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The Relationship between Pleural Fluid Findings and the Development of Pleural
Thickening in Patients with Pleural Tuberculosis
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Carlos R R Carvalho
University of São Paulo
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Chest 1991;100;1264-1267
DOI 10.1378/chest.100.5.1264
The online version of this article, along with updated information and services
can be found online on the World Wide Web at:
http://chestjournal.chestpubs.org/content/100/5/1264
Chest is the official journal of the American College of Chest Physicians. It has
been published monthly since 1935. Copyright1991by the American College of
Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights
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(http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692
The objective of the study was to determine if residual was 5.40±0.58 g/dl for group 1 and 5.17±0.80 g/dl for
pleural thickening after treatment for pleural tuberculosis group 2, while the mean pleural fluid glucose level was
could be predicted from the pleural fluid findings at the 78.6± 19.5 mg/dl for group 1 and 79.5±20.1 mg/dl for
time of the initial thoracentesis. Forty-four patients initially group 2. The
pleural mean
fluid lactate dehydrogenase
diagnosed as having pleural tuberculosis between January (LDH)level in group 1 was 593 ±498 lUlL, while the mean
1986 and January 1988 were separated into two groups: the level for group 2 was 491 ± 198 lUlL. The presence of
23 patients in group 1 had residual pleural disease, while residual pleural thickening was not related to the chemo-
the 21 patients in group 2 had no residual pleural disease therapeutic regimen or the performance of a therapeutic
after treatment for their pleural tuberculosis was corn- thoracentesis. From this study we conclude that approxi-
pleted. Tb. clinical characteristics of the two different mately 50 percent of patients with pleural tuberculosis will
groups did not differ significantly, but the patients in group have residual pleural thickening when their therapy is
1 tended to be a little sicker in that the duration of their completed, but that one cannot predict which patients will
symptoms was longer, their hemoglobin values were lower, have residual pleural thickening from either their clinical
and weight loss and cough were more frequent. There were characteristics or their pleural fluid findings.
no significant differences in the pleural fluid findings in the (Chest 1991; 100:1264-67)
two different groups. The mean pleural fluid protein level
S
group of patients. There was a significant relationship S #{149}5
between the ratio ofthe pleural fluid to serum glucose S. S
S
S
and the ratio of the pleural fluid to serum LDH .5 S
(r = - 0.51, p<O.Ol). The minus sign on the correlation 200- 5 S
1266 Pleural Auid, Pleural Thickenrng and Pleural Tuberculosis (Bathes eta!)
what is it related to? The patients with residual tuberculous pleurisy in the light of a follow-up study. Acts
Tuberc Scand 1964; 44:303-09
thickening tended to have a larger PPD, a lower
3 Lee CH, Wang WJ, Lan RS, Tsai YH, Chiang YC. Corticoste-
incidence ofpositive pleural fluid cultures, and a lower roids in the treatment of tuberculous pleurisy: a double-blind,
incidence ofpositive AFB smears. These observations placebo-controlled, randomized study. Chest 1988; 94:1256-59
suggest that delayed hypersensitivity rather than the 4 Morrone N, Lombardi MC, Machado 0. Prevention of pleural
inflammatory response to infection is responsible for thickening through pleural aspiration in patients with tubercu-
bus effusion. J Pneumologia (San Paulo) 1989; 15:180-84
the fibrosis. The local inflammatory hypersensitivity
5 Martensson C, Bake B, Brolin I, Larsson 5, Pettersson K,
response with tuberculous pleuntis is mediated in Thiringer C. Radiographic appearance and lung function after
part by a number of inflammatory and immunostim- non-malignant pleural efihision. Eur J Bespir Dis 1987; 71:306-
ulatory factors, including complement degradation 13
products, interferon gamma, and interleukin 1.112 6 Light RW, Pleural diseases, 2nd ed. Philadelphia: Lea & Febiger,
1990
Since it is becoming increasingly clear that cytokines
7 Light RW, Girard WM, Jenkinson SC, George RB. The mci-
modulate the development of fibrosis,’3”4 one might dence and significance of parapneumonic effusions. Am J Med
anticipate that there would be some relationship 1980; 69:507-12
between the level of hypersensitivity and the devel- 8 Rodriguez-Panadero F, Lopez Mejias J. Low glucose and pH
opment of pleural fibrosis. levels in malignant pleural effusions. Am Rev Respir Dis 1989;
139:663-67
We had also anticipated that there would be a
9 Roper WH, WaringJJ. Primary serofibrinous pleural effusion in
significant negative correlation between the levels of military personnel. Am Rev Respir Dis 1955; 71:616-34
LDH and the levels of glucose in the pleural fluid. 10 Ellner JJ, Barnes PF, Wallis RS, Modin RL. The immunology of
This has been the case with parapneumonic’5 and tuberculous pleurisy. Sem Respir Infect 1988; 3:335-42
malignant’6 pleural effusions. In the present study, 11 Barnes PF, Mistry SD, Cooper CL, Pirmez C, Rea TH, Modlin
RL. Compartmentalization ofa CD4 T lymphocyte subpopu-
there was not a significant correlation between the
lation in tuberculous pleuritis. J Immunol 1989; 142:1114-19
levels of glucose and LDH in the pleural fluid, 12 Ribera E, Espanol T, Martinez-Vazquez JM, Ocana I, Encabo
although there was a significant relationship between C. Lymphocyte proliferation and gamma-interferon production
the ratios of the pleural fluid to the serum LDH and after in vitro’ stimulation with PPD: differences between
glucose. The lack of a significant correlation with the tuberculous and nontuberculous pleurisy in patients with posi-
tive tuberculin skin test. Chest 1990; 97:1381-85
absolute levels was quite possibly related to the
13 Antony YB, Sahn SA, Antony AC, RepinejE. Bacillus Calmette-
relatively narrow range of pleural fluid glucose levels. Guerin-stimulated neutrophils release chemotaxins for mono-
In conclusion, the results of the present study fail cytes in rabbit pleural spaces and in vitro. J Clin Invest 1985;
to support our hypothesis that residual pleural thick- 76:1514-21
ening would be more common in patients with pleural 14 Libby P, Friedman GB, Salomon RM. Cytokines as modulators
ofcell proliferation in fibrotic disease. Am Rev Respir Dis 1989;
tuberculosis with a higher degree of pleural inflam-
140:1114-17
mation as evidenced by lower pleural fluid glucose
15 Good JT Jr. Taryle DA, Maulitz RM, Kaplan RL, Sahn SA. The
levels and higher pleural fluid LDH levels. The diagnostic value ofpleural fluid pH. Chest 1980; 78:55-9
incidence of residual pleural thickening was slightly 16 Sahn SA, Good JT Jr. Pleural fluid pH in malignant effusions:
above 50 percent, but the presence of the residual diagnostic, prognostic, and therapeutic implications. Ann Intern
Med 1988; 108:345-49
pleural thickening was not associated with clinical
17 Schwartz DA, Calvin JR. Dayton CS, Stanford W, Merchant
symptoms. It is unlikely that the mild degrees of
JA, Hunninghake GW. Determinants ofrestrictive lung function
residual thickening observed in the present study have in asbestos-induced pleural fibrosis. J AppI Physiol 1990;
any clinical significance. Although documentation of 68:1932-37