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Case report: A 60-year old female patient with postmenopausal osteoporosis

presented for evaluation due to PTH-excess (354.4 pg/ml) and serum calcium at the
upper reference range (9.8 mg/dl). The patient had been under 3-year denosumab
treatment and had received the last injection 2 months ago. The neck ultrasound

revealed a hypoechoic lesion below the right thyroid lobe, the adjunctive 99m Tc-

sestamibi scintigraphy turned however non-suggestive for parathyroid adenoma. A
novel PTH estimation at 4 months showed considerable PTH decline (86.3 pg/ml)
with synchronous 25 OH-D3 insufficiency and persistent normocalcaemia. Therefore,

a conservative follow-up was initially decided, presuming that denosumab was
responsible for the initial PTH excess in combination with 25OH-D3 insufficiency. The

biochemical reassessment at 6 months and after denosumab withdrawal revealed
only marginal hyperparathyroidism (72.5 pg/ml). However, mild hypercalcaemia

manifested during the following 3 months with relapse of hyperparathyroidism
despite accomplishment of 25OH-D3 sufficiency. A second 99m Tc-sestamibi

scintigraphy was performed, showing intense tracer retention at the inferior pole of
the right thyroid lobe at the early phase and a normal washout at the late phase,

therefore raising suspicion of a small parathyroid adenoma either rich in p-
glycoprotein or poor in oxyphylic cells. A possible hyperfunctioning thyroid lesion at

this anatomic position was excluded by 99m Tc-pertechnate-thyroid scintigraphy. 1
month later and because of persistent hyperparathyroidism and hypercalcaemia with

new-onset hypercalciuria a third 99m Tc-sestamibi scintigraphy was conducted for
validation. The test suggested presence of a right inferior parathyroid adenoma, thus

correlating with the neck ultrasound. The patient underwent right inferior
parathyroidectomy. PTH and calcium levels normalized directly intraoperatively. The
histopathological analysis confirmed the diagnosis of a small parathyroid adenoma,

consisted exclusively of chief cells.

Conclusion: Denosumab may cause PTH elevation, sustainable months after its

application. This phenomenon may cause misinterpretation of the laboratory tests
and delay definitive diagnosis of primary hyperparathyroidism due to small

parathyroid adenomas without standard scintigraphic pattern. Therefore, a careful
patient follow-up is required, as well as a possible imaging reassessment in order to

detect the underlying cause of PTH excess.

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