(Press-News.org) gastroesophageal reflux disease (GERD) is a prevalent gastrointestinal disorder, with up to 20% of patients developing complications like Erosive esophagitis (EE), Barrett’s esophagus, and esophageal adenocarcinoma. EE, characterized by mucosal necrosis and erosions, presents with symptoms ranging from heartburn to dysphagia and gastrointestinal bleeding. Despite effective pharmacologic treatments, 15% of patients exhibit refractory disease. This review synthesizes current evidence to guide clinicians in diagnosing and managing EE, balancing pharmacologic and procedural interventions.
Pathogenesis
EE results from gastric acid, pepsin, and bile reflux damaging the esophageal mucosa. Key contributing factors include:
Mechanical Dysfunction: Defective lower esophageal sphincter (LES), hiatal hernia, and impaired esophageal motility.
Nocturnal Reflux: Histamine-driven acid secretion exacerbates nighttime symptoms.
Medications/Diseases: Nitrates, anticholinergics, obesity, and neurological disorders (e.g., Parkinson’s) increase EE risk.
Endoscopic Findings: Linear erosions in the distal esophagus with histologic evidence of inflammation and necrosis.
Refractory EE may stem from poor medication adherence, NSAID use, or reduced pain perception in elderly patients.
Clinical Presentation
Symptoms include:
Typical: Heartburn, regurgitation, globus sensation.
Alarm Features: Dysphagia, odynophagia, weight loss, anemia (indicating complications like strictures or malignancy).
Early recognition of alarm symptoms is critical for timely intervention.
Evaluation
Diagnostic tools:
Esophagogastroduodenoscopy (EGD): Gold standard for visualizing erosions and grading severity (Los Angeles classification).
Ambulatory pH Monitoring: Bravo™ wireless system or impedance-pH testing for refractory cases.
High-Resolution Manometry: Assesses motility disorders pre-surgery.
Treatment
Pharmacologic Therapy
Goals: Symptom relief, mucosal healing, and prevention of recurrence.
Lifestyle Modifications: Adjunct to medications (e.g., weight loss, avoiding trigger foods).
Acid-Suppressing Agents:
PPIs: First-line; require proper dosing (30 mins pre-meal). Double-dose PPIs may be needed for refractory EE.
P-CABs (e.g., Vonoprazan): Rapid, potent acid suppression without tachyphylaxis.
H2RAs: Secondary option; limited by tolerance development.
Maintenance Therapy: Long-term PPIs/P-CABs for severe EE (LA grades C/D), with periodic EGD to monitor healing.
Procedural Therapy
For refractory cases:
Laparoscopic Fundoplication: Effective for patients with documented acid reflux and partial PPI response.
Endoscopic Therapies:
Stretta: Controversial efficacy.
Transoral Incisionless Fundoplication (TIF): Comparable to surgery for small hiatal hernias.
Magnetic Augmentation (LINX): Novel LES-strengthening device.
Special Considerations
Pregnancy: H2RAs and PPIs (except omeprazole) are safe; avoid P-CABs.
Long-Term Risks: PPIs/P-CABs may affect nutrient absorption (B12, iron) and increase infection risk (e.g., C. diffici).
Optimal Management Algorithm
Initial EGD to confirm EE and grade severity.
8-Week PPI/P-CAB Therapy: Reassess symptoms; repeat EGD for LA grades C/D.
Refractory Cases: Optimize dosing, switch agents, or add H2RAs. Employ pH monitoring/manometry.
Procedural Options: Consider for persistent symptoms or medication intolerance.
Future Directions
Research priorities include:
Motility Agents: To enhance LES tone without side effects.
Anti-Inflammatory Therapies: Targeting mucosal repair.
Improved Procedural Techniques: Enhanced endoscopic/surgical options.
Conclusion
EE management requires a tailored approach combining pharmacologic and procedural therapies. PPIs and P-CABs remain cornerstone treatments, while emerging endoscopic techniques offer hope for refractory cases. Clinicians must balance efficacy, safety, and patient-specific factors to optimize outcomes.
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