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Dependence of Colonization of the Large Intestine by Candida on the Treatment of Crohn’s Disease
The aim of this study was to determine if there are quantitative differences in Candida fungi between pediatric patients with Crohn’s disease (before and after exclusive enteral nutrition (EEN), and the biologic therapy with anti-tumor necrosis factor alpha – (IFX)), and healthy controls. DNA was is...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Exeley Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7256697/ https://www.ncbi.nlm.nih.gov/pubmed/31050260 http://dx.doi.org/10.21307/pjm-2019-014 |
Sumario: | The aim of this study was to determine if there are quantitative differences in Candida fungi between pediatric patients with Crohn’s disease (before and after exclusive enteral nutrition (EEN), and the biologic therapy with anti-tumor necrosis factor alpha – (IFX)), and healthy controls. DNA was isolated from fecal samples and PCR was used to determine the number of fungal cells. Both therapeutic interventions resulted in a statistically significant decrease in Pediatric Crohn’s Disease Activity Index. The numbers of Candida decreased during both therapeutic intervention but the difference was statistically significant for the IFX intervention only (p = 0.045). Moreover, fungi population in both study groups declined during intervention when compared to the control group but the difference was significant before treatment only in the IFX group (p = 0.013). The total distribution of Candida with both IFX and EEN as well as in the control group differed significantly (p = 0.01) before treatment only. No correlation between the numbers of Candida and disease activity as well as the following biochemical parameters: serum iron concentration, protein or glucose level were found. It cannot be ruled out that, in combination with genetic and immunological disorders, fungi can contribute to the initiation of the disease process and perpetuation of active inflammation. |
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