Esposito Irene, Bergmann Frank, Penzel Roland, di Mola Fabio F, Shrikhande Shailesh, Büchler Markus W, Friess Helmut, Otto Herwart F
Department of Pathology, University of Heidelberg, Im Neuenheimer Feld 220, 69120, Heidelberg, Germany.
Virchows Arch. 2004 Feb;444(2):119-26. doi: 10.1007/s00428-003-0949-1. Epub 2004 Jan 14.
Inflammatory pseudotumors (IPT), also known as inflammatory myofibroblastic tumors (IMT), are benign inflammatory processes that may have an infectious etiology and are very rare in the pancreatico-biliary region. Recent studies suggest a biological distinction between IPT and IMT, the latter being a true neoplastic process. We describe a case of pancreatic IPT, originally diagnosed as malignancy, which presumably recurred 4 months after the operation. Histologically, the tumor consisted of a smooth muscle actin and CD68-positive spindle cell population and a more abundant mononuclear inflammatory cell population, primarily composed of macrophages and T-lymphocytes. Inflammatory cells were the source of connective tissue growth factor and transforming growth factor-beta1 and tended to accumulate around nerves and blood vessels, as well as around residual pancreatic parenchymal elements, where an intense angiogenetic response was detected. Comparative genomic hybridization analysis of the tumor showed no chromosomal imbalances. Polymerase chain reaction-based analysis of T-cell receptor gamma gene rearrangement revealed an oligoclonal pattern. These findings suggest that the pathogenesis of aggressive cases of IPT could be related to the development of an intense and self-maintaining immune response, with the emergence of clonal populations of T-lymphocytes. The relation of the pancreatic IPT to autoimmune pancreatitis is emphasized.
炎性假瘤(IPT),也称为炎性肌纤维母细胞瘤(IMT),是一种可能由感染引起的良性炎症过程,在胰胆管区域非常罕见。最近的研究表明IPT和IMT在生物学上存在区别,后者是一种真正的肿瘤性过程。我们描述了一例胰腺IPT病例,最初被诊断为恶性肿瘤,术后大概4个月复发。组织学上,肿瘤由平滑肌肌动蛋白和CD68阳性的梭形细胞群以及更丰富的单核炎性细胞群组成,主要由巨噬细胞和T淋巴细胞组成。炎性细胞是结缔组织生长因子和转化生长因子-β1的来源,倾向于在神经和血管周围以及残留的胰腺实质成分周围积聚,在这些部位检测到强烈的血管生成反应。对肿瘤进行的比较基因组杂交分析未显示染色体失衡。基于聚合酶链反应的T细胞受体γ基因重排分析显示为寡克隆模式。这些发现表明,侵袭性IPT病例的发病机制可能与强烈且自我维持的免疫反应的发展有关,伴随着T淋巴细胞克隆群体的出现。强调了胰腺IPT与自身免疫性胰腺炎的关系。