Shrikhande S V, Martignoni M E, Shrikhande M, Kappeler A, Ramesh H, Zimmermann A, Büchler M W, Friess H
Department of General Surgery, University of Heidelberg, Heidelberg, Germany.
Br J Surg. 2003 Dec;90(12):1565-72. doi: 10.1002/bjs.4353.
There is increasing evidence that immune mechanisms may be crucial in the development of alcoholic chronic pancreatitis. However, it is not known whether differences in underlying aetiology influence the inflammatory reaction in patients with chronic pancreatitis. The histological features and the pattern of inflammatory cell infiltration were studied in three aetiological forms of chronic pancreatitis: alcoholic, idiopathic and tropical pancreatitis.
Forty-three patients, ten with alcoholic, 12 with idiopathic and 21 with tropical chronic pancreatitis, were evaluated for the pattern of pancreatic inflammatory cell infiltration and histological features. Ten organ donors served as controls. Haematoxylin and eosin-stained tissue sections were used for histological evaluation. For immunohistochemical characterization of the inflammatory reaction, four antibodies-CD4, CD8, CD45 and CD68-were used. Quantitative evaluation of the various cell infiltrates was performed with computer-assisted image analysis. The inflammatory cell infiltration pattern was also evaluated.
The degree of endophlebitis and the overall density of plasma cells were greater in tropical than in alcoholic chronic pancreatitis. The grade of intralobular fibrosis was significantly higher in tropical chronic pancreatitis compared with the idiopathic form. No significant quantitative differences in the specific cellular infiltrates (CD4, CD8, CD45, CD68) were observed in the three different groups. However, the perivascular inflammation number score was significantly higher in alcoholic compared with idiopathic pancreatitis (P = 0.037), and the perivascular inflammation area score was significantly lower in idiopathic than in alcoholic (P = 0.024) or tropical (P = 0.020) pancreatitis.
Different aetiological forms of chronic pancreatitis result in similar histological features and a comparable inflammatory cell reaction, indicating that the disease, independent of the underlying aetiology, reaches a common immunological stage beyond which it appears to progress as a single distinctive entity.
越来越多的证据表明免疫机制在酒精性慢性胰腺炎的发展中可能至关重要。然而，尚不清楚潜在病因的差异是否会影响慢性胰腺炎患者的炎症反应。对三种病因形式的慢性胰腺炎（酒精性、特发性和热带性胰腺炎）的组织学特征和炎症细胞浸润模式进行了研究。
对43例患者进行评估，其中10例为酒精性慢性胰腺炎，12例为特发性慢性胰腺炎，21例为热带性慢性胰腺炎，观察其胰腺炎症细胞浸润模式和组织学特征。10例器官捐献者作为对照。苏木精-伊红染色的组织切片用于组织学评估。为了对炎症反应进行免疫组织化学表征，使用了四种抗体——CD4、CD8、CD45和CD68。采用计算机辅助图像分析对各种细胞浸润进行定量评估。还评估了炎症细胞浸润模式。
热带性慢性胰腺炎的静脉内炎程度和浆细胞总体密度高于酒精性慢性胰腺炎。与特发性慢性胰腺炎相比，热带性慢性胰腺炎的小叶内纤维化程度明显更高。在三个不同组中，未观察到特定细胞浸润（CD4、CD8、CD45、CD68）的显著定量差异。然而，酒精性胰腺炎患者的血管周围炎症数量评分显著高于特发性胰腺炎（P = 0.037），特发性胰腺炎的血管周围炎症面积评分显著低于酒精性（P = 0.024）或热带性（P = 0.020）胰腺炎。
不同病因形式的慢性胰腺炎导致相似的组织学特征和相当的炎症细胞反应，表明该疾病与潜在病因无关，达到了一个共同的免疫阶段，在此阶段之后，它似乎作为一个独特的实体发展。
