Veterinary Medicine - December 2008 - (Page 661)

TABLE 1 Selected Causes of Canine and Feline Non-immune-mediated Hemolytic Anemia* Causes, Underlying Disorders, and Possible Triggers Inherited causes of hemolytic anemia Pyruvate kinase deﬁciency Phosphofructokinase deﬁciency Chondrodysplasia/anemia Osmotic fragility Metabolic causes of hemolytic anemia Hypophosphatemia Notes on Further Investigation and Diagnostic Testing Seen in young basenjis, West Highland white terriers, Cairn terriers, Abyssinians, Somalis, and others; myeloﬁbrosis (in dogs only) may be identiﬁed. Seen in English springer spaniels, cocker spaniels, and mixed-breed dogs; can result in a hemolytic crisis and exertional myopathy. Seen in Alaskan malamutes; dwarﬁsm with mild regenerative anemia may occur. Seen in Abyssinian and Somalis; signs include recurrent anemia, splenomegaly, weight loss, and lymphocytosis. Seen in dogs and cats treated for diabetes mellitus and hepatic lipidosis and can occur with refeeding syndrome; signs include a rapid drop in PCV, mild intravascular lysis, and mild Heinz body formation. Foods, metals, and chemical causes of hemolytic anemia Onion or garlic toxicosis Seen more commonly in dogs; signs include Heinz body hemolytic anemia. Copper toxicosis Acute copper toxicosis can result in intravascular hemolysis and mild methemoglobinemia. Zinc toxicosis Zinc toxicosis is seen from ingestion of pennies (minted since 1983), zinc nuts and bolts, and zinc oxide-containing ointments. Few Heinz bodies and spherocytes are found; intravascular hemolysis is seen; the mechanism of hemolysis is uncertain. Naphthalene poisoning results in intravascular hemolysis, vomiting, seizures, and hepatopathy. Naphthalene toxicosis *Source: References 1, 5, and 24. Heinz body anemia. Heinz bodies are dark-staining refractile material that indicate irreversibly denatured and precipitated hemoglobin in RBCs and can occur from oxidative damage in animals that have ingested onions or received drugs such as methylene blue, dl-methionine, or vitamin K3.1 In some cases of hemolytic anemia, eccentrocytes—cells in which the damaged hemoglobin is clustered together and shifted to one side of the RBC membrane, leaving a clear crescent-shaped region—are also present. Eccentrocytes and cells containing Heinz bodies have less deformability and more rigidity, making them more likely to be lysed or removed from the circulation by the spleen. Feline RBCs are especially sensitive to oxidative damage because of a high number of sulfhydryl groups in their hemogloblin. In addition, feline spleens, because of their nonsinusal conformation, are less effective at removing Heinz bodies than are canine sinusal spleens. Thus, Heinz body anemia is more commonly seen in cats and can be present during toxicosis as well as in a variety of other diseases such as hyperthyroidism, diabetes mellitus, and lymphoma.1 Hypophosphatemia. Hypophosphatemia can also cause hemolytic anemia in patients being treated for diabetes mellitus, hepatic lipidosis, starvation, and other conditions.1 In these cases, it is thought that an abrupt drop in plasma phosphate concentrations can cause a concurrent depletion of RBC adenosine triphosphate, diphosphoglycerate, and reduced glutathione. These depletions lead to less deformability, more osmotic fragility, and more susceptibility to oxidative injury in erythrocytes. A rapid drop in packed cell volume and a mild Heinz body anemia can be seen in animals with hypophosphatemia. Treatment consists of phosphate supplementation (intravenous in cases of severe depletion, oral in mild cases).1 Primary and secondary IMHA IMHA has been described in people, dogs, cats, and a wide range of other species.2 In dogs, it is estimated that 60% to 75% of cases are considered primary (idiopathic), meaning that no underlying cause can be found.3 It is thought that as more intense clinical investigations are conducted in these patients, underlying diseases and triggers will be discovered.3 Any breed can be affected with primary IMHA, but certain breeds—such as cocker spaniels, poodles, Irish setters, and Old English sheepdogs—seem to be overrepresented (Table 2).1 In both people and dogs, there appears to be a linkage between speci c human leukocyte antigen (HLA) and dog leukocyte antigen (DLA) haplotypes and autoimmune disease, although the genes involved may differ for each disease. A recent study in dogs investigated whether a genetic mutation in the DLA of certain breeds predisposes them to IMHA. The results suggest that more than one gene may be involved in these susceptible breeds.4 In secondary IMHA, RBC destruction occurs as a consequence of the immune system reacting to some condition or being activated by an agent. The end result is that the RBCs are destroyed as innocent bystanders. The process is probably the result of several factors, including an animal’s susceptibility to disease and its propensity to form an autoimmune response. Usually, the process results from a combination of environmental factors and a genetic predisposition. The VETERINARY MEDICINE December 2008 661

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Veterinary Medicine - December 2008 Contents Letters Thanking Our Valued Reviewers Practical Matters Idea Exchange Why Do Dogs and Cats Eat Grass? Managing Atypical and Critical Cases of Primary Hypoadrenocorticism in Dogs Behaviors Suggestive of Postoperative Pain in Cats What to Consider When Considering Digital Radiography Avoid Common Bandaging Mistakes in Dogs and Cats IMHA: Diagnosing and Treating a Complex Disease CE Form/Advertiser Index Marketplace/Classifieds Mind Over Miller

Veterinary Medicine - December 2008

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