplinary strategy to guarantee optimal care and mitigate potential adverse outcomes in medically complex patients. Presentation: 6/2/2024

5117 Unusual Sarcoid Presentation as a Case of Hypercalcemia

Abstract Disclosure: M. Salim: None. A. Chauhan: None. S. Avula: None. A. Ahmed: None. K. Zekarias: None. Background: Hypercalcemia may arise from a variety of causes and can pose challenging diagnostic dilemma. Clinical Case: An 89-year-old male presented with worsening malaise related to persistent hypercalcemia. He reported productive cough, polyuria, polydipsia, generalized muscle weakness and weight loss. Physical exam was remarkable for upper and lower extremities weakness. Laboratory tests showed calcium 11.6 (8.8-10.2 mg/dL), phosphorus 2.8 mg/dL (2.5-4.5 mg/dL), albumin 4.2 g/dL (3.5-5.2 g/dL), parathyroid hormone (PTH) 10 pg/mL (15-65 pg/mL), parathyroid hormone-related protein (PTH-rp) 4.5 pmol/L (0.0-2.3 pmol/L), TSH 6.24 (0.30 - 4.20 uIU/mL), free T4 1.10 ng/dL (0.90-1.70 ng/dL), GFR 61 mL/min/1.73m2, 25 OH Vit D 31 ng/mL (20-75 ng/mL), vit D 1,25-dihydroxy 134 pg/mL (19.9-79.3 pg/mL), calcium urine/creatinine 0.54. Hypercalcemia was first noted 11 months before the visit with a level of 14.0 mg/dL (8.8-10.2 mg/dL), phosphorus 3.5 mg/dL, PTH 11, PTH-rp 1.4 pmol/L, 25 OH Vit D 62 ng/mL, Vit D 1,25-dihydroxy 90 pg/mL, angiotensin-1-converting enzyme 12 U/L (16-85 U/L), serum and urine electrophoresis showed no monoclonal gammopathy present, and tuberculosis interferon-gamma test negative. Autoimmune workup was unremarkable, except for weak positive anti-signal recognition particle (SRP) antibodies and anti-Mi-2 antibodies. CT chest/pelvis/abdomen demonstrated peripheral predominant reticular opacities suggestive of interstitial lung disease and no malignant findings. Treatment history included zoledronic acid 11 months before the visit. The patient was referred for a granulomatous disease workup.Upon one month follow-up, the hypercalcemia symptoms were worsening. Repeat calcium was 12.3 mg/dL and fungal serologies were negative. The patient was started on prednisone empirically. PET CT was ordered and revealed patchy inflamed musculature of extremities suspicious of dermatomyositis/polymyositis. Further labs showed unremarkable myomarker panel, u3-Hydroxy-3-Methylglutaryl Coenzyme A reductase (HMGCR) antibody, Anti-cN-1A antibody, ACE 53 U/L, creatine kinase 32 U/L (39-309 U/L), aldolase 5.4 U/L (1.2-7.6 U/L), soluble IL-2R 1,021 U/mL (137-838 U/mL), and lysozyme 3.89 ug/mL (&amp;lt;2.75 ug/mL). A muscle biopsy was done, which showed benign skeletal muscle with patchy myofiber atrophy, patchy interstitial fibrosis, and focal interstitial mild chronic inflammation with no evidence of sarcoid granulomas in the sample. One week lab follow-up post initiation of steroid showed calcium of 10.1 mg/dL and subsequently improvement in his overall labs. Working diagnosis of sarcoid myositis was made. Conclusion: This case report highlights the approach of diagnosing a rare case of hypercalcemia due to sarcoid myositis. In a highly clinical suspicious patient, PET CT scan might be a necessary modality for diagnosis. Presentation: 6/2/2024

8157 Hypercalcemia To Hypocalcemia In Three Days: The Importance Of Asking The Questions

Abstract Disclosure: P. Kachhadia: None. K. Patel: None. S. Khan: None. A. Abu Limon: None. S. Aldasouqi: None. F. Akanbi: None. Z. Ul Abideen: None. Introduction: Severe hypercalcemia needing inpatient hospitalization requires very thorough history taking in order to determine etiology and treatment plan. Causes differ drastically, and misdiagnosis or mistreatment can be life threatening. Here, we present a case of symptomatic hypercalcemia secondary to milk-alkali syndrome that was treated promptly after admission with IV zoledronic acid, leading to severe symptomatic hypocalcemia and prolonged hospitalization. Case presentation: Patient is a 68 year old female with a PMH of breast cancer, osteoporosis and hiatal hernia who presented to the emergency department for fatigue, constipation and lightheadedness. On evaluation, she was found to have a creatinine of 1.54 (0.6-1.1 mg/dL), eGFR 36 (&amp;gt;90 mL/min/1.73 m²), Ca 18.48 (8.6-10.2 mg/dL), albumin 4.7 (3.4-5.4 g/dL), Mg1.4 (1.7-2.2 mg/dL), 25-OHD 18 (30-100), 1,25-Dihydroxy Vitamin D 7.4 (18-78 pg/mL), PTH 11.2 (15-65 pg/mL), phosphorus level 2.4 (2.5-4.5mg/dL), TSH 2.01 (0.4-4.0 mIU/L). SPEP and PTHrP were unremarkable. Due to history of prior breast cancer, imaging was done and CT showed new possible RUL pancoast tumor with RUL spiculated opacity. Patient was started on IV fluids and subsequently received IV zoledronic acid due to concern for severe hypercalcemia secondary to malignancy. By day 3 of treatment, patient's calcium decreased severely, down to a corrected calcium level of 6.4 (8.6-10.2 mg/dL). It was upon further investigation and discussion with the patient that we discovered the patient had received subcutaneous denosumab for her osteoporosis three weeks prior to admission. In addition, she was taking six tums daily (total 1 month duration) for symptoms of dyspepsia secondary her hiatal hernia. The patient’s severe hypocalcemia was treated with high dose oral calcium carbonate and vitamin D along with IV calcium gluconate. Magnesium was replaced daily. Through daily replacement, patient was kept in the hospital for a total of 10 days duration before her calcium levels were deemed safe for return home. Discussion: Hypercalcemia is a common cause of hospitalization worldwide. Testing should be comprehensive and history taking should be thorough to help navigate treatment plans. Bisphosphonates are indicated for hypercalcemia of malignancy, and its use otherwise may be the cause of severe hypocalcemia if not used in the right setting. In our case, the patient’s hypocalcemia was multifactorial from prior denosumab use and then subsequent zoledronic acid use. Additional risk factors included low vitamin D counts and disruption of high amounts of over the counter tums after being admitted to the hospital. Anchoring bias also led clinicians to believe that the hypercalcemia was secondary to malignancy. Consequently, this led to a prolonged 10 day hospitalization for persistently low calcium levels. Presentation: 6/1/2024

12350 A Rare Case Of Giant Parathyroid Adenoma Managed Medically For 8 Months: A Case Report

Abstract Disclosure: S. Labram: None. L. Bilandzic: None. Background: Single parathyroid adenoma is the most common cause of primary hyperparathyroidism, and is attributed to approximately 85% of cases[1]. However, those classified as giant (weighing over 3.5 g and having a size greater than 2cm2) are exceedingly rare. This reports a rare case of primary hyperparathyroidism caused by giant parathyroid adenoma and details biochemical response following medical and surgical management. Case Report: A 64 year old black female presented with severe abdominal pain, confusion and constipation. Investigations revealed severe hypercalcemia of 17.3 mg/dl with massively elevated parathyroid hormone of 1255 pg/mL. Ultrasound showed a large hypoechogenic lobulated mass inferior to the left thyroid lobe representing a giant parathyroid adenoma. Due to delayed surgery the patient was initially treated medically over the course of 8 months. Over these months she was admitted to hospital 3 times for symptomatic hypercalcemia and received a total of 3 zolendronic acid infusions. Despite this she was unable to achieve long term remission of hypercalcemia. Cinacalcet was added and tolerated at the dose of 30 mg daily. Hypercalcemia improved, but remained elevated at a range of 11-13 mg/dL and the symptoms of brain fog and constipation did not subside entirely. She was eventually able to undergo surgical resection, and a giant parathyroid adenoma weighing 8.9 g was excised. Intraoperative intact parathyroid hormone (IOiPTH) sampling showed &amp;gt; 50% reduction (prior to removal 878pg/mL, 10 minutes after removal 132 pg/ml, 20 minutes after removal 96pg/mL). Pathological review showed an atypical parathyroid tumor. As the tumor lacked invasive growth it did not meet criteria for carcinoma. Conclusions: This is a rare case of primary hyperparathyroidism caused by a giant solitary parathyroid adenoma. The gold standard for management of primary hyperparathyroidism secondary to parathyroid adenoma is minimally invasive parathyroidectomy. However in our case, due to inability to access immediate surgery, challenging and prolonged medical treatment of severe hypercalcemia followed for 8 months. Ultimately, normalization of calcium level was achieved only by surgical intervention. IOiPTH measurements showed appropriate decrease confirmatory for the complete removal of the adenoma.

8063 Cystic Parathyroid Adenoma: A Rare Cause Of Severe Hypercalcemia

Abstract Disclosure: M. Owrangi: None. F. Hasan: None. Introduction: Parathyroid adenomas are the most common cause of primary hyperparathyroidism, but within this category, a rare subtype exists - cystic parathyroid adenomas (CPAs). Comprising only 0.5-1% of all parathyroid lesions, CPAs present unique diagnostic and therapeutic challenges. We report a case of a female patient presenting with severe hypercalcemia caused by a CPA. Case presentation: A 44-year-old African American female with a history of nephrolithiasis presented with abdominal pain and signs of dehydration. Labs were remarkable for serum calcium 13.2 mg/dL, albumin 4.0 g/dL, phosphorus 1.8 mg/dL, iPTH 617.7 pg/mL, 25-OH vit D 12.1 ng/mL, creatinine 0.85 mg/dL. She was initially resuscitated aggressively with IV fluids resulting in an improvement in serum calcium level to 10.3 mg/dL. Thyroid US showed a cystic nodule deep to the left thyroid lobe. Sestamibi parathyroid scan was consistent with a left superior parathyroid adenoma. She underwent 2 gland parathyroidectomy 3 months after the initial presentation. Intraoperatively serum PTH decreased by 91% after resection of the 2 parathyroid adenomas. Pathology confirmed the presence of 2 parathyroid adenomas, the larger one measuring 2.8 cm and weighing 3.8 g. Discussion: We describe a case of a middle-aged female presenting with severe hypercalcemia due to CPA. Her initial presentation was concerning for parathyroid carcinoma given the severity of hypercalcemia. However, the radiologic findings, coupled with surgical pathology, indicated that she had CPA. CPAs can be either functional, causing primary hyperparathyroidism (PHPT) with elevated serum calcium levels, or non-functional, remaining asymptomatic. Clinical features of PHPT associated with CPAs are similar to those with solid adenomas and include fatigue, GI symptoms, nephrolithiasis, bone pain, and neuropsychiatric manifestations. However, CPAs may exhibit certain distinct presentations: i) higher pre-operative serum calcium levels; and ii) increased risk of symptomatic hypercalcemia. Despite their rarity, CPAs deserve special attention due to their unique presentation, challenging diagnosis, and potential for severe hypercalcemia. Surgical parathyroidectomy is the definitive treatment for functional CPAs. Accurate localization and complete excision of the adenoma are crucial to avoid recurrence. Most CPAs occur in the fourth and fifth decade of life and are more common in women (female to male ratio of 2.5:1). 65-85% of cases are located in the neck and the majority arise from the inferior parathyroid glands and are left-sided, and may very rarely be intrathyroidal. Presentation: 6/2/2024

7191 When Pain Is Misdiagnosed: A Case of Parathyroid Carcinoma Masked as Fibromyalgia

Abstract Disclosure: H. Pham: None. P.V. Kumar: None. S. Taylor: None. Parathyroid carcinoma is a rare and aggressive cause of hyperparathyroidism, typically associated with &amp;lt;1% of primary hyperparathyroidism cases. Incidence occurs mainly in the 5th decade of life, with less than 4% of all cases presenting in patients under age 30. Here, we highlight a case involving a 28-year-old woman with fibromyalgia who presented for worsening right shoulder pain in the setting of progressive, poorly characterized pain for the past year. Her initial physical exam was unremarkable aside from a non-tender left sided neck enlargement. However, her laboratory results were significant for corrected serum calcium of 15 mg/dL, serum phosphorus of 2.3 mg/dL, parathyroid hormone (PTH) &amp;gt;2500 pg/mL, and alkaline phosphatase 1604 units/L. X-ray of her right shoulder demonstrated mottled bone concerning for degenerative disease. Thyroid ultrasound revealed a complex cystic lesion posterior to the left thyroid lobe measuring 5.3 x 3.9 x 2.9 cm, worrisome for giant parathyroid adenoma. CT abdomen/pelvis showed diffuse osteosclerosis and innumerable lytic lesions, consistent with osteitis fibrosa cystica, as well as bilateral nephrolithiasis, likely medullary nephrocalcinosis. Her hypercalcemia was treated with aggressive hydration with normal saline and IV pamidronate. She underwent surgical resection of her parathyroid adenoma, which was unfortunately complicated by symptomatic hypocalcemia requiring prolonged care in the ICU. Her calcium levels did improve within a few days, and she was subsequently discharged with close outpatient follow-up. Final pathology report showed predominant thickened trabecular growth pattern with focal vascular invasion consistent with parathyroid carcinoma. Our patient’s case represents a rare presentation of parathyroid carcinoma in a young patient without any additional risk factors. Although atypical, her severe symptomatic hypercalcemia, nephrolithiasis, presence of large neck mass, and diffuse skeletal disease warranted immediate concern for malignant hyperparathyroidism instead of benign adenoma. Delayed diagnosis in our patient led to prolonged bone disease and severe complications. While hungry bone syndrome typically manifests post-parathyroidectomy in patients with end-stage renal disease, our patient experienced this complication in the setting of advanced, untreated hyperparathyroidism. We should consider hypercalcemia and hyperparathyroidism in our differential diagnosis for chronic pain, especially if pain remains uncontrolled with conservative measures. The most appropriate initial test for evaluation of hypercalcemia is a PTH level to distinguish between PTH-dependent and PTH-independent etiologies. Parathyroid carcinoma, even in young patients, should be considered when PTH is &amp;gt;3x upper limit of normal, serum calcium is &amp;gt;14, or skeletal and renal involvement is present. Presentation: 6/3/2024

8802 A Rare Case Of Symptomatic Hypercalcemia In A Patient With Untreated Chronic Tophaceous Gout

Abstract Disclosure: S. Avula: None. A. Kumar: None. Z.J. Anderson: None. A. Chauhan: None. L.T. LaFave: None. Background: Hypercalcemia is a medical condition with abnormally high serum calcium levels. There are numerous mechanisms for the development of hypercalcemia, but gout is not well documented.Hypercalcemia attributed to Tophaceous gout is a rare phenomenon that is not well studied. Here we report a case of symptomatic hypercalcemia in a patient with a history of untreated tophaceous gout, leading to hypercalcemia and osteolytic lesions. Clinical Case: The patient is a 52-year-old male with a medical history of hypertension, rheumatoid arthritis, and tophaceous gout who immigrated from Tanzania. He presented with two weeks of abdominal pain that acutely worsened the morning of his presentation. He reported a 16-year history of tophaceous gout, for which he had been treated with allopurinol without success. On physical examination polyarticular subcutaneous nodules were present in the bilateral upper and lower extremities, primarily over the joints. There were similar lesions on the buttocks. Initial laboratory evaluation included a complete blood count which was notable for a hemoglobin of 10.3 g/dL (13.1 - 17.5 g/dL). His albumin was normal at 4 g/dl. (3.8 - 5.1 g/dl). Serum calcium was elevated at 12.9 mg/dL (8.8-10.0 mg/dL), with a serum ionized calcium level of 6.52 mg/dL(4.40-5.20 mg/dL). PTH was low at 15.8 pg/mL (16.0 - 65.0 pg/mL), and PTHrP was 2.9 pg/ml (&amp;lt;4.5 pg/ml). Uric acid level on admission was elevated to 11.4 mg/dL (3.4 - 7.0 mg/dL). 1-25 dihydroxy vitamin D elevated at 93.2 pg/mL (19.9 - 79.3 pg/mL). Computed tomography (CT) with intravenous contrast of the chest, abdomen, and pelvis was notable for axillary, pelvic, and inguinal lymphadenopathy concerning for lymphoproliferative or neoplastic processes. Biopsy of right inguinal node biopsy showed benign-appearing lymphoid tissue. Additional findings included multiple lobulated calcified hyperdense foci throughout the subcutaneous and muscular tissues of the buttocks with resorptive changes of the axial skeleton. Spectral CT reconstruction determined these to be uric acid deposits. Radiographs of his extremities were consistent with advanced gouty arthropathy. Infectious work-up was negative. Patient was given 3 liters of 0.9% sodium chloride. He received four doses of Calcitonin (4 units/kg) followed by one dose of Zoledronic acid 5 mg I.V. He was treated with Febuxostat, solumedrol and Azathioprine for his tophaceous gouty arthritis. Conclusion: Hypercalcemia is a commonly encountered yet a very important clinical condition. Parathyroid and malignant etiologies of hypercalcemia account for approximately 90% of cases of hypercalcemia. Gout as the inciting factor for developing hypercalcemia is a rarely documented phenomenon. This case highlights hypercalcemia as an unusual yet severe manifestation of untreated chronic gout and demonstrates the need for additional studies and reviews. Presentation: 6/2/2024

Hypercalcemia in Hodgkin’s Lymphoma – A Case Report

Hypercalcemia, though rare is an important cause of diffuse aches and pains. More relevant is the cause, which can sometimes be treatable and at other times not. Here, we present a case of 48-year-old man with lymphadenopathy, hypercalcemia and acute kidney injury who was diagnosed with Hodgkin’s lymphoma. This case is about a 48-year-old man who presented with symptoms of hypercalcemia and generalised lymphadenopathy. With a predisposition of EBV infection, Hodgkin’s lymphoma was identified to be the source of hypercalcemia, leading on to the hypercalcemic nephropathy. Hypercalcemia is usually seen with non-hodgkins lymphoma and only a few reports of hypercalcemia associated with Hodgkins lymphoma had been published. The usual mechanism is Vit D dependent, however, in our patient hypercalcemia was probably mediated by PTHrP; since both the vit D and activated vit D levels were normal. The presence of PTHrP mediated hypercalcemia Hodgkin’s lymphoma makes our case rare, as an uncommon presentation of a disease with yet another uncommon mechanism underlying.

Locoregional Treatments in Peritoneal Metastasis from Gastric Cancer

Background: Liver cancer is among the top five causes of cancer death globally. Hepatocellular Carcinoma (HCC) accounts for up to 90% of primary liver neoplasms in adults. The incidence of thyroid me-tastasis from HCC is rare and estimated from 0.8 to 12%. This report describes a 51-year-old man presenting with hypercalcemia and known metastatic HCC with new metastasis to the thyroid gland. Case Report: A 51-year-old male was admitted due to symptomatic hypercalcemia. His medical history included HCC with metastasis to the retroperitoneal lymph nodes diagnosed one year prior. Computed tomography revealed an enlarging liver mass, diffuse lymphadenopathy and many osseous lytic lesions. Ultrasound of the neck revealed abnormal right cervical lymph nodes and a heterogeneous mass replacing the right thyroid gland. Biopsy of the right cervical lymph node immunohistochemical stained positive for PAN-K, Glypican-3, HepPar1 and Anti-Arginase and negative for p40 and CEA-poly, supporting the diagnosis for metastatic HCC. His hospital course was complicated by dysphagia, spontaneous bacterial peritonitis and acute-on-chronic liver failure. Despite aggressive resuscitation, he continued to decline and ultimately pursued hospice care. Conclusion: This case illustrates the need to have a high index of suspicion for thyroid metastasis in HCC patients presenting with a new-onset cervical mass, dysphagia or hypercalcemia. Metastatic cancer to the thyroid gland is generally considered a poor prognostic factor, as seen in this case with the rapid decline. This case demonstrates an extremely rare presentation of HCC with metastasis to the thyroid gland.

An Overview of Familial Hypocalciuric Hypercalcemia

Familial hypocalciuric hypercalcemia (FHH) is one of the rare reasons for hypercalcemia. FHH is an autosomal dominant disease that is inheritable. The most common calcium sensitive receptors (CaSR) develop because of the inactivation of. In addition, they also develop due to the function loss of AP2S1 and GNA11. The FHH sickness is characterized by hypercalcemia, hypocalciuria, the regular or increased level of the parathyroid hormone, and normal renal function. The symptoms of hypercalcemia are usually not observed. It is often diagnosed by calculating the calcium/creatine clearance ratio of a 24-hour urine sample, and then genetically looking at it. FHH is usually a benign disorder, and when symptomatic and rarely complications develop, calcimimetics are used or parathyroidectomy can be performed. In conclusion, FHH is a benign and genetically transmitted, moderate cause of hypercalcemia. It is rare and usually asymptomatic.

A rare case of Isolated hepatic sarcoidosis with symptomatic hypercalcemia

A rare case of Isolated hepatic sarcoidosis with symptomatic hypercalcemia

A Case of Cosecretion of Parathyroid Hormone-Related Protein and 1,25-Dihydroxyvitamin D in Small Cell Lung Carcinoma Presenting as Symptomatic Hypercalcemia

A Case of Cosecretion of Parathyroid Hormone-Related Protein and 1,25-Dihydroxyvitamin D in Small Cell Lung Carcinoma Presenting as Symptomatic Hypercalcemia