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Acute HME syndrome

Medical condition

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Mechanism

The acute severe C. occidentalis poisoning in children affects multiple systems. Functional and biochemical evidences to show toxic effect on the brain, liver and striated muscles. Pathologically there is acute onset massive zonal necrosis of liver and histopathology evidence of acute muscle fibre degeneration. The degenerative changes in the brain are mild, but brain oedema is severe and is believed to be the immediate cause of death.

A team of researchers from IITR, Lucknow, conducted detailed animal and toxicological studies to conclusively demonstrate that the toxin involved in these outbreaks was present in the pods (seeds) of the Cassia occidentalis weed [8-12]. GC-MS analysis of various fractions of methanol extracts from Cassia occidentalis seeds revealed the presence of five anthraquinones (AQs): physcion, emodin, rhein, aloe-emodin, and chrysophanol. Interestingly, these AQs were detected in serum and urine samples from the affected cases and Cassia occidentalis-exposed rats. Cytotoxicity testing of these AQs in rat primary hepatocytes and HepG2 cells showed that rhein is the most toxic compound, followed by emodin, aloe-emodin, physcion, and chrysophanol. It was also demonstrated that 100 nM cyclosporine A was the most effective among various protective agents at preventing apoptosis in hepatocytes [13].

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