Primary hyperparathyroidism due to ectopic parathyroid adenoma with bone lesions mimicking skeletal neoplasm: a case report

Introduction

Primary hyperparathyroidism (PHPT) is characterized biochemically by hypercalcemia, hypophosphatemia, and disturbances in bone metabolism. The clinical spectrum of PHPT is heterogeneous, with variable frequency of manifestations across populations. Updated epidemiological data indicate the following distribution of clinical features: (I) asymptomatic hypercalcemia, 70–80%, most common in Western countries due to routine biochemical screening; (II) nephrolithiasis, 15–20%, often recurrent; (III) osteoporosis and fragility fractures, 20–25%, predominantly affecting cortical bone; (IV) neuropsychiatric symptoms, 10–20%, including fatigue, depression, anxiety, and cognitive dysfunction; (V) gastrointestinal symptoms, 10–15%, such as anorexia, constipation, abdominal pain, and rarely pancreatitis or peptic ulcer; (VI) proximal muscle weakness, ~10%; (VII) polyuria and polydipsia, 5–10%, associated with nephrogenic diabetes insipidus; and (VIII) bone pain or brown tumors, <5%, now considered a rare manifestation typically associated with severe or long-standing disease (1).

The embryological development of the parathyroid glands is uniquely complex and critical to understanding the potential for ectopic locations. In the normal adult, four parathyroid glands originate from the third and fourth pharyngeal pouches. The inferior parathyroid glands, derived from the third pharyngeal pouch, migrate caudally together with the thymus and usually settle near the anterior or inferior aspects of the lower thyroid poles. In contrast, the superior parathyroid glands originate from the fourth pharyngeal pouch, migrate over a shorter distance, and typically localize to the posterior surface of the upper thyroid poles. In contrast, the superior parathyroid glands arise from the fourth pharyngeal pouch and migrate over a shorter distance, typically localizing to the posterior surface of the upper thyroid poles (2,3).

Due to the considerable distance and complexity of their embryologic descent, parathyroid glands are susceptible to aberrant migration, arrest, or misdifferentiation along their developmental pathway. These anomalies may result in ectopic parathyroid tissue being located in atypical sites, including the paratracheal or paraesophageal regions, within the thyroid gland, the mediastinum, retrosternal space, or even within deep cervical musculature (4). It is estimated that approximately 6% to 16% of parathyroid adenomas are ectopic in origin. Among these, adenomas located medial to the sternocleidomastoid muscle or those intimately associated with major cervical vessels and nerves are exceedingly rare (5). Such anatomical variations frequently evade detection on conventional imaging modalities and are prone to misdiagnosis.

Herein, we present a rare case of an ectopic parathyroid adenoma located medial to the left sternocleidomastoid muscle, initially misdiagnosed as a bone tumor due to its clinical presentation with recurrent rib pain and osteolytic lesions. This case underscores the diagnostic challenges associated with ectopic parathyroid lesions and highlights the necessity of a thorough endocrine function and organs evaluation in patients presenting with unexplained skeletal destruction. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-165/rc).

Case presentation

A 60-year-old male tile-layer presented to the Thoracic Surgery Department of Affiliated Hospital of Guangdong Medical University on February 18, 2024, with a 10-month history of persistent left-sided rib pain, which had notably worsened over the preceding 2 months. The patient reported a dull, insidious onset of left chest discomfort without any clear precipitating event. The pain was exacerbated by physical activity and persisted during nighttime rest. Over the past 2 months, the discomfort intensified and became associated with localized tenderness.

The patient’s medical history included multiple fractures resulting from previous trauma, including a right clavicle fracture 12 years prior, a left fifth digit fracture 10 years ago, a left wrist fracture 9 years ago, and an ischial fracture 5 years ago. The patient also described chronic lower back pain recurring over the past 4 years, as well as progressive dental loosening and spontaneous tooth loss beginning 2 years ago (Figure 1). He denied any history of cervical surgery or familial malignancy.

Figure 1 Clinical photograph showing loosening and exfoliation of anterior teeth (arrow). This image is published with the patient’s consent.

On physical examination, his vital signs were as follows: temperature, 36.5 ℃; pulse, 86 beats per minute; respiratory rate, 18 breaths per minute; and blood pressure, 153/102 mmHg. Palpation revealed a firm, enlarged mass over the axillary segment of the left ninth rib. Cardiopulmonary and abdominal examinations were unremarkable.

Initial laboratory tests revealed marked hypercalcemia (serum calcium: 3.07 mmol/L), hypophosphatemia (serum phosphate: 0.62 mmol/L), significantly elevated alkaline phosphatase (639 U/L), and increased serum uric acid (470.5 µmol/L). Comprehensive malignancy screening, including tumor marker panels, serum and urine immunofixation electrophoresis, β2-microglobulin levels, thyroid function tests, serum protein electrophoresis, and bone marrow aspiration, showed no evidence of multiple myeloma or other hematologic malignancies.

Non-contrast computed tomography (CT) of the chest revealed multiple osteolytic lesions involving the ribs—including the left first, second, fifth, ninth, eleventh, and twelfth ribs; the right third, fifth, seventh, ninth, tenth, and eleventh ribs—as well as both scapulae. Several lesions showed expansile features, raising suspicion for a primary osseous neoplasm (Figures 2,3). Based on these findings, the patient underwent surgical excision of the lesion in the left ninth rib several days later.

Figure 2 Three-dimensional reconstruction of chest CT scan demonstrating expansile osteolytic lesion of the left ninth rib (arrow). CT, computed tomography.

Figure 3 Chest CT scan demonstrating osteolytic lesions in both scapulae. CT, computed tomography.

Microscopic examination of the resected rib lesion revealed a tumor divided into lobules by reactive woven bone trabeculae. The lobules were composed of plump fibroblasts, scattered osteoclast-like giant cells, and hemosiderin-laden macrophages—findings consistent with a brown tumor. Tumor involvement was identified at the proximal surgical margin, while the distal margin was free of tumor infiltration.

The patient was referred to the Endocrinology Department several weeks later for further assessment. Laboratory testing at that time revealed severe hypercalcemia (serum calcium: 3.56 mmol/L), hypophosphatemia (serum phosphate: 0.65 mmol/L), and a markedly elevated parathyroid hormone (PTH) level of 1,443.5 pg/mL—this being the patient’s first documented measurement of PTH. Serial biochemical tests at multiple time points confirmed persistently elevated serum calcium, PTH, and alkaline phosphatase levels. However, despite a transient decline, serum calcium levels remained consistently above the normal range.

A non-contrast CT scan of the brain was unremarkable. However, osseous structures including the skull, cervical vertebrae, and surrounding bony elements demonstrated heterogeneous density with multiple radiolucent lesions. These findings, when considered alongside the patient’s clinical history, were consistent with metabolic bone disease secondary to hyperparathyroidism. In addition, dual-energy X-ray absorptiometry (DXA) of the left femur revealed a mean bone mineral density (BMD) of 0.380 g/cm². The femoral neck BMD was 0.414 g/cm², with a T-score of –3.5 and a Z-score of –3.0, while the Ward’s region BMD was 0.199 g/cm², with a T-score of –4.2 and a Z-score of –3.6. Overall, the average T-score was –3.8, consistent with severe osteoporosis.

Conventional neck ultrasonography revealed no obvious abnormalities in the typical parathyroid regions. Contrast-enhanced CT of the neck demonstrated an ovoid, soft-tissue density nodule medial to the left sternocleidomastoid muscle. The lesion was initially suspected to represent Castleman disease (Figure 4).

Figure 4 Contrast-enhanced cervical CT scan showing an oval-shaped soft tissue density lesion adjacent to the medial aspect of the left sternocleidomastoid muscle. CT, computed tomography.

Further localization of the suspected ectopic parathyroid lesion was performed using single-photon emission computed tomography/computed tomography (SPECT/CT) with ^99mTc-sestamibi parathyroid scintigraphy. No definitive uptake was noted in the typical anterior parathyroid regions. However, an ovoid, slightly hyperdense lesion was identified in the left cervical level II–III region, exhibiting patchy areas of lower density. These imaging features were highly suggestive of an ectopic parathyroid adenoma (Figure 5). Although not available in our institution at that time, ¹⁸F-fluorocholine positron emission tomography (PET)/CT has been increasingly recognized as a highly sensitive imaging modality in patients with ectopic or inconclusive parathyroid adenomas.

Figure 5 ^99mTc-sestamibi SPECT/CT demonstrating an oval-shaped, slightly hyperdense lesion in the left cervical region (level II–III), with radiotracer uptake corresponding to the suspected ectopic parathyroid adenoma. SPECT/CT, single-photon emission computed tomography/computed tomography.

The patient was admitted to the Department of Vascular and Thyroid Surgery for definitive surgical intervention. Laboratory investigations revealed persistent hypercalcemia (serum calcium: 2.86 mmol/L), hypophosphatemia (serum phosphate: 0.61 mmol/L), and markedly elevated PTH levels—1,356.8 pg/mL at admission and peaking at 1,912.1 pg/mL prior to surgery. Thyroid autoantibodies [anti-thyroglobulin (TG), anti-thyroid peroxidase, anti-thyroid stimulating hormone (TSH) receptor antibodies], serum TG, 25-hydroxyvitamin D, and standard thyroid function tests were all within normal limits.

The patient underwent surgical exploration and resection of the left cervical mass. Intraoperatively, meticulous dissection was performed to expose the left internal jugular vein, common carotid artery, internal carotid artery, and external carotid artery. A firm, solid mass was identified superior to the carotid bifurcation (Figure 6A), with indistinct margins and dense adhesions to the vagus nerve. Careful separation was carried out to preserve the nerve, and the mass was completely excised (Figure 6B), along with surrounding lymphoadipose tissue.

Figure 6 Intraoperative and pathological findings of the ectopic parathyroid adenoma. (A) Intraoperative view showing the ectopic parathyroid adenoma (arrow) located superior to the carotid bifurcation; (B) complete excision of the tumor measuring approximately 2.5 cm × 1.8 cm × 0.5 cm; (C) histological examination revealing parathyroid tissue with mild cellular atypia and focal nuclear enlargement (H&E staining, magnification ×200). H&E, hematoxylin and eosin.

Intraoperative frozen section analysis revealed histological features consistent with parathyroid tissue, suggestive of a parathyroid neoplasm (Figure 6C). A rapid intraoperative PTH assay performed 10 minutes after tumor removal demonstrated a sharp decline in PTH levels to 119.6 pg/mL, indicating complete and successful excision of the hyperfunctioning gland.

Histopathological examination of the excised left cervical mass confirmed a parathyroid-derived lesion, consistent with an ectopic parathyroid adenoma exhibiting focal hyperplasia. Subcapsular lymphoid tissue was identified locally; however, the possibility of metastatic parathyroid carcinoma involving regional lymph nodes could not be entirely excluded. Immunohistochemical staining demonstrated positivity for PTH and chromogranin A (CgA), while calcitonin, TG, and thyroid transcription factor-1 (TTF-1) were negative. The Ki-67 proliferation index was approximately 5% in hotspot areas. Examination of the resected left cervical lymph nodes revealed no evidence of tumor metastasis.

Serial postoperative biochemical monitoring showed a rapid decline in serum calcium and PTH levels. On postoperative day 1, serum calcium was 2.84 mmol/L, phosphate 0.61 mmol/L, and PTH 7.10 pg/mL. By day 5, serum calcium had decreased to 1.83 mmol/L, phosphate to 0.49 mmol/L, and PTH had risen to 213.70 pg/mL. On day 9, serum calcium remained low at 1.78 mmol/L, phosphate was 0.66 mmol/L, and PTH further increased to 316.70 pg/mL. At 43 days post-surgery, follow-up testing revealed partial biochemical recovery, with serum calcium of 2.07 mmol/L and PTH elevated to 688.70 pg/mL. The dynamic trends of serum calcium and PTH levels are illustrated in Figures 7,8. A timeline summarizing the patient’s clinical course, diagnostic evaluations, surgical intervention, and postoperative follow-up is presented in Figure 9 (reference ranges of laboratory parameters in this report: serum calcium, 2.0–2.50 mmol/L; serum phosphate, 0.81–1.45 mmol/L; alkaline phosphatase, 45–125 U/L; serum uric acid, 210–420 µmol/L; PTH, 12–88 pg/mL).

Figure 7 Trend analysis of PTH levels. PTH, parathyroid hormone.

Figure 8 Trend analysis of serum calcium levels.

Figure 9 Timeline summarizing the patient’s clinical course. ^99mTc-MIBI, technetium-99m methoxy isobutyl isonitrile; CT, computed tomography; DXA, dual-energy X-ray absorptiometry; PTH, parathyroid hormone; SCM, sternocleidomastoid; SPECT/CT, single-photon emission computed tomography/computed tomography.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

PHPT arises predominantly from parathyroid adenomas or diffuse hyperplasia, resulting in dysregulated and excessive secretion of PTH. This hormone excess orchestrates enhanced osteoclastic bone resorption and increased renal tubular calcium reabsorption, culminating in hypercalcemia and hypophosphatemia. In contrast, secondary hyperparathyroidism (SHP) commonly develops as a compensatory response to chronic kidney disease, where sustained hypocalcemia, hyperphosphatemia, and deficient active vitamin D leads to sustained stimulation of the parathyroid glands. Clinically, SHP is characterized by elevated PTH levels accompanied by normocalcemia or hypocalcemia and normal to elevated serum phosphate concentrations (6).

The present case manifested as chronic osteoporosis with overt hypercalcemia at admission. The absence of a medical history of chronic renal pathology, normal renal parenchymal architecture on ultrasonography, and unremarkable urinalysis collectively excluded SHP secondary to renal impairment. Corroborative parathyroid scintigraphy unequivocally localized an ectopic parathyroid adenoma medial to the left sternocleidomastoid muscle (levels II–III), a finding subsequently confirmed by postoperative histopathology, establishing a definitive diagnosis of PHPT.

Literature reports indicate that ectopic parathyroid adenomas constitute approximately 22% of PHPT cases, with the mediastinum being the most prevalent ectopic site. Other documented locations include the suprasternal notch, thymus, retrosternal space, and intrathyroidal parathyroid tissue. Ectopic adenomas situated at high cervical locations—such as medial to the sternocleidomastoid muscle—are comparatively rare. Their aberrant anatomical position frequently complicates preoperative localization, thereby elevating surgical complexity and increasing the risk of misdiagnosis (7).

Ectopic parathyroid adenoma and embryological mechanisms

In this case, the adenoma was located medial to the left sternocleidomastoid muscle, representing an exceedingly rare site of ectopic parathyroid tissue. During embryogenesis, the inferior parathyroid glands and thymus derive from the third pharyngeal pouch and migrate synchronously, whereas the superior parathyroid glands originate from the fourth pharyngeal pouch and exhibit relatively stable, shorter migratory trajectories. Aberrations during this migration process—such as tissue retention or misplacement—may result in ectopic parathyroid tissue residing within deep cervical muscular planes or various intrathoracic locations, including the sternocleidomastoid muscle, retrosternal region, and mediastinum. Approximately 6–16% of parathyroid adenomas arise in ectopic sites (8). Thus, when confronting unexplained osteolytic lesions, heightened clinical vigilance for parathyroid dysfunction grounded in embryological insight is imperative.

Diagnostic challenges of brown tumor

Brown tumors arise secondary to chronic PHPT, reflecting an imbalance in bone remodeling characterized by heightened osteoclastic activity and excessive bone resorption (9). In this patient, CT imaging revealed multiple expansile osteolytic lesions, initially misinterpreted as suspicious osseous neoplasms, prompting surgical resection. Histopathological examination confirmed the diagnosis of brown tumor, typified by increased bone resorption under sustained PTH influence, infiltration by osteoclast-like multinucleated giant cells, and hemosiderin deposition. Radiographically, brown tumors may mimic giant cell tumors or metastatic bone lesions. Consequently, in cases of unexplained bone destruction accompanied by hypercalcemia, differential diagnosis must prioritize metabolic bone disease alongside malignancy to minimize misdiagnosis and inappropriate treatment. Routine assessment of serum calcium, phosphate, alkaline phosphatase, and PTH should be standard in evaluating patients with osteolytic lesions. Elevated calcium concurrent with raised PTH mandates exclusion of PHPT as a primary etiology. Beyond conventional CT-scan and magnetic resonance imaging procedures, early integration of SPECT/CT and, when indicated, four-dimensional computed tomography (4D-CT) enhances precise localization and functional assessment of parathyroid tissue. Histological findings of giant cell infiltration or osteoclastic proliferation in bone biopsies should be interpreted cautiously in the context of metabolic parameters to avoid confusion between brown tumor, giant cell tumor, or metastatic carcinoma (10).

Optimization of diagnostic strategies

The localization of ectopic parathyroid tissue frequently lies beyond the conventional field of view of routine cervical ultrasound or CT, limiting the sensitivity of these singular imaging modalities. In the present case, parathyroid ultrasound examination to detect any abnormalities, underscoring the inherent constraints of standard cervical ultrasonography in identifying ectopic parathyroid adenomas. Sole reliance on individual imaging techniques often proves insufficient to encompass the intricate anatomical variability of ectopic parathyroid glands, predisposing to missed diagnoses or misinterpretations. For patients with suspected ectopic parathyroid tissue, the integration of cervical and mediastinal ^99mTc-sestamibi SPECT/CT substantially enhances detection rates, with reported sensitivity reaching up to 90% and specificity approximating 98% (11). Moreover, 4D-CT serves as a valuable second-line modality, employing dynamic vascular contrast enhancement to delineate characteristic adenoma perfusion patterns—arterial phase hyperenhancement followed by delayed washout—with diagnostic accuracy ranging between 85% and 95% (12). In this case, a combined preoperative imaging approach utilizing SPECT/CT fused with 4D-CT could further refine lesion localization, minimize surgical exploration extent, and mitigate risks of erroneous intervention. Our approach is consistent with current international guidelines. The American Association of Endocrine Surgeons (AAES, 2016) and the European Society of Endocrinology (ESE, 2022) emphasize the importance of concordant dual imaging prior to performing focused or minimally invasive parathyroidectomy (13,14). In this case, both contrast-enhanced CT and ^99mTc-sestamibi SPECT/CT demonstrated findings consistent with an ectopic parathyroid adenoma, thereby satisfying the guideline-recommended principle of dual concordant imaging. Although ¹⁸F-fluorocholine PET/CT was not available at our institution, our diagnostic pathway adhered to accepted standards of care. Future incorporation of PET/CT imaging, where available, could further improve the detection and localization of ectopic adenomas and minimize diagnostic uncertainty. Notably, the markedly elevated PTH level of the patient (1,912 pg/mL) and precipitous postoperative decline validate the completeness of resection and exemplify the utility of multimodal imaging in guiding precise surgical management.

Postoperative dynamics of PTH and calcium-phosphate metabolism

Following parathyroid adenoma excision, the patient showed a rapid and pronounced decline in circulating PTH levels (intraoperative reduction to 119 pg/mL and postoperative day 1 nadir of 7.1 pg/mL), subsequently developing a ‘hungry bone syndrome’ characterized by hypocalcemia (lowest serum calcium of 1.78 mmol/L) and rebound fluctuations in PTH concentrations (elevated to 688 pg/mL at 43 days postoperatively). This phenomenon likely reflects the chronic imbalance induced by sustained hyperparathyroidism, where excessive bone resorption and impaired mineralization lead to depleted skeletal calcium stores. Post-resection, the abrupt cessation of pathological PTH stimulation precipitates rapid skeletal uptake of calcium and phosphate to restore bone mineral homeostasis. However, the residual normal parathyroid tissue may initially be insufficient to maintain adequate PTH secretion to match this heightened mineral demand, necessitating compensatory hyperplasia and a consequent PTH rebound. Vigilant postoperative monitoring, alongside aggressive supplementation with calcium, vitamin D, and calcitriol, is essential to prevent symptomatic hypocalcemia and secondary compensatory PTH elevation, ensuring metabolic stabilization and optimal recovery (15).

Literature comparison and clinical implications

Previous reports predominantly describe ectopic parathyroid adenomas located within the mediastinum, retrosternal space, carotid sheath, and lateral aspect of the sternocleidomastoid muscle. By contrast, adenomas located medial to or within the sternocleidomastoid muscle are exceedingly rare, with only two cases reported in the medical literature to date. In one case, the patient was a 19-year-old with multiple endocrine neoplasia type 2B who had previously undergone total thyroidectomy for medullary thyroid carcinoma; the parathyroid adenoma was subsequently found within the sternocleidomastoid muscle and was hypothesized to result from inadvertent autotransplantation during prior surgery (4). In another case, a middle-aged patient presented with a firm, painless, and slowly enlarging cervical mass; imaging [ultrasound, CT, and technetium-99m methoxy isobutyl isonitrile (^99mTc-MIBI) scintigraphy] demonstrated a well-circumscribed intramuscular lesion, and pathology confirmed a functional parathyroid adenoma (6). The present case, with an adenoma medial to the sternocleidomastoid muscle, represents an even rarer anatomical distribution. This underscores the necessity of proactively broadening the scope of imaging investigations when confronted with chronic bone pain or osteolytic lesions in atypical deep cervical locations. Failure to timely excise ectopic adenomas may lead to persistent or progressive formation of brown tumors, with multifocal skeletal damage that can become irreversible, substantially compromising functional recovery post-tumor resection (16). Future adoption of ¹⁸F-fluorocholine (¹⁸F-FCH) PET/CT, intraoperative nerve monitoring (IONM), and near-infrared autofluorescence (NIRAF) in similar cases could further align practice with evolving international standards and improve both diagnostic accuracy and surgical outcomes.

Conclusions

This case of ectopic parathyroid adenoma situated medial to the left sternocleidomastoid muscle initially presented with brown tumor manifestations and was misdiagnosed as a primary bone tumor, illustrating a prototypical diagnostic and therapeutic trajectory. The case highlights the critical importance of including metabolic bone diseases in the differential diagnosis of multifocal osteolytic lesions, employing a multimodal localization strategy, and closely monitoring postoperative calcium-phosphate metabolism and PTH dynamics to achieve precise diagnosis, personalized treatment, and effective long-term follow-up.

Acknowledgments

The authors thank the multidisciplinary team for their collaboration in the diagnosis and management of this case.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-165/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-165/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-165/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are 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. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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