A 67-Year-Old Male with Hypercalcaemia and Giant Parathyroid Adenoma

 

Fauzia Rehman1, Nyla Ajaz1, , Maham Ashraf1, Nabeeha Noor1, Manahal Zaib1, Sameen Tahir2, Sumayya Ismail1

1Department of Pharmacy, Government College University Faisalabad, Faisalabad, Pakistan

2Department of Pharmacy, Riphah International University, Pakistan

 

METADATA

 

Paper history

Received: 13 August 2026

Revised: 24 September 2026

Accepted: 20 October 2026

Published online: 31 October 2026

 

Corresponding author

Nyla Ajaz

 

Keywords

Primary hyperparathyroidism

Hypercalcaemia

Parathyroid adenoma

DEXA scan

 

Citation

Rehman F, Ajaz N, Ashraf M, Noor N, Zaib M, Tahir S, Ismail S (2026) A 67-year-old male with hypercalcaemia and giant parathyroid adenoma. Innovations in STEAM: Research & Education Innovations in STEAM: Research & Education 4(2): 26040205. https://doi.org/10.63793/ISRE/0040.

ABSTRACT

 

Background: Primary hyperparathyroidism (PHPT) is an endocrine disorder in which the parathyroid glands secrete excess parathyroid hormone (PTH), most often because of a single parathyroid adenoma. Giant parathyroid adenomas (GPAs) are rare and can cause severe hypercalcaemia.

Objective: To highlight the diagnostic challenges and management of severe symptomatic primary hyperparathyroidism caused by a large parathyroid adenoma in an elderly patient, emphasizing the role of biochemical and imaging investigations, surgical excision with intraoperative parathyroid hormone monitoring, and postoperative calcium management to prevent hungry bone syndrome.

Methodology: The pot experiment was carried out in 3 � 4 factorial completely randomized design (3 replicates) with salinity: 0, 150 and 200 mM NaCl and Fe-NP foliar application: 0, 250, 350 and 450 ppm. The growth parameters, photosynthetic pigments, oxidative stress parameters, antioxidant metabolites and mineral nutrients were measured by standard procedures.

Results: After hydration and bisphosphonate therapy, the adenoma was surgically exercised with intraoperative PTH monitoring. Serum calcium and renal function returned to normal after surgery, and the patient was discharged on calcium and vitamin D supplements to prevent hungry bone syndrome.

Conclusion: Early diagnosis of PHPT caused by a giant parathyroid adenoma, using PTH measurement and imaging, followed by surgical excision, can prevent further bone and kidney damage.

 

INTRODUCTION

 

Primary hyperparathyroidism (PHPT) is a common endocrine disorder in which the parathyroid glands secrete excess parathyroid hormone (PTH). It is most often caused by a single parathyroid adenoma (Al-Hassan et al. 2019), a benign tumour of one of the parathyroid glands, which lie in the neck behind the thyroid gland. PTH regulates calcium homeostasis. Excess PTH raises serum calcium by stimulating osteoclast activity and suppressing osteoblast activity in bone, and the resulting hypercalcaemia produces the clinical features of the disease (Mahmodlou et al. 2022). Most parathyroid adenomas are small, usually weighing less than 1 g (Narla et al. 2020), and cause relatively few problems. Larger adenomas are more difficult to diagnose and to treat (Mahmodlou et al. 2022).

A giant parathyroid adenoma (GPA) is a rare, benign tumour that is usually defined by a weight above 3.5 g (Al-Hassan et al. 2019; Mahmodlou et al. 2022). Fewer than 1% of cases are of this type, yet a GPA is a clinically important cause of marked PHPT. Whereas sporadic adenomas are usually smaller than 2 cm, GPAs can be associated with very high PTH and calcium levels and with severe systemic complications, including osteitis fibrosa cystica, renal dysfunction and neuropsychiatric manifestations. Biochemically, a GPA can resemble parathyroid carcinoma, but microscopy shows no invasion of the surrounding tissue (Houas et al. 2023). Diagnosis relies on PTH measurement, ultrasonography and sestamibi scintigraphy, and surgical resection, which is usually curative, is the only definitive treatment. Delayed treatment can cause permanent bone and kidney damage. After surgery, hungry bone syndrome may occur, in which the bones take up large amounts of calcium and cause hypocalcaemia, so postoperative calcium monitoring is mandatory. Here we report a patient with symptomatic hypercalcaemia (fatigue, bone pain and a history of kidney stones) and an imaging-documented GPA. The aim is to highlight the diagnostic and therapeutic approach and the importance of recognising disease early.

 

CASE PRESENTATION

 

Clinical history and examination

 

 

Fig. 1: Case representation
A 67-year-old retired teacher presented to Sir Ganga Ram Hospital, Lahore, with severe fatigue that did not improve with rest. He also reported bone pain, with no history of injury or arthritis, and a four-month history of intermittent vertigo described as a spinning sensation, without ear pain or hearing loss. Vertigo is a nonspecific symptom with many possible causes (Kim 2021). On further questioning, he reported constipation and frequent urination, and he had a previous history of kidney stones. The fatigue and bone pain had been present for about a year and were gradually worsening. This combination of symptoms raised the suspicion of hypercalcaemia.

 

Laboratory investigations

 

Laboratory tests showed severe hypercalcaemia, with a serum calcium of 13.1 mg/dL, and a markedly raised PTH of 537.5 pg/mL (Table 1; Fig 1�3). Serum phosphate was low at 1.5 mg/dL, consistent with the phosphaturic action of

PTH, which reduces renal phosphate reabsorption.

Table 1: Biochemical findings before and after surgery

 

Parameter

Pre-op

Post-op

Reference range

Serum calcium (mg/dL)

13.1

9.0

8.8�10.6

Serum phosphorus (mg/dL)

1.5

4.4

2.5�4.5

Alkaline phosphatase (U/L)

150

113

30�120

Serum creatinine (mg/dL)

1.4

0.9

0.67�1.17

Blood urea (mg/dL)

38

36

17�43

Parathyroid hormone (pg/mL)

537.5

NR

NR

 

 

Fig. 2: Axial neck view of a 67-year-old man showing a giant parathyroid adenoma behind the right thyroid lobe, its effects on bone and kidney, and the clinical course f

 

 

 

Fig. 3: Pre-operative routine biochemistry report of the patient (patient identifiers masked)

 

Fig 4: Neck ultrasonography report showing a 29 � 20 mm solid hyperechoic lesion at the inferior pole of the right thyroid lobe (patient name masked)

 

 

Fig. 5: Parathyroid SPECT/CT report (dual-phase 99mTc-sestamibi scintigraphy) suggesting a parathyroid adenoma posterior to the right thyroid lobe (patient identifiers masked).

 
Imaging

 

Neck ultrasonography showed a well-defined, solid, hyperechoic lesion measuring 29 � 20 mm at the inferior pole of the right thyroid lobe (Fig. 2). The lesion contained a few cystic areas and showed no major vascularity on colour Doppler. Dual-phase 99mTc-sestamibi scintigraphy with SPECT/CT showed focal tracer retention in the lower pole of the right thyroid lobe that persisted on delayed images, confirming a parathyroid adenoma (Figure 3). DEXA scanning showed osteopenia, consistent with chronic PTH-mediated bone resorption (Pandya et al. 2024). Raised PTH increases osteoclast activity, which causes loss

of both cortical and trabecular bone; this explains the bone pain and the increased risk of fracture.

Management and outcome

 

The patient had symptomatic hypercalcaemia, with features such as weakness and dehydration, and surgery was therefore advised. Before surgery, intravenous fluids were given to correct dehydration and control serum calcium, together with a bisphosphonate to lower serum calcium by limiting bone resorption. The adenoma was removed by surgical excision, with intraoperative monitoring of PTH. After the operation, serum calcium (9.0 mg/dL), phosphate (4.4 mg/dL), alkaline phosphatase (113 U/L) and creatinine (0.9 mg/dL) were within the reference ranges (Table 1; Fig. 6). The patient was discharged on calcium and vitamin D supplements to prevent hungry bone syndrome. Histopathology and weight of the excised specimen

 

Fig. 6: Post-operative routine biochemistry report of the patient (patient identifiers masked).

 
DISCUSSION

 

This case shows a severe presentation of PHPT caused by a large parathyroid adenoma. Three points deserve emphasis: the need for timely diagnosis in patients with nonspecific symptoms such as fatigue, bone pain and vertigo; the central role of PTH measurement and imaging (ultrasonography and sestamibi scintigraphy) in localising adenoma; and the role of surgery as a definitive therapy, with medical management reserved for patients who cannot undergo surgery.

The symptoms of our patient were common and nonspecific. Fatigue, bone pain and vertigo occurred daily, together with other vague complaints, and all were ultimately explained by PHPT, in which the parathyroid gland releases excess PTH. Giant adenomas are uncommon, but when they occur the symptoms are usually severe and serum calcium reaches high levels (Singh et al. 2022). PTH measurement, ultrasonography and sestamibi scintigraphy were used for diagnosis. The optimal treatment for parathyroid adenoma is parathyroidectomy. However, if this is not possible then medical management can be used including calcimimetics and bisphosphonates (Leere et al., 2017). The patient's serum calcium and renal function were normal following surgery, which shows a positive response to the surgical treatment. Early identification of clinical symptoms and timely management is vital to prevent long term complications from severe hyperparathyroidism. Monitoring serum calcium levels after surgery can help identify and manage any complications, such as hungry bone syndrome.

 

Follow-up

 

Renal function and bone density will improve over a period of 1-2 years. Regular follow up is required to monitor for any recurrence and hungry bone syndrome.

 

CONCLUSION

 

A giant parathyroid adenoma is a rare but significant cause of primary hyperparathyroidism and can present with non-specific symptoms such as fatigue, vertigo, bone pain, polyuria and constipation. Serum calcium, phosphate and PTH levels alongside ultrasound and sestamibi scans can help make a quick diagnosis and localise the lesion. Surgery is the definitive treatment. Early diagnosis can prevent permanent kidney and bone damage. Careful monitoring and supplementation of calcium can also help to avoid hungry bone syndrome.

 

ACKNOWLEDGEMENTS

 

The authors would like to acknowledge the Department of Pharmacy, Government College University Faisalabad, Faisalabad, Pakistan, for its support and academic contributions to this work

 

AUTHOR CONTRIBUTIONS

 

FR and NA conceived the case report and supervised the work. NA managed the patient and collected the clinical data. MA and NN reviewed the literature and wrote the original draft. MZ analysed and interpreted the laboratory and imaging findings and prepared the table and figures. ST and SI revised the manuscript critically for important intellectual content. All authors read and approved the final manuscript.

 

CONFLICT OF INTEREST

 

The authors declare that there is no conflict of interest.

 

 

ETHICS APPROVAL

 

Authors to confirm written informed consent for publication of this case and the accompanying images was obtained from the patient.

 

FUNDING SOURCE

 

Not applicable

 

REFERENCES

 

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