Twenty-nine dogs were diagnosed with hyperadrenocorticism (HAC). A single determination of endogenous plasma adrenocorticotropic hormone (ACTH) and adrenal ultrasonography were used in a prospective study to differentiate between pituitary-dependent HAC (PDH) and adrenal-dependent HAC (ADH). In 27 out of the 29 dogs (93 per cent), both endogenous plasma ACTH concentrations and adrenal ultrasonography indicated the same cause of HAC. Twenty-one of the 29 cases (72 per cent) were shown to be pituitary-dependent; all had plasma ACTH concentrations of greater than 28 pg/ml (reference range 13 to 46 pg/ml) and both adrenal glands were ultrasonographically of similar size and of normal shape. All 21 cases responded well to mitotane therapy. Six cases (21 per cent) were shown to be adrenal-dependent; all had plasma ACTH concentrations below the limit of the assay (<5 pg/ml) and the presence of an adrenal mass on ultrasonography. The sensitivity and specificity of adrenal ultrasonography and endogenous ACTH determinations to identify the cause of HAC were demonstrated to be 100 per cent and 95 per cent, respectively, for ADH. These discriminatory tests are more accurate than published figures for dexamethasone suppression testing.

An 11-year-old, neutered, female Domestic Long Hair cat had a 3-week history of left forelimb lameness. Conscious proprioception and postural reflexes were absent on the left thoracic limb. The cat had slightly reduced placing and hopping responses on the left pelvic limb, absent cutaneous trunci muscle reflex on the left side, and left triceps muscle atrophy. Magnetic resonance imaging revealed a 2 x 2 x 2 cm mass in the region of the left brachial plexus. The cat was treated by left forelimb amputation and hemilaminectomy. Histopathology of the brachial plexus revealed lymphoma.

Protein-losing enteropathies were diagnosed in two dogs that were initially presented with diarrhoea and weight loss. Plasma biochemistry in both cases revealed low concentrations of albumin, calcium and ionised calcium. Both dogs had an elevated plasma parathyroid hormone concentration and low serum 25-hydroxyvitamin D (25[OH]D) concentration. The first dog was diagnosed with lymphangiectasia on postmortem examination, and the second dog was diagnosed with chronic lymphocytic/ plasmacytic enteritis and severe cystic mucoid changes based on endoscopic duodenal biopsies. While a causal effect was not demonstrated, the protein-losing enteropathies may have caused reduced intestinal absorption of vitamin D leading to low plasma concentrations of ionised calcium and secondary hyperparathyroidism. To the authors' knowledge, this is the first report of low ionised calcium concentrations, low 25(OH)D and 1,25-dihydroxyvitamin D concentrations, and high parathyroid hormone concentrations in dogs with protein-losing enteropathies.

A 13-year-old, male cocker spaniel presented with a history of inappetence, depression and reluctance to stand. The dog had multiple, ulcerated skin lesions which were diagnosed as panniculitis by histopathology. A diagnosis of pancreatitis was made on the basis of markedly elevated serum lipase concentrations, abdominal ultrasonography which showed an abnormal lobulated area of hypoechoic tissue in the body and right lobe of the pancreas, and a fine needle biopsy from this area which revealed large numbers of degenerate neutrophils. After treatment with antibiotics and prednisolone, the dog made a full clinical recovery and was free of clinical signs for four months. The dog was euthanased five months later and postmortem examination revealed chronic, active pancreatitis and a pancreatic adenoma. This is the first report of antemortem diagnosis of pancreatitis and panniculitis in a dog.