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BACKGROUND - Esophageal self-expandable stents (SESs) effectively treat strictures and leaks but may be complicated by a stent-associated esophagorespiratory fistula (SERF). Little is known about SERFs.
OBJECTIVE - To determine the incidence, morbidity, mortality, and risk factors for SERF.
DESIGN - Retrospective case-control study.
SETTING - Single referral center.
PATIENTS - All adults undergoing esophageal SES placement during a 10-year period.
INTERVENTION - Stent placement.
MAIN OUTCOME MEASUREMENTS - Occurrence of SERF, morbidity, and mortality.
RESULTS - A total of 16 of 397 (4.0%) patients developed SERF at a median of 5 months after stent placement (range 0.4-53 months) including 6 of 94 (6%), 10 of 71 (14%), and 0 of 232 (0%) of those with lesions in the proximal, middle, and distal esophagus, respectively (overall P < .001). SERF occurred in 10% of those with proximal and mid-esophageal lesions, including 14% with benign strictures, 9% with malignant strictures, and none with other indications for SES placement (P = .27). The risk was highest (18%) in patients with benign anastomotic strictures. Risk factors for development of SERF included a higher Charlson comorbidity index score (odds ratio [OR] 1.47 for every 1-point increase; P = .04) and history of radiation therapy (OR 9.41; P = .03). Morbidity associated with SERF included need for lifelong feeding tubes in 11 of 22 (50%) and/or tracheostomy or mechanical ventilation in 5 of 22 (23%). Median survival after diagnosis was 4.5 months (range 0.35-67), and 7 patients survived less than 30 days.
LIMITATIONS - Retrospective design, limited statistical power.
CONCLUSION - SERF is a morbid complication of SES placement for strictures of the proximal and mid-esophagus. The dominant risk factors for development of SERF are prior radiation therapy and comorbidity score.
Copyright © 2013 American Society for Gastrointestinal Endoscopy. Published by Mosby, Inc. All rights reserved.
PURPOSE - The NOG protein is a secretory antagonist of bone morphogenetic proteins (BMPs). Nog-/- mouse embryos demonstrate proximal esophageal atresia (EA) and distal tracheoesophageal fistula (TEF) compatible with the most common configuration of EA/TEF observed in humans. Four microdeletions that span the NOG locus at 17q22 have been described in human patients having EA/TEF. We investigated the incidence of point mutations in the coding region of the NOG gene in human EA/TEF.
METHODS - DNA was collected from 50 patients previously treated for EA/TEF. PCR was used to amplify the coding region of NOG. To detect single nucleotide polymorphisms (SNPs), amplicons were subjected to temperature gradient capillary electrophoresis (TGCE). Candidate SNPs were directly sequenced.
RESULTS - TGCE analysis revealed a SNP in the coding region of NOG in 1 of 50 patients (2%). DNA sequencing revealed a synonymous SNP at position 468 (C-T) of the NOG coding region.
CONCLUSION - SNPs in the coding region of the NOG gene are identified infrequently in human cases of EA/TEF. Further investigation of SNPs in the promoter region of NOG is warranted, as is the effect of synonymous SNPs on NOG mRNA stability.