Hypercalcemia episodes caused by ectopic parathyroid adenoma and subsequent gastrointestinal stromal tumor: A case report and literature review

Objective: Ectopic parathyroid gland-induced hypercalcemia is unusual, whereas hypercalcemia from a gastrointestinal stromal tumor (GIST) is extremely rare. This study aims to present a rare case of simultaneous ectopic parathyroid adenoma and GIST, associated with two episodes of hypercalcemia, and to review imaging techniques for ectopic parathyroid localization and the mechanism of hypercalcemia linked to GISTs.

Methods: The clinical manifestations, diagnostic workup, therapeutic interventions, and outcomes of the present case were analyzed. To evaluate advanced imaging modalities, particularly four-dimensional computed tomography (4D-CT) and ¹⁸F-fluorocholine (FCH) PET/CT, for ectopic parathyroid localization, a PubMed search for literature in English from inception to July 2025 was conducted using the terms (“4D-CT” AND “ectopic parathyroid”) or (“¹⁸F-fluorocholine PET/CT” AND “ectopic parathyroid”). Additional keywords related to parathyroid imaging, including “FCH-PET/CT”, “¹⁸F-fluorocholine PET/CT”, and “4D-CT”, were incorporated to broaden the search. Reports of GIST-related hypercalcemia were also identified to summarize underlying mechanisms and management approaches.

Results: An 87-year-old man presented with progressive renal dysfunction and hypercalcemic hyperparathyroidism. ^99mTc-sestamibi single photon emission computed tomography/computed tomography (SPECT/CT) identified an ectopic parathyroid lesion in the anterior mediastinum, which was successfully treated with video-assisted thoracoscopic surgery, resolving hypercalcemia. Two years later, recurrent hypercalcemia occurred with reduced parathyroid hormone levels. A CT scan and biopsy revealed a GIST in the pelvis, an extremely rare cause of hypercalcemia. Imatinib normalized calcium and parathyroid hormone levels and induced tumor regression. Nineteen reports showed that 4D-CT or FCH-PET/CT successfully localized ectopic parathyroid lesions after conventional imaging modalities were inconclusive. In 9 cases of GIST-associated hypercalcemia, pathophysiology may involve parathyroid hormone–related protein (PTHrP) or 1-alpha-hydroxylase, with glucocorticoids having a potential role in treatment.

Conclusions: To our knowledge, this case represents the first reported coexistence of an ectopic parathyroid adenoma and a GIST. 4D-CT and FCH-PET/CT can be used as alternative imaging modalities following ^99mTc-sestamibi SPECT/CT to locate ectopic parathyroid lesions. The mechanism behind GIST-related hypercalcemia may involve the expression of PTHrP or 1-alpha-hydroxylase in tumor tissues.

Introduction

Primary hyperparathyroidism (pHPT) is a common endocrine disorder, with estimated incidences of 233 and 85 per 100,000 women and men in the United States, respectively (1). Ectopic parathyroid glands are present in 10% to 22% of pHPT cases (2, 3), likely due to abnormal embryonic migration. Accurate preoperative localization of ectopic parathyroid adenomas is crucial for optimizing surgical outcomes, and various imaging modalities are available to aid in this process (4). As for gastrointestinal stromal tumors (GISTs), they have an annual global incidence of approximately 1.5 per 100,000, affecting both sexes equally with a peak incidence at age 70 (5). GISTs, the most common type of soft tissue sarcoma, arise from the digestive tract and are primarily driven by gain-of-function mutations in the KIT or PDGFRA genes, which encode receptor tyrosine kinases. The introduction of tyrosine kinase inhibitors has significantly improved the prognosis of this previously chemotherapy-resistant cancer (6).

To date, there are few case reports on hypercalcemia associated with GISTs (7–15). The coexistence of an ectopic parathyroid adenoma and a GIST with two separate episodes of hypercalcemia in a single patient is exceptionally rare. This study aims to present this rare condition and to review the advanced imaging techniques used for localization of ectopic parathyroid lesions and the pathophysiology of GIST-induced hypercalcemia.

Case presentation

An 87-year-old man with a medical history of heart failure with preserved ejection fraction, chronic kidney disease, hypertension, and cerebellar infarction presented with worsening renal function and hypercalcemia in 2022. His regular medications included furosemide 40 mg daily and trichlormethiazide 2 mg daily. There was no family history of endocrine disorders or tumors. The serum calcium level at the time was elevated at 2.99 mmol/L (normal range: 2.15-2.58 mmol/L). Laboratory evaluation showed a serum phosphorus level of 3.0 mg/dL (normal range: 2.5-5.0 mg/dL), markedly elevated intact parathyroid hormone (PTH) level of 505.1 pg/mL (reference range: 15.0-68.3 pg/mL), a 24-hour urine calcium level of 304.8 mg/day, and a high calcium clearance ratio of 0.06, leading to a diagnosis of primary hyperparathyroidism. Bone mineral density showed osteopenia, and renal sonography revealed a small left renal stone. A neck ultrasound did not identify any parathyroid lesion. A ^99mTc-sestamibi single photon emission computed tomography/computed tomography (SPECT/CT) revealed a tracer-avid lesion in the left superior anterior mediastinum, which was successfully excised via video-assisted thoracoscopic surgery (VATS), resulting in normalization of serum calcium during follow-up (Figure 1). The excised lesion measured 3.0 × 2.6 × 1.2 cm and weighed 5.1 g. Histologic examination revealed an ectopic parathyroid gland with hyperplasia, and immunohistochemistry was positive for PTH in the lesional cells.

Figure 1

Figure 1. First episode hypercalcemia (PTH-dependent). ^99mTc-sestamibi SPECT/CT identified an ectopic parathyroid adenoma in the anterior mediastinum (a). The lesion was successfully removed via video-assisted thoracoscopic surgery, leading to resolution of the first, PTH-dependent, episode of hypercalcemia (b). Only serum calcium and creatinine were tested preoperatively; PTH was not included.

Two years after the prior episode of hypercalcemia, he presented with generalized weakness, drowsy consciousness, and abdominal distension, prompting his transfer to our emergency department. Physical examination revealed muscle strength graded 4/5 in all extremities. Laboratory tests showed hypercalcemia (3.31 mmol/L; normal range: 2.15-2.58 mmol/L), acute kidney injury (creatinine: 2.91 mg/dL; normal range: 0.6-1.3 mg/dL), and a suppressed intact PTH level of 9.3 pg/mL (reference range: 15.0-68.3 pg/mL), with normal phosphorus, magnesium, and liver function levels. The serum 25-hydroxyvitamin D was slightly low at 17.3 ng/mL. His home medications included furosemide 40 mg once daily for heart failure. A non-contrast computed tomography (CT) scan of the abdomen and pelvis revealed a 12.8 cm soft tissue mass in the pelvic cavity (Figure 2a). The lesion was further characterized by a MRI with contrast showing intermediate-to-low T1WI signal, heterogeneous high T2WI signal, diffusion restriction, and heterogeneous contrast enhancement. These findings are consistent with a GIST. Whole body bone scintigraphy showed no skeletal metastases. A ultrasound-guided biopsy was performed. Histologically, the specimen shows a spindle cell neoplasm with nor pleomorphism or necrosis, and mitoses are absent (<1/50 HPF). Immunohistochemistry demonstrates diffuse positivity for CD117 and DOG1 and negativity for SMA, desmin, and S100, confirming the diagnosis of a GIST, with a Ki-67 index of 10% (Figure 3). Based on tumor size, low mitotic activity, and uncertain origin, the lesion meets a high-risk category by NIH consensus criteria. Although AFIP (Miettinen–Lasota) assessment is limited, the large size and low mitotic rate suggest intermediate-to-high risk. The tumor corresponds to cT4N0M0, stage IIIA. Given the suppressed intact PTH, elevated serum calcium, and a large GIST, malignancy-associated hypercalcemia was strongly suspected.

Figure 2

Figure 2. Second episode hypercalcemia (PTH-independent). The initial pelvic mass measured 12.8 cm at diagnosis. After three months of imatinib treatment, the tumor size decreased to 8.8 cm (a). During the second, PTH-independent, episode of hypercalcemia, calcium levels normalized within two weeks of imatinib therapy for the gastrointestinal stromal tumor. Transient iPTH elevation due to hypocalcemia resolved with calcium supplementation (b).

Figure 3

Figure 3. Histopathologic findings of the pelvic gastrointestinal stromal tumor. A spindle cell neoplasm shows spindle-shaped tumor cells with monomorphic nuclei and eosinophilic cytoplasm (30×) (a). Tumor cells show diffuse positive staining for C-kit/CD117 (12×) (b) and DOG1 (12×) (c).

The patient was initially treated with intravenous fluids, furosemide, and calcitonin. Hypercalcemia was incompletely resolved, with a corrected calcium level of 3.02 mmol/L. A single dose of subcutaneous denosumab (120 mg) and imatinib therapy (100 mg daily) were administered on the same day following pathological confirmation of GIST (Figure 2b). The imatinib dose was adjusted due to the patient’s advanced age, acute decompensated heart failure, and an estimated creatinine clearance of 20 mL/min. Calcium levels normalized two weeks after denosumab and imatinib administration. Over the next four weeks, the intact PTH level, which had transiently increased due to hypocalcemia, returned to normal with calcium supplementation (Figure 2b). The effect of imatinib on calcium normalization was confounded by denosumab, which can cause hypocalcemia and transient PTH changes. After three months of imatinib therapy, normocalcemia was maintained without calcium supplementation and tumor size was reduced on a follow-up CT scan (Figure 2a), supporting the diagnosis of GIST-associated hypercalcemia. The dosage of imatinib remained unchanged during therapy, and no clinically significant adverse effects were observed.

Discussion

To our knowledge, this is the first reported case demonstrating the coexistence of an ectopic parathyroid adenoma and a GIST associated with two separate episodes of hypercalcemia. In animal studies, certain genetic mutations, such as mafB, have been linked to the development of ectopic parathyroid tissue (16). In contrast, GISTs are associated with genetic alterations in KIT and PDGFRA (6). Currently, there is no evidence to suggest that these two conditions arise from shared genetic mutations. Although no known gene directly links parathyroid neoplasms and GISTs, both conditions predominantly affect individuals over the age of 50 and can independently cause hypercalcemia, which may explain their co-occurrence in this case.

Hypercalcemia with an elevated or inappropriately elevated PTH level is indicative of PTH-dependent hypercalcemia. A thorough medical history and physical examination, including an assessment of symptoms like kidney stones, bone pain, or abdominal issues, are essential to identify underlying causes. Additional tests may include a calcium/creatinine clearance ratio and a 24-hour urine calcium excretion to assess for familial hypocalciuric hypercalcemia, a serum creatinine test to evaluate renal function, and a measurement of 25-hydroxyvitamin D levels to assess for vitamin D deficiency. For the localization of hyperfunctioning glands in pHPT, imaging techniques have traditionally involved neck ultrasound and ^99mTc-sestamibi SPECT/CT (1). Other imaging modalities, such as four-dimensional computed tomography (4D-CT) of the neck, magnetic resonance imaging (MRI), positron emission tomography/computed tomography (PET/CT) with radiotracers such as ¹⁸F-fluorocholine (FCH), and parathyroid venous sampling (PVS) are typically reserved for cases with negative or inconclusive results from conventional methods (17–19). A network meta-analysis (20) of 8,495 patients from 119 studies demonstrated that FCH-PET/CT is superior to the CT category and conventional modalities like ultrasound and MIBI after 2010; however, the selection of preoperative imaging may vary based on availability, cost, and performance.

Ectopic parathyroid adenoma should be suspected in pHPT patients who exhibit an ectopic lesion on imaging studies, negative localization of the parathyroid gland, or persistent disease after surgery (1). Ectopic parathyroid glands have been classically described as occurring anywhere from the angle of the mandible to the mediastinum. They most commonly occur in several locations, including the retro/paraesophageal space, mediastinum, intrathymic or intrathyroidal sites, carotid sheath, and a high undescended cervical position (17). Their wide range of locations can make them challenging to identify accurately. Neck ultrasound is particularly effective for locating intra-thyroid parathyroid glands, but is less accurate for detecting ectopic glands in the mediastinum (3). In contrast, ^99mTc-sestamibi SPECT/CT are particularly effective in identifying ectopic glands, especially in the thymus, mediastinum, or retroesophageal space, with a reported sensitivity of 89% (3). Despite the growing adoption of contemporary tools like 4D-CT and FCH-PET/CT in parathyroid imaging, their effectiveness in individuals with ectopic parathyroid glands remains poorly understood. To date, FCH-PET/CT has successfully localized ectopic parathyroid adenomas in six reported cases, five of which had failed prior localization with ^99mTc-sestamibi SPECT/CT (21–25) (Table 1). Similarly, 4D-CT enabled detection in fifteen cases after conventional imaging modalities, including ultrasound, ^99mTc-sestamibi SPECT/CT, CT, MRI, and PVS, were inconclusive (Table 1), highlighting their critical role in challenging cases (26–39). By contrast, it is impossible to determine whether cases successfully localized by conventional imaging modalities were actually missed by advanced imaging tools like 4D-CT or FCH-PET/CT. Further research is needed to determine the optimal imaging modality for the localization of ectopic parathyroid adenomas.

Table 1

Table 1. Successful 4D-CT and FCH-PET/CT localization of ectopic parathyroid glands.

Hypercalcemia with a reduced PTH level is suggestive of PTH-independent hyperparathyroidism. For PTH-independent hypercalcemia, further evaluation typically involves imaging studies such as chest radiograph, mammogram, or CT scans to rule out malignancy, bone scans to assess for bone metastases or primary bone tumors, and serum and urine protein electrophoresis to evaluate for multiple myeloma. Additional tests may include serum parathyroid hormone–related protein (PTHrP) and serum 1,25-dihydroxyvitamin D levels to assess for malignancy or vitamin D toxicity. The diagnostic flow is then tailored based on the results, with further evaluation and testing as needed to identify the underlying causes of hypercalcemia.

Hypercalcemia induced by GISTs is an extremely rare condition, with only 9 reported cases to date (7–15), as demonstrated in Table 2. Reported cases in GIST-induced hypercalcemia involved patients aged 45 to 77 years, with a female-to-male ratio of six to three. Almost all previously reported patients presented with advanced-stage disease and initially received treatment with tyrosine kinase inhibitors rather than surgery (7–13, 15). In GIST-induced hypercalcemia, earlier studies suggested that PTHrP secretion by the tumor was the primary mechanism (8, 12). However, recent literature increasingly implicates a 1,25-dihydroxyvitamin D–mediated pathway (10, 11, 13, 15). GISTs have been shown to produce 1-alpha-hydroxylase (15), which converts 25-hydroxyvitamin D into its active form, 1,25-dihydroxyvitamin D. This excess active vitamin D subsequently increases intestinal calcium absorption and bone resorption, leading to hypercalcemia. In patients presenting with hypercalcemia, standard hypercalcemia management, along with targeted cancer treatment for GISTs, has been employed. Additionally, three case reports have explored the use of prednisolone for acute hypercalcemia management, with doses of 1.5 mg/kg and 37.5 mg per day, respectively. Calcium levels successfully decreased in two cases (11, 15), while one case showed no response (13). We were unable to definitively elucidate the mechanism of hypercalcemia in our case due to the unavailability of PTHrP/CYP27B1 (1-alpha-hydroxylase) immunohistochemical staining and serum assays for PTHrP and 1,25-dihydroxyvitamin D at our institution. Further research is necessary to determine the underlying mechanisms, the efficacy of steroid therapy, and appropriate dosing strategies.

Table 2

Table 2. The clinical manifestation and possible mechanism of documented cases with hypercalcemia induced by GISTs.

Conclusions

This is the first reported case of concurrent ectopic parathyroid adenoma and GIST-induced hypercalcemia. In this case, ^99mTc-sestamibi SPECT/CT successfully localized the ectopic parathyroid adenoma. In diagnostically challenging cases where conventional imaging modalities are inconclusive, 4D-CT and FCH-PET/CT may serve as complementary tools for localization of ectopic parathyroid adenomas. GIST-related hypercalcemia is rare and may result from tumor secretion of PTHrP or 1-alpha-hydroxylase–mediated overproduction of 1,25-dihydroxyvitamin D, often presenting with suppressed PTH levels. Management includes standard calcium-lowering agents and GIST-directed therapies. Steroids may help in calcitriol-mediated cases, but their efficacy remains uncertain.

Data availability statement

The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding author.

Ethics statement

This study was conducted in accordance with the principles of the Declaration of Helsinki. Ethical approval was obtained from the Research Ethics Committee of National Taiwan University Hospital (IRB No. 202510100W, approval date: November 06, 2025). Written informed consent was obtained for the publication of this case report, including relevant clinical details and images.

Author contributions

Y-CL: Conceptualization, Formal Analysis, Validation, Writing – original draft, Methodology, Data curation, Writing – review & editing. J-CL: Validation, Conceptualization, Methodology, Formal Analysis, Writing – review & editing, Data curation. C-YW: Validation, Conceptualization, Methodology, Writing – review & editing, Data curation, Writing – original draft. W-YC: Validation, Conceptualization, Methodology, Formal Analysis, Supervision, Writing – original draft, Writing – review & editing, Data curation.

Funding

The author(s) declared that financial support was received for this work and/or its publication. This work was supported by the Osteoporosis Prevention and Treatment Research Fund of National Taiwan University Hospital. The funder had no role in the study design, data collection and analysis, decision to publish, or manuscript preparation. No additional external funding was received for this study.

Conflict of interest

The authors declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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References

1. Bilezikian JP, Khan AA, Silverberg SJ, Fuleihan GE, Marcocci C, Minisola S, et al. Evaluation and management of primary hyperparathyroidism: summary statement and guidelines from the fifth international workshop. J Bone Miner Res. (2022) 37:2293–314. doi: 10.1002/jbmr.4677

PubMed Abstract | Crossref Full Text | Google Scholar

2. Albuja-Cruz MB, Allan BJ, Parikh PP, and Lew JI. Efficacy of localization studies and intraoperative parathormone monitoring in the surgical management of hyperfunctioning ectopic parathyroid glands. Surgery. (2013) 154:453–60. doi: 10.1016/j.surg.2013.05.034

PubMed Abstract | Crossref Full Text | Google Scholar

3. Roy M, Mazeh H, Chen H, and Sippel RS. Incidence and localization of ectopic parathyroid adenomas in previously unexplored patients. World J Surg. (2013) 37:102–6. doi: 10.1007/s00268-012-1773-z

PubMed Abstract | Crossref Full Text | Google Scholar

4. Glasgow C, Lau EYC, Aloj L, Harper I, Cheow H, Das T, et al. An approach to a patient with primary hyperparathyroidism and a suspected ectopic parathyroid adenoma. J Clin Endocrinol Metab. (2022) 107:1706–13. doi: 10.1210/clinem/dgac024

PubMed Abstract | Crossref Full Text | Google Scholar

5. Søreide K, Sandvik OM, Søreide JA, Giljaca V, Jureckova A, and Bulusu VR. Global epidemiology of gastrointestinal stromal tumours (GIST): A systematic review of population-based cohort studies. Cancer Epidemiol. (2016) 40:39–46. doi: 10.1016/j.canep.2015.10.031

PubMed Abstract | Crossref Full Text | Google Scholar

6. Serrano C, Martin-Broto J, Asencio-Pascual JM, Lopez-Guerrero JA, Rubio-Casadevall J, Bague S, et al. 2023 GEIS guidelines for gastrointestinal stromal tumors. Ther Adv Med Oncol. (2023) 15:17588359231192388. doi: 10.1177/17588359231192388

PubMed Abstract | Crossref Full Text | Google Scholar

7. Al-Moundhri MS, Al-Thahli K, Al-Kindy S, Salam J, and Rao L. Metastatic gastrointestinal stromal tumor and hypercalcemia in a patient with ulcerative colitis. Saudi Med J. (2006) 27:1585–7.

PubMed Abstract | Google Scholar

8. Beckers MM and Slee PH. Hypercalcaemia in a patient with a gastrointestinal stromal tumour. Clin Endocrinol (Oxf). (2007) 66:148. doi: 10.1111/j.1365-2265.2006.02682.x

PubMed Abstract | Crossref Full Text | Google Scholar

9. George A. Metastatic gastrointestinal stromal tumour presenting as hypercalcaemia–a rare occurrence. Clin Oncol (R Coll Radiol). (2008) 20:317–8. doi: 10.1016/j.clon.2008.02.002

PubMed Abstract | Crossref Full Text | Google Scholar

10. Jasti P, Lakhani VT, Woodworth A, and Dahir KM. Hypercalcemia secondary to gastrointestinal stromal tumors: parathyroid hormone-related protein independent mechanism? Endocr Pract. (2013) 19:e158–62. doi: 10.4158/EP13102.CR

PubMed Abstract | Crossref Full Text | Google Scholar

11. Hygum K, Wulff CN, Harslof T, Boysen AK, Rossen PB, Langdahl BL, et al. Hypercalcemia in metastatic GIST caused by systemic elevated calcitriol: A case report and review of the literature. BMC Cancer. (2015) 15:788. doi: 10.1186/s12885-015-1823-7

PubMed Abstract | Crossref Full Text | Google Scholar

12. Urasaki T, Naito Y, Doi T, and Nishida T. A case of gastrointestinal stromal tumor complicated by hypercalcemia induced by parathyroid hormone-related protein. Ann Oncol. (2016) 27:vii107. doi: 10.1093/annonc/mdw524.011

Crossref Full Text | Google Scholar

13. Barbaryan A, Bailuc S, Poddutoori P, Richardson A, and Mirrakhimov AE. Gastrointestinal stromal tumor induced hypercalcemia. Case Rep Oncol Med. (2017) 2017:4972017. doi: 10.1155/2017/4972017

PubMed Abstract | Crossref Full Text | Google Scholar

14. Hart T, Sinitsky D, Shamsiddinova A, and Rohatgi A. Refractory hypercalcaemia secondary to localised gastrointestinal stromal tumour. Ann R Coll Surg Engl. (2018) 100:e136–e8. doi: 10.1308/rcsann.2018.0064

PubMed Abstract | Crossref Full Text | Google Scholar

15. Herrera-Martinez Y, Contreras Gonzalez MJ, Pedraza-Arevalo S, Guerrero Martinez MDC, Rodrigo Martinez A, Gonzalez Menchen A, et al. Calcitriol-mediated hypercalcemia, somatostatin receptors expression and 25-hydroxyvitamin D₃-1alpha- hydroxylase in GIST tumors. Front Endocrinol (Lausanne). (2021) 12:812385. doi: 10.3389/fendo.2021.812385

PubMed Abstract | Crossref Full Text | Google Scholar

16. Kamitani-Kawamoto A, Hamada M, Moriguchi T, Miyai M, Saji F, Hatamura I, et al. Mafb interacts with gcm2 and regulates parathyroid hormone expression and parathyroid development. J Bone Miner Res. (2011) 26:2463–72. doi: 10.1002/jbmr.458

PubMed Abstract | Crossref Full Text | Google Scholar

17. Naik M, Khan SR, Owusu D, Alsafi A, Palazzo F, Jackson JE, et al. Contemporary multimodality imaging of primary hyperparathyroidism. Radiographics. (2022) 42:841–60. doi: 10.1148/rg.210170

PubMed Abstract | Crossref Full Text | Google Scholar

18. Chiu WY, Chen KY, Shun CT, Wu MH, Tsai KS, Chiu CH, et al. Conventional imaging techniques plus ¹⁸F-fluorocholine PET/CT: A comparative study of diagnostic accuracy in localizing parathyroid adenomas in primary hyperparathyroidism. Front Endocrinol (Lausanne). (2025) 16:1595461. doi: 10.3389/fendo.2025.1595461

PubMed Abstract | Crossref Full Text | Google Scholar

19. Hindie E, Schwartz P, Avram AM, Imperiale A, Sebag F, and Taieb D. Primary hyperparathyroidism: defining the appropriate preoperative imaging algorithm. J Nucl Med. (2021) 62:3S–12S. doi: 10.2967/jnumed.120.245993

PubMed Abstract | Crossref Full Text | Google Scholar

20. Lee SW, Shim SR, Jeong SY, and Kim SJ. Direct comparison of preoperative imaging modalities for localization of primary hyperparathyroidism: A systematic review and network meta-analysis. JAMA Otolaryngol Head Neck Surg. (2021) 147:692–706. doi: 10.1001/jamaoto.2021.0915

PubMed Abstract | Crossref Full Text | Google Scholar

21. Triantafyllidou M, Strobel K, Leiser A, and Fischli S. Localisation of ectopic mediastinal parathyroid adenoma by 18F-fluorocholine PET/CT. BMJ Case Rep. (2018) 2018:bcr2017222089. doi: 10.1136/bcr-2017-222089

PubMed Abstract | Crossref Full Text | Google Scholar

22. Hai R, Xie L-J, You Q, Wu F, Qiu G-C, and Zhou X-Y. Diagnosis of ectopic intrathyroidal parathyroid adenoma with nodular goiter by 18F fluorocholine: A case report. Ear Nose Throat J. (2022) 104:168–72. doi: 10.1177/01455613221103082

PubMed Abstract | Crossref Full Text | Google Scholar

23. Jang H, Lee S, Kim D, and Hong N. Retropharyngeal ectopic parathyroid adenoma localized by ¹⁸F-fluorocholine positron emission tomography/computed tomography: A case report. J Bone Metab. (2022) 29:197–203. doi: 10.11005/jbm.2022.29.3.197

PubMed Abstract | Crossref Full Text | Google Scholar

24. Hakim Tawil JA, Flórez A, Sanabria MC, Palau M, and Santivañez JJ. Submandibular ectopic parathyroid adenoma: A case report. Ear Nose Throat J. (2023) 104:118S-121S. doi: 10.1177/01455613231177193

PubMed Abstract | Crossref Full Text | Google Scholar

25. Aphale R, Dharmashaktu Y, Damle NA, Singareddy CR, Behera A, Wakankar R, et al. Odd sites of parathyroid adenomas: ¹⁸F-fluorocholine PET/CT pointing to the right place. Indian J Nucl Med. (2024) 39:123–5. doi: 10.4103/ijnm.ijnm_13_23

PubMed Abstract | Crossref Full Text | Google Scholar

26. Welling RD, Olson JA, Kranz PG, Eastwood JD, and Hoang JK. Bilateral retropharyngeal parathyroid hyperplasia detected with 4D multidetector row CT. Am J Neuroradiology. (2011) 32:E80–E2. doi: 10.3174/ajnr.A2104

PubMed Abstract | Crossref Full Text | Google Scholar

27. Dhillon VK, Pitukcheewanont P, Yeh M, and Maceri D. Identifying an ectopic parathyroid adenoma using 4DCT in a pediatric patient with persistent primary hyperparathyroidism. Case Rep Otolaryngol. (2013) 2013:1–4. doi: 10.1155/2013/676039

PubMed Abstract | Crossref Full Text | Google Scholar

28. Elhelf IAS, Kademian JC, Moritani T, Capizzano AE, Policeni B, and Maley J. Ectopic mediastinal parathyroid adenoma localized with four-dimensional CT: A case report. Radiol Case Rep. (2017) 12:247–50. doi: 10.1016/j.radcr.2017.01.011

PubMed Abstract | Crossref Full Text | Google Scholar

29. Kim J, Cubangbang M, Adkins L, Chia S, DeKlotz TR, Boyle L, et al. Ectopic parathyroid adenoma in the pyriform sinus. Head Neck. (2017) 39:E110–E3. doi: 10.1002/hed.24878

PubMed Abstract | Crossref Full Text | Google Scholar

30. Binnetoglu A, Demir B, and Mamadli J. Challenges in the management of ectopic parathyroid pathologies: A case series of five patients. Turkish Arch Otorhinolaryngology. (2020) 58:133–6. doi: 10.5152/tao.2020.4782

PubMed Abstract | Crossref Full Text | Google Scholar

31. Hsieh MP, Nemer JS, Beylergil V, and Yeh R. Ectopic parathyroid adenoma of the piriform sinus on parathyroid 4D-CT and ^99mTc-MIBI SPECT/CT. Clin Nucl Med. (2020) 45:e358–e9. doi: 10.1097/RLU.0000000000003163

PubMed Abstract | Crossref Full Text | Google Scholar

32. Unais TM, Gangadhar P, Hameed S, and Kolikkat N. A deceptive preoperative imaging of an ectopic supernumerary parathyroid adenoma in a secondary hyperparathyroidism. Indian J Otolaryngol Head Neck Surg. (2020) 74:2024–6. doi: 10.1007/s12070-020-01978-8

PubMed Abstract | Crossref Full Text | Google Scholar

33. Flokas ME, Ganieva G, Grieco A, and Agdere L. Ectopic parathyroid adenoma in an 11-year-old girl: case report and literature review. AACE Clin Case Rep. (2021) 7:51–6. doi: 10.1016/j.aace.2020.11.013

PubMed Abstract | Crossref Full Text | Google Scholar

34. Badhe PV, Patil S, Vikram Reddy G, Sheshadri H, Jain S, and Nikumbh T. Slipped capital femoral epiphysis as primary presentation in an adolescent with primary hyperparathyroidism due to ectopic mediastinal parathyroid adenoma. Clin Case Rep. (2023) 11:e7498. doi: 10.1002/ccr3.7498

PubMed Abstract | Crossref Full Text | Google Scholar

35. Mwewa TB and Raeymaeckers S. 4DCT differentiation of parathyroid adenoma: A case report. J Belgian Soc Radiol. (2023) 107:61. doi: 10.5334/jbsr.3238

PubMed Abstract | Crossref Full Text | Google Scholar

36. Zenno A, Ramamoorthy B, Hammoud DA, Quezado M, Zeiger MA, and Jha S. Case report: nine-year-old with parathyroid adenoma within the piriform sinus. Front Endocrinol. (2023) 14:1171052. doi: 10.3389/fendo.2023.1171052

PubMed Abstract | Crossref Full Text | Google Scholar

37. Edamadaka Y, Malhotra G, Daga A, Memon SS, Lila AR, and Bandgar T. Multimodality evaluation of persistent hyperparathyroidism in a rare case of ectopic submandibular parathyroid adenoma. Clin Nucl Med. (2024) 49:e670–e3. doi: 10.1097/RLU.0000000000005495

PubMed Abstract | Crossref Full Text | Google Scholar

38. Naik S, Vora K, Solanki V, and Kaur M. Unmasking hidden culprits: the pivotal role of 4DCT in diagnosing parathyroid adenoma presenting as acute pancreatitis. Radiol Case Rep. (2025) 20:3476–83. doi: 10.1016/j.radcr.2025.02.086

PubMed Abstract | Crossref Full Text | Google Scholar

39. Sandakly N, Zreika B, Haddad F, Ghorra C, and Abboud B. Supernumerary ectopic parathyroid adenoma in the aortopulmonary window: navigating diagnostic and surgical challenges. Int J Surg Case Rep. (2025) 131:3476–83. doi: 10.1016/j.ijscr.2025.111326

PubMed Abstract | Crossref Full Text | Google Scholar