Treatment of proliferative feline eosinophilic keratitis with topical 1.5% cyclosporine: 35 cases

Objective  Proliferative feline eosinophilic keratitis is a chronic keratopathy caused by a suspected immune mediated response to an unknown antigenic stimulus. The purpose of this study is to demonstrate the efficacy of topical 1.5% cyclosporine solution in proliferative feline eosinophilic keratitis.
Methods  Thirty-five cats were treated topically with 1.5% cyclosporine A between 1997 and 2007. Eosinophilic keratitis was diagnosed by clinical appearance and evidence of eosinophils and/or mast cells in corneal cytology. The patients were treated with topical cyclosporine (1.5%) twice (26 of 35, 74.3%) and three times (9 of 35, 25.7%) daily. The minimum period for follow-up was 5 months.
Results  The age of the patients ranged from 2 to 13 years with a mean age of 6.0 years. Twenty-two were neutered males, and 13 were females. The represented breeds were 30 DSH, 3 DLH, one Siamese and one Maine Coon. Cytologic examination of a corneal scrape revealed the presence of eosinophils in 34 of 35 specimens, and mast cells in 25 of 35 specimens. Improvement in the treated eyes was seen in 31 cats (88.6%). Four animals (11.4%) did not respond to the treatment with topical cyclosporine. Recurrences were seen in seven (22.6%) cases. Blepharitis was noted as an infrequent side effect.
Conclusion  Based on our findings, topical cyclosporine (1.5%) is an effective treatment of proliferative feline eosinophilic keratitis in the vast majority of cases. Recurrences were mainly associated with poor owner compliance. Chronic, often lifelong therapy with medications is thus recommended.     

Hydrolyzed casein influences intestinal mucin gene expression in the rat

The effect of hydrolyzed casein (HC) on the expression of three mucin genes (Muc2, Muc3, and Muc4) in the rat intestine was investigated using quantitative real-time polymerase chain reaction. After a 10 day acclimatization period, rats received for 8 days the test diets containing either HC or a synthetic amino acid (SAA) mixture as the sole source of nitrogen or a protein-free (PF) diet (n = 12 per treatment). The addition of HC or the SAA mixture to the diet significantly improved average daily gain, average daily food intake, and gain:feed ratio as compared with the PF diet. Terminal ileal endogenous N flow was significantly higher for the HC-fed rats in comparison with either the SAA or the PF rats (p < or = 0.001). HC supported a significant increase of Muc3 mRNA (277 and 229% of that for diets PF and SAA, respectively; p < or = 0.05) in the small intestinal tissue and Muc4 mRNA (325 and 265% of that for diets PF and SAA, respectively; p < or = 0.05) in the colon. In conclusion, HC enhances ileal endogenous N flow and up-regulates in vivo the expression of some individual mucin genes.