Pleural inflammation caused by bacteria, mycobacterium, or autoimmune disease is usually characterized by effusion, fever, malaise, chest pain, nonproductive cough, and dyspnea in the acute phage , or diffuse thickening of the pleura, with or without calcification, in the chronic phase. Therefore, pleural thickening with no subjective symptoms generally implies non-active inflammatory pleural diseases, so-called “residual pleural thickness”, or neoplasm of the pleura. Interestingly, the asymptomatic diffuse pleural thickening in our case showed intense FDG uptake and proved to be caseous granulomatous inflammation.
Duysinx et al. suggested that FDG PET/CT is an effective tool for differentiating between benign and malignant pleural diseases. The uptake of FDG was intense in all cases of mesothelioma and neoplastic pleurisy associated with primary lung cancer. In contrast, FDG PET/CT imaging revealed an absence of FDG uptake within the pleura of 2 of 3 patients with tuberculous pleurisy and the rest showed moderate uptake, although detailed clinical data of these patients were not described . Kramer et al. also evaluated the feasibility of PET in the diagnosis of pleural thickening on CT. They concluded that qualitative assessment with PET discriminates between malignant and benign pleural thickening with high accuracy and a high negative predictive value. However, there has been no description of tuberculous pleurisy . To the best of our knowledge, this is the first reported case of tuberculous pleurisy with intense FDP uptake.
The pathogenesis of primary tuberculous pleurisy is a delayed-type hypersensitivity immunogenic reaction to a few mycobacterial antigens entering the pleural space rather than direct tissue destruction by uncontrolled mycobacterial proliferation . This appears to be the reason for the low rate of positive results in acid-fast staining of pleural fluid and tissue, as seen in this case . Recent findings suggest that the immunogenic reaction in tuberculous pleurisy involves lymphocytes (including CD3, CD4, CCR4, and Th17 cells), neutrophils, mesothelial cells, and various cytokines such as interferon-γ, interleukin (IL)-8, IL-12, and monocyte chemoattractant protein-1 [17, 18]. However, the complex mechanisms that induce high glucose metabolism and show high uptake of FDG in pleural thickening is unclear at this time.
About half of untreated cases of primary tuberculous pleurisy relapse with more severe forms of active pulmonary or extra-pulmonary tuberculosis, which may result in severe disability or death [19, 20]. However, in general, many cases of pleural thickening suspiciously caused by primary tuberculous pleurisy with no subjective symptoms have not received antituberculous chemotherapy. FDG uptake in the pleura with positive QuantiFERON-TB may support the use of antituberculous treatment in such cases.