Chest
Volume 131, Issue 4, April 2007, Pages 1166-1172
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Original Research
Respiratory Infections
Gastroesophageal Reflux Disease, Acid Suppression, and Mycobacterium avium Complex Pulmonary Disease

https://doi.org/10.1378/chest.06-1906Get rights and content

Background

Weekly symptoms of gastroesophageal reflux disease (GERD) occur in 20% of the population, and GERD has been implicated in the pathophysiology of many respiratory diseases. Microaspiration of contaminated water is a potential portal of entry for Mycobacterium avium complex (MAC) organisms into the respiratory tract, and acid-suppression therapy may enhance the survival of mycobacteria in the stomach. This study aimed to assess the prevalence of GERD, swallowing disorders, reflux symptoms, and acid-suppression therapy in patients with MAC lung disease (MAC positive [MAC+]), and to compare these patients to control subjects without MAC lung disease (MAC negative [MAC−]).

Methods

Clinical information was collected on 58 MAC+ patients and 58 age- and sex-matched MAC− patients who were asked to complete a DeMeester questionnaire of reflux symptoms and to identify any acid-suppressive medication consumed.

Results

A clinical diagnosis of GERD was documented in 23 of 52 MAC+ patients (44.2%), compared to 16 MAC− patients (27.6%) [p = 0.019]. MAC+ patients consumed significantly more histamine type 2 receptor antagonists and prokinetic agents, and MAC− patients consumed more antacids. The mean DeMeester questionnaire score (± SD) for MAC+ patients was 1.39 ± 1.8, and for MAC− patients was 0.88 ± 1.4. (p = 0.098). Aspiration was suspected in nine MAC+ patients (15.5%), compared to three MAC− patients (5.2%) [p = 0.032]. There was no association between GERD and radiologic presentation of MAC disease. Consolidation and nodules > 5 mm were more common in those receiving acid suppression than those who were not.

Conclusions

GERD, acid suppression, and clinically suspected aspiration are more common in patients with MAC lung disease than in similar patients without MAC disease.

Section snippets

Materials and Methods

A prospective cohort of 58 patients (cases) with MAC lung disease was identified by laboratory notification of isolates of MAC in Queensland, Australia between January 1 and December 31, 1999. The protocol (138/98) was approved by the Princess Alexandra Hospital Research Ethics Committee in accordance with the Australian National Health and Medical Research Council guidelines. Consent to participate was sought, and clinical features of the disease (including risk factors, symptoms, radiology,

Results

The details of MAC+ cases and MAC− controls are shown in Table 1. Radiologic details of those with disease (MAC+) are shown in Table 2 and bacteriology in Table 3.

Clinical information about reflux disease was returned for 52 of 58 MAC+ patients. Twenty-three MAC+ patients (44.2%) had a diagnosis of GERD recorded by their treating doctor, compared to 16 MAC− patients (27.6%) [p = 0.019]. Confirmatory evidence was provided in 10 MAC+ patients: 6 patients had positive findings on gastroscopy, and

Discussion

GERD is a common problem in patients with a number of respiratory diseases. The mechanics of coughing and the related reduction in lower esophageal sphincter tone encourage the reflux of gastric contents into the lower esophagus. The lower pH in the distal esophagus has been shown to cause further cough. Hence, proving a connection between GERD and MAC lung disease specifically was likely to be difficult.

Patients in this cohort with pulmonary MAC disease have a higher incidence of GERD than is

ACKNOWLEDGMENT

The authors thank Dr. Chris Coulter and David Dawson from the QLD Mycobacterial Reference Laboratory, Dr. Jenny Robson from Sullivan and Nicolaides Pathology, and Dr. Ross LeFeuvre and Robyn Fraser from Queensland Medical Laboratory for their assistance in providing reports of all mycobacterial isolates during 1999, and subsequent isolates from the patients in this cohort. Clinical support was provided by Dr. Tom Konstantinos and the Queensland TB Control Unit, Brisbane, QLD, Australia, for

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    This research was supported by a Research Scholarship from the Princess Alexandra Hospital, South Brisbane, QLD, Australia, and was conducted through the Department of Thoracic Medicine of the Princess Alexandra Hospital.

    The authors have no conflicts of interest to declare.

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