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Home / Equine Research Bank / J Vet Intern Med / Systemic calcinosis in a Quarter Horse gelding homozygous fo...
Journal of veterinary internal medicine2022; 36(4); 1543-1549; doi: 10.1111/jvim.16481

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

Abstract: 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. Results: 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. Results: 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. Conclusions: 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.
© 2022 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC. on behalf of the American College of Veterinary Internal Medicine.
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Publication Date: 2022-07-08 PubMed ID: 35801821PubMed Central: PMC9308413DOI: 10.1111/jvim.16481Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research revolves around the treatment of a nine-year-old Quarter Horse suffering from extreme lethargy, reduced appetite and intense muscle wasting due to systemic calcinosis. The study not only confirms the diagnosis but also records the successful treatment and recovery of the horse, marking a first in veterinary literature.

Case Presentation

  • The research revolves around a nine-year-old Quarter Horse gelding, showing symptoms like decreased appetite, excessive urination and thirst (PU/PD), severe muscle wasting and lethargy, suggesting possible immune-mediated myositis.
  • On further examination, the horse also demonstrated fever, irregular, quickened heartbeat (tachyarrhythmia), loss of appetite, PU/PD, and severe destruction of muscle tissue in the back and gluteal muscle.

Diagnosis

  • The clinicopathologic findings coincided with earlier reported cases of systemic calcinosis in horses. The symptoms included increased muscle enzyme activity, elevated levels of phosphate in the blood (hyperphosphatemia), increased calcium-phosphorus product, reduced protein in the blood (hypoproteinemia), and an inflammatory leukogram, which is a total white blood cell count to help detect infection, inflammation or other conditions that can affect the horse.
  • Systemic calcinosis was diagnosed through the histopathological examination of biopsy specimens taken from the skeletal muscle, lung, and kidney.

Treatment and Outcome

  • Along with symptomatic treatment, intravenous administration of sodium thiosulfate was used to neutralize the calcium-phosphate precipitation in soft tissue, which is one of the effects of systemic calcinosis.
  • Oral medication of aluminum hydroxide was given to the horse to reduce phosphorus absorption in the intestines and decrease the concentration of serum phosphorus which was previously increased due to systemic calcinosis.
  • This research report constitutes the first instance within veterinary literature to describe a living (antemortem) diagnosis and successful treatment of systemic calcinosis in a horse, resulting in a positive long-term outcome.

Cite This Article

APA
Sponseller BT, Wong DM, Ruby R, Ware WA, Wilson S, Haynes JS. (2022). Systemic calcinosis in a Quarter Horse gelding homozygous for a myosin heavy chain 1 mutation. J Vet Intern Med, 36(4), 1543-1549. https://doi.org/10.1111/jvim.16481

Publication

Journal of veterinary internal medicine
ISSN: 1939-1676
NlmUniqueID: 8708660
Country: United States
Language: English
Volume: 36
Issue: 4
Pages: 1543-1549

Researcher Affiliations

Sponseller, Beatrice T
  • Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, Iowa, USA.
Wong, David M
  • Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, Iowa, USA.
Ruby, Rebecca
  • Veterinary Diagnostic Laboratory, College of Agriculture, Food and Environment, University of Kentucky, Lexington, Kentucky, USA.
Ware, Wendy A
  • Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, Iowa, USA.
Wilson, Scott
  • Mid-Atlantic Equine Dentistry, Myrtle Beach, South Carolina, USA.
Haynes, Joseph S
  • Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa, USA.

MeSH Terms

  • Animals
  • Calcinosis / drug therapy
  • Calcinosis / veterinary
  • Calcium
  • Horse Diseases / diagnosis
  • Horse Diseases / drug therapy
  • Horse Diseases / pathology
  • Horses
  • Lethargy / veterinary
  • Male
  • Muscular Diseases / veterinary
  • Mutation
  • Myosin Heavy Chains
  • Phosphorus

Conflict of Interest Statement

Authors declare no conflict of interest.

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Citations

This article has been cited 2 times.
  1. De Luca E, Del Piero F. Animal Tissue Mineralization: An Overview of Disease Processes, Comparative Pathology, and Diagnostic Approaches. Biomolecules 2026 Jan 7;16(1).
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  2. Durward-Akhurst SA, Valberg SJ. Myosin Heavy Chain Myopathy and Immune-Mediated Muscle Disorders. Vet Clin North Am Equine Pract 2025 Apr;41(1):61-75.
    doi: 10.1016/j.cveq.2024.10.005pubmed: 39880733google scholar: lookup
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