PedAM
Pediatric Disease Annotations & Medicines
| Disease | enterovirus infections |
| Phenotype | C0011847|diabetes |
| Sentences | 8 |
| PubMedID- 22315304 | Type 1 diabetes is associated with enterovirus infection in gut mucosa. |
| PubMedID- 22385232 | The hypothesis that under some circumstances enteroviral infections can lead to type 1 diabetes (t1d) was proposed several decades ago, based initially on evidence from animal studies and sero-epidemiology. |
| PubMedID- 20858685 | Furthermore, while biopsy studies and previous cross-sectional or retrospective studies of enterovirus infections in patients with type 1 diabetes cannot exclude the possibility that the disease influenced the risk of infection, our longitudinal design allowed us to draw stronger inference in this regard. |
| PubMedID- 22701454 | For example, prior ebv infections are postulated to increase the predisposition to systemic lupus erythematosus (sle), ra, ms, sjogren’s syndrome, and polyarteritis nodosa (barzilai et al., 2007), while autoimmune diabetes susceptibility is associated with enterovirus infections (richardson et al., 2009). |
| PubMedID- 22355028 | A case of insulin-dependent diabetes associated with enteroviral infections. |
| PubMedID- 25335440 | Aims/hypothesis: this study compared the incidence rate of type 1 diabetes in children diagnosed with enterovirus (ev) infections with that in age- and sex-matched children without ev infection in a population-based cohort. |
| PubMedID- 21292721 | We calculated unadjusted odds ratios with 95% confidence intervals and p values for enterovirus identification in patients with pre-diabetes versus no diabetes and patients with diabetes versus no diabetes from the published figures using the mantel-haenszel method. |
| PubMedID- 23510983 | The observations reported here assume particular significance when considered in the context of immunohistochemical evidence that human islet cells can sustain an enteroviral infection in patients with diabetes13,14 and the finding that enteroviral infection leads to upregulation of islet il-6 generation and a reduction in il-13.12 on this basis, it seems probable that in either type 1 or type 2 diabetes, there may be an altered inflammatory milieu within the islets generated both by influent immune cells and by changing patterns of cytokine secretion by the endocrine cells themselves, which favors β-cell loss. |
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