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.

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The RapidVet-H method agreed with the standard cross-match method on compatible samples, but detected incompatibility in some sample pairs that were compatible with the standard method. Evaluation using larger numbers of incompatible pairings is needed to assess diagnostic utility. The gel tube method results were difficult to categorize due to sample spreading. Weak agglutination reactions or other factors such as centrifuge model may be responsible.

Peritoneal fluid from 10 healthy young male Holstein calves was analyzed three times (2 to 3 days, 12 to 15 days and 27 to 30 days) during the first month of life. A new technique for collection of peritoneal fluid from calves positioned in left lateral recumbency was developed. The technique was found to be reliable and without noticeable complications. Mean peritoneal fluid nucleated cell counts, red blood cell counts, and absolute counts for mononuclear cells, lymphocytes and eosinophils did not change significantly (P

A multicentric prospective study was conducted to monitor the effect of phenobarbital on serum total thyroxine (T4) and thyroid-stimulating hormone (TSH) concentrations in epileptic dogs. Serum T4 concentrations were determined for 22 epileptic dogs prior to initiation of phenobarbital therapy (time 0), and 3 weeks, 6 months, and 12 months after the start of phenobarbital. Median T4 concentration was significantly lower at 3 weeks and 6 months compared to time 0. Thirty-two percent of dogs had T4 concentrations below the reference range at 6 and 12 months. Nineteen of the 22 dogs had serum TSH concentrations determined at all sampling times. A significant upward trend in median TSH concentration was found. No associations were found between T4 concentration, dose of phenobarbital, or serum phenobarbital concentration. No signs of overt hypothyroidism were evident in dogs with low T4, with one exception. TSH stimulation tests were performed on six of seven dogs with low T4 concentrations at 12 months, and all but one had normal responses. In conclusion, phenobarbital therapy decreased serum T4 concentration but did not appear to cause clinical signs of hypothyroidism. Serum TSH concentrations and TSH stimulation tests suggest that the hypothalamic-pituitary-thyroid axis is functioning appropriately.

A homogenous enzyme immunoassay (EIA) for measurement of serum thyroxine (T4) concentration was evaluated for use with canine and feline serum. The EIA method was linear from 0 to 150 nmol T4/L for human serum, 0 to 94 nmol T4/L for feline serum and 10 to 60 nmol T4/L for canine serum. Intra- and interassay precision studies yielded coefficients of variation

Airway reactivity and BAL cytology did not show concordance in this population of horses presenting for unexplained poor performance and/or chronic cough. Failure to include tests of airway reactivity may lead to underdiagnosis of IAD in young Standardbred racehorses that present with clinical signs suggestive of IAD.

A 4.5-year-old Quarter Horse gelding was referred for evaluation of a swollen right hind leg of 3 weeks duration, which had occurred after exercise. Lameness was not observed and cold hydrotherapy had resulted in little improvement. Two weeks before presentation, the gelding developed a swelling over the left zygomatic arch for which a tentative diagnosis of abscessation was made. However, the lesion was unresponsive to antibiotics, became pruritic, ulcerated, and exuded serosanguinous fluid. Two days before presentation, dexamethasone powder a was prescribed to treat the leg swelling. On the day of presentation, the gelding also developed a swelling overlying the xiphoid process and a swelling on the right lateral abdomen.At presentation, the gelding weighed 546 kg and had normal vital signs. The right hind fetlock was swollen circumferentially from the distal third of the metatarsus to the pastern. The swelling was warm, firm, and nonpitting. The gelding was grade 1/5 lame in the affected limb.1 The mass (5 cm diameter, 2 cm depth) over the zygomatic arch was firm, ulcerated, and immoveable. The xiphoid process swelling (1 cm diameter, 1 cm depth) was soft, nonfluctuant, and nonmobile. The soft tissue swelling (15 cm diameter, 1 cm depth) on the right lateral abdomen resembled cutaneous edema.Biochemical and hematologic values were within reference intervals except for mild eosinophilia. Radiographs of the right hind fetlock revealed a discrete osteophyte on the dorso-medial aspect of the 1st phalanx. Skull radiographs showed a discrete soft tissue swelling surrounding the left zygomatic arch.Ultrasonography of the right metatarsal area revealed thickening of the subcutaneous tissues (1.1 cm depth) and distention (3.5 cm diameter, 1.5 cm depth) of the digital flexor tendon sheath with anechoic fluid at the level of the fetlock and pastern.Histopathologic evaluation of a 5-mm-diameter punch biopsy from the mass on the head revealed a poorly defined tumor involving the subcutis and deep dermis. It was composed of multiple, densely cellular islands and nests of pale, neoplastic round cells embedded in large amounts of dense fibrous stroma. Mild-to-moderate infiltrates of eosinophils surrounded these neoplastic aggregates. Tumor cells had pale eosinophilic cytoplasm, uniform oval nuclei with finely stippled chromatin, and inapparent to single small nucleoli. Toluidine-blue staining revealed many fine metachromatic cytoplasmic granules. No mitotic figures were observed. This mass was diagnosed as a cutaneous mast cell tumor. Histopathologic evaluation of two 5-mm-diameter punch biopsies of the mass overlying the xiphoid process revealed marked subcutaneous fibrosis containing mild infiltrates of eosinophils with fewer lymphocytes and plasma cells. There was no evidence of neoplasia. The subcutis contained rare discrete aggregates of cell debris, amorphous hypereosinophilic material, and occasional hyalinized fragmented collagen fibers surrounded by a rim of epithelioid macrophages admixed with eosinophils consisten...