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Case Reports
. 2025 Jan;26(1):e3.
doi: 10.4142/jvs.24246. Epub 2024 Dec 10.

First report of iron-overload myopathy due to secondary hemochromatosis in a dog

Affiliations
Case Reports

First report of iron-overload myopathy due to secondary hemochromatosis in a dog

Jae-Hyuk Yim et al. J Vet Sci. 2025 Jan.

Abstract

Importance: Hemochromatosis is rare in domestic animals, and iron-induced myopathy has not been reported in veterinary medicine. This case is the first report of iron-overload myopathy owing to hemochromatosis in a dog.

Case presentation: A 9-year-old spayed female Donggyeong dog presented with severe forelimb lameness. Necropsy revealed an enlarged liver and hemorrhagic lesions in the forelimb muscle. Microscopy showed iron components accumulation in multiple organs, including the liver, forelimb skeletal muscle, spleen, lymph node, and kidney. Prussian blue staining identified iron deposits in both macrophages and parenchymal cells, indicating that the iron accumulation was acquired rather than hereditary. Furthermore, iron components were observed within muscle fibers, accompanied by severe atrophy and myositis.

Conclusions and relevance: Severe necrosis and mild fibrosis were observed in the liver and forelimb skeletal muscles. Based on histological analysis, we diagnosed iron overload myopathy by secondary hemochromatosis. Secondary hemochromatosis with severe muscle atrophy and myositis is very rare, and this is the first report of iron-overload myopathy in a dog.

Keywords: Iron-overload; animal; hemochromatosis; lameness; muscular diseases; non-transferrin bound iron.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Fig. 1
Fig. 1. Liver and forelimb muscle of a 9-year-old Donggyeong dog. (A) The appearance of the Donggyeong dog, showing no specific gross lesion. (B) The liver and gallbladder were significantly enlarged, with multiple yellow-white patches in the liver (scale bar = 5 cm). (C) The cut surface appears diffusely variegated, with congested regions and tan-brown patches (scale bar = 1 cm). (D, E) Hemorrhage and enlarged intermuscular spaces were evident in the forelimb muscles (scale bar = 1 cm).
Fig. 2
Fig. 2. Representative images of the liver. (A) Centrilobular necrosis, ballooning degeneration, and mild fibrosis disrupt lobular architecture, with numerous black globular pigments visible (hematoxylin & eosin stain, scale bar = 100 µm). (B) Mild fibrosis is evident (Masson’s trichrome stain, scale bar = 200 µm). (C) Iron accumulation primarily observed in Kupffer cells filled with iron components, also called siderotic bodies (inset, arrow). Some iron components are also observed in hepatocytes (inset, arrowhead) (Prussian blue stain, scale bar = 100 µm).
Fig. 3
Fig. 3. Representative images of the forelimb muscle. (A) Severe muscle atrophy, myositis, and hemorrhage are evident (hematoxylin & eosin stain, scale bar = 100 µm). (B) Iron components are observed within muscle fibers (arrows) (Prussian blue stain, scale bar = 50 µm).

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