RESUMEN
Background: Diagnostic delay of pyriform sinus fistula (PSF) continues to challenge clinicians, and the preferred imaging modality is yet to be verified. The purpose of this study was to investigate the preferred imaging modality for PSF and the possible risk factors for a longer diagnostic delay. Methods: Medical records of patients with a surgically confirmed PSF from 2014 to 2018 were retrospectively evaluated. A comparison of the first esophagography timing with a true-positive (TP) result and that with a false-negative (FN) result was made. Data of computed tomography (CT) performed immediately after esophagography were also analyzed. In addition, the factors related to diagnostic delay were analyzed using multivariate regression models. Results: A total of 147 patients ranging in age from 0 to 16 years (median: 5.2 years) were included. The mean time since the symptom onset of the first esophagography with TP result was significantly longer than that of the examination with FN result (95.18 ± 79.12 vs. 52.59 ± 42.40 days, P = 0.032). When the time since the symptom onset was less than 12 weeks, the false-negative rate (FNR) of the first esophagography was declining dramatically with a longer time interval. Among 18 cases with an FN result of the first esophagography, the fistulous tract was finally identified in seven cases using an immediate CT. The mean of diagnostic delay was 12.28 months. Besides, rural residency was an independent risk factor for a longer diagnostic delay. Conclusion: Joint examination of esophagography and an immediate CT is the preferred imaging modality for the diagnosis of PSF in children. It is inadvisable to perform the first esophagography when the time since the symptom onset is less than 12 weeks. Besides, the rural residency is an independent risk factor for a longer diagnostic delay.
RESUMEN
Necrotizing enterocolitis (NEC) is a leading cause of mortality in preterm newborns. Intestinal barrier dysfunction is one key event in NEC pathogenesis. Human ß-defensin-3 (hBD3), one member of cationic host defence peptides, was reported to reduce the development of necrotizing enterocolitis in a neonatal rat model. And autophagy was induced in the intestine of human and animals with NEC. We hypothesized that regulation of autophagy might play a critical role in hBD3-mediated protection against NEC injury. Autophagy activity was evaluated both in intestinal epithelial cells and in NEC models. Newborn Sprague-Dawley rats were divided randomly into four groups: Control + NS, Control + rapamycin, NEC + NS, and NEC + hBD3. Body weight, histological score, survival time, enterocyte migration and mucosal barrier were recorded. Our results showed that hBD3 pretreatment could effectively inhibit autophagy activity in cultured IEC-6 and Caco2 enterocytes, and CXCR4 might be involved in hBD3-mediated autophagy suppression. Moreover, hBD3-induced inhibition of autophagy significantly promoted the intestinal epithelial cell migration by wound healing assay and transwell migration assay. In the rat model of NEC, hBD3 could noticeably reduce the expression of autophagy-activated proteins, down-regulate the expression of inflammatory mediators, and promote the mucosal integrity. Our data suggest an additional role of hBD3-mediated protection against intestinal mucosal injury: inhibition of over-activated autophagy in enterocytes.