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Clinical Endoscopy Sep 2023Achalasia is an esophageal motility disorder characterized by impaired lower esophageal sphincter relaxation and peristalsis of the esophageal body. With the increasing... (Review)
Review
Achalasia is an esophageal motility disorder characterized by impaired lower esophageal sphincter relaxation and peristalsis of the esophageal body. With the increasing prevalence of achalasia, interest in the role of endoscopy in its diagnosis, treatment, and monitoring is also growing. The major diagnostic modalities for achalasia include high-resolution manometry, esophagogastroduodenoscopy, and barium esophagography. Endoscopic assessment is important for early diagnosis to rule out diseases that mimic achalasia symptoms, such as pseudo-achalasia, esophageal cancer, esophageal webs, and eosinophilic esophagitis. The major endoscopic characteristics suggestive of achalasia include a widened esophageal lumen and food residue in the esophagus. Once diagnosed, achalasia can be treated either endoscopically or surgically. The preference for endoscopic treatment is increasing owing to its minimal invasiveness. Botulinum toxins, pneumatic balloon dilation, and peroral endoscopic myotomy (POEM) are important endoscopic treatments. Previous studies have demonstrated excellent treatment outcomes for POEM, with >95% improvement in dysphagia, making POEM the mainstay treatment option for achalasia. Several studies have reported an increased risk of esophageal cancer in patients with achalasia. However, routine endoscopic surveillance remains controversial owing to the lack of sufficient data. Further studies on surveillance methods and duration are warranted to establish concordant guidelines for the endoscopic surveillance of achalasia.
PubMed: 37430397
DOI: 10.5946/ce.2023.001 -
Neurourology and Urodynamics Jan 2024The etiology of ureteral dilation in primary nonrefluxing, nonobstructing megaureters is still not well understood. Impaired ureteral peristalsis has been theorized as...
PURPOSE
The etiology of ureteral dilation in primary nonrefluxing, nonobstructing megaureters is still not well understood. Impaired ureteral peristalsis has been theorized as one of the contributing factors. However, ureteral peristalsis and its "normal" function is not well defined. In this study, using mathematical modeling techniques, we aim to better understand how ureteral peristalsis works. This is the first model to consider clinically observed, back-and-forth, cyclic wall longitudinal motion during peristalsis. We hypothesize that dysfunctional ureteral peristalsis, caused by insufficient peristaltic amplitudes (e.g., circular muscle dysfunction) and/or lack of ureteral wall longitudinal motion (e.g., longitudinal muscle dysfunction), promotes peristaltic reflux (i.e., retrograde flow of urine during an episode of peristalsis) and may result in urinary stasis, urine accumulation, and consequent dilation.
METHODS
Based on lubrication theory in fluid mechanics, we developed a two-dimensional (planar) model of ureteral peristalsis. In doing so, we treated ureteral peristalsis as an infinite train of sinusoidal waves. We then analyzed antegrade and retrograde flows in the ureter under different bladder-kidney differential pressure and peristalsis conditions.
RESULTS
There is a minimum peristaltic amplitude required to prevent peristaltic reflux. Ureteral wall longitudinal motion decreases this minimum required amplitude, increasing the nonrefluxing range of peristaltic amplitudes. As an example, for a normal bladder-kidney differential pressure of 5 cmH O, ureteral wall longitudinal motion increases nonrefluxing range of peristaltic amplitude by 65%. Additionally, ureteral wall longitudinal motion decreases refluxing volumetric flow rates. For a similar normal bladder pressure example of 5 cmH O, refluxing volumetric flow rate decreases by a factor of 18. Finally, elevated bladder pressure, not only increases the required peristaltic amplitude for reflux prevention but it increases maximum refluxing volumetric flow rates. For the case without wall longitudinal motion, as bladder-kidney differential pressure increases from 5 to 40 cmH O, minimum required peristaltic amplitude to prevent reflux increases by 40% while the maximum refluxing volumetric flow rate increases by approximately 100%.
CONCLUSION
The results presented in this study show how abnormal ureteral peristalsis, caused by the absence of wall longitudinal motion and/or lack of sufficient peristaltic amplitudes, facilitates peristaltic reflux and retrograde flow. We theorize that this retrograde flow can lead to urinary stasis and urine accumulation in the ureters, resulting in ureteral dilation seen on imaging studies and elevated infection risk. Our results also show how chronically elevated bladder pressures are more susceptible to such refluxing conditions that could lead to ureteral dilation.
Topics: Humans; Peristalsis; Dilatation; Ureter; Ureteral Obstruction; Urinary Bladder
PubMed: 37961019
DOI: 10.1002/nau.25332 -
Gastroenterology Sep 2023Eosinophilic esophagitis (EoE) is characterized by eosinophilic inflammation, but also heterogeneous presentations involving fibrostenotic esophageal remodeling and...
BACKGROUND & AIMS
Eosinophilic esophagitis (EoE) is characterized by eosinophilic inflammation, but also heterogeneous presentations involving fibrostenotic esophageal remodeling and esophageal dysmotility. We aimed to define and evaluate phenotypes of EoE using functional lumen imaging probe (FLIP) panometry (ie, a PhysioMechanical classification of EoE).
METHODS
Patients with EoE who completed FLIP during endoscopy were included in a cross-sectional study. FLIP studies were analyzed for distensibility plateau and compliance of the esophageal body, maximum esophagogastric junction diameter, and contractile response pattern. These FLIP features were then applied to define PhysioMechanical classifications.
RESULTS
A total of 215 patients with EoE (mean [standard deviation] age 38 [12] years; 31% female) were included. Seven PhysioMechanical classifications were identified that differed by various clinical characteristics, including symptom duration (P < .001) and Endoscopic EoE Reference Scores (EREFS) (P < .001). In particular, patients with "nonreactive fibrostenosis" (n = 14), had greater symptom duration (median [interquartile range] 20 [10-30] years) and more frequently had EREFS grade 2 or 3 ring scores (14 of 14 patients) than patients with a "normal" PhysioMechanical classification (symptom duration: 3 [1-8] years; 4 of 50 [8%] had EREFS grade 2 or 3 rings). In addition, among patients off treatment at cross-sectional evaluation (n = 46), there was a difference between PhysioMechanical classifications in future proton pump inhibitor (PPI) response rates (ie, achieving peak mucosal eosinophil count <15 per high-powered field after PPI treatment); P = .009. PPI response ranged from 87% (13 of 15 patients) with "isolated esophagogastric junction outflow obstruction" to 11% (1 of 9 patients) with "spastic-reactive fibrostenosis."
CONCLUSIONS
Classifying PhysioMechanical esophageal function in EoE based on FLIP panometry features may facilitate defining disease severity and directing management in EoE.
Topics: Female; Male; Humans; Eosinophilic Esophagitis; Cross-Sectional Studies; Endoscopy, Gastrointestinal; Esophageal Motility Disorders
PubMed: 37263308
DOI: 10.1053/j.gastro.2023.05.031 -
Current Gastroenterology Reports Nov 2023Achalasia is one of the most commonly described primary esophageal motility disorders worldwide, but there is significant controversy regarding ideal management of... (Review)
Review
PURPOSE OF REVIEW
Achalasia is one of the most commonly described primary esophageal motility disorders worldwide, but there is significant controversy regarding ideal management of end-stage disease. This article reviews the definition of end-stage achalasia and summarizes past and present surgical treatment.
RECENT FINDINGS
Myotomy of the lower esophageal sphincter remains the mainstay of treatment of achalasia, even in advanced disease. Esophagectomy may have benefit as a primary treatment modality in end-stage achalasia with sigmoid esophagus, but international guidelines recommend consideration of laparoscopic or endoscopic approaches initially in most patients. Novel peroral esophageal plication techniques may provide alternative treatment options in patients with significant esophageal dilation that fail myotomy or esophagectomy.
SUMMARY
End-stage achalasia is characterized by progressive tortuosity and dilation of the esophagus as a failure of primary peristalsis. Up to 20% of patients with achalasia will progress to end-stage disease. In most cases, laparoscopic or endoscopic myotomy is recommended as initial approach to surgical management.
Topics: Humans; Esophageal Achalasia; Esophageal Sphincter, Lower; Laparoscopy; Esophagectomy; Myotomy; Treatment Outcome
PubMed: 37646894
DOI: 10.1007/s11894-023-00889-2 -
Seminars in Immunology Nov 2023The enteric nervous system is an autonomous neuronal circuit that regulates many processes far beyond the peristalsis in the gastro-intestinal tract. This circuit,... (Review)
Review
The enteric nervous system is an autonomous neuronal circuit that regulates many processes far beyond the peristalsis in the gastro-intestinal tract. This circuit, consisting of enteric neurons and enteric glial cells, can engage in many intercellular interactions shaping the homeostatic microenvironment in the gut. Perhaps the most well documented interactions taking place, are the intestinal neuro-immune interactions which are essential for the fine-tuning of oral tolerance. In the context of intestinal disease, compelling evidence demonstrates both protective and detrimental roles for this bidirectional neuro-immune signaling. This review discusses the different immune cell types that are recognized to engage in neuronal crosstalk during intestinal health and disease. Highlighting the molecular pathways involved in the neuro-immune interactions might inspire novel strategies to target intestinal disease.
Topics: Humans; Neuroimmunomodulation; Intestinal Diseases; Homeostasis; Enteric Nervous System
PubMed: 37632991
DOI: 10.1016/j.smim.2023.101819