Systemic Calcinosis in 5 Horses
ACVIM 2008
J. Tan1; S.J. Valberg1; M. Sebastian2; G. Davis3; L. Goehring4;M. Harland5; J. Kelly6; L. Kuebelbeck6; J. Newton5; J. Reimer7; B. Waldridge5
1University of Minnesota, St Paul, MN, USA; 2Livestock Disease Diagnostic Center, Lexington, KY, USA; 3Okotoks Animal Clinic, Okotoks, AB, USA; 4Colorado State University, Fort Collins, CO, USA; 5Auburn University, Auburn, AL, USA; 6Surgi-Care Center for Horses, Brandon, FL, USA; 7Rood and Riddle, Lexington, KY, USA

Systemic calcinosis is a syndrome of calcium deposition in the connective tissue of organs including lungs, kidneys, stomach, heart, and skin, not previously described in horses. The purpose of this study was to characterize the signalment, history, clinical signs, muscle biopsy findings, and postmortem findings of 5 horses with potential systemic calcinosis. Records from the Neuromuscular Diagnostic Laboratory at the University of Minnesota were searched to identify horses with biopsy findings of calcified myofibers (Von Kossa stains) and postmortem findings of dystrophic calcification in other organs.

Five Paint or Quarter Horses fit the criteria and ranged in age from 8 months to 6 yrs (median 3.5 yrs). Duration of clinical signs ranged from 3 to 17 days and in 3 of the 5 horses, respiratory illness was reported in conjunction with clinical signs. Common clinical signs were lethargy (5/5), inappetence (2/5), epaxial and gluteal atrophy (3/5) and stiffness (3/5) or recumbency (2/5). Hyperfibrinogenemia (5/5), hyperphosphatemia (5/5), a Ca*P product of greater than 70 (4/5) and high serum CK activity (1,880-950,000 U/L) were consistently present. Treatment consisted of nonsteroidal antiinflammatories and antibiotics, and frequently included intravenous fluids, dexamethasone, and furosemide. All horses deteriorated despite treatment and developed complications such as colitis (2/5), thrombophlebitis (2/5), laminitis (1/5), respiratory distress (1/5), or prolonged recumbency (1/5). Muscle biopsy findings included acute myofiber necrosis, macrophage infiltration, anguloid atrophy, centrally located myonuclei, rare multinucleated giant fibers, and scattered fibers with dense calcium deposition. All horses were euthanized. Postmortem findings revealed calcification of muscle (5/5) and kidney cells (5/5). Calcification was also present in the heart (3/5), lungs (3/5), liver (1/5), and vascular tunica intima (1/5). Two forms of systemic calcification occur in humans as a consequence of 1° or 2° hyperparathyroidism or elevated Ca*P product. In calciphylaxis, dystrophic calcification occurs in the tunica media of blood vessels, resulting in tissue ischemia and necrosis. In contrast, systemic calcinosis results in calcification of connective tissue and cells within multiple organs. Corticosteroids are suggested to exacerbate calcification. We hypothesize that in some horses, hyperphosphatemia from rhabdomyolysis or hyperparathyroidism may trigger systemic calcinosis. Prospective analysis of parathyroid hormone concentrations are indicated in horses with hyperphosphatemia and calcified fibers in muscle biopsy. Until this condition is better understood, the prognosis remains guarded.

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Jean-Yin Tan


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