Erosive Esophagitis: Causes, Symptoms, and Treatment

Erosive esophagitis is visible damage to the lining of the esophagus, most often caused by repeated exposure to stomach acid that backs up from the stomach. Among people who undergo upper endoscopy, roughly 28% worldwide are found to have it, and it accounts for about 30% of all gastroesophageal reflux disease (GERD) cases. The condition ranges from mild surface breaks in the tissue to deep, circumferential damage, and its treatment depends heavily on which end of that spectrum you fall on.

How Reflux Damages the Esophageal Lining

For a long time, the assumption was straightforward: stomach acid splashes upward, contacts the esophagus, and burns the tissue like a chemical spill. That picture turns out to be incomplete. When acid and bile acids reach the esophageal lining, they trigger the tissue’s own cells to release inflammatory signaling molecules, including interleukin-6, interleukin-8, and tumor necrosis factor-alpha. These signals recruit immune cells to the area, and the resulting inflammation loosens the tight junctions between cells by reducing the proteins that hold them together. Once those junctions widen, corrosive substances can penetrate deeper into the tissue, creating more damage than surface contact alone would explain.¹ In other words, the injury is partly self-inflicted: the body’s own inflammatory response amplifies what the acid started.

Emerging research also implicates the esophageal microbiome. A healthy esophagus hosts a community of bacteria, and disruptions to that community may fuel the inflammatory cascade independently of acid exposure.² This is still an evolving area, but it helps explain why some people with modest acid exposure develop erosive disease while others with more severe reflux do not.

What Raises Your Risk

The barrier between your stomach and esophagus is not a single gate but a two-part system: the muscular lower esophageal sphincter (LES) and the diaphragmatic hiatus, the opening in the diaphragm through which the esophagus passes. When these two structures are properly aligned, they reinforce each other. A hiatal hernia separates them, and that separation independently weakens the barrier in several ways: it reduces LES pressure, increases the frequency of the brief, spontaneous sphincter relaxations that let acid escape, and impairs the esophagus’s ability to clear refluxed material back down.³ One study found that in people with a hiatal hernia, the rate of these transient sphincter relaxations roughly doubled compared to people without one.⁴

Abdominal fat is another significant contributor. A study of adults aged 40 to 69 found that visceral fat area was independently associated with developing erosive esophagitis, roughly doubling the odds even after adjusting for other factors.⁵ The mechanism is partly mechanical: visceral fat increases pressure inside the abdomen, which pushes stomach contents upward. It may also contribute through inflammatory pathways, since visceral fat is metabolically active tissue that produces its own pro-inflammatory signals.

Medications can cause erosive injury too, through a completely different route. Certain pills that lodge in the esophagus on the way down cause direct chemical burns to the tissue. Common culprits include NSAIDs like ibuprofen, bisphosphonates used for osteoporosis, potassium chloride supplements, and some antibiotics.⁶ Pill-induced esophagitis tends to hit a specific spot in the mid-esophagus where the esophagus is compressed by the aortic arch. Taking medications with a full glass of water and staying upright for at least 30 minutes afterward substantially reduces the risk.

Symptoms and the Surprising Number of Silent Cases

The classic symptom is heartburn, a burning sensation behind the breastbone that often worsens after meals, when lying down, or when bending over. Regurgitation of sour or bitter fluid into the throat is the other hallmark. Some people also experience chest pain, difficulty swallowing, or a sensation that food is sticking. Less obviously connected symptoms include chronic cough, hoarseness, and throat clearing.

What many people do not realize is how often erosive esophagitis produces no symptoms at all. One large study found that about 43% of individuals with endoscopically confirmed erosive esophagitis reported no esophageal or throat symptoms.⁷ This means a substantial number of people are walking around with visible esophageal damage and no idea it exists. These silent cases are typically found incidentally during endoscopy performed for other reasons.

Symptoms also cannot reliably distinguish erosive from non-erosive reflux disease. Research comparing the two groups found that heartburn severity, frequency, and associated complaints overlap heavily; non-esophageal symptoms like sleep disturbance and chest discomfort were actually more prominent in the non-erosive group.⁸ The practical upshot: you cannot tell from symptoms alone whether your reflux is causing visible damage. Only endoscopy can answer that question.

How Severity Is Graded

When an endoscopy reveals erosive esophagitis, doctors use the Los Angeles (LA) classification to grade its severity on a scale from A to D. Grade A means one or more mucosal breaks no longer than 5 mm that do not extend between the tops of mucosal folds. Grade B involves breaks longer than 5 mm, still confined within folds. Grade C means breaks that extend between folds but involve less than 75% of the esophageal circumference. Grade D is the most severe, with mucosal breaks involving 75% or more of the circumference.⁹

This grading matters because it directly affects treatment decisions and outcomes. Grade A is by far the most common and responds well to standard doses of acid-suppressing medication. Grades C and D are less common, harder to heal, and more likely to relapse or develop complications. Grade D in particular may involve factors beyond simple acid reflux, including bile reflux or severe motility problems, which is why it sometimes requires more aggressive investigation and treatment.

When the clinical picture is unclear or when symptoms persist despite treatment, additional testing can help. Ambulatory pH monitoring measures how much acid reaches the esophagus over 24 to 48 hours. A more sensitive tool, pH-multichannel intraluminal impedance monitoring, can detect not only acid reflux but also non-acid reflux events, which is particularly useful for evaluating patients whose symptoms do not improve with acid suppression.¹⁰

Acid-Suppressing Medication

Proton pump inhibitors (PPIs) remain the cornerstone of treatment. Drugs like omeprazole, esomeprazole, and lansoprazole reduce stomach acid production at the source, and they work well for most people with erosive esophagitis.¹¹ After eight weeks of PPI treatment, more than 80% of patients show endoscopic healing.¹² Only a small minority fail to heal on a standard once-daily PPI course over that timeframe.¹³

The catch is staying healed. Erosive esophagitis has a high relapse rate once medication is stopped, because the underlying mechanical dysfunction that allows reflux usually persists. Maintenance rates with PPIs at six to twelve months tend to drop below 80%.¹² Many patients with moderate to severe disease end up on long-term or indefinite PPI therapy, which raises practical questions about side effects. Long-term PPI use has been linked in observational studies to slightly increased risks of certain nutrient deficiencies, kidney problems, and bone fractures, though the absolute risk increases are small and the evidence is debated. For most people with confirmed erosive esophagitis, the benefits of continued acid suppression outweigh those risks.

A Newer Class of Acid Suppressant

Vonoprazan, a potassium-competitive acid blocker (P-CAB), represents a different approach to acid suppression. Unlike PPIs, which need to be activated by acid and build up their effect over several days, vonoprazan works immediately and produces deeper, more sustained acid suppression. In a randomized trial of over 1,000 patients, vonoprazan healed erosive esophagitis at a rate of about 93% after eight weeks, compared to roughly 85% for lansoprazole.¹⁴

Where vonoprazan really shines is with severe disease. For patients with LA grade C or D esophagitis, the healing rate was about 92% with vonoprazan versus 72% with lansoprazole, a substantial gap.¹⁵ Maintenance results followed a similar pattern. A meta-analysis found that both the 10 mg and 20 mg doses of vonoprazan were significantly better at keeping erosive esophagitis healed at 24 weeks compared to lansoprazole, though the higher dose also came with a modestly higher rate of adverse events.¹⁶ Vonoprazan was approved in the United States in 2023, and it is particularly worth discussing with your doctor if you have severe erosive esophagitis or have failed PPI therapy.

Lifestyle Adjustments

Lifestyle changes are often recommended alongside medication, though the evidence supporting individual measures varies. One intervention with solid backing is elevating the head of the bed. A systematic review found that raising the head end by six to eight inches improved both reflux symptoms and measurable acid exposure in the esophagus, with a high-quality crossover trial showing a clinically meaningful reduction in symptom scores at six weeks.¹⁷ This works by using gravity to keep stomach contents from traveling upward while you sleep. A wedge pillow or bed risers under the headboard are more effective than simply stacking pillows, which tends to bend you at the waist rather than elevating the entire torso.

Other commonly recommended measures include eating smaller meals, avoiding eating within two to three hours of lying down, losing weight if you carry excess abdominal fat, and limiting foods that relax the LES or irritate the esophagus (alcohol, coffee, chocolate, fatty foods, citrus, and tomato-based products). The evidence for eliminating specific foods is weaker and more individualized than the evidence for weight loss and head-of-bed elevation. Tracking your own triggers tends to be more useful than following a generic avoidance list.

Surgery for Refractory or Severe Cases

When medications do not control erosive esophagitis adequately, or when a patient prefers not to take acid suppressants indefinitely, antireflux surgery becomes a consideration. The standard procedure is fundoplication, in which the top of the stomach is wrapped around the lower esophagus to mechanically reinforce the barrier against reflux. In a large study comparing outcomes in patients with complicated erosive esophagitis, those who underwent fundoplication had lower rates of recurrent esophageal erosions, ulcers, and strictures during follow-up than those managed without surgery.¹⁸

Surgery is not a guaranteed cure. A study examining factors affecting outcomes after laparoscopic fundoplication found that patients who continued to have reflux after surgery tended to have more severe pre-operative acid exposure and weaker esophageal muscle contractions.¹⁹ Pre-operative testing with pH monitoring and manometry helps identify who is most likely to benefit. Newer magnetic sphincter augmentation devices (placed as a ring of magnetic beads around the LES) offer a less invasive alternative, though long-term data is still accumulating.

For patients whose symptoms persist despite PPIs and who are not surgical candidates, a thorough workup for non-acid reflux and bile reflux is warranted. Ambulatory impedance-pH monitoring can detect reflux events regardless of their acidity, and specialized testing for bile can sometimes reveal a component that acid suppression alone will never address.²⁰

What Happens If Erosive Esophagitis Goes Untreated

Left to smolder, erosive esophagitis can lead to several serious complications. In a large Japanese multicenter study, about 8% of patients with erosive esophagitis had complications at the time of diagnosis: roughly 5% had esophageal bleeding, about 3% had strictures (narrowing of the esophagus from scar tissue), and some had both.²¹ Strictures can cause progressive difficulty swallowing and may require dilation procedures. Bleeding is typically slow and chronic rather than dramatic, sometimes presenting as unexplained iron-deficiency anemia rather than obvious blood loss.²²

The complication that gets the most attention is Barrett’s esophagus, a condition in which the normal squamous lining of the esophagus is replaced by a type of tissue that resembles the intestinal lining. Barrett’s is considered a precancerous condition because it raises the risk of esophageal adenocarcinoma. A community-based follow-up study found that having erosive esophagitis at baseline was independently associated with a roughly fivefold higher risk of developing Barrett’s esophagus compared to people without it.²³ The risk appears highest in those with the most severe grades of esophagitis; one study found that all cases of Barrett’s detected during follow-up occurred in patients who initially had the most severe grade of erosive disease.²⁴

Among patients who already have Barrett’s esophagus, ongoing erosive esophagitis appears to further raise the risk of progressing toward cancer. A Dutch cohort study found an increased risk of progression to high-grade dysplasia or adenocarcinoma in Barrett’s patients who had erosive esophagitis at their initial endoscopy.²⁵ Whether treating the esophagitis aggressively prevents that progression is not fully settled, but it is one of the stronger arguments for not ignoring moderate to severe erosive disease.

Conditions That Look Similar

Not every case of esophageal inflammation with visible changes at endoscopy is caused by acid reflux. Eosinophilic esophagitis (EoE) is an immune-mediated condition that can produce its own pattern of mucosal damage and is becoming increasingly recognized. Compared to reflux-driven erosive esophagitis, EoE tends to occur in younger patients, is strongly associated with food allergies, and presents with dysphagia (difficulty swallowing) as the dominant symptom rather than heartburn. Endoscopic clues include rings, linear furrows, and white plaques in the esophagus, and the hallmark on biopsy is a high concentration of eosinophils, a type of immune cell, in the tissue.²⁶ The distinction matters because EoE does not respond to acid suppression alone and requires different treatment, usually dietary elimination or topical corticosteroids.

Infectious esophagitis, caused by Candida, herpes simplex, or cytomegalovirus, is another mimic that typically appears in people with weakened immune systems. And as mentioned earlier, pill-induced esophagitis can produce erosions that look similar to reflux damage but are localized to a specific spot and resolve once the offending medication is stopped or taken differently. If your esophagitis is not responding to standard reflux treatment, one of these alternative diagnoses should be considered.

How Erosive Esophagitis Affects Sleep

Anyone who has been woken by a surge of acid into the throat already knows that reflux and sleep do not mix well. Research has quantified this relationship more precisely. A study of working-age adults found that erosive esophagitis in men was associated with poorer sleep quality, longer time to fall asleep, and more frequent nighttime awakenings. Even mild LA grade A disease showed these associations.²⁷ Interestingly, the same study did not find a significant association between erosive esophagitis and sleep disturbance in women, a sex difference that remains unexplained and warrants further study.

The sleep connection creates a vicious cycle. Poor sleep increases sensitivity to pain, including esophageal pain, and may worsen reflux by altering esophageal motility and lowering the threshold for sphincter relaxation during the night. Addressing nocturnal reflux through head-of-bed elevation, avoiding late meals, and ensuring acid suppression covers the overnight period can break this cycle. Some PPIs and vonoprazan provide more consistent overnight acid control than others, which is worth discussing with a gastroenterologist if nighttime symptoms are a major problem.

Who Gets It Around the World

Erosive esophagitis is not evenly distributed across populations. A large meta-analysis covering data from 1997 to 2022 found an overall pooled prevalence of 28% among endoscopy patients, but with striking regional variation. Africa and the Middle East had the highest rates, at roughly 47% and 43% respectively, while Asia had the lowest at about 24%. The Americas and Europe fell in between, at around 36% and 34%.²⁸ These numbers reflect endoscopy populations rather than the general public, so they overestimate how common erosive esophagitis is in the broader population. Still, the geographic pattern is real and likely reflects differences in diet, obesity prevalence, Helicobacter pylori infection rates (which paradoxically appear to protect against reflux disease in some populations), and access to early treatment.

The broader GERD landscape is also shifting. Global GERD cases nearly doubled between 1990 and 2021, and the fastest growth in prevalence has been in younger adults aged 25 to 34, challenging the traditional assumption that reflux disease is primarily a condition of middle and older age.²⁹ Rising obesity rates and changing dietary patterns in low- and middle-income countries are likely contributors. For younger adults experiencing persistent heartburn, these trends reinforce that the symptom is worth taking seriously rather than dismissing as a minor nuisance.