Non-steroidal anti-inflammatory drugs (NSAIDs) are in common use worldwide. These drugs may sometimes be used in high or toxic doses by mistake. In this study we investigated the effects of different doses of diclofenac sodium on liver and renal tissues. Forty albino adult male Wistar rats weighing 200 to 220 g were divided equally into four groups. The rats in the control group (n = 10) were each intramuscularly injected with 1 cc of physiologic saline. The other three groups were given diclofenac sodium doses. The rats in the first (n = 10), second (n = 10) and third (n = 10) groups were intramuscularly injected with diclofenac sodium at a low, medium and high dose of 50, 100 and 150 mg/kg live weight/day, respectively, every day for 5 days. At the end of the experimental period (5 days), after the animals were sacrificed, they were autopsied and liver and kidney tissue samples were prepared for histopathologic assessment. No significant (P > 0.05) changes were observed in the histopathology of the liver or kidney tissues of the control rats. The diclofenac sodium treatment significantly (P < 0.001) affected the histopathology of both the liver and kidney. Histopathologic changes in the liver sections stained with hematoxylin and eosin in all diclofenac groups included claudy swelling and hydropic degeneration of the liver cells, focal sinusoidal and vena centralis dilatation, proliferation of the bile duct in portal areas, enlargement of the periportal area with mononuclear cell infiltration, hyperemia and dose-dependent fibrous tissues proliferation and focal necrosis. Cloudy swelling and hydropic degeneration were seen in the tubular epithelial cells of the kidney tissue of all diclofenac sodium treated groups. Necrosis, peritubular lymphocyte infiltration, stromal fibrous tissue proliferation and hyperemia were observed in the second and third groups. In the liver and kidney tissue of the third group, which was given a high dose of diclofenac sodium, necrosis, cloudy swelling and hydropic degeneration and inflammation were rather widespread and intensive, as compared to the group given a low dose. The increase in fibrous tissue in the kidney and liver that caused irregularities in the periportal areas was only seen in the group given a high dose. These results suggest that a high dose of diclofenac sodium causes meaningful changes in liver and kidney tissue.

Non-steroidal anti-inflammatory drugs (NSAIDs) are in common use worldwide. These drugs may sometimes be used in high or toxic doses by mistake. In this study we investigated the effects of different doses of diclofenac sodium on liver and renal tissues. Forty albino adult male Wistar rats weighing 200 to 220 g were divided equally into four groups. The rats in the control group (n = 10) were each intramuscularly injected with 1 cc of physiologic saline. The other three groups were given diclofenac sodium doses. The rats in the first (n = 10), second (n = 10) and third (n = 10) groups were intramuscularly injected with diclofenac sodium at a low, medium and high dose of 50, 100 and 150 mg/kg live weight/day, respectively, every day for 5 days. At the end of the experimental period (5 days), after the animals were sacrificed, they were autopsied and liver and kidney tissue samples were prepared for histopathologic assessment. No significant (P > 0.05) changes were observed in the histopathology of the liver or kidney tissues of the control rats. The diclofenac sodium treatment significantly (P < 0.001) affected the histopathology of both the liver and kidney. Histopathologic changes in the liver sections stained with hematoxylin and eosin in all diclofenac groups included claudy swelling and hydropic degeneration of the liver cells, focal sinusoidal and vena centralis dilatation, proliferation of the bile duct in portal areas, enlargement of the periportal area with mononuclear cell infiltration, hyperemia and dose-dependent fibrous tissues proliferation and focal necrosis. Cloudy swelling and hydropic degeneration were seen in the tubular epithelial cells of the kidney tissue of all diclofenac sodium treated groups. Necrosis, peritubular lymphocyte infiltration, stromal fibrous tissue proliferation and hyperemia were observed in the second and third groups. In the liver and kidney tissue of the third group, which was given a high dose of diclofenac sodium, necrosis, cloudy swelling and hydropic degeneration and inflammation were rather widespread and intensive, as compared to the group given a low dose. The increase in fibrous tissue in the kidney and liver that caused irregularities in the periportal areas was only seen in the group given a high dose. These results suggest that a high dose of diclofenac sodium causes meaningful changes in liver and kidney tissue.