Bird G L, Sheron N, Goka A K, Alexander G J, Williams R S
King's College Hospital, Denmark Hill, London, United Kingdom.
Ann Intern Med. 1990 Jun 15;112(12):917-20. doi: 10.7326/0003-4819-112-12-917.
To determine whether elevated tumor necrosis factor levels contribute to the clinical manifestations and complications of severe acute alcoholic hepatitis and to evaluate the relation between tumor necrosis factor and plasma levels of endotoxin and interleukin-1 beta.
Prospective, controlled study.
The liver unit of a university teaching hospital.
We studied 21 patients with acute severe alcoholic hepatitis. There were four control groups: patients with inactive alcoholic cirrhosis, alcoholic persons without liver disease, patients with impaired renal function, and normal subjects.
With one exception, patients with alcoholic hepatitis had higher tumor necrosis factor levels (mean, 26.3 ng/L; 95% CI, 21.7 to 30.9) than normal subjects (6.4 ng/L; CI, 5.4 to 7.4). Patients who subsequently died had a higher tumor necrosis factor level (34.7 ng/L; CI, 27.8 to 41.6) than survivors (16.6 ng/L; CI, 14.0 to 19.2). In patients with alcoholic hepatitis, tumor necrosis factor levels correlated positively with serum bilirubin (r = 0.74; P = 0.0009) and serum creatinine (r = 0.81; P = 0.0003). Patients with alcoholic hepatitis had higher tumor necrosis factor levels than patients with inactive alcoholic cirrhosis (11.1 ng/L; CI, 8.9 to 13.3) and severely alcoholic persons without liver disease (6.4 ng/L; CI, 5.0 to 7.8). Patients with abnormal renal function had lower tumor necrosis factor levels (14.1 ng/L; CI, 5.4 to 22.8) than patients with alcoholic hepatitis. Serial samples obtained during a 1-week period from patients with alcoholic hepatitis showed no significant change in tumor necrosis factor when patients who died were compared with survivors. No correlation was found between tumor necrosis factor and plasma endotoxin. Levels of interleukin-1 beta did not exceed 20 ng/L.
Elevations in tumor necrosis factor in alcoholic hepatitis are most marked in severe cases, suggesting that tumor necrosis factor plays a role in the pathogenesis.
确定肿瘤坏死因子水平升高是否会导致严重急性酒精性肝炎的临床表现及并发症，并评估肿瘤坏死因子与内毒素及白细胞介素-1β血浆水平之间的关系。
前瞻性对照研究。
一所大学教学医院的肝病科。
我们研究了21例急性重症酒精性肝炎患者。有四个对照组：非活动性酒精性肝硬化患者、无肝病的酗酒者、肾功能受损患者和正常受试者。
除1例患者外，酒精性肝炎患者的肿瘤坏死因子水平（均值为26.3 ng/L；95%可信区间为21.7至30.9）高于正常受试者（6.4 ng/L；可信区间为5.4至7.4）。随后死亡的患者肿瘤坏死因子水平（34.7 ng/L；可信区间为27.8至41.6）高于存活者（16.6 ng/L；可信区间为14.0至19.2）。在酒精性肝炎患者中，肿瘤坏死因子水平与血清胆红素呈正相关（r = 0.74；P = 0.0009），与血清肌酐也呈正相关（r = 0.81；P = 0.0003）。酒精性肝炎患者的肿瘤坏死因子水平高于非活动性酒精性肝硬化患者（11.1 ng/L；可信区间为8.9至13.3）和无肝病的重度酗酒者（6.4 ng/L；可信区间为5.0至7.8）。肾功能异常患者的肿瘤坏死因子水平（14.1 ng/L；可信区间为5.4至22.8）低于酒精性肝炎患者。在1周内从酒精性肝炎患者采集的系列样本显示，将死亡患者与存活者相比，肿瘤坏死因子无显著变化。未发现肿瘤坏死因子与血浆内毒素之间存在相关性。白细胞介素-1β水平未超过20 ng/L。
酒精性肝炎中肿瘤坏死因子的升高在重症病例中最为明显，提示肿瘤坏死因子在发病机制中起作用。
