BackgroundGastroGard, an omeprazole powder paste formulation, is considered the standard treatment for gastric ulcers in horses and is highly effective. Gastrozol, an enteric‐coated omeprazole formulation for horses, has recently become available, but efficacy data are controversial and sparse.ObjectivesTo investigate the efficacy of GastroGard and Gastrozol at labeled doses (4 and 1 mg of omeprazole per kg bwt, respectively, PO q24h) in healing of gastric ulcers.Animals40 horses; 9.5 ± 4.6 years; 491 ± 135 kg.MethodsProspective, randomized, blinded study. Horses with an ulcer score ≥1 (Equine Gastric Ulcer Council) were randomly divided into 2 groups and treated for 2 weeks each with GastroGard followed by Gastrozol (A) or vice versa (B). After 2 and 4 weeks, scoring was repeated and compared with baseline. Plasma omeprazole concentrations were measured on the first day of treatment after administration of GastroGard (n = 5) or Gastrozol (n = 5).ResultsCompared with baseline (squamous score (A) 1.65 ± 0.11, (B) 1.98 ± 0.11), ulcer scores at 2 weeks ((A) 0.89 ± 0.11, (B) 1.01 ± 0.11) and 4 weeks ((A) 1.10 ± 0.12, (B) 0.80 ± 0.12) had significantly decreased in both groups (P < .001), independent of treatment (P = .7). Plasma omeprazole concentrations were significantly higher after GastroGard compared with Gastrozol administration (AUCGG = 2856 (1405‐4576) ng/mL × h, AUCGZ = 604 (430‐1609) ng/mL × h; P = .03). The bioavailability for Gastrozol was 1.26 (95% CI 0.56–2.81) times higher than for GastroGard.Conclusions and Clinical ImportanceBoth Gastrozol and GastroGard, combined with appropriate environmental changes, promote healing of gastric ulcers in horses. However, despite enteric coating of Gastrozol, plasma omeprazole concentrations after single labeled doses were significantly higher with GastroGard.

No abstract

Vascular hamartomas are non-neoplastic developmental anomalies of vessels. Cases of cerebral vascular hamartomas have been previously reported in dogs and cats. A 4-week-old Freiberger foal had shown persistent problems with breathing and swallowing since birth, and bilateral laryngeal paralysis was diagnosed. The foal subsequently developed left sided facial nerve paralysis and a secondary corneal ulcer in the left eye. Necropsy revealed a pinkish mass in the obex region of the brain. The mass was further investigated by histology and immunohistochemistry. Histologically, the mass consisted of many thin-walled, blood-filled vascular structures of variable diameter involving the white matter of the obex. The lining cells were immunohistochemically positive for factor VIII (von Willebrand factor) interpreted as endothelial cells. The endothelial lining showed also variable immunoreactivity for smooth muscle actin and vimentin. Normal neural parenchyma labeled with antibodies directed against glial fibrillary acidic protein and neuron-specific enolase was present between the vascular proliferations. A diagnosis of focal vascular hamartoma in the obex was made. The development of clinical signs is attributed to the compression of the surrounding neural parenchyma.