Reasons for performing study:To present the first report of a case series concerning equine idiopathic muscular hypertrophy of the oesophagus (IMHO). Objectives: To investigate the clinical and pathological features of the disorder. Methods: The medical records of 31 horses suffering from the disorder were reviewed retrospectively. In all these animals the diagnosis was confirmed at post mortem examination. Results: The median age of the affected horses was 12.5 ± 5.6 years (range 1-26) without sex or breed predilection. Only 2 out of 31 horses showed clinical signs associated with oesophageal dysfunction, indicating that the muscular hypertrophy was rather a coincidental post mortem finding. Histology revealed thickening of the distal portion of the oesophagus mainly involving the circular layer of the tunica muscularis without fibrosis or inflammation. In 8 cases, the disorder was seen in concurrence with idiopathic hypertrophy of the tunica muscularis of various other parts of the gastrointestinal tract. Conclusions: In the majority of patients, IMHO was a coincidental finding at post mortem examination usually confined to the smooth, circular muscle layer of the tunica muscularis externa. Potential relevance: Further research is necessary to study the precise effect of IMHO on oesophageal function.

Data suggest that the decreased plasma glucose curve obtained in horses with EMND during OGTTs (compared with control horses) is a result of overall enhanced glucose metabolism or abnormalities in the facilitated glucose transporters; definitive identification of the underlying mechanisms could aid in the development of appropriate treatments of EMND in horses.

SINCE Estepa and others (1998) validated a human radioimmunoassay for intact parathyroid hormone (iPTH) for use in the equine species, this method has contributed considerably to the diagnosis of secondary hyperparathyroidism and should be used in preference to the carboxyl-terminal assay (C-terminal PTH) (Capen 1989). High iPTH concentrations are often seen in primary or secondary hyperparathyroidism; Frank and others (1998) described a pony with primary hyperparathyroidism confirmed on the basis of a high iPTH concentration.Secondary hyperparathyroidism can be due to renal failure, which is rare in horses, or to nutritional secondary hyperparathyroidism (NSH). NSH is related to a persistent unbalanced diet causing hypocalcaemia (Krook and Lowe 1964, Krook 1968, Joyce and others 1971, Schryver and others 1971, Argenzio and others 1974, Walthall and McKenzie 1976, Capen 1989, Palmer 1993. This short communication describes a case in which the iPTH concentration was measured to support the diagnosis of secondary hyperparathyroidism.A five-year-old Shetland pony mare was referred to the Department of Equine Sciences, Utrecht University, because ofweight loss, anorexia and a stiff gait over the previous three days, for which it had been treated with vedaprofen (Quadrisol; Janssen-Cilag BV) and corticosteroids. The mare was pastured with 10 other clinically normal ponies and fed a free choice of maize silage and hay. The owner had bought the mare three months previously.On physical examination the pony was in poor body condition. It had bilateral forelimb shifting-leg lameness, seemed dull and showed a great reluctance to move. The upper face had a swollen appearance with bilateral firm enlargement of the maxilla and mandible, not associated with any clinical signs of pain. The mare had a respiratory rate of 100 breaths/minute, a regular pulse of 96 beats/minute and a body temperature of 38-6°C. The mucous membranes were reddish, moist and some haemorrhages were present. The sclerae were yellow. There was an increased digital pulse.Laboratory evaluation included a complete blood count and serum biochemical analysis; the findings are shown in Table 1. Haematology revealed a slightly decreased packedcell volume (Pcv). The plasma calcium concentration was normal and the plasma ionised calcium concentration was slightly decreased, whereas the plasma phosphorus concentration was increased. Alkaline phosphatase activity was high, probably due to the increased bone resorption. Urinalysis revealed a low normal calcium concentration and hyperphosphaturia. For reference, the calcium and phosphorus concentrations in the urine were determined in 11 clinically healthy warmbloods. The creatinine concentration in the urine was not available for calculation of the fractional excretion of calcium and phosphorus due to FIG 1: Lateral radiograph of the left front foot showing a generalised loss of bone density with a clear number and loss of definition of bone trabeculae errors on the application form.The basal plasma iPTH concentratio...