Sherri L. Ihle

Liver Histopathology and Liver and Serum Alanine Aminotransferase and Alkaline Phosphatase Activities in Epileptic Dogs Receiving Phenobarbital

Phenobarbital (PB) therapy is frequently associated with elevated serum alanine aminotransferase (ALT) and alkaline phosphatase (AP) activities in dogs without clinical signs of liver disease. The goal of this study was to determine if increased serum ALT and AP activities in clinically healthy PB-treated epileptic dogs are due to hepatic enzyme induction or to subclinical liver injury. Liver biopsies were obtained from 12 PB-treated dogs without clinical signs of liver disease but with elevated serum ALT and/or AP activities or both. Liver biopsies were obtained from eight healthy control dogs not receiving PB. Biopsies were evaluated histopathologically (all dogs) and liver homogenates were assayed for ALT (all dogs) and AP (six treated dogs, all controls) activities. As a positive control, liver cytochrome P4502B, an enzyme known to be induced by PB, was measured by benzyloxyresorufin-O-dealkylase activity and immunoblotting (five treated dogs, all controls). Serum AP isoenzyme analyses were performed. Results showed that ALT and AP activities in liver homogenates were not increased in treated dogs compared with controls, whereas the positive control for induction, CYP2B, was dramatically increased in treated dogs. Histopathological examination of liver biopsies revealed more severe and frequent abnormalities in treated dogs compared to controls, but similar types of abnormalities were found in both groups. Serum AP isoenzyme analyses in treated dogs demonstrated increased corticosteroid-induced and liver isoenzyme activities compared to controls. Results do not support induction of ALT or AP in the liver as the cause of elevated serum activities of these enzymes due to PB.

Association between excess body weight and urine protein concentration in healthy dogs

BACKGROUND Markedly overweight people can develop progressive proteinuria and kidney failure secondary to obesity-related glomerulopathy (ORG). Glomerular lesions in dogs with experimentally induced obesity are similar to those in people with ORG. OBJECTIVES The aim of this study was to evaluate if urine protein and albumin excretion is greater in overweight and obese dogs than in dogs of ideal body condition. METHODS Client-owned dogs were screened for underlying health conditions. These dogs were assigned a body condition score (BCS) using a 9-point scoring system. Dogs with a BCS of ≥ 6 were classified as being overweight/obese, and dogs with a BCS of 4 or 5 were classified as being of ideal body weight. The urine protein:creatinine ratio (UPC) and urine albumin:creatinine ratio (UAC) were then determined, and compared between 20 overweight/obese dogs and 22 ideal body weight control dogs. RESULTS Median UPC (0.04 [range, 0.01-0.14; interquartile range, 0.07]) and UAC (0.41 [0-10.39; 3.21]) of overweight/obese dogs were not significantly different from median UPC (0.04 [0.01-0.32; 0.07]) and UAC (0.18 [0-7.04; 1.75]) in ideal body weight dogs. CONCLUSIONS Clinicopathologic abnormalities consistent with ORG were absent from overweight/obese dogs in this study.

Pituitary corticotroph macrotumors. Diagnosis and treatment

Pituitary corticotroph macrotumors occur in 10% to 50% of dogs with PDH. Clinical signs may be only those of hypercortisolism or may include neurologic signs such as stupor, inappetance, circling, or pacing. Currently, CT and MRI are the only tests that can confirm the presence of a pituitary macrotumor in these patients. Results of endocrine testing are not significantly different from those of dogs with a microtumor. When a macroscopic pituitary tumor is identified in a dog with neurologic signs, or if a larger tumor is found in a dog even in the absence of neurologic signs, radiation therapy is currently the treatment of choice. Unfortunately, success rates with treatment are variable. A better response may be seen if the tumor is smaller and neurologic signs are minimal or absent at the time of treatment.

Nutritional Therapy for Diabetes Mellitus

Dietary therapy affects diabetes management in the dog and cat directly through control of blood glucose and indirectly through control of obesity and lipid abnormalities. Caloric intake, the feeding schedule, food form, macronutrient composition of the diet, and the presence of any concurrent problems must all be considered when planning the dietary regime. Generally, the healthy diabetic dog or cat should be fed a diet with increased fiber and moderate carbohydrate in a quantity sufficient to attain and maintain optimal body weight; whenever possible, the daily food allotment should be divided into multiple small meals that are fed through the day and evening when the physiologic effects of administered insulin are present. Once established, the dietary regime should be kept constant from day to day. Following these guidelines will help minimize postprandial hyperglycemia and may lead to a decreased exogenous insulin requirement. However, if a concurrent disorder has dietary requirements that conflict with those for the diabetic pet, nutritional management of the other disorder should usually take precedence.

Failure to Grow

Failure to grow in pups and kittens can be the result of many factors. Dietary, metabolic, endocrine, parasitic, neoplastic, and genetic diseases may be responsible for a failure to thrive alone or in concert with other disorders. A complete history, physical examination, complete blood cell count, biochemistry profile, and urinalysis are the initial steps to define the underlying disorder(s). Subsequent tests may be needed based on these initial diagnostic results.