Parathyroid adenoma causing hypercalcemic crisis masquerading as acute abdomen in a 7-year-old: a case report

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.Her 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 timely diagnosis and focused parathyroidectomy can effectively reverse biochemical abnormalities, alleviate skeletal symptoms, and mitigate the risk of serious long-term 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.Subsequent analysis revealed that these symptoms may represent acute gastrointestinal syndrome in the context of a hypercalcemic crisis.We describe her clinical course, diagnostic workup, and treatment. Laboratory tests revealed severe hypercalcemia (4.67 mmol/L; reference range: 2.1–2.7mmol/L), along with hypophosphatemia, hypomagnesemia, and markedly elevated PTH (268.1 pg/mL).Thyroid ultrasound revealed a nodule in the inferior aspect of the right lobe of the thyroid gland, which was subsequently confirmed by contrast-enhanced CT.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 PA. Serum calcium and PTH levels normalized within 24 hours postoperatively, with complete resolution of clinical symptoms. Marked hypocalcemia developed within several days postoperatively and was corrected. During follow-up to date, serum calcium,PTH levels, and ultrasound examination of the parathyroid have been normal.

Conclusions

PA represents an uncommon yet manageable cause of hypercalcemic crisis in pediatric patients. Timely assessment of serum calcium and PTH 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.Surgical resection of the PA is the first-line treatment. Postoperatively, prevention of hungry bone syndrome and long-term follow-up are required.

Background

Hypercalcemic crisis is a rare but life-threatening condition in the pediatric population, often caused by primary hyperparathyroidism (PHPT) from a functioning PA [1]. PA account for the majority of PHPT 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]. Early diagnosis is critical because delayed recognition leads to severe complications such as renal impairment, neurological symptoms, and cardiovascular instability [1, 3].

The urgency of clinical management necessitates a multidisciplinary approach. This includes prompt biochemical evaluation, such as serum calcium and PTH levels, and urgent surgical intervention to reduce morbidity and mortality [1, 4]. This case report underscores the importance of considering parathyroid disorders in children with unexplained gastrointestinal symptoms [5]. Firstly, it highlights the role of imaging and histopathological confirmation. Additionally, it emphasizes that timely intervention can effectively reverse abnormalities in metabolic indices (including serum calcium, phosphorus, and PTH levels), alleviate associated symptoms, and mitigate the risk of long-term complications [6].

Case report

A previously healthy girl aged 7 years and 3 months was admitted to The First Affiliated Hospital of Dali University on 31 January 2025 following transfer from the local 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. She underwent surgical repair of an atrial septal defect nine months prior to admission. One month prior to admission, a minor fall resulted in a left tibial fracture. There was no personal or family history of similar disorders.

The child exhibited progressively worsening fatigue but did not have itchy skin or neuropsychiatric symptoms. 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, magnesium decreased to 0.51 mmol/L, and 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. 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. Further testing demonstrated elevated 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, elevated urine calcium (0.35 mmol/kg/24 h), and elevated urine magnesium (5.59 mmol/24 h), while urinary potassium, sodium, chloride, 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. Thyroid and cervical lymph node ultrasound identified a hypoechoic area (approximately 17.8 × 6.6 × 10 mm in size) located inferior to the right thyroid lobe, suggestive of a PA. Neck contrast-enhanced CT identified a nodule (the maximum diameter was 0.6 cm)located posterior and inferior to the right thyroid lobe, findings that are highly suggestive of a parathyroid lesion, likely a parathyroid adenoma. Abdominal ultrasound focusing on the liver, gallbladder, pancreas, spleen, kidneys, ureters, and mesenteric lymphnodes showed no abnormalities. Echocardiography revealed normal findings. Additionally, pituitary MRI was unremarkable. Whole-exome sequencing was performed, and no pathogenic mutations were identified.

When the child was admitted, Her blood pressure was 85/57mmHg and skin elasticity was weakened, indicating a low volume state. We immediately hydrated and added furosemide diuretics after full volume recovery on the second day. Afterwards, blood pressure remained normal. During the use of diuretics, we observed daily that the skin was not dry or swollen, and the capillary refilling was normal. At the same time, we monitored the inflow and outflow daily, and the urine output was maintained at 3.56-4.27 ml/kg/h. The weight gradually and steadily increased from 19.5 kg upon admission, reaching 20 kg when transferred to pediatric surgery. However, CVP monitoring was not performed in this case, which is a limitation. The day after admission, salmon calcitonin was started to be used. After 5 consecutive days of use, the blood calcium remained high at 3.46mmol/L, so it was replaced with pamidronate disodium. After using one dose, the blood calcium decreased to 2.65mmol/L. MDT discussed that PHPT was caused by PA and decided to perform exploratory surgery. Therefore, the patient was transferred to pediatric surgery and blood calcium was measured at 2.32mmol/L. During the operation, an isolated, hard textured, dark brown parathyroid gland measuring 1.5 × 1.0 × 0.4 cm was removed. Within 10 min after glandular resection, PTH decreased from 268.1pg/ml to 120.3 pg/ml. Both frozen section and formalin-fixed paraffin-embedded (FFPE) section confirmed a benign PA, which is mainly composed of main cells and has a complete capsule.The patient had no hoarseness, choking, or twitching/convulsions postoperatively. On the third day after surgery, low blood calcium (2.01mmol/L) was observed, the PTH monitored in the morning dropped significantly to 5.02pg/ml, it returned to normal upon repeat testing in the afternoon, and treatment with oral calcium carbonate D3 and calcitriol was administered. No numbness, tetany or convulsions; Chvostek’s sign and Trousseau’s sign were negative. Serum calcium and PTH were persistently normal starting from postoperative day 6.The important nodes and temporal trends of serum calcium and PTH are shown in Fig. 1a and b, respectively. The patient was advised to continue oral calcium. Rechecks of electrolytes and PTH at 1 month, 3 months, 6 months, 12 months after discharge showed no abnormalities. One month after discharge, DAX bone densitometry showed recovery to normal levels, and subsequent follow‑ups every three months remained within normal limits. After discharge, thyroid ultrasound examinations every 3–6 months showed no significant abnormalities. The entire diagnosis and treatment timeline for this child is shown in Table 1.

Fig. 1.

a Serum calcium level monitoring. Upper limit of normal serum calcium. b PTH level monitoring. PTH crash phrase, PTH nadir phrase, PTH recovery phrase, this represents a typical biochemical pattern following parathyroid surgery in children

Table 1.

Clinical course

Date (2025)	Event	Key value / Intervention
01–19	Pathological fracture	dreduced bone mineral density
01–21	Onset of vomiting and diarrhea	Plain abdominal film: incomplete intestinal obstruction
01–31	Admission to our paediatric ward Severe dehydration.BP:85/57mmHg; AKP247U/L; Mg 0.63↓mmol/L; K(N)	Chief complaint:10-day history of abdominal pain and vomiting; Ca: 4.67 mmol/L(critical value) Intravenous hydration
02 − 01	Initiation of diuretic therapy	BP normal; positive fluid balance was maintained; a dequate urine output; steady weight gain
02−01 to 02–05	Salmon calcitonin	Calcium remained high at 3.46mmol/L
02−01	PTH:268.1 pg/ml ↑	PHPT was suspected
02–02	Neck ultrasound: a hypoechoic nodule inferior to right thyroid lobe. Ca 3.5 mmol/L↑ ; Mg 0.51 mmol/L↓; P 0.71 mmol/L ↓	Parathyroid lesion suspected Diagnosis: hypercalcaemic crisis; hypomagnesaemia; hypokalaemia. Whole-exome sequencing was performed.
02–03	Contrast-enhanced neck CT: a nodule at postero-inferior margin of right thyroid lobe.	PHPT due to PA was suspected. Whole-exome sequencing was performed.
02–05	One dose of bisphosphonate	Serum calcium fell to 2.65 mmol/L.
02–08	MDT	Diagnosis: PHPT du to PA→ surgery planned
02–10	Pituitary MRI: normal. Ca:2.32 mmol/L.	Pituitary tumor ruled out; transferred to surgical department.
02–12	Pre-operative ultrasound: a well-defined, hypoechoic nodule; Ca:2.55 mmol/L.	Adequate preoperative preparation.
02–14	An adenoma of 1.5 × 1.0 × 0.4 cm was excised; intraoperative PTH dropped to 120.3 pg/ml .	Preoperative diagnosis confirmed; parathyroid function restored.
02–15	PTH:68 pg/ml; Ca: 2.23 mmol/L; Serum AKP and phosphorus were normal.	Serum calcium declined.
02–17	PTH:5↓↓pg/ml; Ca :2.01↓ mmol/L.	transient hypofunction, Possible hungry bone syndrome; oral calcium supplement started
02–20	Histopathology repor: right PA with intact capsule; chiefly clear-cell pattern	In accordance with preoperative diagnosis.
02–24	No positive symptoms or signs; All parameters within normal limits.	Discharged; regular follow-up advised.

Discussion

Hypercalcaemia should be ruled out in any child presenting with persistent abdominal pain and vomiting. Beyond common causes such as dehydration or malignancy, functional parathyroid disorders should also be considered [7, 8]. PHPT caused by a functional 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 [9]. Unlike adults, where solitary PA accounts for 80–90% of PHPT cases, pediatric cases are more often linked to hereditary syndromes or multiglandular disease [10]. Severe hypercalcaemia can lead to intestinal pseudo-obstruction (a condition mimicking bowel obstruction) by impairing intestinal smooth muscle contractility and neural conduction.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 [7, 11], as exemplified in our case.

PHPT is caused by excessive synthesis and secretion of PTH due to abnormal parathyroid tissue (tumor or hyperplasia), with PA accounting for 85% of its etiology [12]. On the one hand, excessive PTH promotes bone resorption by increasing osteoclast activity and inhibiting osteoblasts, leading to hypercalcemia [13]. In the early stage, intermittent hypercalcemia may occur, and in the later stage, blood calcium continues to increase. Patients experience extensive bone resorption and decalcification, leading to a decrease in bone density, increased risk of osteoporosis and fractures, and in severe cases, fibrocystic osteitis. Elevated blood calcium can also lead to migratory calcification [14]. On the other hand, PTH can stimulate renal 1α-hydroxylase, converting 25-hydroxyvitamin D into the active form 1,25-dihydroxyvitamin D, which can enhance intestinal absorption and increase renal tubular reabsorption of calcium, thereby exacerbating hypercalcemia. However, long-term hyperparathyroidism may impair kidney function, affect 1 α - hydroxylase activity, and lead to insufficient production of active vitamin D. In addition, hypercalcemia may inhibit the expression of vitamin D receptors, further weakening the effect of vitamin D. Vitamin D deficiency can also exacerbate hyperparathyroidism. Vitamin D deficiency reduces intestinal calcium absorption, making it difficult to maintain blood calcium levels. The parathyroid gland perceives insufficient blood calcium and compensates by secreting more PTH, exacerbating symptoms of hyperparathyroidism [15]. In addition, PTH can increase the reabsorption of calcium by distal renal tubules and reduce the reabsorption of phosphorus by proximal tubules, leading to increased excretion of urinary calcium and phosphorus. The decomposition products of bone matrix are excreted through urine, which can easily form urinary tract stones or renal calcium deposition. PTH can also inhibit the reabsorption of bicarbonate by renal tubules, leading to hyperchloroacidosis. High concentrations of calcium ions can stimulate gastrin secretion, increase gastric acid, form gastric and duodenal ulcers, and may also activate trypsinogen to cause acute pancreatitis [14].

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 [16]. Upon detection of hypercalcemia, the differential diagnosis should include familial hypocalciuric hypercalcemia (FHH), malignancy, vitamin D intoxication, and renal osteodystrophy [17, 18]. A markedly elevated PTH level, combined with suppressed 25-hydroxyvitamin D and normal-to-low urinary calcium, strongly supports the diagnosis of PHPT [1].The core of PHPT diagnosis relies on biochemical markers: the classic phenotype consists of hypercalcemia, elevated PTH, and a fractional excretion of calcium (FeCa) > 2%. Atypical presentations (e.g., hypercalcemia with normal PTH, or normocalcemia with elevated PTH) require exclusion of secondary causes. The oral calcium loading test and Pro-FHH score can assist in differentiating PHPT from FHH [19]. Urinary creatinine measurement is not currently available at our institution, so FeCa could not be calculated. Given the classic phenotype of hypercalcemia, hypercalciuria, and elevated PTH, imaging suggestive of PA, and a negative CaSR genetic test, FHH was essentially ruled out. Therefore, calculation of FeCa or the calcium/creatinine clearance ratio (CCCR) was not performed. After confirming PHPT, further evaluation of the underlying etiology is required. The patient was aged over 7 years with a history of atrial septal defect. Although no family history was reported, hereditary parathyroid disorders such as multiple endocrine neoplasia type 1 (MEN1), hyperparathyroidism-jaw tumor syndrome (HPT-JT), and familial isolated primary hyperparathyroidism (FIHP) still needed to be ruled out. Notably, MEN1 is the most common syndrome associated with solitary adenoma in children [20].Therefore, genetic screening for MEN1, CDC73/HRPT2, CDKN1B, and CaSR was indicated. Localization of the PA can be reliably achieved using high-resolution cervical ultrasound and contrast-enhanced CT, which together provide a sensitivity that exceeds 90% [21].

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. Loop diuretics (e.g., furosemide 1 mg/kg every 6–8 h) should be administered only after adequate volume repletion has been achieved to enhance renal calcium excretion. Calcitonin (4–6 IU/kg every 12 h) suppresses osteoclast function and is used to rapidly lower calcium levels, although its effect is transient [22].Administer intravenous bisphosphonate, such as pamidronate, at 0.5 mg/kg as a single dose if serum calcium concentration remains severely elevated—greater than 3.5mmol/L—despite initial treatments [23].Hemodialysis or cinacalcet may be considered for refractory cases. The use of bisphosphonates in pediatric hypercalcemic crisis requires a risk-benefit assessment, taking into account the unique characteristics of active bone growth in children. By inhibiting farnesyl pyrophosphate synthase, bisphosphonates rapidly reduce serum calcium, creating a safe window for elective surgery [24].However, the high bone turnover rate in children leads to more pronounced postoperative hungry bone syndrome, resulting in a higher risk of hypocalcemia than in adults [25]. In our patient, calcitonin was administered initially but showed suboptimal efficacy. Treatment was therefore switched to pamidronate, which achieved a marked reduction in serum calcium. Nevertheless, severe hypocalcemia occurred postoperatively, confirming the superimposed risk between the long half-life of bisphosphonates and the hungry bone effect [13]. Current clinical guidelines recommend bisphosphonate use when serum calcium remains above 3.5 mmol/L despite hydration and calcitonin therapy. Dosage must be accurately calculated based on body weight. Postoperatively, prophylactic calcium supplementation is warranted, and monitoring should be prolonged until bone mineral density recovers. Long-term follow-up of linear growth is also recommended to evaluate potential effects on the growth plate. 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. In hypercalcemic crisis, salmon calcitonin is generally only used for emergency management during the initial 48–72 h. Tachyphylaxis develops rapidly, and its efficacy diminishes significantly with continued use. Furthermore, early combination with bisphosphonates produces an additive or synergistic hypocalcemic effect, allowing rapid control of serum calcium. Clearly, the period of observation in our case was excessively long, and bisphosphonate intervention was delayed. Although bisphosphonates reduce serum calcium through potent inhibition of bone resorption, their maximal effect typically occurs 2–4 days after administration [22]. Initiating bisphosphonates only after salmon calcitonin has lost efficacy creates a dangerous therapeutic “window period”. Hypercalcemic crisis is particularly harmful in children, and delayed effective treatment may lead to severe complications such as irreversible renal injury. Definitive treatment is surgical excision of the adenoma [13]. Early definitive surgery is indicated. Nevertheless, parental hesitation over surgical risk–benefit assessment and hospital selection delayed preoperative management. 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 [26]. Intraoperative PTH monitoring, defined as a drop of 50% or more from baseline measured 10 min after excision [10], serves as a reliable predictor of surgical success and was used effectively in our case.

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 [25, 27]. Long-term follow-up is essential for patients who have undergone surgical resection due to reported recurrence rates of 2–5%, even after seemingly curative surgical resection [28]. Monitor for symptoms of hypercalcemia and disease recurrence [7]. Serum calcium and PTH were measured daily during the first 3 postoperative days. Discharge was considered safe when serum calcium was > 2.1 mmol/L and stable for 48 h [27].In this case, prophylactic calcium supplementation was not initiated immediately after surgery, and monitoring frequency was insufficient, resulting in delayed detection of hypocalcemia. Systematic follow-up was performed at 1, 3, 6 months, 1 year, and 2 years postoperatively, including serum calcium, PTH, and DXA bone mineral density [29]. Establish a comprehensive and individualized follow-up system is of great necessity [7].

In summary, a hormone-secreting PA 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 [12]. 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.

This case report has certain limitations. Firstly, this study is only an observation and summary of a single case, lacking support from control groups and large sample data. Therefore, it is difficult to rule out the interference of individual specificity on the results, which limits the extrapolation and universality of the conclusions. The clinical manifestations and treatment responses observed in this case may only represent a minority of cases and cannot be directly generalized to a wider patient population. Secondly, as this case is a rare disease with certain particularities, its diagnosis and treatment experience may not be applicable to routine clinical situations. At the same time, the basic conditions of patients vary in different medical environments, so there may be differences in the implementation details and evaluation criteria of treatment plans, further weakening the reproducibility and promotional value of the conclusions.

Conclusion

PA remains an exceptionally rare cause of PHPT in children, however, it must be considered in any child who presents with persistent gastrointestinal symptoms, and unexplained hypercalcemia. The clinical presentation, often resembles an acute abdominal emergency. Early assessment of serum calcium and PTH is essential for the timely recognition. 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. Hungry bone syndrome should be vigilant for. Long-term surveillance is necessary to monitor recurrence. The overall prognosis is excellent when the condition is timely identified and appropriately treated.

Abbreviations

ALT

Alanine aminotransferase

AST

Aspartate aminotransferase

CCCR

Calcium/creatinine clearance ratio

FFPE

Formalin-fixed paraffin-embedded

FIHP

Familial isolated primary hyperparathyroidism

FHH

Familial hypocalciuric hypercalcemia

FeCa

Fractional excretion of calcium

HPT-JT

Hyperparathyroidism-jaw tumor syndrome

MEN1

Multiple endocrine neoplasia type 1

PA

Parathyroid adenoma

PHPT

Primary hyperparathyroidism

PTH

Parathyroid hormone

Authors’ contributions

WHZ: Study conception, data collection, drafting of the manuscript; WNZ: Study conception, data collection, critical revision; XYZ: Study conception, data collection, Laboratory analysis, critical revision; MJZ: Laboratory analysis, drafting of the manuscript.Final approval of the version to be published: all authors. All authors agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Funding

There was no external financial support for this study.

Data availability

The raw sequence data reported in this paper have been deposited in the Genome Sequence Archive [30, 31] (Genomics,Proteomics & Bioinformatics 2025) in National Genomics Data Center (Nucleic Acids Res 2025), China National Center for Bioinformation / Beijing Institute of Genomics,Chinese Academy of Sciences (GSA-Human: HRA018423) that are publicly accessible at https://ngdc.cncb.ac.cn/gsa-human. De-identified clinical data, imaging files and laboratory results are available upon reasonable request to the corresponding author (286673424@qq.com).

Declarations

Ethics approval and consent to participate

The study received ethical approval from the First Affiliated Hospital of Dali University, with the approval number DFY20251208001. Additionally, written informed consent for study participation was obtained from her legal guardians of the patient.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.