To Investigate Diagnostic Aid of the Inflammation and Apoptosis-associated Markers and Apoptosis Pattern of PE Neutrophil for Tuberculous Pleurisy Clinical Trial
Official title:
Evaluating the Diagnostic Validity of Inflammation-associated Markers for Tuberculous Pleurisy
1. To investigate the difference of PE inflammation/apoptosis-associated markers between
TB pleurisy and non-TB pleurisy
2. To investigate the difference of neutrophil apoptosis in exudative PE between TB
pleurisy and non-TB pleurisy
3. To investigate the change of apoptosis pattern of PE neutrophil, before and after TB
antigen stimulation, and compare the difference between TB pleurisy and non-TB pleurisy
4. To investigate diagnostic aid of the inflammation/apoptosis-associated markers and
apoptosis pattern of PE neutrophil for tuberculous pleurisy
Tuberculosis (TB) remains a global health problem even though it has nearly been eradicated
in some developed countries. Because of variable manifestations and the difficulty in
collecting clinical samples, extra-pulmonary TB is usually difficult to early diagnose.
Tuberculous pleurisy (TP) is one of the most common extra-pulmonary infection and accounts
for approximately 5% of all forms of TB. The gold standard for diagnosing TP is
mycobacterial culture of pleural effusion (PE), pleura tissue, which requires weeks to
yield. The treatment could thus be delayed, resulting in an increased mortality rate. In
addition, mycobacterial culture is not so sensitive for PE and with positivity in less than
two thirds of cases with TB pleurisy.
For diagnosing TP, PE biomarkers are required to be investigated in addition to traditional
PE cell counting and biochemistry. In particularly, inflammation-associated cytokines and
apoptosis-associated markers may be important because the two pathways involve in TB
infection/defense mechanism. For inflammation-association markers, current literature is not
comprehensive except IFN-gamma and IFN-gamma release assay (IGRA). However, the result of
IGRA using PE is disappointed. We should study other PE inflammation markers such as
IFN-induced protein-10, interleukin [IL]-2, IL-12 and so on. On the other hand, apoptosis
suppression is one of escape mechanisms in TB pathogenesis. Macrophage, dendritic cell, and
neutrophil are reportedly inhibited for apoptosis in TB infection. But the apoptosis of PE
neutrophil are rarely studied. Moreover, the role of apoptosis-associated markers (Fas
ligand [FasL], decoy receptor 3, lipoxin, prostaglandin E2, caspases) in PE has rarely been
investigated in diagnosing TP except FasL. Therefore, we conduct a prospective study to
investigate inflammation/apoptosis-associated markers in exudative PE and apoptosis of PE
neutrophil to analyze their diagnostic usefulness for TP.
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Observational Model: Case Control, Time Perspective: Prospective