Diagnostic Evaluation of Suspected Calciphylaxis

1. Serum calcium, phosphate, blood urea nitrogen, cre-atinine, glucose.

2. Serum albumin.

3. Serum intact parathyroid hormone.

4. Protein S and C levels, quantitative and functional.

5. Skin biopsy of indurated plaque or ulcer margin.

6. Evaluation for large vessel arterial disease (in distal subset).

7. Consider radiographic evaluation of soft tissue for subcutaneous calcifications.

Treating calciphylaxis is far more challenging than establishing the diagnosis. Treatment is directed at reversing metabolic derangements favoring calcification. In early series, the focus of treatment was parathyroidec-tomy. Literature favoring parathyroidectomy reported higher survival rates in surgically treated patients, but these were uncontrolled studies with limited follow-up (18). Use of parathyroidectomy is likely to be beneficial only in cases with striking elevations in parathyroid hormone. It may be that secondary hyperparathyroidism is less relevant than it was in earlier reports because of ever-improving metabolic control in patients with endstage renal disease. The incidence of calciphylaxis appears be increasing, and this may be, in part, due to a switch from aluminum-containing phosphate binders to those containing calcium. In the patient with calciphylaxis, calcium-containing phosphate binders should be changed to non-calcium ones such as sevelamer. Increased frequency of dialysis from three to five times a week with a low calcium bath has been advocated to reduce calcium burden (21). This requires careful monitoring for hypocalcemia. While the use of vitamin D would be expected to worsen disease based on Selye's model, it has a theoretical advantage of suppressing parathyroid hormone levels while limiting gastrointestinal absorption of calcium and phosphorous in the patient with secondary hyperparathyroidism (21). Hyperbaric oxygen has been reported to be of benefit in healing of cutaneous ulcers (22). Even oxygen administration by nasal cannula may increase cutaneous oxygen tension in patients with calciphylaxis (11). Bisphos-phonates have been found to suppress experimental calciphylaxis, and intravenous treatment with the bisphos-phonate, pamidronate, was reported to result in dramatic disease resolution in a case report (23,24). Intravenous sodium thiosulfate, which may solubilize tissue calcium deposits, was used with striking beneficial effect in a case report (25). Another case report noted good response to low-dose tissue plasminogen activator in a patient with calciphylaxis, history of deep venous thrombosis, low protein C and antithrombin III, and elevated fibrinogen levels, suggesting that this is a therapy to consider in cal-ciphylaxis patients with evidence of a hypercoagulable state (26). A summary of possible tools in calciphylaxis treatment is suggested:

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