Bély Miklós, Apáthy Agnes
Department of Pathology, Policlinic of the Hospitaller Brothers of St. John of God, Budapest, Hungary.
Pathol Oncol Res. 2008 Dec;14(4):473-80. doi: 10.1007/s12253-008-9026-z. Epub 2008 Oct 31.
The aim of this study was to determine: the prevalence, and histological characteristics of vasculitis in the pancreas, and to follow the formal pathogenesis of multifocal pancreatitis due to arteritis and/or arteriolitis (multifocal vasculogenic pancreatitis). A randomized autopsy population of 161 in-patients with rheumatoid arthritis (RA) was studied. Systemic vasculitis (SV) complicated RA in 36 (22.36%) of 161 cases; tissue samples of pancreas were available for histologic evaluation in 28 patients. Pancreatitis and vasculitis were characterized histologically and immunohistochemically. Vasculogenic, multifocal pancreatitis was not recognized clinically. Vasculitis of the pancreatic arterioles and small arteries (branches of splenic artery, upper and lower gastroduodenal arteries) can lead to local ischaemia and to regressive changes in the pancreas. This vasculogenic process is more or less widespread and multifocal, depending on the number of involved vessels and is followed by reactive inflammation, depending on the stages of the pathological process. Because of the recurrent nature of vasculitis with time these regressive changes accumulate within the pancreas and may contribute to an unexpected circulatory failure and sudden death of the patient. Vasculogenic microinfarcts in the pancreas may be clinically characterized by unexplained recurrent abdominal symptoms and spontaneous remissions which insidiously may lead to metabolic failure resistant to therapy.
胰腺血管炎的患病率和组织学特征,并追踪由动脉炎和/或小动脉炎引起的多灶性胰腺炎(多灶性血管源性胰腺炎)的正式发病机制。对161例类风湿关节炎(RA)住院患者的随机尸检人群进行了研究。161例中有36例(22.36%)的系统性血管炎(SV)并发RA;28例患者有胰腺组织样本可用于组织学评估。对胰腺炎和血管炎进行了组织学和免疫组织化学特征分析。血管源性多灶性胰腺炎在临床上未被识别。胰腺小动脉和小动脉(脾动脉分支、胃十二指肠上下动脉)的血管炎可导致局部缺血和胰腺的退行性改变。这种血管源性过程或多或少广泛且多灶性,取决于受累血管的数量,并根据病理过程的阶段伴有反应性炎症。由于血管炎随时间反复发生,这些退行性改变在胰腺内积累,可能导致患者意外循环衰竭和猝死。胰腺血管源性微梗死在临床上可能表现为无法解释的反复腹部症状和自发缓解,可能会隐匿地导致对治疗有抵抗性的代谢衰竭。