A one-year-old, intact male Maltese was referred with dehydration, anorexia, and marked hyperglycemia. The dog had been managed due to meningoencephalitis of unknown etiology (MUE) for three months. The dog had been treated with long-term prednisolone administration. Diabetic ketoacidosis (DKA) was identified based on the blood chemistry and venous gas analyses, and intensive treatments including insulin administration were initiated. On further examinations, there was no any other disease that contributed to the occurrence of DKA. Insulin resistance resulted from the administration of prednisolone was highly suspected, but the agent could not be tapered due to managing MUE. Following resolution of DKA, the dog was discharged with life-long insulin and prednisolone therapy. Over the next two years, the dog continued to be routinely re-evaluated and was managed with permanent insulin therapy (0.8–1.4 units/kg SC 12 hourly) and medications including prednisolone (0.4–1.1 mg/kg PO 12 hourly). Because MUE severely progressed, the dog was euthanized by owner’s request. Histopathologic examination of pancreas obtained by post-mortem revealed that both endo- and exocrine pancreas was within normal limit. The case described herein showed the risk of ketoacidosis as well as hyperglycemia after long-term prednisolone administration in a dog without pancreatic islet pathology.

This study was carried out to investigate the protective effect of prednisolone in rabbit primary cultured articular chondrocytes treated with sodium nitroprusside (SNP), a nitric oxide donor. After a cell phenotype was determined, the MTT assay and Western blot analysis of type II collagen, cylooxygenase-2 (COX-2) and phosphorylated extracellular regulated kinase (pERK) were performed in the control, SNP (298 μg/ml) alone or SNP plus prednisolone (0.05-50 μg/ml)-treated rabbit articular chondrocytes. Immunofluorescence staining of type II collagen was also performed. Cell morphology indicated that SNP treatment induced cytotoxicity, and that the SNP-induced cytotoxicity was inhibited by prednisolone treatment. MTT assay showed that the SNP treatment resulted in a significant decrease in the level of cell viability compared with that of control (p<0.01), and that the prednisolone treatment resulted in a decrease in the SNP-induced cytotoxicity. SNP treatment resulted in a decrease in the level of type II collagen, compared with the control chondrocytes. The prednisolone treatment recovered the down-regulated expression of type II collagen induced by SNP, showing a significant level in 5 μg/ml of the prednisolone treatment group compared to the SNP treatment group (p<0.05). A significant increase in COX-2 was significantly induced by the SNP treatment compared to control chondrocytes (p<0.01). The COX-2 expression was decreased by the prednisolone treatment, showing a significant level in 50 μg/ml of the prednisolone treatment group compared to the SNP treatment group (p<0.05). These phenomena was confirmed by immunofluorescence staining. Furthermore, the SNP treatment significantly induced a decrease of pERK expression compared to the control chondrocytes (p<0.01). The prednisolone treatment recovered its expression, showing a significant level in 0.5 μg/ml of the prednisolone treatment group compared to the SNP treatment group (p<0.05). Taken the above results together, prednisolone is considered to inhibit SNP-induced cell death and dedifferentiation, and modulated expression of COX-2 and pERK in rabbit articular chondrocytes.

A 2-year-old, spayed male Bengal cat was referred to our clinic due to a mass lesion on the upper lip, as well as lower lip swelling and redness. Furthermore, well-circumscribed, raised, pink lesions were found in the oral cavity. Complete blood counts (CBC) and serum biochemistry profiles revealed no remarkable findings. Bacterial and fungal cultures of the lesion in the oral cavity were negative. Fine needle aspiration of the lesions revealed numerous eosinophils. Based on both clinical examination and cytological evaluation, the cat was diagnosed with feline eosinophilic granuloma. As an initial treatment, oral prednisolone (PDS) with cyclosporine was administered. However, the cyclosporine caused the cat to vomit. The lesion was markedly improved after 2 weeks of PDS-only therapy; this was subsequently tapered for 2 months and discontinued. However, one month later, the lesion had relapsed. The cat was then treated for one month using tacrolimus with PDS, and the clinical signs of eosinophilic granuloma gradually improved. The tacrolimus was gradually tapered for 1 month, and the PDS was gradually tapered for 4 months. There is no standard protocol for the investigation and treatment of feline eosinophilic granuloma. The cat in this report was administered immunosuppressive therapies to treat eosinophilic granuloma. This case report provides evidence the combination of PDS and tacrolimus is effective for reducing relapse in feline eosinophilic granuloma.