752

Radiologic-Pathologic

Conferences

of the Massachusetts

General

Hospital

Brown
Felix S. Chew1

Tumor
and Frank Huang-Hellinger

A mass in the anterior chest wall was revealed by the chest radiograph of a 48-year-old man with chronic renal insufficiency, previous renal transplant, and elevated serum parathormone level (Fig. 1). CT showed an expansile lesion of heterogeneous attenuation centered in the medullary space of the fifth rib with thinned overlying bony cortex. The differential diagnosis included brown tumor, giant cell tumor, and giant cell reparative granuloma, as well as metastasis and myeloma. Features of hyperparathyroidism were present elsewhere in the skeleton. After resection, the gross pathologic examination revealed a rib mass with intact cortex. Microscopy showed hemorrhage, multinucleated giant cells, and proliferating fibrous tissue. The final pathologic diagnosis was brown tumor in secondary hypenparathyroidism. Brown tumors represent a reparative cellular process rather than a neoplastic process. In chronic renal disease, continual, excessive urinary calcium excretion can lower the serum calcium level and lead to a rise in parathonmone secretion so that skeletal calcium can be mobilized to maintain normal serum calcium levels. This mobilization occurs through rapid osteoclastic turnover of bone, a direct effect of parathormone on bone. In localized regions where bone loss is particularly rapid, hemorrhage, reparative granulation tissue, and active, vascular, proliferating fibrous tissue may replace the normal marrow contents, resulting in a brown tumor [1]. Hemosidenin imparts the brown color.

On nadiographs, brown tumors are well-defined, purely lytic lesions that provoke little reactive bone [2, 3]. The cortex may be thinned and expanded, but will not be penetrated. Attenuation values on CT will be in the range of blood and fibrous tissue. Brown tumors are hypervascular on angiograms [4] and intensely active on bone scans. Although they may progress alarmingly, once the underlying metabolic condition is corrected, rapid healing with sclerosis is usual unless there has been cyst formation [2]. Brown tumors have a slightly greater frequency in primary hyperparathyroidism than in secondary hyperparathyroidism (3% vs 2%). However, secondary hyperparathyroidism is much more common than primary hypenparathyroidism so that most brown tumors are associated with secondary hyperparathyroidism [3]. Biopsy or resection may be required to resolve diagnostic uncertainty.
REFERENCES
1. Enneking WF. Clinical musculoskeletal pathology, 3rd ed. Gainesville, FL: University of Florida Press, 1990 2. Steinbach HL, Gordan GS, Eisenberg E, et al. Primary hyperparathyroidism: a correlation of roentgen, clinical, and pathologic features. AJR 1961; 86:329-343 3. Hayes CW, Conway WF. Hyperparathyroidism. Radiol Clin North Am 199i;29:85-96 4. Doppman JL, Marx 5, Spiegel A, et al. Differential diagnosis of brown tumor vs. cystic osteitis by arteriography and computed tomography. Radiology 1979:131:339-340

Fig. 1.-Brown tumor. A, Chest radiograph shows mass (arrow) in chest wail, osteoporosis, and multiple rib fractures. B and C, CT scans of fifth rib show expansile intramedullary mass with heterogeneous attenuation. D, Cut section of gross specimen shows multilocular, expansile, hemorrhagic lesion. From 1Both dence the weekly authors: radiologic-pathologic Department of Radiology, correlation conferences conducted Hospital by Jack Wittenberg. and Harvard Pathology School, editor: Andrew E. Rosenberg. MA 02114. Address correspon-

Massachusetts

General

Medical

32 Fruit St., Boston,

to F. S. Chew. 0361-803X/93/1604-0752 American Roentgen Ray Society

AJR i993;160:752