CASE 25

By: Dr. Khalid Abdullah AL-Ismail MD and Dr. Nizar
Al-Nakshabandi MD, FRCPC

HISTORY: 31-year-old female complaining of a discharging mass in the right hip region and pain.

What are your findings?

What is the differential diagnosis?

What are the causes?

FINDINGS:

The AP radiograph of the right hip demonstrate multilobulated cloudlike calcification in an amorphous type of calcification in a lumpy bumpy appearance. It is particularly located adjacent to a joint and hip in this case.

Axial T2 Fat sat weighted sequence gadolinium administration shows inhomogeneous lesions with low signal intensity and marked fascial enhancement.

Similarly, the coronal T1 with gadolinium shows similar findings.

DIFFERENTIAL DIAGNOSIS:

• Hyperparathyroidism: most frequently in chronic renal failure.

• Calcium pyrophosphate deposition disease (CPPD).

• Myositis ossificans.

• Calcinosis circumscripta.

• Calcinosis universalis.

• Milk-alkali syndrome.

• Hypervitaminosis D.

• Calcinosis of chronic renal failure.

• Calcific tendonitis.

• Synovial osteochondromatosis.

• Synovial sarcoma.

• Osteosarcoma.

• Calcific myonecrosis.

• Tophaceous gout.

DIAGNOSIS:

Tumoral calcinosis.

PEARLS AND DISCUSSION:

Tumoral calcinosis is a rare condition characterized by painless periarticular masses.

The cases are autosomal dominant with abnormality in gene FGF 23.

Patient’s are usually of African descent. Progression occurs in the first and second decade of life. In addition, periarticular tumors reduce the range of motion of the joint. The lesions are usually painless. Late stages occur with ulcers.

Hyperphosphatemia occurs. Normal calcium levels are observed. Elevated vitamin D levels are noted. Parathyroid hormone levels are normal. As is the glomerular filtration rate. Treatment largely depends on the underlying cause. Surgical resection of tumoral calcinosis is well documented. But recurrence can occur if there are poor margins. Prostate deprivation using aluminum hydroxide in conjunction with acetazolamide synergistically lowers hyperphosphatemia.

FURTHER READING:

1. Olsen KM, Chew FS. Tumoral calcinosis: pearls, polemics, and alternative possibilities. Radiographics. 2006;26 (3): 871-85

2. Carmichael KD, Bynum JA, Evans EB. Familial tumoral calcinosis: a forty-year follow-up on one family. J Bone Joint Surg Am. 01;91 (3): 664-71.

3. Chefetz I, Sprecher E. Familial tumoral calcinosis and the role of O-glycosylation in the maintenance of phosphate homeostasis. Biochim. Biophys. Acta. 2009;1792 (9): 847-52.