Serum Complement Levels and Endothelial Markers in Patients with Exertional Heat Stroke

運動性熱中暑血清補體及內皮細胞傷害之研究

林裕峰(Yuh-Feng Lin) ； 陳金順(Gieen-Shuen Chen) ； 萬國良(Guo-Liang Wann) ； 林石化(Shih-Hua Lin) ； 謝善德(Shang-Der Shieh) ； 王家儀(Jia-Yi Wang)

《Journal of Medical Sciences》 19卷1期 (1998/08) Pp. 39-46

摘要

Exhaustive exercise or training in a humid and hot environment can cause exertional heat stoke in military recruits and lead to hyperthermia, shock, disseminated intravascular coagulation (DIC), adult respiratory distress syndrome (ARDS), acute renal failure and multiple organ failure. It has well been known that endothelial cell damage might be the original pathogenesis resulting in systemic organ dysfunction. Complement activation, endothelial cell marker changes as well as cytokine production might all be cascades contribute to the clinical manifestation of exertional heat stroke (ExHS). However, only cytokine production has been studied in patients with ExHS. We then investigated endothelial cell marker changes and complement components in 20 patients with ExHS and 10 normal controls for further understanding of the pathophysiology of severe heat injury. Our results showed that angiotensin converting enzyme levels were significantly lower in patients with ExHS on admission (10.12 ± 1.95 vs 21.21 ± 3.18 nmol hippuric acid min^(-1) ml^(-1), p＜0.05) while von Willebrand's factor antigen (vWf:Ag) (1.34 ± 0.06 vs 0.63 ± 0.05%, p＜0.001) and thrombomodulin (79.12 ± 7.34 vs 63.47 ± 4.21 ng/mL, p＜0.05) were significantly higher on admission than those at recovery phase. Serum complement C3 (86.6 ± 1.5 vs 103.4 ± 3.3 mg/dL, p＜0.001), C4 (17.9 ± 0.7 vs 23.5 ± 1.4 mg/dL, p＜0.05) and CH50 (125.2 ± 11.9 vs 156.4 ± 9.3 mg/dL, p＜0.01) were significantly lower on admission than those at recovery phase. C3a des Arg was significantly elevated on admission as compared to that at recovery phase (15.5 ± 1.6 vs 13.2 ± 1.7x10^4 mg/dL, p＜0.05). There were good correlation between C3 and angiotensin converting enzyme (ACE) (r=0.64, p＜0.05), C3a and ACE (r=-0.58, p＜0.05), and C3 and vWf;Ag (r=-0.68, p＜0.05). From the above data, we might conclude that complement activation in ExHS could play important role in the pathogenesis of endothelial cell injury as well as endothelial marker changes. On the other hand, endothelial cell injury probably induced by heat itself, coagulation activation, endotoxin and oxidant injury might also contribute to complement activation.

關鍵字

熱中暑 ； 補體活化 ； 內皮細胞標記

並列摘要

Exhaustive exercise or training in a humid and hot environment can cause exertional heat stoke in military recruits and lead to hyperthermia, shock, disseminated intravascular coagulation (DIC), adult respiratory distress syndrome (ARDS), acute renal failure and multiple organ failure. It has well been known that endothelial cell damage might be the original pathogenesis resulting in systemic organ dysfunction. Complement activation, endothelial cell marker changes as well as cytokine production might all be cascades contribute to the clinical manifestation of exertional heat stroke (ExHS). However, only cytokine production has been studied in patients with ExHS. We then investigated endothelial cell marker changes and complement components in 20 patients with ExHS and 10 normal controls for further understanding of the pathophysiology of severe heat injury. Our results showed that angiotensin converting enzyme levels were significantly lower in patients with ExHS on admission (10.12 ± 1.95 vs 21.21 ± 3.18 nmol hippuric acid min^(-1) ml^(-1), p＜0.05) while von Willebrand's factor antigen (vWf:Ag) (1.34 ± 0.06 vs 0.63 ± 0.05%, p＜0.001) and thrombomodulin (79.12 ± 7.34 vs 63.47 ± 4.21 ng/mL, p＜0.05) were significantly higher on admission than those at recovery phase. Serum complement C3 (86.6 ± 1.5 vs 103.4 ± 3.3 mg/dL, p＜0.001), C4 (17.9 ± 0.7 vs 23.5 ± 1.4 mg/dL, p＜0.05) and CH50 (125.2 ± 11.9 vs 156.4 ± 9.3 mg/dL, p＜0.01) were significantly lower on admission than those at recovery phase. C3a des Arg was significantly elevated on admission as compared to that at recovery phase (15.5 ± 1.6 vs 13.2 ± 1.7x10^4 mg/dL, p＜0.05). There were good correlation between C3 and angiotensin converting enzyme (ACE) (r=0.64, p＜0.05), C3a and ACE (r=-0.58, p＜0.05), and C3 and vWf;Ag (r=-0.68, p＜0.05). From the above data, we might conclude that complement activation in ExHS could play important role in the pathogenesis of endothelial cell injury as well as endothelial marker changes. On the other hand, endothelial cell injury probably induced by heat itself, coagulation activation, endotoxin and oxidant injury might also contribute to complement activation.

並列關鍵字

heat stroke ； complement activation ； endothelial markers