The Role of Tumor Necrosis Factor-alpha and Interleukin-1beta as Predictable Markers for Development of Adult Respiratory Distress Syndrome in Septic Syndrome.
10.4046/trd.1994.41.5.452
- Author:
Youn Suck KOH
;
Yun Hae JANG
;
Woo Sung KIM
;
Won Dong KIM
;
Jae Dam LEE
;
Soon Hwan OH
- Publication Type:Original Article
- Keywords:
Adult respiratory distress syndrome;
Septic syndrome;
Tumor necrosis factor-alpha;
Interleukin-1beta
- MeSH:
Acute Lung Injury;
Adult*;
Chungcheongnam-do;
Enzyme-Linked Immunosorbent Assay;
Humans;
Intensive Care Units;
Interleukin-1beta*;
Lung;
Lymphotoxin-alpha;
Necrosis;
Plasma;
Respiratory Distress Syndrome, Adult*;
Respiratory Insufficiency;
Shock;
Shock, Septic;
Tumor Necrosis Factor-alpha*
- From:Tuberculosis and Respiratory Diseases
1994;41(5):452-461
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Tumor necrosis factor(TNF)-alpha and Interleukin(IL)-1beta are thought to play a major role in the pathogenesis of the septic syndrome, which is frequently associated with adult respiratory distress syndrome(ARDS). In spite of many reports for the role of TNF-alpha in the pathogenesis of ARDS, including human studies, it has been reported that TNF-alpha is not sensitive and specific marker for impending ARDS. But there is a possibility that the results were affected by the diversity of pathogenetic mechanisms leading to the ARDS because of various underlying disorders of the study group in the previous reports. The purpose of the present study was to evaluate the roles of TNF-alpha and IL-lbeta as a predictable marker for development of ARDS in the patients with septic syndrome, in which the pathogenesis is believed to be mainly cytokine-mediated. METHODS: Thirty-six patients of the septic syndrome hospitalized in the intensive care units of the Asan Medical Center were studied. Sixteens suffered from ARDS, whereas the remaining 20 were at the risk of developing ARDS(acute hypoxemic respiratory failure, AHRF). In all patients venous blood sample were collected in heparin-coated tubes at the time of enrollment, at 24 and 72 h thereafter. TNF-alpha and IL-lbeta was measured by an enzyme-linked immunosorbent assay (ELISA). All data are expressed as median with interquartile range. RESULTS: 1) Plama TNF-alpha levels: Plasma TNF-beta levels were less than 10pg/mL, which is lowest detection value of the kit used in this study within the range of the mean+/-2SD, in all of the normal controls, 8 of 16 subjects of ARDS and in 8 in 20 subjects of AHRF. Plasma TNF-alpha levels from patients with ARDS were 10.26pg/mL(median;<10-16.99pg/mL, interquartile range) and not different from those of patients at AHRF(10.82, <10-20.38pg/mL). There was also no significant difference between pre-ARDS(<10, <10-15.32pg/mL) and ARDS(<10, <10-10.22pg/mL). TNF-alpha levels were significantly greater in the patients with shock than the patients without shock(12.53pg/mL vs. <10pg/mL) (P<0.01). There was no statistical significance between survivors(< 10, <10-12.92pg/mL) and nonsurvivors(11.80, <10-20.8pg/mL) (P=0.28) in the plasma TNF-alpha levels. 2) Plasma IL-lbeta levels: Plasma IL-1beta levels were less than 0.3ng/mL, which is the lowest detection value of the kit used in this study, in one of each patients group. There was no significant difference in IL-1beta levels of the ARDS(2.22, 1.37-8.01ng/mL) and of the AHRF(2.13, 0.83-5.29ng/mL). There was also no significant difference between pre-ARDS(2.53, <0.3-8.34ng/mL) and ARDS(5.35, 0.66-11.51ng/mL), and between patients with septic shock and patients without shock (2.51, 1.28-8.34 vs 1.46, 0.15-2.13ng/mL). Plasma IL-19 levels were significantly different between survivors(1.37, 0.4-2.36ng/mL) and nonsurvivors(2.84, 1.46-8.34ng/mL). CONCLUSION: Plasma TNF-alpha and IL-1beta level are not a predictable marker for development of ARDS. But TNF-alpha is a marker for shock in septic syndrome. These result could not exclude a possibility of pathophysiologic roles of TNF-alpha and IL-1beta in acute lung injury because these cytokine could be locally produced and exert its effects within the lungs.
