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Tracheal penetration and tracheoesophageal fistula caused by an esophageal self-expanding metallic stent.

ABSTRACT: Tracheal penetration of esophageal self-expanding metallic stents (SEMS) with/without tracheoesophageal fistula (TEF) formation is a rare occurrence. We report the case of a 66-year-old female patient with advanced esophageal squamous cell carcinoma who had undergone palliative esophageal stenting on three occasions for recurrent esophageal stent obstruction. On evaluation of symptoms of breathing difficulty and aspiration following third esophageal stent placement, tracheal erosion and TEF formation due to the tracheal penetration by esophageal stent were diagnosed. The patient was successfully managed by covered tracheal SEMS placement under flexible bronchoscopy.

SUBMITTER: Madan K

PROVIDER: S-EPMC4167813 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Tracheal penetration and tracheoesophageal fistula caused by an esophageal self-expanding metallic stent.

Madan Karan K Venuthurimilli Arun A Ahuja Vineet V Hadda Vijay V Mohan Anant A Guleria Randeep R

Case reports in pulmonology 20140903

Tracheal penetration of esophageal self-expanding metallic stents (SEMS) with/without tracheoesophageal fistula (TEF) formation is a rare occurrence. We report the case of a 66-year-old female patient with advanced esophageal squamous cell carcinoma who had undergone palliative esophageal stenting on three occasions for recurrent esophageal stent obstruction. On evaluation of symptoms of breathing difficulty and aspiration following third esophageal stent placement, tracheal erosion and TEF form ...[more]

PMID: 25276461

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Tracheoesophageal fistula characterisation

Project description:Esophageal atresia and tracheoesophageal fistula (EA/TEF) are relatively frequently occurring foregut malformations with a largely unknown etiology. EA/TEF is thought to have a strong genetic component and several genes have been proven to be involved in syndromic EA/TEF. However, it is not clear which biological processes or gene networks are disturbed. To gain more insight in the origin of the TEF, we aimed to examine and describe TEF composition using a combination of whole-genome transcription profiling and (immuno-) histochemical stainings. We hypothesized that such characterization of human TEFs provides insight in the molecular and mechanistic etiology of EA/TEF. Data analysis was carried out using BRB-array tools version 4.6.0 (October 2018) in combination with R version 3.5.1 (July 2018). For each probe set, the geometric mean of the hybridization intensities of all samples was calculated. The level of expression of each probe set was determined relative to this geometric mean and logarithmically transformed (on a base 2 scale) to ascribe equal weight to gene-expression levels with similar relative distances to the geometric mean.

2020-10-30 | GSE148247 | GEO

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Project description:Esophageal atresia and tracheoesophageal fistula (EA/TEF) are major congenital malformations affecting 1:3500 live births. Current research efforts are focused on understanding the etiology of these defects. We describe well-known animal models, human syndromes, and associations involving EA/TEF, indicating its etiologically heterogeneous nature. Recent advances in genotyping technology and in knowledge of human genetic variation will improve clinical counseling on etiologic factors. This review provides a clinical summary of environmental and genetic factors involved in EA/TEF.

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Malignant gastrotracheal fistula treated by self-expandable metallic stent: First case report from India.

Project description: Not available

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Retrospective analysis of pneumothorax after repair of esophageal atresia/tracheoesophageal fistula.

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Project description:The various malformations of the aerodigestive tract collectively known as esophageal atresia/tracheoesophageal fistula (EA/TEF) constitute a rare group of birth defects of largely unknown etiology. Previous studies have identified a small number of rare genetic variants causing syndromes associated with EA/TEF. We performed a pilot exome sequencing study of 45 unrelated simplex trios (probands and parents) with EA/TEF. Thirteen had isolated and 32 had nonisolated EA/TEF; none had a family history of EA/TEF. We identified de novo variants in protein-coding regions, including 19 missense variants predicted to be deleterious (D-mis) and 3 likely gene-disrupting (LGD) variants. Consistent with previous studies of structural birth defects, there is a trend of increased burden of de novo D-mis in cases (1.57-fold increase over the background mutation rate), and the burden is greater in constrained genes (2.55-fold, p = 0.003). There is a frameshift de novo variant in EFTUD2, a known EA/TEF risk gene involved in mRNA splicing. Strikingly, 15 out of 19 de novo D-mis variants are located in genes that are putative target genes of EFTUD2 or SOX2 (another known EA/TEF gene), much greater than expected by chance (3.34-fold, p value = 7.20e-5). We estimated that 33% of patients can be attributed to de novo deleterious variants in known and novel genes. We identified APC2, AMER3, PCDH1, GTF3C1, POLR2B, RAB3GAP2, and ITSN1 as plausible candidate genes in the etiology of EA/TEF. We conclude that further genomic analysis to identify de novo variants will likely identify previously undescribed genetic causes of EA/TEF.

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Tracheoesophageal fistula characterisation

Project description:Tracheoesophageal fistula characterisation

| PRJNA623592 | ENA

Risk Factors for Recurrent Tracheoesophageal Fistula After Gross Type C Esophageal Atresia Repair.

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Use of Mitomycin C for Refractory Esophageal Stricture following Tracheoesophageal Fistula Repair.

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