Experimental murine schistosomiasis: reduced hepatic morbidity after pre- and/or post-infection treatment with ibuprofen or diclofenac sodium.

Arachidonic-acid metabolites appear to participate in skin penetration by and transformation of schistosome cercariae and in the pathogenesis of schistosomiasis. With this in mind, mice were treated with one of two cyclooxygenase inhibitors before and/or after infection with Schistosoma mansoni. The effects of the treatment on liver morbidity and the parasitic infection were then evaluated, using infected, untreated and uninfected, treated mice as controls. Treatment with ibuprofen (20 mg/kg.day) or diclofenac sodium (2.5 mg/kg.day) for 7 days before infection led to significantly lower liver weights, worm loads and hepatic hydroxyproline contents than in the untreated mice. If treatment with either drug was continued after infection, for 28 days, there was an additional significant decrease in hepatic gamma-glutamyl transpeptidase activity. All these parameters except liver weight were similarly affected when treatment with either drug was begun on the day of infection and continued for 28 days. There was no significant change in liver weight or worm load when treatment was delayed until day 28 post-infection but faecal egg counts were reduced in the treated groups. In additional experiments, using a smaller dose of diclofenac sodium (1.25 mg/kg.day), all the measured parameters of infection were significantly decreased when the treatment was initiated 7 days before infection and continued until day 28 post-infection. The results indicate that the treatment of S. mansoni-infected mice with ibuprofen or diclofenac sodium was effective in reducing the severity of infection and in attenuating hepatic fibrosis, particularly when the treatment was started early in relation to the time of infection.