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. Author manuscript; available in PMC: 2022 Mar 15.
Published in final edited form as: Am Surg. 2020 Sep 15:3134820951460. doi: 10.1177/0003134820951460

A Rare Case of Metastatic Adenocarcinoma Involving a Parathyroid Adenoma

Anna R Kahkoska 1, Renee L Betancourt 2, Lawrence T Kim 3
PMCID: PMC8212554  NIHMSID: NIHMS1713522  PMID: 32931303

A 54-year-old female presented for a nephrology clinic follow-up visit complaining of fatigue, nausea, and anorexia. She had a 2-year history of stage IV adenocarcinoma of the lung, intermittent hypercalcemia with elevated parathyroid hormone (PTH), and new-onset focal segmental glomerulosclerosis of unclear etiology. Labs demonstrated a calcium of 12.6 mg/dL with a PTH of 693 pg/nL.

She was admitted and treated with intravenous fluid and cinacalcet. Her calcium transiently decreased to 10.3 mg/dL. However, attempts to wean intravenous fluids failed as her calcium levels increased. Bone scan was unremarkable. PTH-related peptide was normal. Tc-99m sestamibi scan showed a 1.7 × 1.4-cm hypermetabolic nodule consistent with left superior parathyroid adenoma. The patient underwent an uncomplicated excision of a 26 × 20 × 15 mm-left superior parathyroid adenoma with subsequent normalization of calcium and PTH concentration. A pathology examination of the parathyroid nodule showed a well-circumscribed, encapsulated proliferation of cells comprised of 2 disparate populations (Figure 1). The first was at the periphery and was composed of sheets, nests, and trabeculae of chief and oncocytic cells with no intervening adipose tissue, consistent with parathyroid adenoma. The second population infiltrated the center of the nodule and showed a pseudopapillary architecture and anastomosing cords composed of markedly pleomorphic cells that were positive for cytokeratin 7 (CK7) and thyroid transcription factor-1 (TTF-1) on immunohistochemical (IHC) staining. An area of necrosis and evidence of mitosis was also identified within the latter cell population. This population was consistent with metastatic lung cancer.

Figure 1.

Figure 1.

(A) High-power view (40×) of the parathyroid adenoma portion of the specimen. (B) High power-view (40×) of the metastatic lung adenocarcinoma within the specimen. (C) Low-power view (10×) showing both populations of cells. The parathyroid adenoma is to the left. (D) Similar section as (C), showing IHC staining for chromogranin. The parathyroid portion of the specimen is positive (brown staining). (E) Similar section as (C), showing IHC staining for CK7. The adenocarcinoma portion of the specimen is positive (brown staining). (F) Similar section as (C), showing IHC staining for TTF-1. The adenocarcinoma portion of the specimen is positive (brown staining). IHC, immunohistochemical.

We present the case of a middle-aged women with advanced adenocarcinoma of the lung who was found to have metastasis to a benign parathyroid adenoma. Metastatic cancer to the parathyroid gland typically occurs by direct extension from regional cancers, such as thyroid or other head and neck tumors or by spread from distant disease1 and are almost always associated with widely metastatic primary disease.2 The epidemiology of metastases to the parathyroid is not well characterized. In 1 autopsy series, the prevalence of parathyroid metastases was surprisingly high (11.9%). The most common site of origin were breast, leukemia, melanoma, and lung.2,3 One potential explanation for this is the high blood flow through parathyroid glands, which is typical of endocrine organs.

A unique aspect of the case is the tumor-to-tumor pattern of metastasis. A total of 7 previous cases of metastasis to parathyroid adenomas have been reported in the English literature.2 While there is a report of lung adenocarcinoma to parathyroid hyperplasia, to our knowledge there is only 1 other case reported of lung adenocarcinoma with metastasis to a benign parathyroid adenoma.4

Metastases to the parathyroid glands are probably under-recognized in patients with widely metastatic disease.2,3 In most cases, these metastases are not clinically important. Rarely, the metastases may result in hypoparathyroidism due to tumor replacement of the glands.3 In this case, the metastasis was to a benign parathyroid adenoma, and it was the intractable hypercalcemia of primary hyperparathyroidism that prompted surgical intervention. Her calcium level normalized by postoperative day 2, and she remains in treatment for her lung cancer. This case illustrates the potential benefit of surgical treatment of hyperparathyroidism even in the setting of metastatic cancer. In this case, the resolution of hypercalcemia made her medical management easier and improved her quality of life. The serendipitous removal of the metastasis was interesting and unexpected but will not impact the course of her cancer.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Footnotes

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

References

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