GERD, Microaspiration and Pulmonary Fibrosis: Can Reflux Affect Lung Fibrosis?
Gastroesophageal reflux disease, or GERD, is surprisingly common in people with pulmonary fibrosis.
For years, researchers have questioned whether this relationship is simply coincidence or whether repeated reflux and microaspiration could contribute to ongoing lung injury.
The biological hypothesis sounds reasonable:
stomach contents reflux into the esophagus ↓ small amounts reach the throat or airway ↓ microaspiration occurs ↓ repeated epithelial injury develops ↓ fibrotic pathways may be activated
But the clinical evidence is much more complicated.
GERD is unquestionably common in idiopathic pulmonary fibrosis.
A major systematic review and meta-analysis published in June 2026 analyzed 33 studies involving 35,807 patients with IPF and estimated the pooled prevalence of GERD at approximately 47%. (PubMed)
Older physiological studies have reported even higher rates of abnormal reflux when patients undergo objective reflux testing.
But a high prevalence of GERD does not prove that reflux causes pulmonary fibrosis.
Nor has treating reflux convincingly been shown to slow IPF progression.
In fact, current international IPF guidelines recommend against using antacid medication solely for the purpose of improving respiratory outcomes in IPF, while still recognizing that GERD should be treated when there is a conventional gastrointestinal indication. (PubMed Central (PMC))
So where does this leave the reflux–lung hypothesis?
The most accurate interpretation is:
GERD and pulmonary fibrosis are strongly associated, microaspiration remains biologically plausible as a contributor to lung injury, but reflux has not been established as a primary cause of IPF and antacid therapy has not been proven to modify IPF progression.
The relationship becomes even more interesting in systemic sclerosis-associated ILD, where esophageal dysmotility, reflux and impaired clearance are extremely common.
This article examines the latest evidence.
What Is GERD?
Gastroesophageal reflux occurs when stomach contents travel upward into the esophagus.
Occasional reflux can occur normally.
GERD refers to reflux that causes troublesome symptoms, mucosal injury or other complications.
Typical symptoms include:
heartburn
acid regurgitation
sour taste
chest discomfort
But reflux does not always cause classic symptoms.
Some people experience:
chronic cough
hoarseness
throat clearing
throat irritation
nocturnal symptoms
Others may have significant abnormal reflux on physiological testing without obvious symptoms at all.
This is particularly relevant to pulmonary fibrosis.
What Is Silent Reflux?
The term silent reflux is often used when clinically significant reflux occurs without classic heartburn or regurgitation.
In pulmonary disease, this matters because relying exclusively on symptoms can miss abnormal reflux.
Historical IPF studies found that many patients with abnormal reflux did not report typical GERD symptoms.
This is one reason investigators became interested in reflux as a potentially overlooked contributor to chronic pulmonary injury.
What Is Microaspiration?
Aspiration occurs when material enters the respiratory tract instead of remaining within the digestive tract.
Large-volume aspiration can cause obvious respiratory illness.
Microaspiration refers to much smaller amounts of material repeatedly entering the airway.
Potential aspirated material may include:
gastric acid
pepsin
bile acids
food particles
oral secretions
bacteria
Repeated microaspiration may not produce an obvious choking event.
The exposure may be subtle.
This is the biological mechanism most commonly proposed to connect GERD with pulmonary fibrosis.
Why Could Microaspiration Affect the Lungs?
The alveolar epithelium is delicate.
Repeated exposure to gastric or esophageal contents could theoretically cause:
epithelial injury
oxidative stress
inflammatory signaling
altered epithelial repair
macrophage activation
Pulmonary fibrosis already involves repeated alveolar epithelial injury followed by abnormal repair.
Therefore, researchers have hypothesized that recurrent aspiration might act as one of several possible epithelial insults.
A simplified model is:
GERD ↓ proximal reflux ↓ microaspiration ↓ alveolar epithelial injury ↓ abnormal repair ↓ fibroblast activation ↓ fibrosis
This is a plausible mechanism.
But plausibility is not the same as proof.
How Common Is GERD in Idiopathic Pulmonary Fibrosis?
Very common.
The most updated quantitative evidence comes from the 2026 systematic review and meta-analysis evaluating 33 studies and 35,807 patients with IPF.
The pooled prevalence of GERD was:
47.0%
with substantial variability between studies. (PubMed)
The investigators also found variations according to:
study design
geography
time period
methods used to diagnose GERD
This matters because GERD prevalence depends heavily on how it is measured.
Questionnaire-based diagnosis may identify a different group of patients from physiological reflux monitoring.
Why Have Older Studies Reported GERD Rates as High as 90%?
Some older IPF studies using objective esophageal testing reported abnormal acid reflux in very high proportions of patients.
This led earlier international guidelines to consider reflux potentially important in IPF.
The 2015 guideline noted that abnormal acid GER had been observed in up to approximately 90% of selected IPF populations. (OUP Academic)
However, these studies often involved:
small cohorts
selected patients
different definitions of reflux
varying diagnostic methods
Therefore, a single percentage should not be applied to every patient with IPF.
The newer 2026 meta-analysis provides a broader estimate across a much larger patient population. (PubMed)
Does GERD Cause Idiopathic Pulmonary Fibrosis?
This has not been established.
Several possibilities could explain the association.
Possibility 1: Reflux contributes to pulmonary injury
Repeated microaspiration could injure alveolar epithelial cells and amplify fibrosis.
Possibility 2: Pulmonary fibrosis causes reflux
Fibrotic lungs become stiff.
Changes in intrathoracic pressure mechanics may potentially promote reflux.
Chronic cough may also increase abdominal and thoracic pressure changes.
Possibility 3: Shared risk factors influence both
Age, obesity, hiatal hernia and medications may influence GERD and pulmonary disease independently.
Possibility 4: The relationship is bidirectional
This is probably the most realistic model.
Pulmonary fibrosis may increase reflux susceptibility, while reflux and aspiration may provide additional pulmonary epithelial injury in selected patients.
What Is the Evidence for Microaspiration in IPF?
Directly demonstrating repeated microaspiration is difficult.
Researchers have explored several approaches, including measurement of:
pepsin
bile acids
reflux episodes
proximal reflux
in association with pulmonary disease.
The presence of gastric components in respiratory samples provides biological evidence that material originating in the stomach can reach the respiratory tract.
But determining whether this causes progressive fibrosis is considerably more difficult.
A patient may aspirate because advanced lung disease alters mechanics.
Therefore, even documented aspiration does not automatically establish the direction of causality.
Acid Reflux Is Only Part of the Story
One major limitation of the early GERD hypothesis is its focus on stomach acid.
Refluxate can also be:
weakly acidic
non-acid
gaseous
mixed with bile or digestive enzymes
This matters because proton-pump inhibitors decrease gastric acid production.
They do not necessarily stop reflux itself.
A person receiving a PPI may continue to experience:
stomach contents moving upward
but the refluxate may simply contain less acid.
This has major implications for pulmonary disease.
PPIs Do Not Prevent Microaspiration Mechanically
Proton-pump inhibitors such as omeprazole or esomeprazole primarily reduce acid production.
They do not correct:
hiatal hernia
weak lower esophageal sphincter
absent esophageal contractility
delayed gastric emptying
Therefore:
acid suppression ≠ elimination of reflux
and:
acid suppression ≠ guaranteed prevention of aspiration.
This helps explain why trials of antacid treatment have not definitively established pulmonary benefit.
What Did Earlier IPF Guidelines Recommend?
The recommendations have changed over time.
Earlier guidelines suggested treating asymptomatic reflux in many patients with IPF.
That recommendation was based largely on:
high prevalence of GERD
biological plausibility of microaspiration
retrospective observational studies suggesting possible benefit
The quality of evidence was very low.
As more data accumulated, the recommendation changed.
What Do Current IPF Guidelines Say?
The 2022 ATS/ERS/JRS/ALAT clinical practice guideline states:
patients with IPF should not routinely receive antacid medication solely for the purpose of improving respiratory outcomes.
This is a conditional recommendation based on very low-quality evidence. (PubMed Central (PMC))
However, the guideline makes an equally important point:
patients who have symptomatic GERD can still receive appropriate GERD therapy according to conventional GERD indications.
Therefore, the recommendation is not:
“Do not treat reflux in IPF.”
The recommendation is:
Do not prescribe antacid medication solely because you expect it to slow IPF.
Why Did the Recommendation Change?
Early observational studies suggested possible benefit from antacid therapy.
But subsequent analyses did not consistently demonstrate improvement in clinically important IPF outcomes.
Potential concerns with chronic acid suppression also became relevant.
These can include altered:
gastrointestinal microbial ecology
infection susceptibility
nutrient absorption
depending on the patient and duration of therapy.
Therefore, the balance of evidence no longer supported universal antacid therapy solely for pulmonary purposes.
What Does the Newer Mortality Evidence Show?
A 2025 systematic review and meta-analysis examined antireflux therapy and mortality in patients with IPF and GERD.
Six studies involving 2,874 patients were included.
Antireflux therapy did not produce a statistically significant reduction in overall mortality.
For IPF-related mortality, the pooled estimate suggested a possible benefit, but the confidence interval crossed the threshold for statistical significance.
The authors concluded that more rigorous randomized trials are required. (PubMed)
This reinforces the current position:
the possibility of benefit remains unresolved, but it is not proven.
What About Antireflux Surgery?
If reflux itself rather than acidity is the relevant pulmonary exposure, mechanically preventing reflux could theoretically be more meaningful than acid suppression.
This has generated interest in procedures such as fundoplication.
However, surgical antireflux treatment has not been definitively established as disease-modifying therapy for IPF.
Surgical decisions also require careful assessment of:
esophageal motility
aspiration risk
operative risk
overall pulmonary status
This becomes particularly complicated in patients with advanced ILD.
Why Is Esophageal Motility Important?
Normal reflux clearance depends partly on effective esophageal contractions.
If the esophagus cannot efficiently push refluxed material back toward the stomach, exposure becomes prolonged.
This is particularly important in systemic sclerosis.
Systemic Sclerosis: A Different Reflux–Lung Scenario
The relationship between reflux and ILD may be particularly relevant in systemic sclerosis, or SSc.
Gastrointestinal involvement is extremely common.
Patients may develop:
weak or absent esophageal contractions
lower esophageal sphincter dysfunction
delayed gastric emptying
reflux
esophageal dilation
SIBO
This creates a strong physiological basis for prolonged reflux and possible microaspiration.
How Common Is GERD in Systemic Sclerosis-ILD?
A large recent analysis from the EUSTAR cohort included 5,462 patients with systemic sclerosis-associated ILD.
GERD was present in approximately:
80.6%
of those patients.
Patients with GERD had:
lower FVC
lower DLCO
poorer six-minute walk performance
more severe systemic disease
compared with SSc-ILD patients without GERD. (PubMed Central (PMC))
This is a striking association.
But once again:
association does not prove that reflux caused the worse ILD.
Does Reflux Predict SSc-ILD Progression?
The relationship remains complex.
Data from the Scleroderma Lung Study II cohort found that greater reflux symptom severity was independently associated with greater radiological progression of ILD and fibrosis over two years.
Interestingly, objective CT measurements of esophageal dilation were not associated with progression. (PubMed Central (PMC))
This suggests that esophageal involvement may matter, but the optimal marker of pulmonary risk is not yet clear.
Esophageal Dysmotility and Pulmonary Disease
Recent data continue to show relationships between severe esophageal motor dysfunction and pulmonary involvement in systemic sclerosis.
A 2025 analysis reported that esophageal dysmotility was associated with ILD and lower gas-transfer measures, while acknowledging that the direction of causality remains uncertain. (PubMed Central (PMC))
The proposed mechanism is:
dysmotility ↓ poor reflux clearance ↓ more proximal reflux ↓ greater aspiration opportunity ↓ possible lung injury
But the reverse relationship may also contribute.
Reduced lung compliance may modify intrathoracic mechanics and worsen reflux.
Why PPIs May Not Be Enough in Systemic Sclerosis
This is particularly important.
The main problem in systemic sclerosis may not simply be excessive acid.
It may be:
impaired motility and impaired clearance.
A recent study of patients with systemic sclerosis undergoing detailed physiology while taking twice-daily PPIs found:
GERD remained highly prevalent
esophageal dysmotility occurred in 80%
absent contractility was common
gastric dysmotility was also frequent
Poor esophageal clearance was associated with longer reflux exposure, while gastric dysmotility was associated with greater reflux burden. (PubMed Central (PMC))
This highlights an important clinical principle:
acid suppression may not fully address reflux when the fundamental problem is dysmotility.
Acid Versus Non-Acid Reflux
This is why pH testing alone may be insufficient in selected patients.
A person taking a PPI may have:
normal acid exposure
continued non-acid reflux
If the pulmonary concern is aspiration of gastric contents rather than acid exposure alone, non-acid reflux becomes relevant.
Testing that combines:
pH monitoring + impedance
can detect both acid and non-acid reflux episodes.
What Tests Can Evaluate Reflux?
Depending on the clinical problem, assessment may include:
Upper endoscopy
Can identify:
erosive esophagitis
Barrett’s esophagus
structural lesions
But normal endoscopy does not exclude reflux.
Ambulatory pH monitoring
Measures acid exposure.
pH-impedance monitoring
Measures both acid and non-acid reflux and can characterize reflux episodes more comprehensively.
High-resolution esophageal manometry
Assesses:
esophageal contractility
sphincter function
motility disorders
This may be particularly valuable in systemic sclerosis.
Does a Hiatal Hernia Matter?
Hiatal hernia can promote reflux by altering the anatomy of the gastroesophageal junction.
Hiatal hernia is relatively common in patients with IPF.
But its presence does not prove aspiration or determine whether reflux is contributing to fibrosis.
It should be interpreted within the full clinical context.
Can Chronic Cough Be Caused by Reflux?
Yes, reflux can contribute to chronic cough in selected patients.
But cough in pulmonary fibrosis has many possible mechanisms.
These include:
mechanical distortion of the lungs
airway hypersensitivity
fibrosis-related neural changes
GERD
upper airway disease
medications
Therefore, cough should not automatically be attributed to reflux.
Could Treating Reflux Improve Cough Without Changing Fibrosis?
Yes.
This distinction is important.
A patient may experience improvement in:
heartburn
regurgitation
nocturnal cough
after treating GERD.
That is clinically useful.
But symptom improvement does not necessarily mean that lung fibrosis has slowed.
Gastrointestinal outcomes and pulmonary fibrosis outcomes should be assessed separately.
Where Does the Gut Microbiome Fit Into This?
GERD and the gut–lung axis are related but distinct concepts.
The reflux–lung pathway is primarily:
stomach/esophagus → reflux → microaspiration → lung
The gut microbiome–lung pathway is primarily:
intestinal microbiome → microbial metabolites and immune signaling → systemic circulation → lung
Both may influence respiratory disease.
But they should not be combined into one mechanism.
Could PPIs Influence the Gut Microbiome?
Yes.
Proton-pump inhibitors can alter intestinal microbial composition.
This is relevant because the 2026 CleanUP-IPF microbiome study found that PPI use itself was associated with gut microbiome characteristics in patients with IPF. (PubMed)
This creates an important research challenge.
If a study finds dysbiosis in IPF, researchers need to distinguish microbial effects related to:
IPF itself
age
diet
PPI exposure
antibiotics
other medications
This is one reason microbiome associations must be interpreted cautiously.
Does This Mean PPIs Should Be Avoided?
No.
A medication should not be stopped simply because it may influence the microbiome.
PPIs have established indications.
They can be highly effective in:
erosive esophagitis
symptomatic GERD
selected Barrett’s esophagus management
other acid-related disorders
The appropriate question is:
Does this patient have a good indication for the medication?
not:
Does the medication change gut bacteria?
Functional and Integrative Medicine Perspective
GERD is an area where integrative evaluation can be useful—provided it remains physiologically grounded.
Instead of assuming all reflux is caused by “too much stomach acid,” evaluation should consider:
lower esophageal sphincter function
hiatal hernia
esophageal dysmotility
gastric emptying
meal timing
body weight
nocturnal reflux
medications
food triggers
In systemic sclerosis, motility deserves particular attention.
Lifestyle Measures for GERD
Depending on the patient, supportive strategies may include:
avoiding large meals close to bedtime
remaining upright after meals
identifying individual food triggers
reducing excess body weight where appropriate
elevating the head of the bed for nocturnal reflux
These strategies may improve reflux symptoms.
They have not been proven to reverse pulmonary fibrosis.
Should Everyone With Pulmonary Fibrosis Be Tested for GERD?
Not necessarily.
Testing should depend on the clinical context.
Potential reasons for further assessment may include:
troublesome reflux symptoms
unexplained regurgitation
significant nocturnal symptoms
recurrent aspiration suspicion
dysphagia
systemic sclerosis with severe esophageal involvement
evaluation before lung transplantation
The appropriate investigation varies between patients.
Reflux and Lung Transplantation
GERD and aspiration are also important considerations in lung transplantation.
After transplantation, aspiration and reflux may potentially contribute to allograft injury.
Many transplant programs therefore pay close attention to:
reflux
aspiration
esophageal motility
gastric emptying
This is a distinct clinical context from native-lung IPF, but it reinforces how closely gastrointestinal physiology can interact with pulmonary health.
What We Know
Current evidence supports several conclusions.
We know that:
GERD is common in IPF
a 2026 meta-analysis estimated GERD prevalence around 47% across more than 35,000 patients
reflux may occur without typical symptoms
microaspiration is biologically capable of injuring lung tissue
GERD and severe esophageal dysfunction are highly prevalent in SSc-ILD
greater reflux burden or symptoms have been associated with worse pulmonary disease in several observational SSc studies
(PubMed)
What We Do Not Know
We do not know:
whether GERD causes IPF
how much microaspiration contributes to IPF progression
which IPF patients are most vulnerable to aspiration-mediated injury
whether treating reflux slows FVC decline
whether acid or non-acid reflux is more important
whether antireflux surgery improves long-term IPF outcomes
whether reflux is a cause or consequence of more severe SSc-ILD
What Does This Mean Clinically?
The practical approach is not to ignore reflux.
Nor is it to assume that every patient with pulmonary fibrosis needs a PPI.
Instead:
identify clinically meaningful reflux or dysmotility → characterize the mechanism when necessary → treat GERD appropriately → continue evidence-based ILD therapy
Treatment of reflux should be directed toward its established gastrointestinal or aspiration-related indications.
It should not be presented as a replacement for antifibrotic or immunomodulatory therapy.
What Treatments Still Matter for IPF?
Depending on the patient, evidence-based pulmonary care may include:
antifibrotic therapy
oxygen when indicated
pulmonary rehabilitation
vaccination
treatment of comorbidities
lung transplantation evaluation
Reflux management should complement this framework.
What About Autoimmune ILD?
In autoimmune ILD, especially systemic sclerosis, the gastrointestinal component may deserve more active assessment.
Potentially relevant issues include:
esophageal dysmotility
severe GERD
delayed gastric emptying
SIBO
nutritional compromise
swallowing dysfunction
But management should remain individualized.
Frequently Asked Questions
Can acid reflux cause pulmonary fibrosis?
There is no definitive evidence that GERD causes idiopathic pulmonary fibrosis.
Repeated microaspiration is a biologically plausible contributor to lung injury, but causality remains unproven.
How common is GERD in IPF?
A 2026 meta-analysis of 33 studies involving 35,807 patients estimated the prevalence at approximately 47%. (PubMed)
Can you have reflux without heartburn?
Yes.
Some patients have clinically significant reflux without typical heartburn or regurgitation.
What is microaspiration?
Microaspiration refers to small amounts of oral, esophageal or gastric material entering the respiratory tract, often without an obvious choking episode.
Does taking a PPI prevent aspiration?
Not necessarily.
PPIs reduce gastric acidity but do not mechanically stop reflux.
Should all patients with IPF take PPIs?
No.
Current international guidelines suggest against prescribing antacid therapy solely to improve respiratory outcomes in IPF. PPIs remain appropriate when there is a separate GERD indication. (PubMed Central (PMC))
Can treating reflux reverse pulmonary fibrosis?
No clinical evidence demonstrates that treating GERD reverses established pulmonary fibrosis.
Is reflux important in systemic sclerosis-ILD?
Yes.
GERD and esophageal dysmotility are extremely common in systemic sclerosis, and observational studies have linked reflux with more severe pulmonary involvement. (PubMed Central (PMC))
How can non-acid reflux be detected?
Combined pH-impedance monitoring can detect acid and non-acid reflux.
Can diet help reflux?
Meal timing, avoiding individual triggers, weight management where appropriate and other lifestyle strategies can help selected patients with GERD.
They have not been proven to alter pulmonary fibrosis progression.
Key Takeaway
The most accurate interpretation is:
GERD is common in pulmonary fibrosis and repeated microaspiration is a biologically plausible source of additional lung injury, but current evidence does not prove that GERD causes IPF or that routine antacid treatment slows pulmonary fibrosis.
Conclusion
The relationship between GERD, microaspiration and pulmonary fibrosis remains one of the most intriguing and debated areas in interstitial lung disease.
GERD is clearly common in IPF.
The most recent large systematic review, published in 2026 and including 35,807 patients, estimated that approximately 47% of patients with IPF have GERD. (PubMed)
The biological rationale linking reflux with pulmonary fibrosis is also credible.
Repeated proximal reflux may permit small amounts of gastric or esophageal material to enter the respiratory tract.
That exposure could theoretically contribute to:
epithelial injury
inflammation
abnormal repair
fibroblast activation
But important questions remain unanswered.
We do not know whether reflux initiates IPF.
We do not know how much microaspiration contributes to disease progression.
And we have not demonstrated that routinely suppressing gastric acid improves meaningful pulmonary outcomes.
This is why current international guidelines recommend against using antacid medication solely to improve respiratory outcomes in IPF, while continuing to support appropriate treatment of symptomatic GERD. (PubMed Central (PMC))
Systemic sclerosis presents a different and particularly important scenario.
Large contemporary cohorts show GERD in the majority of patients with SSc-ILD, while reflux severity and esophageal dysfunction are associated with more severe pulmonary disease in observational studies. (PubMed Central (PMC))
Recent physiological research also demonstrates why acid suppression alone may sometimes be inadequate in systemic sclerosis: severe esophageal and gastric dysmotility can cause persistent reflux even during intensive PPI therapy. (PubMed)
This points toward a more sophisticated clinical model.
Instead of asking simply:
“Does the patient have too much stomach acid?”
we may need to ask:
“Is reflux occurring, how proximal is it, is it acid or non-acid, is esophageal clearance impaired, is gastric emptying abnormal, and is there reason to suspect aspiration?”
That framework is especially important in autoimmune ILD and lung transplantation.
The reflux–lung relationship also needs to be distinguished from the gut–lung microbiome axis.
Reflux primarily creates a potential physical route of exposure from the gastrointestinal tract to the lung through aspiration.
The microbiome pathway primarily involves immune and metabolic communication between intestinal microbes and distant organs.
Both may eventually prove relevant to pulmonary fibrosis.
But they represent different mechanisms and require different clinical approaches.
For now, the appropriate strategy is balanced:
identify and treat clinically important reflux and gastrointestinal dysfunction while continuing evidence-based pulmonary fibrosis care.
Reflux management may improve gastrointestinal symptoms and potentially reduce aspiration exposure.
What has not yet been demonstrated is that it can replace—or reliably enhance—the disease-modifying treatment of pulmonary fibrosis.
Future studies combining:
pH-impedance monitoring
esophageal manometry
aspiration biomarkers
lung microbiome analysis
HRCT progression
pulmonary function
may eventually identify the subgroup of patients in whom reflux truly acts as a pulmonary disease modifier.
That would move the field from a general association toward precision treatment.
About Dr. Samar Shadly
Dr. Samar Shadly is a Consultant Pulmonologist and Certified Functional Medicine Practitioner, with advanced subspecialty training in interstitial lung disease, pulmonary fibrosis, pulmonary hypertension and lung transplantation at the University of Toronto.
Her clinical and academic interests include Integrative and Functional Pulmonology, pulmonary fibrosis, autoimmune-associated ILD, the gut–lung axis, gastrointestinal–pulmonary interactions, nutrition and emerging microbiome science.
Looking for a Comprehensive Approach to Pulmonary Fibrosis or ILD?
If you are living with pulmonary fibrosis, systemic sclerosis-associated ILD or another form of interstitial lung disease and would like a comprehensive assessment that considers your pulmonary condition together with relevant reflux, gastrointestinal, nutritional, metabolic and lifestyle factors, online consultation options are available.
The goal is to integrate these factors with—not replace—established pulmonary and rheumatological care.
Contact us through the consultation page or WhatsApp to learn more.
Functional and integrative care is intended to complement—not replace—appropriate evidence-based pulmonary treatment.
Medical Disclaimer: This article is intended for educational purposes only and does not constitute individualized medical advice. Patients with pulmonary fibrosis or interstitial lung disease should remain under appropriate specialist care.
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