Health & Medical Health & Medicine Journal & Academic

A Costal Mass Mistaken for Giant-cell Bone Tumor

A Costal Mass Mistaken for Giant-cell Bone Tumor

Abstract and Introduction

Abstract


Introduction Primary hyperparathyroidism is a common endocrine disorder characterized by elevated parathyroid hormone levels, which cause continuous osteoclastic bone resorption. Giant cell tumor of bone is an expansile osteolytic tumor that contains numerous osteoclast-like giant cells. There are many similarities in the radiological and histological features of giant cell tumor of bone and brown tumor. This is a rare benign focal osteolytic process most commonly caused by hyperparathyroidism.
Case presentation We report the unusual case of a 40-year-old Caucasian woman in which primary hyperparathyroidism was diagnosed after surgical ablation of a costal mass. The mass was suspected of being neoplastic and histopathology was compatible with a giant cell tumor of bone. On the basis of the biochemical results (including serum calcium, phosphorous and intact parathyroid hormone levels) primary hyperparathyroidism was suspected and a brown tumor secondary to refractory hyperparathyroidism was diagnosed.
Conclusions Since giant cell tumor is a bone neoplasm that has major implications for the patient, the standard laboratory tests in patients with bone lesions are important for a correct diagnosis.

Introduction


Primitive hyperparathyroidism (PHPT) is the third most common endocrine disorder after diabetes mellitus and thyroid dysfunction. The estimated incidence of cases of PHPT is 0.2% to 0.3%. The diagnosis of PHPT has classically been based on the demonstration of high plasma calcium and low plasma phosphorus concentrations. In recent years, however, it has been recognized that patients with PHPT may present with plasma calcium concentrations within the normal range. About 75% to 80% of cases of PHPT are diagnosed when a routine assay shows hypercalcemia in patients who are asymptomatic or during evaluation for osteoporosis. Surgical ablation is the treatment of choice for PHPT. Persistent hyperparathyroidism leads to altered osseous metabolism involving bone resorption and tissue changes that are collectively known as osteitis fibrosa cystica (OFC). Today, < 5% of patients display evidence of OFC. Osteitis fibrosa cystica is characterized by the presence of subperiosteal resorption in the digits, skull and long bones, diffuse osteopenia, and brown tumor.

Brown tumor is an extremely rare osseous lesion that constitutes a focal manifestation of OFC induced by hyperparathyroidism, independently of its cause. The reported prevalence of brown tumors is 0.1%, and they have been reported to occur in 4.5% of patients with PHPT and in 1.5% to 1.7% of those with secondary disease. The disease can manifest itself at any age, but is more common among people older than 50 years, and is three times more common in women than in men. Brown tumor may be the first clinical sign of hyperparathyroidism. Histologically, brown tumors are made up of mononuclear stromal cells mixed with multinucleated giant cells, among which recent hemorrhagic infiltrates and hemosiderin deposits (hence the brown color) are often found. Brown tumors may appear in any of the bones. However, when the same type of lesion is found in patients without PHPT, the differential diagnosis becomes more complex.

Many of the radiological and histological features of brown tumor, a benign osteolytic process, are similar to those of giant cell tumor (GCT) of bone. Giant cell tumor of bone is an uncommon primary bone tumor that accounts for around 5% of all primary bone tumors. Giant cell tumor is a locally aggressive tumor characterized by a high number of multinuclear giant cells that exhibit the features of mature osteoclasts. Clinically, most patients with GCT are asymptomatic or present with bone pain due to enlargement of the tumor. Malignant transformation of GCT is a rare event, occurring in less than 1% of all cases. The treatment of primary GCT is essentially surgical. The differential diagnosis is based on biochemical analysis.

Here, we report the case of a patient with an incidentally discovered costal mass, the diagnostic investigation of which led to an unexpected diagnosis.

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