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. 2010 Apr;2(1):106-110.
doi: 10.5539/gjhs.v2n1p106.

Identification of Intrinsic Airway Acidification in Pulmonary Tuberculosis

Lina Ngamtrakulpanit  1 , Yuanlin Yu, Andrew Adjei, George Amoah, Ben Gaston, John Hunt
Affiliations

Identification of Intrinsic Airway Acidification in Pulmonary Tuberculosis

Lina Ngamtrakulpanit et al. Glob J Health Sci. 2010 Apr.

Abstract

Exhaled breath condensate acidification reflects the presence of airway acidification. Mycobacterium tuberculosis is an organism particularly sensitive to acidity. We aimed to determine if there is evidence of airway acidification in a cross section of patients with active tuberculosis.We enrolled 51 subjects with active tuberculosis in Ghana and Thailand, and compared them to control subjects. We collected exhaled breath condensate, and assayed for pH after gas standardization.Exhaled breath condensate pH from the control group revealed a median of 7.9 (7.7 - 8.0, n = 21), significantly higher than the active pulmonary tuberculosis patients who had a median pH of 7.4 (7.0 - 7.7; n = 51; p=0.002). Presence or absence of antibiotic therapy did not affect EBC pH values.These exhaled breath condensate data support the theory that airways become acidic in active tuberculosis infection. This may be a mechanism of immune response and pathology not previously considered.

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Figures

Figure 1
Figure 1
Exhaled breath condensate pH measurements obtained in Ghana and Thailand reveal airway acidity in patients with pulmonary tuberculosis
Figure 2
Figure 2
Exhaled breath condensate pH measurements from Ghana and Thailand were reproducible over time (same samples, repeated assays)
See this image and copyright information in PMC

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