Pulmonary Fibrosis Associated with Tracheobronchial Aspiration

Mays, Edward E.; Dubois, James J.; Hamilton, G

doi:10.1378/chest.69.4.512

Cited by 200 publications

(37 citation statements)

References 15 publications

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“…In a study of 48 patients with radiographic evidence of PF of unknown aetiology, MAYS et al [14] reported a higher prevalence of GER by contrast radiographic upper gastrointestinal series. RAIHA et al [25] performed oesophageal pH probe studies in 137 elderly patients (aged .60 yrs) with abdominal complaints and noted that bilateral scarring of the lung parenchyma on chest radiograph was significantly more common in patients with acid GER.…”

Section: Discussionmentioning

confidence: 97%

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High prevalence of abnormal acid gastro-oesophageal reflux in idiopathic pulmonary fibrosis

Han¹

2006

European Respiratory Journal

579

406

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The aim of this prospective study was to determine the prevalence and characteristics of acid gastro-oesophageal reflux (GER) in patients with idiopathic pulmonary fibrosis (IPF).Sixty-five consecutive patients with well-defined IPF were subjected to 24-h pH monitoring and oesophageal manometry. A total of 133 consecutive patients with intractable asthma and symptoms of GER were used as comparisons.The prevalence of abnormal acid GER in IPF patients was 87%, with 76% and 63% demonstrating abnormal distal and proximal oesophageal acid exposures, respectively. Abnormal acid GER was significantly more common in IPF patients than asthma patients. Only 47% of IPF patients experienced classic GER symptoms. Despite treatment with standard doses of proton pump inhibitors (PPIs), 12 out of 19 patients receiving PPIs during the 24-h pH monitoring had abnormal oesophageal acid exposures by pH probe. There was no correlation between IPF severity and acid GER severity.In conclusion, abnormal acid gastro-oesophageal reflux is highly prevalent, but often clinically occult in patients with idiopathic pulmonary fibrosis. Standard doses of proton pump inhibitors may not suppress the acid gastro-oesophageal reflux in this population. Therefore, further studies are needed to determine if acid abnormal gastro-oesophageal reflux represents an important risk factor for idiopathic pulmonary fibrosis development or progression, and if optimal suppression of acid gastro-oesophageal reflux slows the progression of idiopathic pulmonary fibrosis and/or decreases episodic exacerbations of idiopathic pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 97%

“…Several studies have suggested that IPF may be related to repeated aspiration of gastric contents over long periods of time [14,15]. Pulmonary fibrosis (PF) has been induced by direct instillation of acid into the airways of animals in experimental models of PF [16][17][18].…”

mentioning

confidence: 99%

High prevalence of abnormal acid gastro-oesophageal reflux in idiopathic pulmonary fibrosis

Han¹

2006

European Respiratory Journal

579

406

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“…calcineurin inhibitors) or iatrogenic vagal nerve injury at surgery or it may even be present as a preoperative condition. In fact, interstitial lung disease secondary to connective tissue disorders, idiopathic pulmonary fibrosis and cystic fibrosis have all been associated with GER (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24). We have previously documented the association between BOS and bile acid aspiration along with the association between alveolar neutrophilia and IL-8.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Reflux and Bile Acid Aspiration on the Lung Allograft and Its Surfactant and Innate Immunity Molecules SP-A and SP-D

D’Ovidio

Mura

Ridsdale

et al. 2006

American Journal of Transplantation

170

116

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Gastro-esophageal reflux and related pulmonary bile acid aspiration were prospectively investigated as possible contributors to postlung transplant bronchiolitis obliterans syndrome (BOS). We also studied the impact of aspiration on pulmonary surfactant collectin proteins SP-A and SP-D and on surfactant phospholipids-all important components of innate immunity in the lung. Proximal and distal esophageal 24-h pH testing and broncho-alveolar lavage fluid (BALF) bile acid assays were performed prospectively at 3-month posttransplant in 50 patients. BALF was also assayed for SP-A, SP-D and phospholipids expressed as ratio to total lipids: phosphatidylcholine; dipalmitoylphosphatidylcholine; phosphatidylglycerol (PG); phosphatidylinositol; sphingomyelin (SM) and lysophosphatidylcholine. Actuarial freedom from BOS was assessed.Freedom from BOS was reduced in patients with abnormal (proximal and/or distal) esophageal pH findings or BALF bile acids (Log-rank Mantel-Cox p < 0.05). Abnormal pH findings were observed in 72% (8 of 11) of patients with bile acids detected within the BALF. BALF with high levels of bile acids also had significantly lower SP-A, SP-D, dipalmitoylphosphatidylcholine; PG and higher SM levels (Mann-Whitney, p < 0.05). Duodeno-gastro-esophageal reflux and consequent aspiration is a risk factor for the development of BOS postlung transplant. Bile acid aspiration is associated with impaired lung allograft innate immunity manifest by reduced surfactant collectins and altered phospholipids.

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“…Similar to scleroderma, patients with IPF have a high prevalence of GERD [12,65,[73][74][75], leading to the hypothesis that recurrent occult microaspiration may drive the ongoing inflammation characteristic of this disease. This should not be confused with acute exacerbation of IPF (progression of symptoms over weeks with radiographic airspace disease), as biopsies may also reveal organising pneumonia with underlying UIP in this syndrome [76,77].…”

Section: Ipfmentioning

confidence: 99%

“…This should not be confused with acute exacerbation of IPF (progression of symptoms over weeks with radiographic airspace disease), as biopsies may also reveal organising pneumonia with underlying UIP in this syndrome [76,77]. MAYS et al [73] reported 131 patients with radiographic pulmonary fibrosis, of which six had recurrent aspiration as their primary diagnosis. 63 were ultimately diagnosed as ''idiopathic'' fibrosis, and 79% of this group had symptoms of GERD.…”

Section: Ipfmentioning

confidence: 99%

Gastro-oesophageal reflux disease and non-asthma lung disease

Morehead¹

2009

European Respiratory Review

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Gastro-oesophageal reflux disease (GERD) is a common disorder in Western countries, and its relationship to airways disorders (e.g. asthma) has been well established. Lung diseases other than asthma have also been associated with GERD, but the nature and scope of this relationship has not been fully defined. Diseases that have been associated with GERD include bronchiolitis syndromes, idiopathic pulmonary fibrosis, scleroderma and nontubercular mycobacterial infection.Diagnostic evaluation centres upon proving both reflux and pulmonary aspiration, which may be accomplished in some cases by lung biopsy. However, in many cases a compatible clinical and radiographic picture coupled with proof of proximal reflux by combined oesophageal probe testing may suffice for a provisional diagnosis and allow institution of anti-reflux measures.Proton-pump inhibitors are the medications of choice for GERD; other interventions shown to reduce reflux are weight loss, elevation of the head of the bed and avoidance of recumbency after meals. However, acid suppression therapy does not address non-acid reflux that may be important in disease pathogenesis in select patients, and lifestyle modifications often fail.Laparoscopic fundoplication is the procedure of choice for medically refractory GERD with excellent short-term results with respect to respiratory symptoms associated with GERD; however, long-term studies document a significant percentage of patients requiring ongoing acid suppression therapy.

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Pulmonary Fibrosis Associated with Tracheobronchial Aspiration

Cited by 200 publications

References 15 publications

High prevalence of abnormal acid gastro-oesophageal reflux in idiopathic pulmonary fibrosis

High prevalence of abnormal acid gastro-oesophageal reflux in idiopathic pulmonary fibrosis

The Effect of Reflux and Bile Acid Aspiration on the Lung Allograft and Its Surfactant and Innate Immunity Molecules SP-A and SP-D

Gastro-oesophageal reflux disease and non-asthma lung disease

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