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Poster Presentations: Wednesday, October 26, 2011 |

Role of Latent Tuberculosis Infection in the Pathogenesis and Severity of COPD FREE TO VIEW

Hridaya Ghimire, MBBS; Jian Li, MD
Chest. 2011;140(4_MeetingAbstracts):564A. doi:10.1378/chest.1118939
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Abstract

PURPOSE: To identify pulmonary tuberculosis infection as a risk factor of COPD and to find out any structural and functional changes in lungs as well as to assess any inflammatory and nutritional changes in tuberculosis infected COPD patients.

METHODS: 207 COPD cases diagnosed with their clinical features along with post-bronchodilator FEV1/FVC<70% were reviewed. These COPD patients were divided into two groups; one with latent tuberculosis infection (according to radiologic feature of inactive tuberculosis) and other group without the infection of tuberculosis. Control cases include 190 patients who had done chest X-ray for routine check-up prescribed from departments.

RESULTS: Out of 207 COPD patients, 87 of them had radiological feature of inactive tuberculosis but only 22 out of 190 control patients had those features in their chest X-ray, with OR=5.5, 95% CI [3.3-9.3] and Pearson Chi Square value 46.1, p=0.000. Out of total 207 COPD patients, 36 of them had bullae in their radiologic examination, among which 21 of them had latent tuberculosis features in their radiologic examination, with OR=2.23, 95% CI [1.07-4.62] and Pearson Chi Square value 4.8, p=0.029. In case of lung function parameters, tuberculosis infected group had lower FEV1/FVC compared to non-tuberculosis group {45(35-58) % vs. 49(39.2-58.0) %, p=0.040}. Tuberculosis infected COPD patients had higher high sensitive C reactive protein (hsCRP) level {23.9(4.4-98.5) mg/L vs. 9.4(2.1-56.1) mg/L, p=0.036}, lower plasma albumin {37.7±3.6g/L vs. 38.8±3.1g/L, p=0.019}, lower serum iron {8.8(5.6- 17.3) µmol/L vs. 12.6 (7.8-18.9) µmol/L, p=0.031} and lower transferrin {1.75(1.56-2.01)g/L vs. 1.98(1.74-2.18)g/L, p=0.026} compared to COPD patients without tuberculosis infection.

CONCLUSIONS: Tuberculosis infection increases the risk of COPD. Its coexistence with COPD results in greater inflammation and damage to lung tissue (determined by increase in bullae formation, higher hsCRP level) with decrease in basic nutritional elements.

CLINICAL IMPLICATIONS: Tuberculosis resulted in greater inflammation and damage to lung tissue in COPD patients. It may be necessary to recognize tuberculosis infected COPD groups as a new phenotype of COPD and should be treated accordingly.

DISCLOSURE: The following authors have nothing to disclose: Hridaya Ghimire, Jian Li

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