Two cats from two separate clinics were submitted to the Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) and were both diagnosed with hepatic amyloidosis. The whole body of the first cat was submitted for necropsy and histopathology. Formalin-fixed sections of liver, gallbladder, and kidney from the second cat were submitted for histopathology following a necropsy that was performed by the practicing veterinarian. The necropsy findings described by the submitting veterinarian in that case were nearly identical to those seen at TVMDL during necropsy of the first cat.
Both cats were 2.5 to 4 years old and were castrated males. They both presented with vague clinical signs of lethargy and anorexia which failed to improve upon hospitalization. One of these cats developed severe icterus that was notable in the clinic and at necropsy. At necropsy, the abdomens contained small to moderate amounts of non-clotted blood, indicating a hemoabdomen. The source of the blood was from the liver, which both had multifocal clots of blood on the surface and in the parenchyma (Figure 1). The rest of the liver was pale and extremely friable, especially when compared to the other organs.
Histologically, both cats had mild to severe amounts of amyloid in the liver. This amyloid was determined to be the cause of the hepatic rupture and hemorrhage. One of the cats also had a tremendous amount of amyloid in the thyroid gland (Figure 2) with small amounts also seen in the kidney and spleen.
Amyloid is a misfolded protein that can be deposited in various organs and in many species. In cats, systemic or generalized amyloidosis is seen as a familial condition in various breeds. In this condition, the amyloid typically has primary deposition in either the kidney or liver, though many other organs can also have variable amounts. Hepatic amyloidosis is seen most often in Siamese and Oriental shorthair breeds. Affected cats may show intermittent vague signs of disease, fulminant signs of liver failure, or can present with sudden death. Large accumulations of amyloid disrupt the hepatic architecture, making it exceedingly fragile and prone to rupture. The specific mode of inheritance and pathogenesis of this disease are not well understood.
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