Records from 101 dogs presented for investigation of unexplained pyrexia were reviewed. The most common diagnosis was immune-mediated disease (22 per cent of cases), with immune-mediated polyarthritis accounting for 20 per cent of all diagnoses. The frequency of positive results obtained in investigative tests was also assessed. Cytological and radiological examinations provided a high diagnostic success rate, although routine haematology and plasma biochemistry were also useful screening tests. On the basis of these results it is suggested that, in the investigation of unexplained pyrexia, a diagnosis of immune-mediated polyarthritis should be excluded before less common diagnoses are considered.
The case records of 26 dogs with nasal tumours, treated either with radiation alone or surgery and radiation, were compared. One‐ and two‐year actuarial survival rates for 12 dogs treated with radiotherapy were 58 and 13 per cent, respectively, compared to 71 and 38 per cent, respectively, for 14 dogs which were treated with surgery before radiotherapy. Sixty‐seven per cent of the dogs treated with radiotherapy had recurrent clinical signs by 52 weeks compared to 36 per cent of the dogs treated with surgery and radiotherapy. The longer disease‐free interval of the dogs treated with surgery and radiotherapy was statistically significant. When dogs with sarcomas were compared to those with carcinomas, there was no significant difference in disease‐free interval or survival time.
The case histories of 60 dogs with hyperadrenocorticism were reviewed. Fifty-four of the dogs were treated with mitotane at a mean daily dose rate of 48.8 mg/kg (range 25.6 to 84 mg/kg) for between four and 21 days. The mean weekly maintenance dose of mitotane was 48.8 mg/kg. An adrenocorticotrophic hormone (ACTH) stimulation test was performed before the treatment began, and in 30 cases at the end of the induction course, and the response to ACTH was measured at regular intervals thereafter. Nine of the treated dogs developed complete hypoadrenocorticism during treatment and required permanent mineralocorticoid replacement therapy. Twelve of the dogs had normal responses to an ACTH stimulation test before treatment, and the diagnosis of hyperadrenocorticism was based on the result of a low-dose dexamethasone suppression test. These 12 dogs had consistently lower cortisol levels before and after stimulation with ACTH and four of them developed complete hypoadrenocorticism. In general the clinical signs were well controlled when the cortisol levels were less than 105 nmol/litre before and after the stimulation test. Dogs in which the clinical signs recurred had cortisol levels between 210 and 580 nmol/litre after the test, a level which is within the normal pretreatment range. Twenty-seven of the treated dogs died and six of these deaths were attributable directly to the disease or therapy. The median survival time of the 54 treated dogs was 30 months; eight dogs died during the first 16 weeks of treatment, and the dogs which survived this period had a median survival time of 39 months (mean 50 months).
A radiological assessment of 35 canine nasal tumours using an objective scoring system was carried out and related to patient survival. The scoring system demonstrated significant increases in disease-free interval and survival for dogs with scores of less than 12 compared to those with scores of 12 or above.
A four-year-old Labrador retriever was presented with lethargy and exercise intolerance. Clinical examination was unremarkable. A subnormal cortisol response to adrenocorticotrophin hormone (ACTH) was demonstrated (plasma cortisol concentrations before and after administration of ACTH were both below the detection limit of the assay) but plasma aldosterone concentrations were within the normal range. Endogenous plasma ACTH concentrations were high, indicating primary adrenocortical disease. Following glucocorticoid supplementation at a replacement dose (prednisolone 0.1 mg/kg) the dog made a full clinical recovery.
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