Caffeic acid phenethyl ester modulates gentamicin-induced oxidative nephrotoxicity in kidney of rats.

In this study, the modulator effect of caffeic acid phenethyl ester (CAPE) on the oxidative nephrotoxicity of gentamicin in the kidneys of rats was investigated by determining indices of lipid peroxidation and the activities of antioxidant enzymes as well as by histological analyses. Forty female Wistar albino rats were randomly divided into four groups, namely control, gentamicin, CAPE, and gentamicin plus CAPE. On the 12th day of the study, all rats were sacrificed and then blood samples and kidneys were taken. Lipid peroxidation and nitric oxide levels, glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) enzyme activities, and histological evaluation were measured in kidneys of rats. Levels of blood urea nitrogen and creatinine were studied in serum. CAPE with gentamicin caused decreases in lipid peroxidation, nitric oxide, urea nitrogen, and creatinine levels, although it caused increases in CAT, GSH-Px, and SOD activities when compared with gentamicin alone. In addition, on histological evaluation, the renal damage caused by gentamicin alone appeared much higher than that caused by CAPE plus gentamicin. It is concluded that oxidative stress plays a critical role in causing gentamicin nephrotoxicity and that this nephrotoxicity may be significantly reduced by CAPE.

DRESS like severe drug rash with eosinophilia, atypic lymphocytosis and fever secondary to ceftriaxone.

We report a case in a 50-year-old male who had been treated with ceftriaxone for 3 weeks to treat meningitis. He was admitted 4 days after cessation of the ceftriaxone treatment with fever, headache, nausea, vomiting, myalgia, arthralgia, pruriginous skin rashes, and with edema on face. Blood tests showed marked eosinophilia and atypic lymphocytosis. He was successfully treated with prednisone p.o. We report this case as we could not recognize a case like this which was induced by ceftriaxone.