Parathyroid Adenoma Causing Hypercalcemic Crisis Masquerading as Acute Abdomen in a 7-Year-Old: Case Report and Systematic Literature Review

Parathyroid Adenoma Causing Hypercalcemic Crisis Masquerading as Acute Abdomen in a 7-Year-Old: Case Report and Systematic Literature Review | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Parathyroid Adenoma Causing Hypercalcemic Crisis Masquerading as Acute Abdomen in a 7-Year-Old: Case Report and Systematic Literature Review Wanhua Zhang, Weina Zhang, Xinyi Zi, Manjun Zhang This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8366828/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 12 You are reading this latest preprint version Abstract Background: Hypercalcemic crisis from a functioning parathyroid adenoma (PA) is exceptionally rare in prepubertal children and typically presents with a non-specific complaint such as polyuria or lethargy. We report a 7-year-old girl who was urgently referred for acute, colicky abdominal pain and repeated vomiting, which clinically mimicked acute appendicitis. During the work-up, extensive metabolic tests incidentally revealed severe hypercalcemia and elevated intact parathyroid hormone (PTH), which led to the diagnosis of PA-induced hypercalcemic crisis.This is the youngest girl reported in Asia whose initial manifestation was an acute abdomen rather than renal or neuropsychiatric symptoms. The case underscores that functioning PA should be included in the differential diagnosis of children presenting with unexplained gastrointestinal distress, and illustrates that prompt recognition and focused parathyroidectomy can achieve rapid normalization of calcium levels without complications. Case Presentation: We report the case of a seven-year-old female patient who was hospitalized due to complaints of abdominal discomfort accompanied by episodes of recurrent vomiting.These symptoms were later found to be related to an underlying fracture. We describe her clinical course, diagnostic workup, and treatment. Laboratory tests revealed severe hypercalcemia (4.67 mmol/L; reference range: 2.1–2.7), along with hypophosphatemia, hypomagnesemia, and markedly elevated parathyroid hormone (268 pg/mL).Contrast-enhanced CT imaging identified a 2.1 cm nodule located posterior to the right thyroid lobe. After urgent management of hypercalcemia—including intravenous fluids, furosemide, salmon calcitonin, and pamidronate—the patient underwent surgical excision of the right inferior parathyroid gland.Histopathological examination confirmed the diagnosis of a benign parathyroid adenoma. Serum calcium and PTH levels normalized within 24 hours postoperatively, with complete resolution of clinical symptoms.During follow-up to date, serum calcium, parathyroid hormone levels, and color Doppler ultrasound examination of the parathyroid have been normal. Conclusions: Parathyroid adenoma represents an uncommon yet manageable cause of hypercalcemic crisis in pediatric patients. Timely assessment of serum calcium and parathyroid hormone levels in individuals presenting with unexplained gastrointestinal symptoms—such as nausea, vomiting, or abdominal pain—facilitates swift diagnosis, thereby reducing the need for unnecessary diagnostic procedures like extensive imaging or invasive tests.. parathyroid adenoma hypercalcic crisis hyperthyroidism case report Figures Figure 1 Figure 2 BACKGROUND Hypercalcemic crisis is a rare but life-threatening condition in the pediatric population, often caused by primary hyperparathyroidism from a functioning parathyroid adenoma( 1 ). Parathyroid adenomas account for the majority of primary hyperparathyroidism cases in adults. However, they are exceptionally rare in children and often pose diagnostic challenges. This is because their nonspecific symptoms, such as abdominal pain and vomiting, can mimic acute abdominal emergencies, frequently leading to misdiagnosis or delayed diagnosis ( 2 , 3 ). Early diagnosis is critical because delayed recognition leads to severe complications such as renal impairment, neurological symptoms, and cardiovascular instability( 4 ). The urgency of clinical management necessitates a multidisciplinary approach. This includes prompt biochemical evaluation, such as serum calcium and parathyroid hormone (PTH) levels, and urgent surgical intervention to prevent morbidity and mortality( 5 ). This case report underscores the importance of considering parathyroid disorders in children with unexplained gastrointestinal symptoms. Firstly, it highlights the role of imaging and histopathological confirmation. Additionally, it emphasizes that timely intervention can lead to complete resolution of symptoms and normalization of metabolic parameters such as calcium and parathyroid hormone levels( 6 , 7 ). CASE REPORT A previously healthy girl aged 7 years and 3 months of Wa ethnicity was admitted to A hospital in Dali on 31 January 2025 following transfer from the local county hospital.She presented with a 10-day history of periumbilical colicky abdominal pain and non-bilious vomiting, which occurred 5 to 8 times daily and was accompanied by a 2 kg weight loss. She also had no bowel movements for 3 days. Her medical history included surgical repair of an atrial septal defect nine months prior to admission. Twelve days before admission, she underwent immobilization of a left tibial fracture using plaster casting. The child exhibited progressively worsening fatigue but did not have itchy skin or psychiatric or neurological symptoms. One month prior to admission, a minor fall resulted in a left tibial fracture. The past medical history included one previous fracture following a fall. There was no personal or family history of similar musculoskeletal disorders. On admission, physical examination revealed altered mental status and signs of malnutrition. The child was also dehydrated, characterized by slightly dry, cold skin with reduced elasticity. No sternal tenderness was noted. On palpation, the abdomen was flat and soft, with no visible peristalsis. Abdominal tenderness was generalized, with the most pronounced tenderness in the epigastric and periumbilical regions. There was no rebound tenderness or shifting dullness. No masses were palpated, bowel sounds were diminished, and there was no tenderness on percussion over the spinous processes. Emergency electrolyte analysis revealed a hypercalcemic crisis, with serum calcium elevated at 4.67 mmol/L. Additionally, hypomagnesemia was observed, with magnesium decreased to 0.51 mmol/L, and hypophosphatemia, with phosphate decreased to 0.67 mmol/L. Potassium, sodium, and chloride levels were within normal limits. Serum 25-hydroxyvitamin D was 12.5 ng/mL . High-sensitivity C-reactive protein exceeded 10.00 mg/L, indicating a level above the clinical warning threshold. No abnormalities were detected in the complete blood count or thyroid function. Liver function tests—including albumin, alkaline phosphatase, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and bilirubin—were normal. Renal function and serum amylase were within normal limits. Serum carbon dioxide levels, fasting blood glucose, and blood gas analysis showed no abnormalities. Erythrocyte sedimentation rate and cardiac enzymes were unremarkable. Stool analysis and urinalysis revealed no abnormalities. Abdominal ultrasound focusing on the liver, gallbladder, pancreas, spleen, kidneys, ureters, and mesenteric lymph nodes showed no abnormalities. Additionally, echocardiography revealed normal findings. Further testing demonstrated elevated parathyroid hormone (PTH 268.1 pg/mL; reference range: 15–65 pg/mL). Moreover, 24-hour urine electrolyte analysis showed a urine volume of 2.4 L and elevated urinary magnesium (5.59 mmol/24 hours), while urinary potassium, sodium, chloride, calcium, and phosphorus levels were within normal ranges. Bone density assessment indicated osteoporosis, which was further confirmed by a tibial X-ray showing specific osteoporotic changes such as cortical thinning and trabecular bone loss. The patient was continuously treated with salmon calcitonin, intravenous fluid hydration, diuretic therapy, potassium supplementation, vitamin D therapies, and nutritional support. Despite these interventions, serial monitoring was consistently performed and showed elevated serum calcium levels. Subsequent thyroid and cervical lymph node ultrasound identified multiple cystic nodular lesions classified as C-TIRADS Category 2 in the left thyroid lobe. Additionally, a hypoechoic area located inferior to the right thyroid lobe was observed, suggestive of a parathyroid adenoma（As shown in fig. 1）. Neck contrast-enhanced CT revealed heterogeneous enhancement in both thyroid lobes and identified a nodule located posterior and inferior to the right thyroid lobe, findings that are highly suggestive of a parathyroid lesion, likely a parathyroid adenoma（As shown in fig. 2） We diagnosed primary hyperparathyroidism (PHPT) caused by a parathyroid adenoma(Other diagnoses include hyperparathyroidism, multiple electrolyte imbalances—such as abnormalities in sodium and potassium levels—and a left tibial fracture.). Multidisciplinary consultation developed a calcium reduction plan, and the plan was discussed among the team before the operation. Following administration of a dose of pamidronate disodium, the child's serum calcium levels returned to normal, so she was transferred to pediatric surgery for the operation. She underwent exploratory surgery for suspected parathyroid adenoma. During the operation, a solitary, firm, dark brown parathyroid gland measuring 2.0 × 1.8 × 0.4 cm was removed from the right inferior pole.Intraoperative PTH monitoring showed a decline from 120 pg/mL to 5 pg/mL within 10 minutes after gland excision. Both frozen and formalin-fixed paraffin-embedded sections confirmed the diagnosis of a benign parathyroid adenoma, which was predominantly composed of chief cells and had an intact capsule.The postoperative recovery was uneventful, with no complications observed. To prevent Hungry Bone Syndrome, oral calcium carbonate and calcitriol therapy were initiated on the first postoperative day.The serum total calcium level was 2.23 mmol/L on postoperative day 1 and remained within the normal range throughout the hospitalization period.The patient has tolerated standard diet and was discharged on the 10th postoperative day.At the outpatient follow-up four weeks after discharge, she remained asymptomatic with a serum calcium level of 2.25 mmol/L and a PTH level of 42 pg/mL.Long-term monitoring after hospital discharge has shown that electrolyte and parathyroid function levels have remained within the normal range，The monitoring results of serum calcium and PTH levels are shown in Figure 3（a，b）.The child's post-discharge whole exome sequencing report indicated the following: (1) No pathogenic point mutations (single nucleotide variants, SNVs) or clinically significant copy number variations (CNVs), such as segmental deletions or duplications, were detected. (2) Other suspicious variants, including a heterozygous deletion of exons 8–21 of the AARS1 gene, were identified; however, these variants are considered unrelated to the patient's clinical phenotype. The entire diagnosis and treatment timeline for this child is shown in Table 1. Date (2025) Event Key value / Intervention Jan 19 Left tibial fracture in county hospital Cast immobilisation for 5 d Jan 28 Plain abdominal film Suggestive of incomplete intestinal obstruction Jan 31 Admission to our paediatric ward Chief complaint:10-day history of abdominal pain and vomiting; serum Ca 4.67 mmol/L (critical value) Jan 31 Emergency laboratory WBC10.35×10⁹/L,CRP12mg/L;signs of dehydration Jan 31 – Feb 7 Initial antibiotic course Ceftazidime 50 mg/kg q8h i.v. Feb 1 Calcitonin therapy started Salmon calcitonin 4 IU/kg q12h i.m. Feb 2 First neck ultrasound Electrolytes recheck Additional diagnoses made Hypoechoic nodule inferior to right thyroid(parathyroid lesion suspected) Ca 3.5 mmol/L ↓, Mg 0.51 mmol/L↓, PO₄ 0.71 mmol/L ↓ Hypercalcaemic crisis hypomagnesaemia / hypokalaemia Feb 3 Contrast-enhanced neck CT PTH result Nodule at postero-inferior margin of right thyroid—parathyroid adenoma likely 268.1 pg/ml ↑ Feb 5 Bisphosphonate added Pamidronate disodium 0.5 mg/kg i.v. single dose Feb 6 Calcitonin stopped After 5 days; serum Ca fallen to 2.65 mmol/L Feb 8 Multidisciplinary team meeting Diagnosis: parathyroid adenoma → surgery planned Feb 10 Pituitary MRI No abnormality;serum Ca 2.32 mmol/L Feb 11 Transfer to paediatric surgery Electrolytes nearly normal; operative indication confirmed Feb 12 Pre-operative ultrasound Nodule 2.0 cm × 1.8 cm, well circumscribed Feb 13 Pre-op summary Serum Ca 2.55 mmol/L; 1 U packed RBC reserved Feb 14 Surgery Intra-operative PTH Complete excision of right parathyroid adenoma (size 1.5 × 1 × 0.4 cm) 120pg/ml→ confirms hyper-function corrected Feb 15 Post-op day 1 PTH 68 pg/ml; serum Ca 2.23 mmol/L Feb 17 Post-op day 3 PTH 5pg/ml(transient hypofunction), serum Ca 2.01mmol/L→oral calcium supplement started Feb 20 Histopathology report Right parathyroid adenoma with intact capsule; chiefly clear-cell pattern Feb 21 Calcium monitoring 2.13 mmol/L (lower normal limit) Feb 24 Discharge Serum Ca 2.23 mmol/L; no vomiting or abdominal pain; wound dry DISCUSSION Hypercalcaemia should be ruled out in any child presenting with persistent abdominal pain and vomiting( 8 ). Beyond common causes such as dehydration or malignancy, functional parathyroid disorders should also be considered( 9 ). Our case demonstrates that severe hypercalcaemia can lead to intestinal pseudo-obstruction (a condition mimicking bowel obstruction) by impairing intestinal smooth muscle contractility and neural conduction.PHPT caused by a functional parathyroid adenoma (PA) is an extremely rare endocrine disorder in children. Its estimated incidence is 0.5–1.0 per million among children under 15 years of age( 10 ). Unlike adults, where solitary PA accounts for 80–90% of PHPT cases, pediatric cases are more often linked to hereditary syndromes or multiglandular disease. As a result, single-adenoma PHPT is particularly rare in children.( 11 ). The nonspecific manifestations of hypercalcemic crisis—such as abdominal pain, vomiting, and weight loss—often cause it to be misdiagnosed as acute gastroenteritis or intestinal obstruction( 12 ), as exemplified in our case. Early recognition depends critically on the systematic measurement of the serum calcium and PTH levels during the initial laboratory evaluation of children presenting with persistent gastrointestinal symptoms accompanied by dehydration( 13 ). Upon detection of hypercalcemia, the differential diagnosis should include familial hypocalciuric hypercalcemia (FHH), malignancy, vitamin D intoxication, and renal osteodystrophy( 14 , 15 ). A markedly elevated PTH level, combined with suppressed 25-hydroxyvitamin D and normal-to-low urinary calcium, strongly supports the diagnosis of PHPT( 16 ). Localization of the parathyroid adenoma can be reliably achieved using high-resolution cervical ultrasound and contrast-enhanced CT, which together provide a sensitivity that exceeds 90%( 17 ). Urgent management of the hypercalcemic crisis follows a stepwise approach: Aggressive intravenous rehydration with isotonic saline at 1.5 to 2 times the standard maintenance rate is used to restore volume and promote calcium excretion( 18 ).Loop diuretics (e.g., furosemide 1 mg/kg every 6–8 hours) should be administered only after adequate volume repletion has been achieved to enhance renal calcium excretion.Calcitonin (4–6 IU/kg every 12 h) is used to rapidly lower calcium levels, although its effect is transient( 19 ).Administer intravenous bisphosphonate, such as pamidronate, at 0.5 mg/kg as a single dose if serum calcium concentration remains severely elevated—greater than 3.0 mmol/L—despite initial treatments( 20 ).Although the final prognosis of the patient in this case is good, the preoperative calcium reduction protocol can be further optimized; moreover, the duration of calcium reduction can be shortened.Definitive treatment is surgical excision of the adenoma. While minimally invasive, radio-guided parathyroidectomy is established in adults, open bilateral neck exploration remains the preferred approach in most pediatric centers, particularly when preoperative localization is unclear or inconclusive( 21 ). Intraoperative parathyroid hormone monitoring, defined as a drop of 50% or more from baseline measured 10 minutes after excision, serves as a reliable predictor of surgical success and was used effectively in our case( 22 ). After parathyroidectomy, hungry bone syndrome occurs more frequently in children than in adults. Therefore, prophylactic oral calcium (30–50 mg/kg/day) and calcitriol (0.25 µg/day) treatment should be initiated on the first postoperative day, and both medications should be gradually tapered over 4–6 weeks( 23 ). Long-term follow-up is essential for patients who have undergone surgical resection. This follow-up should include annual measurements of serum calcium and parathyroid hormone for a minimum of five or more years due to reported recurrence rates of 2–5%, even after seemingly curative surgical resection( 24 ). In summary, a hormone-secreting parathyroid adenoma is a treatable cause of hypercalcemic crisis in children. however, it can still pose a potentially life-threatening risk, highlighting the importance of early diagnosis and treatment( 25 ). High clinical suspicion, timely biochemical confirmation, and a well-coordinated multidisciplinary surgical approach can achieve complete metabolic remission of the condition and prevent long-term complications. CONCLUSION Parathyroid adenoma remains an exceptionally rare cause of primary hyperparathyroidism in children, however, it must be considered in any child who presents with persistent gastrointestinal symptoms, such as nausea or abdominal pain, and unexplained hypercalcemia. The clinical presentation, which includes abdominal pain, recurrent vomiting, weight loss, and dehydration, often resembles an acute abdominal emergency, such as a surgical emergency.This similarity to other conditions often leads to unnecessary investigations and delayed diagnosis. Therefore, early assessment of serum calcium and parathyroid hormone is essential for the timely recognition of related disorders. Once the diagnosis is established, prompt medical management of hypercalcemic crisis is initiated. This is followed by surgical excision of the adenoma, which achieves rapid biochemical cure and complete resolution of clinical symptoms. Our clinical case confirms that a single functioning parathyroid adenoma can be safely removed in pediatric patients. This procedure results in normalization of calcium and parathyroid hormone levels within 24 hours postoperatively. Long-term surveillance is necessary to monitor recurrence. The overall prognosis is excellent when the condition is timely identified and appropriately treated. Declarations ETHICS AND PATIENT CONSENT The study received ethical approval from the First Affiliated Hospital of Dali University, with the approval number DFY20251208001. Additionally, written informed consent was secured from the legal guardian of the patient for the publication of anonymized clinical data and images. DISCLOSURE The authors declare that there are no competing interests to disclose. CLINICAL TRIAL NUMBER Clinical trial number: not applicable. ACKNOWLEDGEMENTS The authors express their gratitude to the family of the patient for their collaboration. In order to enhance the language quality and readability of the manuscript during its preparation, the authors utilized tools such as DeepSeek and ChatGPT. Following this, they meticulously reviewed and revised the content as necessary, assuming complete responsibility for the material presented in the published article. It is important to note that artificial intelligence (AI) was not employed in the creation of any figures, tables, or raw research data. FUNDING There was no external financial support for this study. DATA SHARING STATEMENT De-identified clinical data, imaging files and laboratory results are available upon reasonable request to the corresponding author ( [email protected] ). References Dong JY, Guan H, Zhu Y. Clinical symptoms in 455 hyperparathyroidism patients. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2011;33(3):330-3. Dror N, Greenberg M, Perl L, Eliakim A. Primary Hyperparathyroidism due to Parathyroid Adenoma in Children and Adolescents. Endocr Pract. 2024;30(6):564-8. Bin Yahib SM, Algarni B, Alghamdi A, Nassan S. Primary Hyperparathyroidism as a Rare Cause of Unexplained Recurrent Abdominal Pain: Case Presentation and Literature Review. Cureus. 2021;13(10):e19155. Wilson RM, Sturridge L. Phosphate, Fractures, and Frustration-A Missed Diagnosis of Oncogenic Osteomalacia Leading to Multisystem Complication. Clin Case Rep. 2025;13(8):e70790. Mariassunta P, G P, V V, J T, T F, G O. [Calciphylaxis: a multidisciplinary approach]. G Ital Nefrol. 2009;26(4). Francesco Rosario C, Federico DS, Antonio DA, Edoardo I, Fabio C, Vanna B, et al. Mega solid bone cyst in iliac region from primary hyperparathyroidism: a case report. J Med Case Rep. 2025;19(1). Mohammed Shafi A, Sivagnanasundaram D, Rajan S, Vijaya G, Maya M, Shelley S. Mediastinal parathyroid adenoma removal by video-assisted thoracoscopic surgery. Ann Afr Med. 2021;20(2). Stepan K, Ivana P, Viktor C. Two Different Causes of Paediatric Hypercalcaemia. Sultan Qaboos Univ Med J. 2019;18(3). Richard C, Glenn M. Endocrine and metabolic emergencies: hypercalcaemia. Ther Adv Endocrinol Metab. 2010;1(5). Roberta M, Alessia L, Roberto M, Elio B, Giuseppe C, Gianfranco DI, et al. Neuroendocrine Tumors and Survival Rates in Multiple Endocrine Neoplasia Type 1 Patients: Impact of Gender Difference. Neuroendocrinology. 2024;115(5). Carole G, Nunzia Cinzia P, Aoife L, Fréderic C, David T, Fréderic S. Persistent and recurrent hyperparathyroidism. Updates Surg. 2017;69(2). Dorota R, Aleksander K, Anna W, Magdalena O, Alicja K, Anna T-N, et al. Long-Term Consequences of Misdiagnosis of Parathyroid Adenomas in Pediatric Patients. Case Rep Pediatr. 2025;2025(0). Mara C, Mihaela S, Florina Ligia P, Ana-Maria G, Adrian C, Claudiu N. Pediatric Neuroendocrine Neoplasia of the Parathyroid Glands: Delving into Primary Hyperparathyroidism. Biomedicines. 2023;11(10). Abdullah A-R, Abdullah A-A, Hanan A, Ahmed A, Eman F, Hassan A, et al. Case report: familial hypocalciuric hypercalcemia. AME Case Rep. 2024;8(0). Janet Y L, Dolores M S. Familial hypocalciuric hypercalcemia and related disorders. Best Pract Res Clin Endocrinol Metab. 2018;32(5). Liubov G Y, Tatiana K, Ilya V S, Marina Evgenevna B, Aluza Ramilevna B, Roman A C, et al. Clinical phenotypes of primary hyperparathyroidism in hospitalized patients who underwent parathyroidectomy. Endocr Connect. 2021;10(2). Ethan F, Daniela A-S, Joshua P, Yuan L, Alfred Jr S, Jared C I. Preoperative imaging for parathyroid localization in patients with concurrent thyroid disease: A systematic review. Head Neck. 2018;40(7). Erol D, Cagla K, Gulcin Y, Betul S, Halil Y, Aydin T, et al. Extreme hypercalcemia in a kidney transplant recipient. CEN Case Rep. 2018;7(2). S E, Y N, Y O. [Medical treatment of malignant hypercalcemia]. Gan To Kagaku Ryoho. 1993;20(15). A M M. Pamidronate (Aredia, Ciba) in malignant hypercalcaemia. Intensive Crit Care Nurs. 1997;13(1). Julie Ann S, Robert U. Minimally invasive parathyroidectomy. Surg Oncol. 2003;12(2). Pietro Giorgio C, Giuseppe P, Giulia L, Fabio M, Lucia B, Matteo A, et al. Intraoperative parathyroid hormone assay during focused parathyroidectomy: the importance of 20 minutes measurement. BMC Surg. 2013;13(0). Mara C, Claudiu N. Forestalling Hungry Bone Syndrome after Parathyroidectomy in Patients with Primary and Renal Hyperparathyroidism. Diagnostics (Basel). 2023;13(11). Inga M-G, Franz-Tassilo M-G, Katharina R, Matthias L, Holger S W, Clemens S, et al. Long-term recurrence after parathyroidectomy in primary hyperparathyroidism-do predictors exist? Gland Surg. 2025;13(12). Veronica D G, Jarreau C. Atypical Parathyroid Tumor and Hyperparathyroidism, and Their Association With the CDC73 Mutation in a Pediatric Patient. Cureus. 2025;17(9). Additional Declarations No competing interests reported. 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01:02:56","extension":"xml","order_by":12,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":69658,"visible":true,"origin":"","legend":"","description":"","filename":"1a7e899fecf54d148642ed8eeb1927a01structuring.xml","url":"https://assets-eu.researchsquare.com/files/rs-8366828/v1/3a80259f61df5e35adc37a27.xml"},{"id":99192198,"identity":"66b6ccee-01d8-4aba-aa7f-f19ec6edb62b","added_by":"auto","created_at":"2025-12-30 01:02:56","extension":"html","order_by":13,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":81289,"visible":true,"origin":"","legend":"","description":"","filename":"earlyproof.html","url":"https://assets-eu.researchsquare.com/files/rs-8366828/v1/fa6bd785433dbc36e6093cdb.html"},{"id":99192189,"identity":"1dc77bee-fbd2-478e-96fe-830d6aa9eb11","added_by":"auto","created_at":"2025-12-30 01:02:56","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":51615,"visible":true,"origin":"","legend":"\u003cp\u003eUltrasound image of the right thyroid lobe showing hypoechoic areas, possibly corresponding to the parathyroid gland.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8366828/v1/19f86e0abf7f6567fcc943ef.png"},{"id":99192190,"identity":"1f8a9480-1ac0-4a4f-9031-1c6dcb923c8e","added_by":"auto","created_at":"2025-12-30 01:02:56","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":41621,"visible":true,"origin":"","legend":"\u003cp\u003eThe cervical CT scan revealed an enhancing nodular focus on the posterior lower edge of the right thyroid gland, with a diameter of about 0.6 cm and a clear edge. These findings suggest the possibility of a parathyroid adenoma.\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-8366828/v1/a7bb164b1a2f07ef7870c872.png"},{"id":99323803,"identity":"9105b6ab-61bd-40e8-8902-a41da1082652","added_by":"auto","created_at":"2025-12-31 16:46:18","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":436860,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8366828/v1/ff99c951-175a-4ca5-9c68-ede3cb00fe8c.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Parathyroid Adenoma Causing Hypercalcemic Crisis Masquerading as Acute Abdomen in a 7-Year-Old: Case Report and Systematic Literature Review","fulltext":[{"header":"BACKGROUND","content":"\u003cp\u003eHypercalcemic crisis is a rare but life-threatening condition in the pediatric population, often caused by primary hyperparathyroidism from a functioning parathyroid adenoma(\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). Parathyroid adenomas account for the majority of primary hyperparathyroidism cases in adults. However, they are exceptionally rare in children and often pose diagnostic challenges. This is because their nonspecific symptoms, such as abdominal pain and vomiting, can mimic acute abdominal emergencies, frequently leading to misdiagnosis or delayed diagnosis (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). Early diagnosis is critical because delayed recognition leads to severe complications such as renal impairment, neurological symptoms, and cardiovascular instability(\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThe urgency of clinical management necessitates a multidisciplinary approach. This includes prompt biochemical evaluation, such as serum calcium and parathyroid hormone (PTH) levels, and urgent surgical intervention to prevent morbidity and mortality(\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). This case report underscores the importance of considering parathyroid disorders in children with unexplained gastrointestinal symptoms. Firstly, it highlights the role of imaging and histopathological confirmation. Additionally, it emphasizes that timely intervention can lead to complete resolution of symptoms and normalization of metabolic parameters such as calcium and parathyroid hormone levels(\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e).\u003c/p\u003e"},{"header":"CASE REPORT","content":"\u003cp\u003eA previously healthy girl aged 7 years and 3 months of Wa ethnicity was admitted to A hospital in Dali on 31 January 2025 following transfer from the local county hospital.She presented with a 10-day history of periumbilical colicky abdominal pain and non-bilious vomiting, which occurred 5 to 8 times daily and was accompanied by a 2 kg weight loss. She also had no bowel movements for 3 days. Her medical history included surgical repair of an atrial septal defect nine months prior to admission. Twelve days before admission, she underwent immobilization of a left tibial fracture using plaster casting.\u003c/p\u003e\n\u003cp\u003eThe child exhibited progressively worsening fatigue but did not have itchy skin or psychiatric or neurological symptoms. One month prior to admission, a minor fall resulted in a left tibial fracture. The past medical history included one previous fracture following a fall. There was no personal or family history of similar musculoskeletal disorders. On admission, physical examination revealed altered mental status and signs of malnutrition. The child was also dehydrated, characterized by slightly dry, cold skin with reduced elasticity. No sternal tenderness was noted. On palpation, the abdomen was flat and soft, with no visible peristalsis. Abdominal tenderness was generalized, with the most pronounced tenderness in the epigastric and periumbilical regions. There was no rebound tenderness or shifting dullness. No masses were palpated, bowel sounds were diminished, and there was no tenderness on percussion over the spinous processes.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;Emergency electrolyte analysis revealed a hypercalcemic crisis, with serum calcium elevated at 4.67 mmol/L. Additionally, hypomagnesemia was observed, with magnesium decreased to 0.51 mmol/L, and hypophosphatemia, with phosphate decreased to 0.67 mmol/L. Potassium, sodium, and chloride levels were within normal limits. Serum 25-hydroxyvitamin D was 12.5 ng/mL . High-sensitivity C-reactive protein \u0026nbsp;exceeded 10.00 mg/L, indicating a level above the clinical warning threshold. No abnormalities were detected in the complete blood count or thyroid function. Liver function tests\u0026mdash;including albumin, alkaline phosphatase, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and bilirubin\u0026mdash;were normal. Renal function and serum amylase were within normal limits. Serum carbon dioxide levels, fasting blood glucose, and blood gas analysis showed no abnormalities. Erythrocyte sedimentation rate and cardiac enzymes were unremarkable. Stool analysis and urinalysis revealed no abnormalities. Abdominal ultrasound focusing on the liver, gallbladder, pancreas, spleen, kidneys, ureters, and mesenteric lymph nodes showed no abnormalities.\u003c/p\u003e\n\u003cp\u003eAdditionally, echocardiography revealed normal findings. Further testing demonstrated elevated parathyroid hormone (PTH 268.1 pg/mL; reference range: 15\u0026ndash;65 pg/mL). Moreover, 24-hour urine electrolyte analysis showed a urine volume of 2.4 L and elevated urinary magnesium (5.59 mmol/24 hours), while urinary potassium, sodium, chloride, calcium, and phosphorus levels were within normal ranges. Bone density assessment indicated osteoporosis, which was further confirmed by a tibial X-ray showing specific osteoporotic changes such as cortical thinning and trabecular bone loss.\u003c/p\u003e\n\u003cp\u003eThe patient was continuously treated with salmon calcitonin, intravenous fluid hydration, diuretic therapy, potassium supplementation, vitamin D therapies, and nutritional support. Despite these interventions, serial monitoring was consistently performed and showed elevated serum calcium levels. Subsequent thyroid and cervical lymph node ultrasound identified multiple cystic nodular lesions classified as C-TIRADS Category 2 in the left thyroid lobe. Additionally, a hypoechoic area located inferior to the right thyroid lobe was observed, suggestive of a parathyroid adenoma（As shown in fig. 1）. Neck contrast-enhanced CT revealed heterogeneous enhancement in both thyroid lobes and identified a nodule located posterior and inferior to the right thyroid lobe, findings that are highly suggestive of a parathyroid lesion, likely a parathyroid adenoma（As shown in fig. 2）\u003c/p\u003e\n\u003cp\u003eWe diagnosed primary hyperparathyroidism (PHPT) caused by a parathyroid adenoma(Other diagnoses include hyperparathyroidism, multiple electrolyte imbalances\u0026mdash;such as abnormalities in sodium and potassium levels\u0026mdash;and a left tibial fracture.). Multidisciplinary consultation developed a calcium reduction plan, and the plan was discussed among the team before the operation. Following administration of a dose of pamidronate disodium, the child\u0026apos;s serum calcium levels returned to normal, so she was transferred to pediatric surgery for the operation.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;She underwent exploratory surgery for suspected parathyroid adenoma. During the operation, a solitary, firm, dark brown parathyroid gland measuring 2.0 \u0026times; 1.8 \u0026times; 0.4 cm was removed from the right inferior pole.Intraoperative PTH monitoring showed a decline from 120 pg/mL to 5 pg/mL within 10 minutes after gland excision. Both frozen and formalin-fixed paraffin-embedded sections confirmed the diagnosis of a benign parathyroid adenoma, which was predominantly composed of chief cells and had an intact capsule.The postoperative recovery was uneventful, with no complications observed. To prevent Hungry Bone Syndrome, oral calcium carbonate and calcitriol therapy were initiated on the first postoperative day.The serum total calcium level was 2.23 mmol/L on postoperative day 1 and remained within the normal range throughout the hospitalization period.The patient has tolerated standard diet and was discharged on the 10th postoperative day.At the outpatient follow-up four weeks after discharge, she remained asymptomatic with a serum calcium level of 2.25 mmol/L and a PTH level of 42 pg/mL.Long-term monitoring after hospital discharge has shown that electrolyte and parathyroid function levels have remained within the normal range，The monitoring results of serum calcium and PTH levels are shown in Figure 3（a，b）.The child\u0026apos;s post-discharge whole exome sequencing report indicated the following: (1) No pathogenic point mutations (single nucleotide variants, SNVs) or clinically significant copy number variations (CNVs), such as segmental deletions or duplications, were detected. (2) Other suspicious variants, including a heterozygous deletion of exons 8\u0026ndash;21 of the AARS1 gene, were identified; however, these variants are considered unrelated to the patient\u0026apos;s clinical phenotype.\u003c/p\u003e\n\u003cp\u003eThe entire diagnosis and treatment timeline for this child is shown in Table 1.\u003c/p\u003e\n\u003cdiv align=\"center\"\u003e\n \u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" class=\"fr-table-selection-hover\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eDate (2025)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eEvent\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eKey value / Intervention\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eJan 19\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eLeft tibial fracture in county hospital\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eCast immobilisation for 5 d\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eJan 28\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003ePlain abdominal film\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eSuggestive of incomplete intestinal obstruction\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eJan 31\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eAdmission to our paediatric ward\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eChief complaint:10-day history of abdominal pain and vomiting; serum Ca 4.67 mmol/L (critical value)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eJan 31\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eEmergency laboratory\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eWBC10.35\u0026times;10⁹/L,CRP12mg/L;signs of dehydration\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eJan 31 \u0026ndash; Feb 7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eInitial antibiotic course\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eCeftazidime 50 mg/kg q8h i.v.\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eCalcitonin therapy started\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eSalmon calcitonin 4 IU/kg q12h i.m.\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 2\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFirst neck ultrasound\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003eElectrolytes recheck\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003eAdditional diagnoses made\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eHypoechoic nodule inferior to right thyroid(parathyroid lesion suspected)\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003eCa 3.5 mmol/L \u0026darr;, Mg 0.51 mmol/L\u0026darr;, PO₄ 0.71 mmol/L \u0026darr;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003eHypercalcaemic crisis hypomagnesaemia / hypokalaemia\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eContrast-enhanced neck CT\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003ePTH result\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eNodule at postero-inferior margin of right thyroid\u0026mdash;parathyroid adenoma likely\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e268.1 pg/ml \u0026uarr;\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eBisphosphonate added\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003ePamidronate disodium 0.5 mg/kg i.v. single dose\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eCalcitonin stopped\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eAfter 5 days; serum Ca fallen to 2.65 mmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eMultidisciplinary team meeting\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eDiagnosis: parathyroid adenoma \u0026rarr; surgery planned\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003ePituitary MRI\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eNo abnormality;serum Ca 2.32 mmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 11\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eTransfer to paediatric surgery\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eElectrolytes nearly normal; operative indication confirmed\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 12\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003ePre-operative ultrasound\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eNodule 2.0 cm \u0026times; 1.8 cm, well circumscribed\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003ePre-op summary\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eSerum Ca 2.55 mmol/L; 1 U packed RBC reserved\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 14\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eSurgery\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003eIntra-operative PTH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eComplete excision of right parathyroid adenoma (size 1.5 \u0026times; 1 \u0026times; 0.4 cm)\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e120pg/ml\u0026rarr; confirms hyper-function corrected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 15\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003ePost-op day 1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003ePTH 68 pg/ml; serum Ca 2.23 mmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 17\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003ePost-op day 3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003ePTH 5pg/ml(transient hypofunction), serum Ca 2.01mmol/L\u0026rarr;oral calcium supplement started\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 20\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eHistopathology report\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eRight parathyroid adenoma with intact capsule; chiefly clear-cell pattern\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 21\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eCalcium monitoring\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003e2.13 mmol/L (lower normal limit)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eFeb 24\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eDischarge\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 197px;\"\u003e\n \u003cp\u003eSerum Ca 2.23 mmol/L; no vomiting or abdominal pain; wound dry\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eHypercalcaemia should be ruled out in any child presenting with persistent abdominal pain and vomiting(\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). Beyond common causes such as dehydration or malignancy, functional parathyroid disorders should also be considered(\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). Our case demonstrates that severe hypercalcaemia can lead to intestinal pseudo-obstruction (a condition mimicking bowel obstruction) by impairing intestinal smooth muscle contractility and neural conduction.PHPT caused by a functional parathyroid adenoma (PA) is an extremely rare endocrine disorder in children. Its estimated incidence is 0.5\u0026ndash;1.0 per million among children under 15 years of age(\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). Unlike adults, where solitary PA accounts for 80\u0026ndash;90% of PHPT cases, pediatric cases are more often linked to hereditary syndromes or multiglandular disease. As a result, single-adenoma PHPT is particularly rare in children.(\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e). The nonspecific manifestations of hypercalcemic crisis\u0026mdash;such as abdominal pain, vomiting, and weight loss\u0026mdash;often cause it to be misdiagnosed as acute gastroenteritis or intestinal obstruction(\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e), as exemplified in our case.\u003c/p\u003e \u003cp\u003eEarly recognition depends critically on the systematic measurement of the serum calcium and PTH levels during the initial laboratory evaluation of children presenting with persistent gastrointestinal symptoms accompanied by dehydration(\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Upon detection of hypercalcemia, the differential diagnosis should include familial hypocalciuric hypercalcemia (FHH), malignancy, vitamin D intoxication, and renal osteodystrophy(\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). A markedly elevated PTH level, combined with suppressed 25-hydroxyvitamin D and normal-to-low urinary calcium, strongly supports the diagnosis of PHPT(\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eLocalization of the parathyroid adenoma can be reliably achieved using high-resolution cervical ultrasound and contrast-enhanced CT, which together provide a sensitivity that exceeds 90%(\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eUrgent management of the hypercalcemic crisis follows a stepwise approach:\u003c/p\u003e \u003cp\u003eAggressive intravenous rehydration with isotonic saline at 1.5 to 2 times the standard maintenance rate is used to restore volume and promote calcium excretion(\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e).Loop diuretics (e.g., furosemide 1 mg/kg every 6\u0026ndash;8 hours) should be administered only after adequate volume repletion has been achieved to enhance renal calcium excretion.Calcitonin (4\u0026ndash;6 IU/kg every 12 h) is used to rapidly lower calcium levels, although its effect is transient(\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e).Administer intravenous bisphosphonate, such as pamidronate, at 0.5 mg/kg as a single dose if serum calcium concentration remains severely elevated\u0026mdash;greater than 3.0 mmol/L\u0026mdash;despite initial treatments(\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e).Although the final prognosis of the patient in this case is good, the preoperative calcium reduction protocol can be further optimized; moreover, the duration of calcium reduction can be shortened.Definitive treatment is surgical excision of the adenoma. While minimally invasive, radio-guided parathyroidectomy is established in adults, open bilateral neck exploration remains the preferred approach in most pediatric centers, particularly when preoperative localization is unclear or inconclusive(\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e). Intraoperative parathyroid hormone monitoring, defined as a drop of 50% or more from baseline measured 10 minutes after excision, serves as a reliable predictor of surgical success and was used effectively in our case(\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eAfter parathyroidectomy, hungry bone syndrome occurs more frequently in children than in adults. Therefore, prophylactic oral calcium (30\u0026ndash;50 mg/kg/day) and calcitriol (0.25 \u0026micro;g/day) treatment should be initiated on the first postoperative day, and both medications should be gradually tapered over 4\u0026ndash;6 weeks(\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e). Long-term follow-up is essential for patients who have undergone surgical resection. This follow-up should include annual measurements of serum calcium and parathyroid hormone for a minimum of five or more years due to reported recurrence rates of 2\u0026ndash;5%, even after seemingly curative surgical resection(\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn summary, a hormone-secreting parathyroid adenoma is a treatable cause of hypercalcemic crisis in children. however, it can still pose a potentially life-threatening risk, highlighting the importance of early diagnosis and treatment(\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e). High clinical suspicion, timely biochemical confirmation, and a well-coordinated multidisciplinary surgical approach can achieve complete metabolic remission of the condition and prevent long-term complications.\u003c/p\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eParathyroid adenoma remains an exceptionally rare cause of primary hyperparathyroidism in children, however, it must be considered in any child who presents with persistent gastrointestinal symptoms, such as nausea or abdominal pain, and unexplained hypercalcemia. The clinical presentation, which includes abdominal pain, recurrent vomiting, weight loss, and dehydration, often resembles an acute abdominal emergency, such as a surgical emergency.This similarity to other conditions often leads to unnecessary investigations and delayed diagnosis. Therefore, early assessment of serum calcium and parathyroid hormone is essential for the timely recognition of related disorders. Once the diagnosis is established, prompt medical management of hypercalcemic crisis is initiated. This is followed by surgical excision of the adenoma, which achieves rapid biochemical cure and complete resolution of clinical symptoms. Our clinical case confirms that a single functioning parathyroid adenoma can be safely removed in pediatric patients. This procedure results in normalization of calcium and parathyroid hormone levels within 24 hours postoperatively. Long-term surveillance is necessary to monitor recurrence. The overall prognosis is excellent when the condition is timely identified and appropriately treated.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003eETHICS AND PATIENT CONSENT\u003c/p\u003e\n\u003cp\u003eThe study received ethical approval from the First Affiliated Hospital of Dali University, with the approval number DFY20251208001. Additionally, written informed consent was secured from the legal guardian of the patient for the publication of anonymized clinical data and images.\u003c/p\u003e\n\u003cp\u003eDISCLOSURE\u003c/p\u003e\n\u003cp\u003eThe authors declare that there are no competing interests to disclose.\u003c/p\u003e\n\u003cp\u003eCLINICAL TRIAL NUMBER\u003c/p\u003e\n\u003cp\u003eClinical trial number: not applicable.\u003c/p\u003e\n\u003cp\u003eACKNOWLEDGEMENTS\u003c/p\u003e\n\u003cp\u003eThe authors express their gratitude to the family of the patient for their collaboration. In order to enhance the language quality and readability of the manuscript during its preparation, the authors utilized tools such as DeepSeek and ChatGPT. Following this, they meticulously reviewed and revised the content as necessary, assuming complete responsibility for the material presented in the published article. It is important to note that artificial intelligence (AI) was not employed in the creation of any figures, tables, or raw research data.\u003c/p\u003e\n\u003cp\u003eFUNDING\u003c/p\u003e\n\u003cp\u003eThere was no external financial support for this study.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eDATA SHARING STATEMENT\u003c/p\u003e\n\u003cp\u003eDe-identified clinical data, imaging files and laboratory results are available upon reasonable request to the corresponding author ([email protected]).\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eDong JY, Guan H, Zhu Y. Clinical symptoms in 455 hyperparathyroidism patients. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2011;33(3):330-3.\u003c/li\u003e\n\u003cli\u003eDror N, Greenberg M, Perl L, Eliakim A. Primary Hyperparathyroidism due to Parathyroid Adenoma in Children and Adolescents. Endocr Pract. 2024;30(6):564-8.\u003c/li\u003e\n\u003cli\u003eBin Yahib SM, Algarni B, Alghamdi A, Nassan S. Primary Hyperparathyroidism as a Rare Cause of Unexplained Recurrent Abdominal Pain: Case Presentation and Literature Review. Cureus. 2021;13(10):e19155.\u003c/li\u003e\n\u003cli\u003eWilson RM, Sturridge L. Phosphate, Fractures, and Frustration-A Missed Diagnosis of Oncogenic Osteomalacia Leading to Multisystem Complication. Clin Case Rep. 2025;13(8):e70790.\u003c/li\u003e\n\u003cli\u003eMariassunta P, G P, V V, J T, T F, G O. [Calciphylaxis: a multidisciplinary approach]. G Ital Nefrol. 2009;26(4).\u003c/li\u003e\n\u003cli\u003eFrancesco Rosario C, Federico DS, Antonio DA, Edoardo I, Fabio C, Vanna B, et al. Mega solid bone cyst in iliac region from primary hyperparathyroidism: a case report. J Med Case Rep. 2025;19(1).\u003c/li\u003e\n\u003cli\u003eMohammed Shafi A, Sivagnanasundaram D, Rajan S, Vijaya G, Maya M, Shelley S. Mediastinal parathyroid adenoma removal by video-assisted thoracoscopic surgery. Ann Afr Med. 2021;20(2).\u003c/li\u003e\n\u003cli\u003eStepan K, Ivana P, Viktor C. Two Different Causes of Paediatric Hypercalcaemia. Sultan Qaboos Univ Med J. 2019;18(3).\u003c/li\u003e\n\u003cli\u003eRichard C, Glenn M. Endocrine and metabolic emergencies: hypercalcaemia. Ther Adv Endocrinol Metab. 2010;1(5).\u003c/li\u003e\n\u003cli\u003eRoberta M, Alessia L, Roberto M, Elio B, Giuseppe C, Gianfranco DI, et al. Neuroendocrine Tumors and Survival Rates in Multiple Endocrine Neoplasia Type 1 Patients: Impact of Gender Difference. Neuroendocrinology. 2024;115(5).\u003c/li\u003e\n\u003cli\u003eCarole G, Nunzia Cinzia P, Aoife L, Fr\u0026eacute;deric C, David T, Fr\u0026eacute;deric S. Persistent and recurrent hyperparathyroidism. Updates Surg. 2017;69(2).\u003c/li\u003e\n\u003cli\u003eDorota R, Aleksander K, Anna W, Magdalena O, Alicja K, Anna T-N, et al. Long-Term Consequences of Misdiagnosis of Parathyroid Adenomas in Pediatric Patients. Case Rep Pediatr. 2025;2025(0).\u003c/li\u003e\n\u003cli\u003eMara C, Mihaela S, Florina Ligia P, Ana-Maria G, Adrian C, Claudiu N. Pediatric Neuroendocrine Neoplasia of the Parathyroid Glands: Delving into Primary Hyperparathyroidism. Biomedicines. 2023;11(10).\u003c/li\u003e\n\u003cli\u003eAbdullah A-R, Abdullah A-A, Hanan A, Ahmed A, Eman F, Hassan A, et al. Case report: familial hypocalciuric hypercalcemia. AME Case Rep. 2024;8(0).\u003c/li\u003e\n\u003cli\u003eJanet Y L, Dolores M S. Familial hypocalciuric hypercalcemia and related disorders. Best Pract Res Clin Endocrinol Metab. 2018;32(5).\u003c/li\u003e\n\u003cli\u003eLiubov G Y, Tatiana K, Ilya V S, Marina Evgenevna B, Aluza Ramilevna B, Roman A C, et al. Clinical phenotypes of primary hyperparathyroidism in hospitalized patients who underwent parathyroidectomy. Endocr Connect. 2021;10(2).\u003c/li\u003e\n\u003cli\u003eEthan F, Daniela A-S, Joshua P, Yuan L, Alfred Jr S, Jared C I. Preoperative imaging for parathyroid localization in patients with concurrent thyroid disease: A systematic review. Head Neck. 2018;40(7).\u003c/li\u003e\n\u003cli\u003eErol D, Cagla K, Gulcin Y, Betul S, Halil Y, Aydin T, et al. Extreme hypercalcemia in a kidney transplant recipient. CEN Case Rep. 2018;7(2).\u003c/li\u003e\n\u003cli\u003eS E, Y N, Y O. [Medical treatment of malignant hypercalcemia]. Gan To Kagaku Ryoho. 1993;20(15).\u003c/li\u003e\n\u003cli\u003eA M M. Pamidronate (Aredia, Ciba) in malignant hypercalcaemia. Intensive Crit Care Nurs. 1997;13(1).\u003c/li\u003e\n\u003cli\u003eJulie Ann S, Robert U. Minimally invasive parathyroidectomy. Surg Oncol. 2003;12(2).\u003c/li\u003e\n\u003cli\u003ePietro Giorgio C, Giuseppe P, Giulia L, Fabio M, Lucia B, Matteo A, et al. Intraoperative parathyroid hormone assay during focused parathyroidectomy: the importance of 20 minutes measurement. BMC Surg. 2013;13(0).\u003c/li\u003e\n\u003cli\u003eMara C, Claudiu N. Forestalling Hungry Bone Syndrome after Parathyroidectomy in Patients with Primary and Renal Hyperparathyroidism. Diagnostics (Basel). 2023;13(11).\u003c/li\u003e\n\u003cli\u003eInga M-G, Franz-Tassilo M-G, Katharina R, Matthias L, Holger S W, Clemens S, et al. Long-term recurrence after parathyroidectomy in primary hyperparathyroidism-do predictors exist? Gland Surg. 2025;13(12).\u003c/li\u003e\n\u003cli\u003eVeronica D G, Jarreau C. Atypical Parathyroid Tumor and Hyperparathyroidism, and Their Association With the CDC73 Mutation in a Pediatric Patient. Cureus. 2025;17(9).\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-pediatrics","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bped","sideBox":"Learn more about [BMC Pediatrics](http://bmcpediatr.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bped/default.aspx","title":"BMC Pediatrics","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"parathyroid adenoma, hypercalcic crisis, hyperthyroidism, case report","lastPublishedDoi":"10.21203/rs.3.rs-8366828/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8366828/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground: Hypercalcemic crisis from a functioning parathyroid adenoma (PA) is exceptionally rare in prepubertal children and typically presents with a non-specific complaint such as polyuria or lethargy. We report a 7-year-old girl who was urgently referred for acute, colicky abdominal pain and repeated vomiting, which clinically mimicked acute appendicitis. During the work-up, extensive metabolic tests incidentally revealed severe hypercalcemia and elevated intact parathyroid hormone (PTH), which led to the diagnosis of PA-induced hypercalcemic crisis.This is the youngest girl reported in Asia whose initial manifestation was an acute abdomen rather than renal or neuropsychiatric symptoms. The case underscores that functioning PA should be included in the differential diagnosis of children presenting with unexplained gastrointestinal distress, and illustrates that prompt recognition and focused parathyroidectomy can achieve rapid normalization of calcium levels without complications.\u003c/p\u003e\n\u003cp\u003eCase Presentation: We report the case of a seven-year-old female patient who was hospitalized due to complaints of abdominal discomfort accompanied by episodes of recurrent vomiting.These symptoms were later found to be related to an underlying fracture. We describe her clinical course, diagnostic workup, and treatment. Laboratory tests revealed severe hypercalcemia (4.67 mmol/L; reference range: 2.1–2.7), along with hypophosphatemia, hypomagnesemia, and markedly elevated parathyroid hormone (268 pg/mL).Contrast-enhanced CT imaging identified a 2.1 cm nodule located posterior to the right thyroid lobe. After urgent management of hypercalcemia—including intravenous fluids, furosemide, salmon calcitonin, and pamidronate—the patient underwent surgical excision of the right inferior parathyroid gland.Histopathological examination confirmed the diagnosis of a benign parathyroid adenoma. Serum calcium and PTH levels normalized within 24 hours postoperatively, with complete resolution of clinical symptoms.During follow-up to date, serum calcium, parathyroid hormone levels, and color Doppler ultrasound examination of the parathyroid have been normal.\u003c/p\u003e\n\u003cp\u003eConclusions: Parathyroid adenoma represents an uncommon yet manageable cause of hypercalcemic crisis in pediatric patients. Timely assessment of serum calcium and parathyroid hormone levels in individuals presenting with unexplained gastrointestinal symptoms—such as nausea, vomiting, or abdominal pain—facilitates swift diagnosis, thereby reducing the need for unnecessary diagnostic procedures like extensive imaging or invasive tests..\u003c/p\u003e","manuscriptTitle":"Parathyroid Adenoma Causing Hypercalcemic Crisis Masquerading as Acute Abdomen in a 7-Year-Old: Case Report and Systematic Literature Review","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-12-30 01:02:51","doi":"10.21203/rs.3.rs-8366828/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-03-26T07:17:53+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-23T16:21:42+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"25473578663891679148628771532071961991","date":"2026-03-18T14:19:52+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"155122911054292250497736377087812689865","date":"2026-01-30T19:33:48+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-12-27T03:45:29+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"197291509378803756338676209632309120304","date":"2025-12-27T02:53:57+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"236115685366875911997429366440947344417","date":"2025-12-24T10:36:33+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-12-22T07:48:14+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-12-19T10:15:35+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-12-19T07:01:25+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-12-19T06:56:59+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Pediatrics","date":"2025-12-15T13:25:29+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-pediatrics","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bped","sideBox":"Learn more about [BMC Pediatrics](http://bmcpediatr.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bped/default.aspx","title":"BMC Pediatrics","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"1cf049c7-813a-4952-a360-96dcc670bb3b","owner":[],"postedDate":"December 30th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-05-26T11:53:35+00:00","versionOfRecord":[],"versionCreatedAt":"2025-12-30 01:02:51","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8366828","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8366828","identity":"rs-8366828","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}