Clinical diagnosis
Case 152
【Progress】
His sputum culture revealed Guffky scale 4 or 5 indicative of active pulmonary tuberculosis. He was transported to the expert hospital where Tbc ward was served.
【Discussion】
When tuberculosis mycobacteria are infected, they are attacked by macrophages living in the pulmonary alveoli and engulfed into macrophages. They are not killed but survived in the macrophages. They can stay in macrophages for long. It is believed that they increase in number in macrophages in case of the weak immune response of the host, inducing active pulmonary tuberculosis with infectious potency (1). The healthy macrophages engulf the infected macrophages, forming Langerhans giant cells. When tuberculosis bacteria meet lymphocytes, lymphocytes secret cytokines; B cells secrete adenosine deaminase (ADA); T cells secrete interferon γ (INF-γ), which can be markers for tuberculosis infection (2, 3).
T cells, B cells, macrophages and fibrocytes form granulation nodule called tuberculoma which plays a role of defense, repressing contiguous potency from a point of a host view. However, it allows Tbc mycobacteria survive in the tuberculoma. When the infection activates, tissue destruction and necrosis occur forming cavities which contain vital tuberculosis mycobacteria (1-3). The sputum from the cavities can spread the infection. Besides, the necrosis evades the major vessel wall, inducing massive hemoptysis.
In a healthy condition, plural fluid produces from mesothelial cells and drains via pores of lymphatic channels at parietal pleura. Lymphatic channels at the visceral pleura outflow to the pulmonary lymph-nodes or the extra-pulmonary nodes along with extrapulmonary arteries such as intercostal artery, internal thoracic artery and so on. In an unhealthy situation, visceral lymphatic channels communicate with pleural space. Pleural effusion results from overproduction of pleural fluid or drainage disorder. Tuberculous pleurisy most occurs hemi-lateral. It is believed tuberculous pleurisy results from the peripheral pulmonary infected lesion invading directly to the visceral pleura or hematopoietic metastasis, inducing overproduction of pleural fluid (4-7).
As diseases causing unilateral pleural effusion, cardiac failure, liver failure and renal failure, metastatic plural tumor, pulmonary artery embolism, primary mesothelioma, bacterial pleuritis and tuberculous pleurisy are listed. Sputum examination or thoracentesis is necessary for differentiation. Namely, first, it is necessary to distinct whether pleural effusion is transudate or exudate. If transudate, it comes from chronic heart failure, liver cirrhosis or nephrosis. If exudate, further examination is necessary since it may come from pulmonary embolism, malignancy from mesothelioma or metastatic pleural tumor, or mycobacterium tuberculosis. In case of pulmonary tuberculosis, ADA and INF-γ are crucial markers for tuberculosis infection. The cutoff value to predict tuberculosis pleurisy is 40 U/L (2, 3). In our case, the pleura effusion obtained from thoracentesis revealed exudate and the value of ADA of the pleural effusion was 54.5 U/L, indicative diagnosis of tuberculosis pleurisy.
【Summary】
We present a seventy nine year-old male presented in our hospital suffering from cough, sputum, chest pain, nausea and slight fever for several days. He had experienced right pleural effusion eight months before. It revealed total protein 5.5 g/dL, lymphocytes 90%, adenosine deaminase (ADA) level 54.5 U/L, indicative diagnosis of tuberculosis of pleurisy. When tuberculosis mycobacteria are infected into pulmonary alveola, macrophages engulf them and lymphocytes secret cytokine: B cells secret ADA, T cells secret interferon γ. Besides, macrophages engulf the infected macrophage, forming Langerhans giant cells. Macrophages, T cells, B cells and fibrocytes form a tuberculoma which can be either defensive for the host or protective for tuberculosis mycobacterium. However, when the infection surpasses, it forms necrosis and evades the vessel wall, namely cavity which indicates the potency of spreading infection and causes hemoptysis, respectively. Tuberculous pleurisy most occurs hemi-lateral via the route of direct infection to the pleura from the peripheral pulmonary focus or via the hemopoietic route.
When pleural effusion is transudate, it comes from chronic heart failure, liver cirrhosis or nephrosis. If exudate, it comes from pulmonary embolism, malignancy from mesothelioma or metastatic pleural tumor, or mycobacterium tuberculosis. The cutoff value to predict tuberculosis pleurisy is 40 U/L. In our case, the value of ADA of the pleural effusion was 54.5 U/L, indicative diagnosis of tuberculosis pleurisy.
【References】
1.Houben EN, et al. Interaction of pathogenic mycobacteria with the host immune system. Current Opinion in Microbiology. 2006; 9: 76–85.
2.Doosoo Je on, M.D. Tuberculous Pleurisy: An Update. Tuberc Respir Dis 2014; 76: 153–159
3.Porcel JM, et al. Advances in the diagnosis of tuberculous pleuritis. Ann Transl Med. 2016; 4(15): 282
4.Berger HW, et al. Tuberculous pleurisy. Chest. 1973;63:88–92.
5.Epstein DM, et al. Tuberculous pleural effusions. Chest. 1987;91:106–9.
6.Ilsen B, et al. Comparative Interpretation of CT and Standard Radiography of the Pleura. Journal of the Belgian Society of Radiology. 2016;100(1):106
7.Patel A, et al. Pleural tuberculosis presented as multiple pleural masses: An atypical presentation. Lung India. 2013 Jan-Mar; 30(1): 54–56
2019.7.10