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Tuberculosis associated pulmonary hypertension: The revelation of a clinical observation

BACKGROUND: Pulmonary tuberculosis is not listed as a cause of pulmonary hypertension (PH). Scanty information is available in the literature regarding this issue. METHODS: A group of patients with a history of pulmonary tuberculosis were diagnosed to have PH on the basis of a novel clinico-radio-ec...

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Detalles Bibliográficos
Autores principales: Bhattacharyya, Parthasarathi, Saha, Dipanjan, Bhattacherjee, Pratyaya Deep, Das, Soumen Kumar, Bhattacharyya, Pinak Pani, Dey, Ratna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4797429/
https://www.ncbi.nlm.nih.gov/pubmed/27051098
http://dx.doi.org/10.4103/0970-2113.177433
Descripción
Sumario:BACKGROUND: Pulmonary tuberculosis is not listed as a cause of pulmonary hypertension (PH). Scanty information is available in the literature regarding this issue. METHODS: A group of patients with a history of pulmonary tuberculosis were diagnosed to have PH on the basis of a novel clinico-radio-echocardiographic criteria. Subdivided into two groups on the basis of the history of smoking, we looked for their demographic, spirometric, radiological characteristics along with the quality of life assessment. RESULTS: A total of 40 patients (21 smokers and 19 nonsmokers) were found to have PH with history of pulmonary tuberculosis. The two groups were similar radiologically including the extent of fibrosis. The nonsmoker group had lower age range (52.16 ± 14.81 vs. 63.1 ± 10.05, P = 0.01), worse chronic obstructive pulmonary disease (COPD) assessment test score (16.11 ± 6.24 vs. 13.9 ± 5.6, P = 0.25) and higher pulmonary artery (PA) pressure (46.39 ± 7.44 vs. 44.55 ± 8.04, P = 0.46) compared to the smokers. Overall and for the smoker group, in particular, the spirometric pictures were favoring obstruction without reversibility as in COPD (forced expiratory volume in 1 second [FEV(1)] % as 64.26 ± 18.38 and 58.85 ± 14.61 with % of predicted FEV(1) being 43.74 ± 17.26 and 42.38 ± 16.64 respectively). However, those with no history of smoking had restrictive changes as in diffuse parenchymal lung disease (DPLD) in their spirometry (FEV(1)/forced vital capacity [FVC] of 79.33 ± 19.93 and FVC as 49.67 ± 11.54% of predicted). The smoker group had far more obvious involvement of the small airways in terms of change in FEF(25-75) compared to nonsmokers (FEF(25-75) = 22.85 ± 19.68 vs. 63.83 ± 48.61). CONCLUSION: PH appears associated with the history of pulmonary tuberculosis. With or without a history of smoking, they pose two distinct phenotypes in spirometry as COPD and DPLD. The DPLD phenotype had worse quality of life.