Evaluation of plasma-ionized magnesium concentration in 122 dogs with diabetes mellitus: a retrospective study.

The goal of this study was to evaluate plasma-ionized magnesium (iMg2+) concentration in a large group of dogs with naturally occurring diabetes mellitus and to determine whether dogs with diabetes mellitus have hypomagnesemia, as reported in diabetic humans and cats. Plasma iMg2+ concentrations were retrospectively evaluated at the time of initial examination of 122 diabetic dogs at the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania. Diabetic dogs were defined as having uncomplicated diabetes mellitus (DM, 78 dogs) diabetic ketoacidosis (DKA, 32 dogs), or ketotic nonacidotic diabetes mellitus (DK, 12 dogs) on the basis of presence or absence of metabolic acidosis or ketonuria. Twenty-two control dogs were used to determine reference values for plasma iMg2+ concentration in healthy dogs. Plasma iMg2+ concentration also was evaluated in 19 nondiabetic dogs with acute pancreatitis because many of the dogs with DKA had concurrent acute pancreatitis. Plasma iMg2+ concentration was significantly higher in dogs with DKA (median 0.41 mmol/L, reference range 0.14-0.72 mmol/L) than in dogs with DM (0.33 mmol/L, 0.17-0.65 mmol/L; P = .0002) or the control group (0.32 mmol/L, 0.26-0.41 mmol/L; P = .006). There were no significant differences between plasma iMg2+ concentrations in dogs with DM or DK compared with control dogs. We conclude that dogs with naturally occurring diabetes mellitus do not have marked hypomagnesemia on initial examination at a tertiary care center.

Detection of Bartonella henselae and Bartonella clarridgeiae DNA in hepatic specimens from two dogs with hepatic disease.

A 4-year-old Basset Hound and a 6-year-old Doberman Pinscher were referred for diagnostic evaluation following documentation of persistently increased hepatic enzyme activities and hepatic dysfunction. Histologic evaluation of hepatic biopsy specimens from the 2 dogs revealed granulomatous hepatitis in the Basset Hound and lymphocytic hepatitis with fibrosis and copper accumulation in the Doberman Pinscher. No etiologic agents were identified histologically. Bartonella henselae DNA was subsequently amplified from hepatic tissue from the Basset Hound and Bartonella clarridgeiae was amplified from hepatic tissue from the Doberman Pinscher. Amplification was performed with a polymerase chain reaction assay incorporating primers that target a portion of the 16S-23S rRNA intergenic spacer region. Both dogs were treated with azithromycin, in combination with a variety of other medications and herbal treatments, and improved clinically. Identification of Bartonella DNA in these dogs indicates the need for future prospective studies to determine the clinical relevance of Bartonella spp infection in dogs with hepatic disease.