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Objective The aim of this study was to assess incidence, risk factors, and outcomes of distal recurrent tracheoesophageal fistula (RTEF) after repair of esophageal atresia (EA). Methods Ethical consent was obtained. Data collection was done by review of hospital records of 286 patients (268 in-house and 18 referred) who underwent repair of type C or D EA from 1980 to 2021. Spitz class, long-gap (tracheoesophageal fistula at carina), fundoplication, leakage, and stricture were assessed as RTEF risk factors. Outcome measures were long-term closure of RTEF, retainment of native esophagus, and survival. Results RTEF occurred in 23 patients (19 in-house) with type C (n = 22) or type D (n = 1) EA with median 4.4 (interquartile range [IQR]: 1.7–13) months after repair. Five patients had late RTEF 3.5 to 16 years after repair. Nineteen (7.3%) in-house patients developed RTEF. Presenting symptoms, age at diagnosis, and presence of anastomotic stricture (AS) are listed. No statistically significant risk factors were found, risk ratio of 0.5 to 2.7 (IQR: 0.1–8.7), p-value of 0.25 to 0.75. Detached closure clip and esophageal foreign body contributed to RTEF in two patients. Sixteen patients underwent rethoracotomy for closure of RTEF, 5 (22%) with AS eventually underwent esophageal reconstruction after a period with cervical esophagostomy. Two patients with late-manifested RTEFs underwent closure with laser cauterization. In 22 patients, treatment of RTEF succeeded, whereas 1 (4%) premature patient died of instant re-RTEF. Conclusion RTEF had an incidence of 7% with diverse patterns of manifestation and predicting factors. Closure rate and patient survival were excellent, but RTEF with AS predicted loss of native esophagus.

Aim To assess the risk factors for anastomotic stricture (AS) in end-to-end anastomosis (EEA) in patients with esophageal atresia (EA). Methods With ethical consent, hospital records of 341 EA patients from 1980 to 2020 were reviewed. Patients with less than 3 months survival (n = 30) with Gross type E EA (n = 24) and with primary reconstruction (n = 21) were excluded. Outcome measures were revisional surgery for anastomotic stricture (RSAS) and number of dilatations required for anastomotic patency without RSAS. The factors that were tested for risk of RSAS or dilatations were distal tracheoesophageal fistula (TEF) at the carina in C-type EA (congenital TEF [CTEF]), type A/B EA, antireflux surgery (ARS), anastomotic leakage, recurrent TEF, and Spitz group and congenital heart disease. Main Results A total of 266 patients, Gross type A (n = 17), B (n = 3), C (n = 237), or D (n = 9) underwent EEA (early n = 240, delayed n = 26). Early anastomotic breakdown required secondary reconstruction in five patients. Of the remaining 261 patients, 17 (6.1%) had RSAS, whereas 244 patients with intact end to end required a median of five (interquartile range: 2–8) dilatations for anastomotic patency. Main risk factors for RSAS or (> 8) dilatations were CTEF, type A/B, ARS, and anastomotic leakage that increased the risk of RSAS or dilatations from 4.6- to 11-fold. Conclusion The risk of severe AS is associated with long-gap EA, significant gastroesophageal reflux, and anastomotic leakage.

Dioxins, e.g. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), use the aryl hydrocarbon receptor (AHR)/aryl hydrocarbon receptor nuclear translocator (ARNT) receptor complex to mediate their toxic actions. In addition to interaction with environmental pollutants, several transcription factors, steroid receptors, and growth factors are capable interacting with the AHR/ARNT complex, which suggests a constitutive role for the receptor complex.The testis has been reported to be among the most sensitive organs to TCDD exposure. Our experiments revealed a complex distribution of AHR and ARNT mRNAs and proteins in rat and human testis. AHR and ARNT immunoreactivities could be detected in the nuclei of interstitial and tubular cells. The incubation of seminiferous tubules in a serum-free culture medium resulted in up-regulation of AHR mRNA, which could be depressed by adding FSH to the culture medium. Furthermore, the incubation of tubular segments with a solution of 1 or 100 nm TCDD resulted in a 2- to 3-fold increase in apoptotic cells. Thus, up-regulation of AHR in cultured tubular segments and consecutive depression by FSH suggest a role for AHR in controlled cell death during spermatogenesis. We suggest that AHR and ARNT mediate effects by direct action on testicular cells in the rat and human testis.