RESUMEN
In canine and feline populations, the number of neoplasm cases continues to increase around the world. Attempts are being made in centres of research to identify new biomarkers that speed up and improve the quality of oncological diagnostics and therapy in human and animal tumour patients. Cyclooxygenase-2 (COX-2) is a promising biomarker with increasing relevance to human oncology, but as yet with less application in veterinary oncology. The expression of COX-2 increases significantly during pathological processes involving inflammation, pain or fever. It is also overexpressed in humans presenting various types of tumours and in selected types of tumours in animals, particularly in dogs. This article discusses the expression of COX-2 in canine and feline tumours, the importance of COX-2 as a biomarker with diagnostic, therapeutic, prognostic and predictive relevance in oncology, and the clinical significance of inhibiting COX-2 overexpression in tumours.
RESUMEN
BACKGROUND: Idiopathic lymphoplasmacytic rhinitis (LPR) is a common inflammatory disorder of the nasal cavity in dogs due to unknown etiology. It is characterised by non-specific clinical signs, including nasal discharge, epistaxis and breathing problems. Diagnosis is usually based on the histopathologic identification of infiltrating plasmocytes and lymphocytes in the nasal mucosa and the exclusion of other underlying diseases. Treatment strategies include glucocorticoids, non-steroidal anti-inflammatory drugs, antibiotics and antifungal medications. The aim of this study was to evaluate the efficacy of various therapeutic protocols for managing canine lymphoplasmacytic rhinitis based on the results of clinical, endoscopic and histological examinations, and to determine the relapse rate for LPR in dogs.Twenty dogs of different breeds and both sexes, aged 1 to 14 years, were divided into four groups, each consisting of five dogs, including three experimental groups diagnosed with LPR and a control group.The dogs from the first experimental group were administered prednisone orally at 1 mg/kg/day in the first 4 weeks and 0,5 mg/kg/day in the following 2 weeks. The second group of dogs was administered meloxicam orally at 0,1 mg/kg/day in the first 3 weeks, followed by prednisone at 1 mg/kg/day in the following 2 weeks and 0,5 mg/kg/day in the last week of the treatment. The dogs from the third experimental group were administered meloxicam orally at 0,1 mg/kg/day for 6 weeks. The control group of dogs was administered empty gelatin capsules (placebo) orally for 6 weeks. Clinical signs, endoscopic and histopathologic lesions were scored before and after treatment. Groups were compared using Chi- squared statistics in a 2 × 2 table for pre- versus post-treatment scores. RESULTS: Clinical signs persisted in the group treated with meloxicam and were mostly resolved in prednisone-treated dogs. However, endoscopic and histological changes were still observed in these two groups after treatment. The severity of all diagnostic features was reduced in the group treated with meloxicam for 3 weeks followed by prednisone for 3 weeks. The significant differences (p < 0.05) were noted between experimental and control groups. The dogs showed a statistically significant reduction in characteristics of the LPR before and after treatment, as measured by clinical signs (Group 1vs.4 p = 0.00, group 2 vs 4 p = 0.00, group 3 vs 4 p = 0,01), by endoscopy (1 vs 4 p = 0,01, 2 vs 4 p = 0,00, 3 vs 4 p = 0,03), and by histopathology (groups 1 vs 4 p = 0,00, 2 vs 4 p = 0,00, 3 vs 4 p = 0,03). The significant differences were noted between experimental groups, as measured by endoscopy (group 2vs 3 p = 0,04), and by relapse rate (groups 1 and 2 p = 0,03, groups 2 and 3 p = 0,01). CONCLUSIONS: The three treatment protocols administered to dogs improved clinical, endoscopic and histological status. However, oral administration of meloxicam for 3 weeks, followed by prednisone for 3 weeks, appeared to be the most successful treatment. These patients remained asymptomatic for 6 months.
