The effect of single dietary fibre (DF) on lowering uric acid (UA) level has been reported in the literature. However, the potential protective mechanism of DF against potassium oxybate-induced hyperuricaemia (HUA), as modelled by prophylactic administration, remains unclear. The data demonstrate that DF significantly decreased serum and cerebral tissue UA concentrations, inhibited xanthine oxidase expression and activity in the liver and reduced levels of creatinine and urea nitrogen in the serum. Additionally, it mitigated the deposition of amyloid-β in cerebral tissue. Correlation analysis showed that DF modulated the Toll-like receptor 4/NF-κB signalling pathway, attenuating oxidative stress and inflammatory responses in HUA mice. Additionally, DF helps to maintain the composition of the gut microbiota, reducing harmful Desulfovibrio and enriching beneficial Akkermansia and Ruminococcus populations. The results of the faecal metabolomics analysis indicate that DF facilitates the regulation of metabolic pathways involved in oxidative stress and inflammation. These pathways include pyrimidine metabolism, tryptophan metabolism, nucleotide metabolism and vitamin B6 metabolism. Additionally, the study found that DF has a preventive effect on anxiety-like behaviour induced by HUA. In summary, DF shows promise in mitigating HUA and cognitive deficits, primarily by modulating gut microbiota and metabolites.

We evaluated the effect of chemotherapy with a sequential combined treatment of a low dose of benznidazole and allopurinol, in different schedules of administration, in experimental models of acute and chronic Trypanosoma cruzi infection. Mice were infected with Nicaragua T. cruzi isolate, a virulent parasite from an endemic area of Nicaragua, genotyped as TcI (Grosso et al. 2010). We assessed survival rate, IgG levels, histopathological studies and quantified parasitaemia. A 15% survival rate was recorded in untreated mice during the acute phase of T. cruzi infection. Allopurinol administered immediately after benznidazole treatment was able to reduce parasitaemia and attenuate tissue damage by reducing inflammation. Trypanosoma cruzi-specific antibodies also decreased in 40–50% of the treated mice. The addition of allopurinol during the chronic phase showed the highest beneficial effect, not only by reducing parasitaemia but also by lowering the degree of inflammation and fibrosis.

The diagnosis of visceral leishmaniasis must be based upon a demonstration of the parasite in tissues of the patient. The best diagnostic test is a splenic aspirate, which is safe, highly sensitive and specific if the technique described in this paper is used and both smears and cultures of the aspirate are performed. Peripheral blood and nasal exudate have parasites in smears and/or cultures in 75 and 40% of Kenyan visceral leishmaniasis patients, respectively. Sodium stibogluconate (Pentostam) is the preferred treatment for visceral leishmaniasis. Recent Clinical Research Centre trials of different schedules of treatment with sodium stibogluconate are discussed. Currently, we recommend sodium stibogluconate, 20 mg/kg once daily for 30 days, for initial treatment. For patients who have not responded to initial treatment with sodium stibogluconate or have relapsed after initially responding to this treatment, we recommend sodium stibogluconate, 20 mg/kg once daily for 60 days. Further studies are now underway comparing the combination of allopurinol plus sodium stibogluconate versus sodium stibogluconate alone for unresponsive or relapsed patients.