RESUMEN
This study sought to investigate the effects of kolaviron on diclofenac-induced hepatotoxicity in rats. Sixty male Wistar rats were divided into 6 groups of 10 rats each as follows: a control group that received oral propylene glycol and treatment groups that received diclofenac alone, diclofenac followed by Livolin Forte (a reference drug), or diclofenac followed by kolaviron at three different doses. At the end of the study period, five rats per group were sacrificed under ketamine hydrochloride anesthetic, 24h after treatment, while the other 5 rats in the group were allowed to recover for 2 weeks before being sacrificed. Liver enzyme activities, total bilirubin levels, and the concentrations of several pro-inflammatory cytokines were determined using plasma samples, while liver tissue samples were used for antioxidant analysis and histopathological examination. Compared with the control group, plasma liver enzyme activities, along with bilirubin levels, were higher in the groups that received diclofenac alone or diclofenac+the highest dose of kolaviron, respectively. These groups had higher plasma concentrations of pro-inflammatory cytokines than did the control group. However, the administration of Livolin Forte and kolaviron (at the lower doses) ameliorated diclofenac-induced hepatic injury by improving antioxidant status, preventing an increase in inflammatory mediators, decreasing malondialdehyde, and attenuating the adverse effect of diclofenac on hepatic tissues. In addition, there was a significant difference in the histological scores between the groups that received either diclofenac alone or diclofenac followed by the highest dose of kolaviron when compared with the other three groups (Livolin Forte or lower doses of kolaviron). In conclusion, kolaviron appears to be as effective as Livolin in attenuating DCLF-induced hepatotoxicity in rats. However, high doses of kolaviron seem to cause damage to the liver.
RESUMEN
Right atrial myxomas are rare primary tumors of the heart. They may remain asymptomatic or eventually cause constitutional signs and symptoms. Less frequently, obstruction of the tricuspid valve occurs, resulting in exertional dyspnea, syncope, or sudden death. Neurological manifestation as initial presentation of atrial myxomas is rarely, if ever, associated with right atrial myxomas and may be secondary to cerebral infarction, cerebral hemorrhage and, more rarely subarachnoid hemorrhage. We review the case of a previously unknown, middle-aged Nigerian man who presented to hospital with severe headache and sudden loss of consciousness. A clinical diagnosis of hypertensive hemorrhagic cerebrovascular accident was made. The patient died suddenly a few hours after presentation. Post-mortem examination revealed a small intracerebral hemorrhage in the left superior temporal lobe as well as a large right atrial myxoma, a ventricular septal defect in the muscular septum, and right ventricular hypertrophy. The liver showed fatty change while the kidneys showed evidence of benign nephrosclerosis. Right atrial myxomas may, therefore, be remotely considered as a cause of intracranial hemorrhage, especially in the presence of predisposing cardiac anomalies such as a ventricular septal defect. Similarly, being a known cause of right heart failure, sudden death, and other constitutional derangements, it may contribute significantly to disease outcome. Hence, it should be given due consideration in the differential diagnosis of cerebrovascular accidents.
