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Involvement of the gastrointestinal (GI) tract is an infrequent extrathoracic presentation of sarcoidosis. We reviewed 305 cases of GI involvement reported in 238 patients, in whom GI sarcoidosis was the first sign of the disease in half the cases. The disease does not affect the GI tract uniformly, with a clear oral-anal gradient (80% of reported cases involved the esophagus, stomach, and duodenum). Clinicopathological mechanisms of damage may include diffuse mucosal infiltration, endoluminal exophytic lesions, involvement of the myenteric plexus, and extrinsic compressions. Ten percent of patients presented with asymptomatic or subclinical disease found on endoscopy. The diagnosis is relevant clinically because 22% of cases reviewed presented as life threatening. In addition, initial clinical/endoscopic findings may be highly suggestive of GI cancer. The therapeutic approach is heterogeneous and included wait-and-see or symptomatic approaches, glucocorticoid/immunosuppressive therapy, and surgery. Sarcoidosis of the gut is a heterogeneous, potentially life-threatening condition that requires a multidisciplinary approach and early clinical suspicion to institute personalized therapeutic management and follow-up.

These recommendations provide an evidence-based approach to the role of esophageal stents in the management of benign and malignant diseases. These guidelines have been developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee and approved by the Board of Trustees. The following guidelines are based on a critical review of the available scientific literature on the topic identified in Medline and PubMed (January 1992-December 2008) using search terms that included stents, self-expandable metal stents, self-expandable plastic stents, esophageal cancer, esophageal adenocarcinoma, esophageal squamous cell carcinoma, esophageal stricture, perforations, anastomotic leaks, tracheoesophageal fistula, and achalasia. These guidelines are intended for use by health-care providers and apply to adult, but not pediatric, patients. As with other practice guidelines, these guidelines are not intended to replace clinical judgment but rather to provide general guidelines applicable to the majority of patients. Clinicians need to integrate recommendations with their own clinical judgment, and with individual patient circumstances, values, and preferences. They are intended to be flexible, in contrast to standards of care, which are inflexible policies designed to be followed in every case. Specific recommendations are based on relevant published information. The quality of evidence and strength of recommendations have been assessed using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system, which is a system that has been adopted by multiple national and international societies. The GRADE system is based on a sequential assessment of quality of evidence, followed by assessment of the balance between benefits vs. downsides (harms, burden, and costs) and subsequent judgment regarding the strength of recommendation.

Proton pump inhibitor-responsive esophageal eosinophilia (PPI-REE) is diagnosed in at least one-third of patients with suspected eosinophilic esophagitis (EoE). We aimed to evaluate the durability and factors influencing long-term efficacy of PPI therapy. Retrospective multicenter cohort study of patients with PPI-REE who had at least 12 months of follow-up. PPI therapy was tapered to the lowest dose, which maintained clinical remission. Primary outcomes were the proportion of patients with loss of histological response (<15 eos/HPF) and predictors of loss of response. CYP2C19 polymorphisms were determined from blood samples in a subset of patients. Seventy-five PPI-REE patients were included (mean follow-up 26 months (12-85)), of whom fifty-five (73%) had sustained histological remission on low-dose PPI therapy. Loss of response was significantly higher in those patients with a CYP2C19 rapid metabolizer genotype (36% vs. 6%, P = 0.01) and with rhinoconjunctivitis (40% vs. 13%, P = 0.007). On the multivariate analysis, a CYP2C19 rapid metabolizer genotype (odds ratio (OR) 12.5; 95% confidence interval (CI): 1.3-115.9) and rhinoconjunctivitis (OR 8.6; 95% CI: 1.5-48.7) were independent predictors of loss of response. Among relapsing patients, eosinophilia was limited to the distal esophagus in 14/20 (70%). Nine of ten relapsers, with distal eosinophilia, all showing a CYP2C19 rapid metabolizer genotype, regained histological remission after PPI dose intensification. Most PPI-REE patients remain in long-term remission on low-dose PPI therapy. CYP2C19 rapid metabolizer genotypes and rhinoconjunctivitis were independent predictors of loss of response to PPI, but patients frequently responded to PPI dose escalation.

Background Primary esophageal tuberculosis is an uncommon manifestation of Mycobacterium tuberculosis infection in Asian adults, often presenting with nonspecific symptoms that can complicate diagnosis. This report details a case of primary esophageal tuberculosis in middle age female, emphasizing the diagnostic value of computed tomography (CT) imaging. Case presentation The patient, a 46-year-old female from Sichuan Province, China, experienced recurrent choking and mild retrosternal pain postprandially. She exhibited a weight loss of approximately 1 kg over a week, without additional symptoms such as dysphagia or fever. Esophagoscopy disclosed a small ulcer, and CT imaging revealed esophageal wall thickening with mucosal ulceration. A left thoracic lower and middle esophagectomy was conducted, with postoperative pathology confirming granulomatous inflammation, indicative of tuberculosis. Conclusions This case highlights the pivotal role of CT imaging in diagnosing primary esophageal tuberculosis. The imaging modality’s ability to delineate subtle mucosal ulcerations and wall thickening provides a crucial diagnostic advantage, facilitating accurate and timely diagnosis of this rare condition.

Background Esophageal ulcers can arise not only from malignant lesions but also from benign diseases, such as tuberculosis. These ulcers may mimic the radiological features of esophageal malignancy or tuberculosis on PET/CT, leading to diagnostic challenges. Case presentation A 59-year-old woman was admitted to our hospital with a month-long history of progressive painful swallowing, fatigue, and loss of appetite. Whole-body 18 F-FDG PET/CT revealed a lesion in the mid-esophagus and swollen mediastinal lymph nodes with high FDG uptake, showing a maximum standardized uptake value (SUVmax) of 17.10 for the lymph nodes and 8.08 for the esophageal lesion. Esophageal cancer was initially suspected based on PET/CT findings. However, pathological examination of the esophageal lesion obtained via esophagoscopy showed only inflammation and granulation tissue, with no malignancy. A biopsy of the lymph nodes obtained through endoscopic ultrasonography revealed caseous necrosis but no atypical cells, and microbiological tests were positive for Mycobacterium tuberculosis. A final diagnosis of esophageal tuberculosis was made. Conclusions Esophageal lesions can result from both malignant and benign conditions, including tuberculosis, and may mimic the radiological features of esophageal malignancy on PET/CT or other imaging studies. When esophageal lesions resemble malignancy, pseudotumoral esophagus and esophageal tuberculosis should be considered as differential diagnoses. Endoscopy, particularly endoscopic ultrasonography, is strongly recommended to accurately distinguish between benign and malignant esophageal lesions, helping to avoid unnecessary invasive treatments and reduce potential physical and psychological harm to patients.

Background: With the recent development of endoscopic submucosal dissection (ESD), large oesophageal cancers can be removed with a single procedure, with few limits on the resectable range. However, after aggressive ESD, a major complication that arises is postoperative inflammation and stenosis that can considerably affect the patient’s quality of life. Aims: To examine a novel treatment combining ESD and the endoscopic transplantation of tissue-engineered cell sheets created using autologous oral mucosal epithelial cells, in a clinically relevant large animal model. Methods: Oral mucosal epithelial cells, harvested from beagle dogs, were cultured under normal conditions at 37°C, on temperature-responsive dishes. After ESD (5 cm in length, 180° in range), cell sheets were harvested by a simple reduction in temperature to 20°C, and transplanted by endoscopy. Results: The transplanted cell sheets were able to adhere to and survive on the underlying muscle layers in the ulcer sites, providing an intact, stratified epithelium. Four weeks after surgery, complete wound healing, with no observable stenosis, was seen in the animals receiving autologous cell sheet transplantation. By contrast, noticeable fibrin mesh and host inflammation, consistent with the intermediate stages of wound healing, were observed in the control animals that received only ESD. Conclusions: These findings in a clinically relevant canine model show the effectiveness of a novel combined endoscopic approach for the potential treatment of oesophageal cancers that can effectively enhance wound healing and possibly prevent postoperative oesophageal stenosis.

Recently, incidence of Mycobacterium abscessus (Mab) pulmonary disease (Mab-PD) is increasing worldwide. We aimed to identify factors associated with severity of Mycobacterium abscessus (Mab) pulmonary disease (Mab-PD). All patients diagnosed as Mab-PD based on the official ATS/IDSA statement between 2017 January 1 and 2021 July 31 were included (n = 13). We reviewed medical records, bacteriological and laboratory data of the patients. Severity of lung lesions and esophageal diameters in chest CT were quantitatively evaluated. Gaffky score in the sputum was used as airway mycobacterial burden. We explored the factors associated with high CT score and high Gaffky score. Maximum diameter of esophagus (MDE) in severe disease (CT score≧10) was greater than that in milder disease (CT score<10) (18.0±7.9mm, 9.3±3.1mm, respectively, p = 0.01), and MDE was well correlated with CT score (R = 0.69, p = 0.007). MDE in high mycobacterial burden group (Gaffky score ≧5) tended to be greater than that in low mycobacterial burden group (Gaffky score <5) (16.1±6.8mm, 10.1±5.5mm, respectively, p = 0.12), and MDE was well correlated with Gaffky score (R = 0.68, p = 0.009). Lung lesions were bilateral and predominant in middle or lower lobes. Esophageal dilatation was correlated with severity of Mab-PD and airway mycobacterial burden. Gastroesophageal reflux might be associated with Mab disease progression.

Esophageal epidermoid metaplasia is a rare condition that involves the proximal-to-middle third of the esophagus. It is sharply demarcated and defined histologically by epithelial hyperplasia, a prominent granular cell layer, and superficial hyperorthokeratosis. In addition, preliminary studies have suggested an association between esophageal epidermoid metaplasia and esophageal squamous neoplasia (squamous dysplasia and esophageal squamous cell carcinoma). To further characterize esophageal epidermoid metaplasia and better define its relationship to squamous neoplasia of the esophagus, we performed targeted next-generation sequencing on uninvolved esophageal squamous mucosa and matching esophageal epidermoid metaplasia specimens from 18 patients. Further, we evaluated both synchronous and metachronous high-grade squamous dysplasia/esophageal squamous cell carcinoma by next-generation sequencing from 5 of the 18 (28%) patients, and compared these findings to corresponding esophageal epidermoid metaplasia specimens. Targeted next-generation sequencing revealed 12 of 18 (67%) esophageal epidermoid metaplasia specimens’ harbored alterations in genes often associated with esophageal squamous cell carcinoma. The most frequently mutated genes consisted of TP53 ( n =10), PIK3CA ( n =2), EGFR ( n =2), MYCN ( n =1), HRAS ( n =1), and the TERT promoter ( n =1). Sequencing of synchronous and metachronous high-grade squamous dysplasia/esophageal squamous cell carcinoma identified shared genetic alterations with corresponding esophageal epidermoid metaplasia specimens that suggests a clonal relationship between these entities. In addition, the presence of a TP53 mutation in esophageal epidermoid metaplasia specimens correlated with concurrent or progression to high-grade squamous dysplasia/esophageal squamous cell carcinoma. No genetic alterations were detected in uninvolved esophageal squamous mucosa. On the basis of these findings, we conclude esophageal epidermoid metaplasia is a precursor to in situ and invasive esophageal squamous neoplasia. Further, the detection of TP53 mutations in esophageal epidermoid metaplasia specimens may serve as an early detection biomarker for high-grade squamous dysplasia/esophageal squamous cell carcinoma.

Esophageal Crohn's disease (CD) is challenging and often a disabling phenotype of disease. We aimed to report the clinical, endoscopic, histologic features, and treatment outcomes of esophageal patients with CD.MethodsEsophageal patients with CD evaluated at the Mayo Clinic in Rochester, MN, between January, 1998, and December, 2012, were identified.ResultsTwenty-four cases of esophageal CD were identified. The median age of diagnosis was 23 years (range, 12–60). Twenty-one patients (88%) had extraesophageal CD and 8 patients (33%) had oral ulcers at the time of esophageal CD symptom onset. The majority of patients had esophageal-specific symptoms. Mid (29%) or distal (29%) esophagus was the most common site of involvement. Inflammatory esophageal CD (75%) was marked by superficial ulcerations (58%), erythema and/or erosions (50%), deep ulcerations (13%), and pseudopolyps (4%) on endoscopy. Four patients (17%) were found to have esophageal strictures and 2 patients (8%) had fistulizing disease. Chronic inflammation (83%) was seen on biopsy in the majority of cases with 5 patients having associated granulomas. In our series, inflammatory esophageal CD responded to prednisone, topical budesonide, or biologics. Stricturing esophageal CD was successfully treated with a combination of biologic therapy, immunomodulators, and serial dilations with/without steroid injections. Aggressive medical therapy with biologics and endoscopic therapy was used for fistulizing esophageal CD, however, was not universally effective.ConclusionsEsophageal CD should be considered in all patients with CD with upper gastrointestinal symptoms. Early recognition, diagnosis, and aggressive medical and/or endoscopic treatment are needed for successful outcomes.