SERUM LEVELS OF INTERLEUKIN-1-BETA AND INTERLEUKIN-6 IN PATIENTS WITH CHRONIC-PANCREATITIS

被引:17
作者
BAMBA, T
YOSHIOKA, U
INOUE, H
IWASAKI, Y
HOSODA, S
机构
[1] The Second Department of Internal Medicine, Shiga University of Medical Science, Ohtsu, Shiga, 520-1, Tsukinowa, Seta
关键词
INTERLEUKIN-1-BETA; INTERLEUKIN-6; CHRONIC PANCREATITIS;
D O I
10.1007/BF02358371
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
To investigate the role prayed by cytokines in chronic pancreatitis, we examined serum levels of interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) by radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA) in 33 patients with definitively diagnosed chronic pancreatitis. All the patients, who had received either no treatment or only digestive enzyme products for their chronic pancreatitis, had significantly elevated serum IL-1beta levels (38.5 +/-28.8 pg/ml, mean +/- SD), compared to normal controls (16.0 +/- 6.7 pg/ml; P < 0.01); however they showed no changes in serum IL-6 levels. Changes in IL-1beta and IL-6 serum levels were not correlated with the etiological features of pancreatitis or with complications due to liver diseases. Serum IL-1beta and IL-6 levels were also not correlated with the activity of any pancreatic enzymes in blood or urine. However, in the patients with chronic pancreatitis, serum IL-6 levels were correlated with C-reactive protein (CRP), whereas serum IL-1beta levels were not correlated with CRP or with erythrocyte sedimentation rate. These results suggest that serum IL-1beta is involved in the progression and reduction of chronic inflammation of the pancreas, and that the serum IL-1beta level may be useful as a marker for chronic pancreatitis.
引用
收藏
页码:314 / 319
页数:6
相关论文
共 28 条
  • [1] Creutzfeldt W., Schmidt H., Aetiology and pathogenesis of pancreatitis, Scand J Gastroenterol, 6, pp. 47-62, (1970)
  • [2] Steer M.L., Etiology and pathophysiology of acute pancreatitis, The exocrine pancreas: Biology, pathophysiology, and diseases, pp. 465-474, (1986)
  • [3] Warren J.S., Ward P.A., Johnson K.J., Oxygen radicals as mediators of inflammation, Mediators of the inflammatory process, pp. 159-176, (1989)
  • [4] Brigham K.L., Mediators of the inflammatory process: Prostanoids, Mediators of the inflammatory process, pp. 1-14, (1989)
  • [5] Henderson W.R., Products of 12- and 15-lipoxygenase, Mediators of the inflammatory process, pp. 45-76, (1989)
  • [6] Vargaftig B.B., Pretolani M., Coeffier E., Chignard M., Platelet-activating factor: Biology, receptors, and antagonists, Mediators of the inflammatory process, pp. 113-146, (1989)
  • [7] Shaw R.J., Clark R.A.F., Interleukins and their interactions in inflammation, Mediators of the inflammatory process, pp. 245-268, (1989)
  • [8] Singer M.V., Gyr K., Sarles H., Revised classification of pancreatitis. Report of the second international symposium on the classification of pancreatitis in Marseille, France, March 28–30, 1984, Gastroenterology, 89, pp. 683-690, (1985)
  • [9] Schmidt J.A., Oliver C.N., Lepe-Zuniga J.L., Et al., Silica-stimulated monocytes release fibroblast proliferation factors identical to interleukin 1. A potential role for interleukin 1 in the pathogenesis of silicosis, J Clin Invest, 73, pp. 1462-1472, (1984)
  • [10] Canalis E., Interleukin-1 has independent effects on deoxyribonucleic acid and collagen synthesis in cultures of rat calvariae, Endocrinology, 118, pp. 74-81, (1986)