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Brazilian Journal of Pharmaceutical Sciences

On-line version ISSN 2175-9790

Abstract

SHAH, Rehmat; SUBHAN, Fazal; SULTAN, Syed Muhammad  and  ALI, Gowhar. Short-term oral administration of risperidone induces pancreatic damage and hyperamylasemia in Sprague-dawley rats. Braz. J. Pharm. Sci. [online]. 2018, vol.54, n.4, e17841.  Epub Apr 08, 2019. ISSN 2175-9790.  https://doi.org/10.1590/s2175-97902018000417841.

Risperidone is an atypical antipsychotic acting mainly as a dopamine D2 and serotonin 5-HT2 receptors antagonist prescribed in the treatment of schizophrenia and various affective disorders. Risperidone has been reported to be associated with weight gain, panreatitis and type 2 diabetes mellitus. Various mechanisms of risperidone-induced toxicities have been reported but the histology of tissues especially pancreas has never been studied. Therefore, the current study was designed to elucidate the toxic effects of chronic administration of risperidone on pancreas, liver and kidneys. Animals (rats) of either gender were divided into two groups, the risperidone and control groups. Risperidone was administered in a dose of 2.5 mg/kg/d for three weeks. The controls received acidified saline only. Both the groups received restricted diet (20 g/12 h). The body weight and level of random blood sugar (RBS) were measured on a weekly basis. The levels of lipase and amylase were determined at the conclusion of the experiment. At the end of the experiment, the tissues were dissected out for histopathological evaluation. Risperidone showed no weight gain, hyperglycemia or rise in the level of lipase (P> 0.05); however, the level of amylase was raised (***P<0.05). Histological examination under light microscope showed no hepatotoxicity, nephrotoxicity but did show damage to the pancreas. The findings of this study indicated that the incidence of adverse effects associated with risperidone could be prevented/alleviated/delayed by allowing restricted diet.

Keywords : Risperidone/antipsychotics/oral administration/effects; Histopathology; D2 antagonist; Pancreas.

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