Idiopathic hyperostosis of the calvaria in five young bullmastiffs.

A new calvarial hyperostotic syndrome (CHS) in young bullmastiffs is described. Calvarial hyperostotic syndrome clinically resembles canine craniomandibular osteopathy (CMO) and human infantile cortical hyperostosis (ICH), but it is unique in that there is progressive and often asymmetric skull bone involvement, and the population affected appears to be only young, male bullmastiff dogs. Characteristic radiographic findings consist of cortical thickening of the calvaria with irregular, bony proliferation over the frontal, temporal, and occipital bones. Histopathological examination shows that the trabeculae of the calvarial diploë are thickened and contiguous with a sunburst-like pattern of subperiosteal trabeculae composed of woven and lamellar bone tissue, accompanied by loose fibrovascular tissue and a variable inflammatory response comprised predominantly of neutrophils. In 80% of the cases presented, the lesion was self-limiting. The etiology remains unknown; however, traumatic, neoplastic, and degenerative conditions do not appear to be primary factors in the etiopathogenesis of the syndrome. It may be that this syndrome has a familial component, similar to that described for CMO and ICH.

Fragmented medial coronoid process of the ulna in the dog.

Fragmented medial coronoid process of the ulna is an important cause of elbow dysplasia in the dog. Etiologic factors that have been identified include osteochondrosis, ulnar trochlear notch incongruity or dysplasia, and asynchronous growth of the radius and ulna. Treatment options that are discussed are conservative medical management, surgical removal of the coronoid fragments, and ulnar osteotomy or ostectomy. Prognosis is variable and depends on etiologic factors and response to therapy.

Effect of cimetidine on aspirin-induced gastric hemorrhage in dogs.

Efficacy of cimetidine in the prevention of aspirin-induced gastric hemorrhage was evaluated, using 4 groups of 6 dogs given: Group 1--controls; group 2-7.5 mg of cimetidine/kg of body weight every 8 hours; group 3-7.5 mg of cimetidine/kg every 8 hours and 35 mg of nonbuffered aspirin/kg every 8 hours; and group 4-35 mg of nonbuffered aspirin/kg every 8 hours. All medication was given orally for 10 days at the time of feeding a commercial dry food. The gastric mucosa was evaluated endoscopically before treatment, on treatment day 5, and 36 hours after the final treatment. The dogs were given halothane inhalation anesthesia and were evaluated, using a grading system. Total 24-hour fecal hemoglobin (Hb) concentration was measured, using a quantitative fluorometric analysis for Hb-derived porphyrins. Control dogs and dogs given cimetidine only had no endoscopically visible gastric lesions and no increase in fecal Hb concentration. All dogs given aspirin or aspirin and cimetidine had a similar marked increase in endoscopically visible gastric hemorrhage and marked increases in fecal Hb concentration; however, there was no significant (P = 0.48) difference between the 2 groups. Seemingly, cimetidine given at an oral dosage of 7.5 mg/kg every 8 hours was not effective in preventing aspirin-induced gastric hemorrhage in clinically normal dogs.

Serum salicylate concentrations and endoscopic evaluation of the gastric mucosa in dogs after oral administration of aspirin-containing products.

The serum salicylate concentration produced by oral administration of plain aspirin and several aspirin-containing products given at 8-hour intervals for 7 treatments was measured in 36 laboratory-conditioned adult dogs. The dogs were randomly allotted to 6 groups of 6 dogs each: group 1 was given plain aspirin at a dosage of 25 mg/kg of body weight: group 2 was given plain aspirin at a dosage of 10 mg/kg; group 3 was given buffered aspirin at a dosage of 25 mg/kg; group 4 was given enteric-coated aspirin at a dosage of 25 mg/kg; group 5 was given buffered aspirin at a dosage of 25 mg/kg; and, group 6 was given a placebo. Serum salicylate concentration was measured at 2-hour intervals for the first 8 hours, and then at 8-hour intervals for the next 40 hours. Following the last dosing, serum salicylate concentration was measured at 2-hour intervals until 56 hours; the final 2 samples were measured at 64 and 72 hours. The effect of aspirin on the gastric mucosa was studied in 12 dogs, 3 each randomly selected from groups 1, 3, 4, and 5. The gastric mucosa of each dog was examined with a fiberoptic gastroscope 3 days before the beginning of treatment; lesions were not seen. The drugs were administered as described and the gastric mucosa of each dog was reexamined at 72 hours. Administration of the aspirin-containing products at 8-hour intervals resulted in sustained therapeutic serum salicylate concentrations (greater than 5 mg/dl) in all dogs, except those of group 2. The greatest fluctuation in serum salicylate concentration was found in dogs of group 4. Gastric lesions were seen only in the 3 dogs of group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of a fluorometric method for the quantitative assay of fecal hemoglobin in the dog.

Feces from 27 dogs were evaluated to establish baseline fecal hemoglobin (Hb) concentrations when the dogs were fed diets containing varying amounts of Hb. Fecal Hb concentration was measured, using a quantitative fluorometric assay that was based on the conversion of nonfluorescing Hb heme to fluorescing porphyrins. Mean fecal Hb concentration was 0.31 mg/g of feces when the dogs were fed a dry diet low in Hb. This corresponded to a daily fecal blood loss of 0.043 ml/kg of body weight. The fecal Hb concentration was directly related to the dietary Hb concentration. The average recovery of orally ingested blood was 41% in 4 dogs. This fluorometric assay quantitatively detected small amounts of gastrointestinal bleeding over a wide range of fecal Hb concentrations for which feces appeared normal. Results of this study establish dietary conditions necessary for quantitative evaluation of experimental and clinical gastrointestinal bleeding.

Effect of dietary calcium, magnesium, and phosphorus on phosphate urolithiasis in rats.

Female Wistar rats were fed a basal diet containing various concentrations of calcium, phosphorus, and magnesium: calcium and phosphorus at 0.4, 0.5, 0.8, 1.0, 1.5, and 2 per cent and magnesium at 0.2, 0.4, 0.8, and 1 per cent of the diet dry matter. Two types of uroliths developed: magnesium phosphate in the renal pelves, bladders, and/or ureters of rats fed rations containing 1 per cent magnesium with either 1.0 or 0.5 per cent phosphorus and calcium phosphate uroliths in the renal tubules at the corticomedullary junction of rats fed rations containing phosphorus equal to or greater than 0.8 per cent and magnesium equal to or less than 0.8 per cent. The incidence and severity of calcium phosphate uroliths were reduced by increasing the magnesium concentration in the diet from 0.2 to 0.8 per cent and by increasing the calcium-to-phosphorus ratio to greater than 1. Results of this study indicated that the interactions among dietary calcium, magnesium, and phosphorus seemed to affect the incidence, severity, and type of uroliths in rats.

Prevention of oxalate urolithiasis by some compounds.

Male Wistar rats were fed a basal diet, Purina Laboratory Chow, and an oxalate calculi-producing diet (CPD). The CPD was the basal diet containing 3 per cent glycolic acid. Sodium pyruvate, DL-alanine, alpha-keto glutaric acid, thiamine pyrophosphate, and L-glutamic acid were added to the CPD to determine their effectiveness in preventing calculi formation. The effectiveness of methyl glyoxal was determined by adding it to the drinking water. Rats fed CPD for 4 weeks developed calculi in the ureters, bladder, renal tubules, and/or renal pelvis and papilla. Rats in groups fed alanine and/or pyruvate had no calculi in their renal tubules or ureters; additionally, these rats had a significant reduction in incidence and amount of deposits in the renal pelvis and bladder. Rats in groups fed alpha-keto glutaric acid, thiamine pyrophosphate, L-glutamic acid, and methyl glyoxal developed equally or more severe oxalate urolithiasis than those on CPD alone. Results of this study show that either pyruvate or alanine at appropriate levels may be beneficial in preventing oxalate urolith formation.