The physical, clinicopathologic, and survival rates of 77 cats with severe spontaneous hepatic lipidosis are detailed in this report. Cats were subdivided into groups designated as idiopathic lipidosis if no other disease process was recognized, or secondary lipidosis if another disease process was diagnosed. Cats were also subdivided into groups designated a s survivors or nonsurvivors on the basis of successful recuperation at 4 months after initial diagnosis. Differences between disease and survival groups were evaluated for significance. Overall, more female cats and middle-aged cats were affected. Presenting complaints of vomiting, anorexia, weakness, and weight loss were common. Physical assessment of most cats showed obvious hepatomegaly, jaundice, dehydration, and a weight loss 2 25% of usual body weight. Neurobehavioral signs indicative of hepatic encephalopathy, other than ptyalism and depression, were rare. Clinicopathologic features are characterized by hyperbilirubinemia and increased activities of serum ALT, AST, and ALP, with only small if any increase in yGT activity, Clinical features distinguishing cats with hepatic lipidosis from those with other serious cholestatic disorders include absence of hyperglobulinemia and low y C T activity relative to ALP activity. Although coagulation tests were abnormal in 45% of cats tested (n = 44), few cats showed clinical bleeding tendencies. Most cats received prophylactic vitamin K, therapy. Forty two cats received aggressive nutritional and supportive care and of these 55% survived. Cats with idiopathic disease were significantly younger, had significantly higher ALP activity and bilirubin concentration, and had a slightly better survival rate than cats with secondary lipidosis. Low PCV, hypokalemia, and an older age were significantly related to nonsurvival. Because of the variety of diets and food supplements used in case management, the influence of nutritional factors on survival could not be evaluated. THE FELINE HEPATOCYTE appears to have a pro-. . pensity for lipid vacuole formation in a variety of systemic disease processes.' Mild to moderate hepatic lipi-
Two patients with thrombotic thrombocytopenic purpura (TTP) have recovered completely after intensive plasmapheresis. The mechanisms responsible for the improvement in these instances are most likely related to the removal of an inciting or damaging agent. The possibility that this agent may be an immune complex is discussed. Plasmapheresis appears to be useful therapy for some patients with this syndrome.
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