Systemic calcinosis in a Quarter Horse gelding homozygous for a myosin heavy chain 1 mutation

Abstract

Case description: A 9-year-old Quarter Horse gelding was presented for lethargy, decreased appetite, polyuria and polydipsia (PU/PD), and severe muscle wasting suggestive of immune-mediated myositis.

Clinical findings: The horse displayed lethargy, fever, tachyarrhythmia, inappetence, PU/PD, and severe epaxial and gluteal muscle wasting. Clinicopathologic findings were consistent with previously reported cases of systemic calcinosis in horses, including increased muscle enzyme activity, hyperphosphatemia, increased calcium-phosphorus product, hypoproteinemia, and an inflammatory leukogram. A diagnosis of systemic calcinosis was established by histopathologic evaluation of biopsy specimens from skeletal muscle, lung, and kidney.

Treatment and outcome: Symptomatic treatment was complemented by IV treatment with sodium thiosulfate to reverse calcium-phosphate precipitation in soft tissue and PO aluminum hydroxide to decrease intestinal phosphorus absorption and serum phosphorus concentration.

Clinical relevance: This is the first report in the veterinary literature of an antemortem diagnosis of systemic calcinosis in the horse that was successfully treated and had favorable long-term outcome.

Keywords: calcium-phosphorus product; immune mediated myositis; polydipsia; polyuria; sodium thiosulfate.

FIGURE 1

Transrectal sonogram of the left kidney showing overall increased echogenicity and fine hyperechoic speckling in the renal medulla suggestive of calcification. Image obtained with a transrectal linear 7.5 MHz probe at a maximal depth of 8 cm

FIGURE 2

Base‐apex lead ECG tracing showing multiform ventricular tachyarrhythmia. Three initial sinus complexes are followed by a ventricular tachycardia with wide negative QRS complexes (*). A sinus complex then occurs (middle of bottom strip; P wave buried in the preceding T wave), followed by another ventricular premature (complex) and a run of positive QRS ventricular complexes (arrows). Nonconducted P waves can be seen intermittently between ectopic complexes. Paper speed 25 mm/s

FIGURE 3

A, Lung tissue showing thickening of the alveolar wall with basophilic mineral and mononuclear cells (arrow). Hematoxylin and eosin stain, ×200 magnification. B, Areas of calcification are highlighted in the alveolar walls (arrow). Von Kossa stain, ×200 magnification. C, Biopsy specimen from the gluteus medius in a 9‐year‐old Quarter Horse. Multiple myocytes are calcified (arrow). Other myocytes are shrunken or necrotic (arrowhead). A cellular population of fibroblasts and low numbers of macrophages are present. Hematoxylin and eosin stain, ×400 magnification. D, Areas of calcification are highlighted in calcified myocytes (arrow). Von Kossa stain, ×400 magnification. E, Mineralization of the glomerular tuft and basement membrane characterized by multifocal basophilic stippling (arrow). Hematoxylin and eosin stain, ×400 magnification. F, Renal tubules contain neutrophilic and cellular debris (arrow). Adjacent tubules contain variable amounts of basophilic, crystalline material (arrow head). Hematoxylin and eosin stain, ×200 magnification

FIGURE 4

A, Patient on the day of presentation. Notice the marked epaxial and gluteal muscle atrophy. B, Patient 11 weeks after initial presentation. Notice the marked improvement in overall body condition, especially the epaxial and gluteal muscle mass