Endocrine Abstracts

Introduction: Although calcifications are a relatively common finding on a thyroid ultrasound, present in both benign and malign lesions, osseous metaplasia (OM) is a peculiar discovery, with only a few described cases in literature so far. Common pathophysiological explanations include abnormalities of bone morphogenetic protein family members and basic fibroblast growth factor. Most of the case reports are presenting OM in association with malign lesions, often with papillary thyroid carcinoma and even suggest this could be a sign of increased aggressivity. Other reports show OM accompanied by extramedullary hematopoiesis in patients with hematological disorders, but cases of bone formation in benign thyroid pathologies are extremely rare. We describe the case of a middle-aged female with histological findings of osseous metaplasia in a benign solitary nodule.

Case report: A 54-year-old female presented for endocrinologic evaluation, asymptomatic and with no prior thyroid pathology. Personal history included a meningioma and a breast hamartoma. A thyroid ultrasound revealed a 1.3/1.5 cm nodule in her right thyroid lobe, with micro and macrocalcifications and ill-defined borders (TIRADS 5). The remaining thyroid was homogenous, isoechoic and it had normal vascularization. Thyroid function tests and calcitonin levels were within normal range and antithyroglobulin antibodies were negative. TPOAb were unfortunately not available. Serum calcium, phosphorus and 25 hydroxy-vitamin D3 levels were also normal and no parathyroid lesion was found. In addition, complete blood count and coagulation panel showed no abnormalities. Total thyroidectomy was performed. Histopathologic examination of the right lobe revealed a nodular area, markedly sclero-hyalinized, composed of a few follicular structures, alongside dystrophic calcifications, osseous metaplasia and small hemorrhagic foci. The rest of the thyroid parenchyma showed hyperactive follicles, with no signs of nuclear atypia nor hematopoietic cells, but with rare, small lymphoid aggregates. At follow-up, the patient had a benign evolution. Although personal history was indicative for a possible Cowden syndrome, the patient did not meet the diagnostic criteria and further genetic evaluation was not performed.

Conclusion: OM is an uncommon finding in thyroid tissue and its pathophysiology is yet to be completely understood. Here we reported a case of OM in a patient without signs of malignity, hematological or parathyroid abnormalities and with an unusual association of tumor growths. Apart from its rare occurrence, this could also lead to new pathophysiological explanations of this phenomenon, involving the PTEN gene mutations.