This study compared the effects of a moderate carbohydrate-high fiber (MC-HF) food and a low carbohydrate-low fiber (LC-LF) food on glycemic control in cats with diabetes mellitus. Sixty-three diabetic cats (48 male castrated, 15 female spayed) were randomly assigned to be fed either a canned MC-HF (n = 32) food or a canned LC-LF (n = 31) food for 16 weeks. Owners were blinded to the type of diet fed. CBC, urinalysis, serum chemistry panel, fructosamine concentration and thyroxine concentration were determined on initial examination, and a complete blood count, serum chemistry panel, urinalysis and serum fructosamine concentration were repeated every 4 weeks for 16 weeks. Insulin doses were adjusted as needed to resolve clinical signs and lower serum fructosamine concentrations. Serum glucose (P = 0.0001) and fructosamine (P = 0.0001) concentrations significantly decreased from week 0 to week 16 in both dietary groups. By week 16, significantly more of the cats fed the LC-LF food (68%, 22/31), compared to the cats fed the MC-HF food (41%, 13/32), had reverted to a non-insulin-dependent state (P = 0.03). Cats in both groups were successfully taken off of insulin regardless of age, sex, type of insulin administered or duration of clinical disease before entering the study. There was no significant difference in the initial or final mean body weights or in the mean change in body weight from week 0 to week 16 between dietary groups. Diabetic cats in this study were significantly more likely to revert to a non-insulin-dependent state when fed the canned LC-LF food versus the MC-HF food.

Background: Flow cytometry has been used to detect anti-red blood cell (RBC) antibodies in dogs with immune-mediated hemolytic anemia (IMHA), but the prevalence of anti-RBC antibodies in anemic and nonanemic dogs with a variety of different diseases has not been assessed previously.Hypothesis: We hypothesized that anti-RBC antibodies would be more common in anemic dogs and in dogs with immunemediated disorders and cancer.Animals: Blood samples from 292 dogs were analyzed prospectively by flow cytometry for anti-RBC antibodies.Methods: Blood samples from 147 anemic and 145 nonanemic dogs were evaluated by flow cytometry to detect surfacebound immunoglobulin (Ig) G and IgM antibodies on RBC. Disease associations with RBC antibodies were determined, as was the correlation between disease status and the percentage of Ig 1 RBC. The specificity and sensitivity of flow cytometry and clinical variables for the diagnosis of IMHA were compared by Bayesian analysis.Results: Anemic dogs were significantly more likely to be positive for anti-RBC antibodies (IgG, IgM, or both) than nonanemic dogs. Anemic dogs also had significantly higher percentages of Ig 1 RBC than nonanemic dogs, whereas dogs with IMHA had significantly higher percentages of Ig 1 RBC than dogs with all other diseases. Dogs with IMHA, infectious diseases, and immune-mediated thrombocytopenia were significantly more likely to have anti-RBC antibodies than dogs with other medical or surgical diseases.Conclusions: Anemic dogs with immune-mediated diseases and infectious diseases were at the highest risk for the development of anti-RBC antibodies, and flow cytometry for the detection of IgG on RBC was highly sensitive and specific for the diagnosis of IMHA.

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Immune-Mediated Hemolytic Anemia (IMHA) is a spontaneously occurring disease of man and dogs in which immunoglobulin-coated erythrocytes are destroyed in the spleen. Immunosuppressive therapies and splenectomy have been previously used to combat premature destruction of erythrocytes. Liposomal clodronate has been previously shown to be a potent anti-macrophage agent when administered intravenously in a murine model. Splenic macrophages were selectively depleted through the induction of apoptosis following phagocytosis of liposomes containing clodronate. We hypothesized that such an approach might be useful in blocking clearance of erythrocytes in dogs with spontaneous IMHA. Clodronate (dichloromethyl bisphosphonate) was formulated in liposomes (phosphatidyl choline, cholesterol and mannose), according to a previously published technique. The liposomal clodronate was evaluated in vitro for activity using canine and murine histiocytic cell lines, as assessed by cell killing and blocking of erythrophagia. Cell killing was monitored using microscopic evaluation of cell change, MTT and by propidium iodide staining. Blocking of erythophagia was monitored using flow cytometry. In vivo in normal dogs, increasing doses of liposomal clodronate were administered intravenously and evaluated to determine efficacy in blocking erythrocyte clearance and toxicity. Twenty-four hours post infusion, dye-labeled erythrocytes were opsonized using rabbit anti-canine erythrocyte antibody. Erythrocytes clearance was monitored using flow cytometry. The safe and effective dose of liposomal clodronate was determined to be 0.5 ml/kg administered IV via CRI over a 90 minute time period. After administration of intravenous liposomal clodronate in normal dogs, clearance of opsonized erythrocytes was nearly completely blocked at the 0.5 ml/kg dose. In vitro assays indicated that liposomal clodronate induced death of canine macrophage and dendritic cell lines. Five dogs with spontaneous IMHA were treated once with liposomal clodronate at the 0.5 ml/kg dose. Though erythrocyte clearance was not completely blocked, the drug was well-tolerated and all 5 dogs survived to leave the hospital. These studies suggest that liposomal clodronate may be an effective agent for temporary suppression of erythrocyte destruction in IMHA. Additional studies, including evaluation of higher doses of liposomal clodronate, are warranted in dogs with spontaneous IMHA.