INT J TUBERC LUNG DIS 6(6):516–522 © 2002 IUATLD The effect of pleural fluid content on the development of pleural thickness E. Kunter,* A. Ilvan,* E. Kilic,* K. Cerrahoglu,* T. Isitmangil, F. Capraz,* K. Avsar Departments of * Respiratory Diseases, Thoracic Surgery and Clinical Biochemistry, GATA Camlica Chest Diseases SUMMARY Hospital, Istanbul, Turkey SETTING: Residual pleural thickness (RPT) is a com- mon complication of tuberculous pleurisy (TP), and the degree of RPT cannot be predicted in advance. OBJECTIVES: To determine whether pleural fluid con- tent has an effect on the development of RPT. DESIGN: Forty-seven patients with TP were enrolled in the study. A set of biochemical tests: lactate dehydro- genase, glucose, total proteins, adenosine deaminase, tumour necrosis factor alpha (TNF-), alpha-1 acid glycoprotein (AAG), alpha-2 macroglobulin, C-reactive protein (CRP), complement 3 and complement 4 were studied in the pleural fluid samples. After 6 months of anti-tuberculosis treatment, patients were re-evaluated for RPT. RPT was defined in a posteroanterior chest radiograph as a pleural space of 2 mm or 10 mm mea- sured in the lower lateral chest at the level of an imaginary horizontal line intersecting the diaphragmatic dome. RESULTS: Seventeen patients (36.17%) had an RPT of 2 mm, 18 (38.29%) had an RPT of 2–10 mm, and 12 (25.53%) had an RPT of 10 mm. TNF-levels were lower in patients with an RPT of 2 mm than in patients with an RPT of 2–10 mm or 10 mm (P 0.05 and P 0.01, respectively). The level of TNF-was higher in patients with an RPT of 10 mm compared to the 2–10 mm group (P 0.05). Meanwhile, pleural fluid glucose, AAG and CRP concentrations were signifi- cantly higher in patients with an RPT of 10 mm than in patients with 2 mm RPT (P 0.05, P 0.01, and P 0.05, respectively). CONCLUSION: In TP, the development and degree of RPT are significantly correlated to the glucose, CRP, AAG, and TNF-levels in the pleural fluid. KEY WORDS: tuberculous pleurisy; pleural thickness; pleural fluid content TUBERCULOUS pleural effusion is estimated to con- stitute approximately 5–30% of all diseases due to Mycobacterium tuberculosis. 1,2 Patients with tuber- culous pleurisy (TP) almost invariably have a small subpleural nidus of tuberculosis, even if there is no radiologically apparent parenchymal disease, show- ing fibrous and granulomatous inflammation and leakage into the pleural space. 3 It has been reported that about half of tuberculous pleurisy patients develop residual pleural thickness (RPT) despite appropriate treatment. 4 Depending on the size of the RPT, from a blunted costophrenic angle to wide- spread pachypleuritis, post treatment clinical out- comes of individuals may vary greatly, and surgical removal of the thickened pleura may sometimes be inevitable. Generally, treatment options to prevent thickening of pleura are far from being satisfactory. Corticosteroids, which have been used widely for this purpose, are also thought to be of little use. 5 There are currently no established criteria to predict the development and/or degree of RPT after the treat- ment of TP. The aim of this study was to determine whether residual pleural thickening after treatment for pleural tuberculosis was related to the parameters detected at the time of the initial thoracentesis. There is no doubt that RPT is a consequence of an inflammatory mech- anism in TP. In this regard, we assessed the value of some well known variables, including lactate dehy- drogenase (LDH), glucose, total proteins, adenosine deaminase (ADA) activity, tumour necrosis factor alpha (TNF-), some acute phase reactant (APR) pro- teins such as alpha-1 acid glycoprotein (AAG), alpha- 2 macroglobulin (AMG), C-reactive protein (CRP), complement 3 (C3) and complement 4 (C4) in the pleural fluid. The erythrocyte sedimentation rate (ESR) was also considered. MATERIALS AND METHODS A total of 47 consecutive patients with TP referred to our department from October 2000 to June 2001 were enrolled in the study. Within 24 hours of admis- sion, just before pleural biopsy, a sample of 20 mL of Correspondence to: Dr Erdogan Kunter, GATA Camlica Gogus Hastaliklari Hastanesi, Gogus Hastaliklari Servisi, 81020 Uskudar, Istanbul, Turkey. Tel: (90) 0216-325 72 50. Fax: (90) 0216-325 72 57. e-mail: erkunter@hotmail.com Article submitted 9 January 2002. Final version accepted 21 March 2002.