慢性胰腺炎癌变研究进展与鉴别诊断

慢性胰腺炎与胰腺癌关系密切,慢性胰腺炎病人胰腺癌发生风险增加。其癌变机制尚不明确,多种细胞因子及信号通路参与慢性胰腺炎癌变过程。肿块型慢性胰腺炎与胰腺癌临床表现及影像学特征相似,术前鉴别诊断困难,内镜超声引导下细针穿刺活检（EUS-FNA）及PET/CT具有很好的鉴别诊断价值。     

肿块型胰腺炎与胰腺癌的鉴别诊断

肿块型胰腺炎是慢性胰腺炎的一种特殊类型，临床及影像学检查表现为胰腺局限性肿块，往往难以与胰腺癌相鉴别。本文回顾性分析了本院1997年1月至2004年7月收治的肿块型胰腺炎16例以及胰腺癌32例患者的临床资料，对肿块型胰腺炎与胰腺癌的鉴别诊断进行系统的探讨，为临床工作提供参考。     

3.0 T MR弥散加权成像对鉴别胰腺癌与慢性肿块型胰腺炎的价值

目的探讨在3．0T磁共振（MR）平台上应用弥散加权成像（diffusion—weighted imaging，DWI）鉴别诊断胰腺癌与慢性肿块型胰腺炎的价值。方法纳入经手术病理和临床随访证实的胰腺癌患者13例、慢性肿块型胰腺炎患者7例和健康志愿者14例，在行上腹部常规MR扫描后进行胰腺DWI检查。采用自旋回波回波平面成像技术和空间敏感性编码技术，分别取弥散梯度b值=400、600、800和1000s／mm^2获得相应的DWI图像，测量感兴趣区（ROI）的ADC值，并进行统计学分析。结果①健康志愿者胰腺DWI呈中等信号。②胰腺癌患者癌组织在DWI上呈均匀高信号，边界较清楚；各b值（400、600、800和1000s／mm^2）下，测得ADC值分别为（1．63±0．235）、（1．42±0．126）、（1．36±0．170）及（1．26±0．178）×10^-3mm^2／s，明显低于癌周胰腺组织[（2．11±0．444）、（1．83±0．230）、（1．81±0．426）及（1．60±0．230）×10^-3mm^2／s]及健康志愿者胰腺的ADC值[（1．85±0．350）、（1．69±0．290）、（1．67±0．268）及（1．42±0．221）×10^-3mm^2／s]，P〈0．05。③慢性肿块型胰腺炎在DWI上呈不均匀稍高信号，边界不清；各b值下测得ADC值分别为（1．69±0．150）、（1．56±0．119）、（1．59±0．172）及（1．35±0．080）×10^-3mm^2／s，均高于胰腺癌组织的ADC值，但仅当b值-800s／mm^2时，与胰腺癌组织间差异有统计学意义（P〈0．05）。结论DWI可以清楚显示胰腺肿瘤病灶及范围，结合ADC的测量值能够为鉴别胰腺癌与慢性肿块型胰腺炎提供一定的信息。     

胰头部肿块型胰腺炎与胰腺癌的关系

胰头部肿块型慢性胰腺炎与胰头癌难以鉴别,虽然其属于良性病变,但有一定的恶变率。慢性胰腺炎基础上的组织增生、萎缩以及癌变过程中,癌基因激活和抑癌基因失活可以导致胰腺癌的发生。影像医学的发展为两者的鉴别诊断提供了直观的影像学证据,但是,目前的诊断方法包括CT、MRI、ERCP、EUS（FNA）和PET-CT都存有一定的不足,导致诊断困难。因此,手术是最终诊断胰腺癌和肿块型慢性胰腺炎的惟一手段。     

MRI-DWI鉴别诊断肿块型自身免疫性胰腺炎与胰腺导管腺癌

目的分析肿块型自身免疫性胰腺炎(AIP)和胰腺导管腺癌(PC)的影像学表现,探讨MRI-DWI在鉴别诊断二者方面的价值。方法收集2016年3月至2019年6月中山大学孙逸仙纪念医院经病理诊断的胰腺导管腺癌30例,达到临床诊断标准的肿块型自身免疫性胰腺炎15例,回顾性分析上述患者的影像学特征,在DWI上的表现及ADC值的区别。结果肿块型胰腺炎患者中,大部分病灶T2WI呈不均匀的高信号,T1WI表现为等信号和低信号,DWI为等或高信号,不均匀较明显强化。胰腺导管腺癌患者中,大多数病灶T2WI病灶呈稍高信号,T1WI呈低信号,少部分的病灶呈现混杂信号或者等信号,DWI为低信号为主,不均匀低强化为主。二者均可伴有主胰管的扩张,胰腺导管腺癌同时可伴有主胰管的中断。当b值=800 s/mm~2时,肿块型AIP的ADC平均值为(1.38±0.11)×10-3mm~2/s(平均值±标准差),胰腺导管腺癌的ADC平均值为(1.03±0.15)×10-3mm~2/s(平均值±标准差),P0.05,二者间差异有统计学意义。结论肿块型自身免疫性胰腺炎(AIP)和胰腺导管腺癌(PC)的影像学表现有差异,DWI序列及ADC值有助于鉴别诊断二者。     

磁共振功能成像鉴别胰腺癌与肿块型慢性胰腺炎的价值

目的总结各种磁共振(MR)功能成像的原理及在胰腺癌及肿块型慢性胰腺炎诊断中的应用价值。方法回顾分析国内、外近年来关于MR波谱成像、MR弥散成像及MR灌注成像在胰腺癌及慢性胰腺炎诊断和鉴别诊断中应用的文献。结果胰腺癌与慢性胰腺炎在分子扩散、生化代谢、组织灌注等方面存在差异,MR功能成像方法能反映这些差异而用于鉴别诊断。结论MR功能成像作为一种非侵入性的影像检查方法,能够提供鉴别胰腺癌与肿块型慢性胰腺炎有价值的信息。     

肿块型胰腺炎临床特点11例分析

临床上多数胰腺癌合并有慢性阻塞性胰腺炎,而某些肿块型胰腺炎仅凭影像学资料,甚至术中所见仍难以和胰腺癌相鉴别。作者自1987～1989年共诊治肿块型胰腺炎11例,报告如下。     

Whipple手术治疗胰头部肿块型慢性胰腺炎一例及文献分析

胰头部肿块型慢性胰腺炎（pancreatic head mass type chronic pancreatitis,PHMTCP）于1973年由Bekeker首先描述,是慢性胰腺炎的一种特殊类型,因其酷似胰腺癌,故术前鉴别困难,但预后与胰腺癌截然相反,值得临床医师引起高度重视。本科室2012年收治该病例1例,将其临床资料报道如下。     

胰头部肿块型慢性胰腺炎诊断与治疗

胰头部肿块型慢性胰腺炎从临床表现上很难与胰头癌相鉴别,目前已将发生于胰头部的肿块型慢性胰腺炎视为胰腺癌发生的癌前病变。影像学检查在肿块型慢性胰腺炎诊断中起着重要作用,对于手术指征的掌握、胰头部肿块的可切除性、手术方式的选择以及手术困难程度的估计很有帮助。胰头部肿块型慢性胰腺炎的手术方式是直接针对胰头的,不同的手术方法包括胰十二指肠切除术（保留或不保留幽门的Whipple手术）和胰头部分切除加胰管引流术（Frey 手术,Beger 手术）。胰头肿块型慢性胰腺炎一旦诊断明确即应积极手术治疗,手术方式尽可能采用胰十二指肠切除术,因为它不仅切除了胰头部肿块、解除了胆道和胰管及十二指肠的梗阻,而且也去除了胰头癌的潜在病因;如胰头肿块巨大,行胰十二指肠切除有极大风险,可考虑行保留十二指肠的胰头切除术。     

磁共振DWI及动态增强对前列腺癌的诊断

目的 探讨磁共振弥散加权成像及动态增强在前列腺癌诊断中的价值.方法 分别对24例前列腺癌（PCa）患者、30例前列腺增生（BPH）患者行前列腺DWI及动态增强扫描,15名健康志愿者进行前列腺DWI扫描.分析3组DWI图、ADC图的信号表现,测量ADC值,比较PCa组及BPH组动态增强曲线.所有PCa病例、BPH病例均经手术或穿刺活检病理证实.结果 DWI上PCa表现为高信号影,BPH呈混杂信号,志愿者外周带呈稍高信号.PCa癌灶平均ADC值0.98×10-3mm2/s,增生结节平均ADC值1.46×10-3mm2/s,志愿者前列腺外周带平均ADC值1.85×10-3mm2/s,三者之间的差异互有统计学意义（P＜0.05）.动态增强PCa主要表现为早期强化,BPH主要表现为逐渐强化,PCa与BPH的时间-信号强度曲线类型差异有统计学意义（P＜0.05）.结论 在DWI图像上,PCa癌灶信号较高.PCa癌灶的ADC值低于正常前列腺外周带及前列腺增生.动态增强时PCa癌灶以早期强化为主.这二者均可作为前列腺癌的诊断依据.     

�׿������������׵�Ӱ��ѧ����

??Imaging features of mass-forming pancreatitis ZENG Meng-su?? YAO Xiu-zhong. Department of Radiology, Zhongshan Hospital of Fudan University and Shanghai Institute of Medical Imaging, Shanghai 200032, China
Corresponding author: ZENG Meng-su??E-mail:zeng.mengsu@zs-hospital.sh.cn
Abstract Chronic mass-forming pancreatitis usually included two pathological types: Ordinary chronic mass-forming pancreatitis, characterized by granulation tissue with fibrosis and mass-forming autoimmune pancreatitis, characterized by a dense lymphoplasmacytic infiltration with extensive fibrosis and proliferation. Sometimes it was very difficult to identify pancreatic cancer from chronic mass-forming pancreatitis in the clinical practice. Accurate preoperative diagnosis and differentiation were extremely important for their treatment and prognosis. Chronic mass-forming pancreatitis and pancreatic cancer had their own characteristic imaging findings in CT and MRI respectively, especially in the dynamic contrast-enhanced MRI and DWI. A signal intensity-time (SI-T) curve with a slow rise followed by a slow decline usually indicated chronic mass-forming pancreatitis, while a SI-T curve with a gradual rise indicated pancreatic cancer. ADC values in chronic mass-forming pancreatitis usually was lower than that in pancreatic cancer.     

胰头肿块型胰腺炎诊断和外科治疗进展

随着慢性胰腺炎发病率的逐年升高,胰头肿块型胰腺炎发病率也逐年升高。在临床工作中,胰头肿块型胰腺炎与胰腺癌较难鉴别。但是两者的治疗方案决然不同,且预后差别大。因此胰头肿块型胰腺炎越来越多的受到临床工作者关注。笔者就胰头肿块型胰腺炎的诊断和外科治疗做一综述,以期望为临床提供一些参考。     

胰头十二指肠切除治疗慢性胰腺炎

目的探讨胰头十二指肠切除术在胰头肿块型慢性胰腺炎诊治中可行性。方法回顾分析18例胰头肿块型慢性胰腺炎行胰头十二指肠切除术的临床资料。结果手术方式包括：Whipple法3例,Child法11例,保留十二指肠水平段胰头十二指肠切除术法4例;平均手术时间5．5±0．68h,平均出血量400±125ml;手术并发症：胆漏、胰漏2例,左膈下积液2例,肺部感染1例,其中死亡1例为胰漏伴感染出血,发生率占27．7％;平均住院日27．3±3d。结论肿块型慢性胰腺炎行胰头十二指肠切除术效果确切,是可行的,但有一定的风险。     

慢性肿块型胰腺炎的18F-FDG PET/CT影像学表现

目的探讨慢性肿块型胰腺炎18F-FDG PET/CT影像学表现。方法回顾性分析6例经手术病理证实的慢性肿块型胰腺炎的18F-FDG PET/CT影像资料和临床资料。结果 6例共检出6个病灶,3个位于胰头,3个位于胰尾;平均大小3.0cm×2.7cm。CT平扫6个病灶呈均匀等密度,未见钙化灶,平均CT值约为36HU;增强扫描全部病灶呈延迟期强化。全部病灶18F-FDG摄取呈局灶性增高,最大标准摄取值（SUVmax）1.6～5.3,平均SUVmax3.92±1.49,高于正常胰腺组织的2.05±0.39（t=-3.648,P=0.015）。3例病灶累及胰头,胆总管及胰管不同程度扩张,呈双管征,胰体尾部轻度萎缩;3例病灶累及胰尾,胆总管及胰管未见扩张,胰体尾部未见萎缩。病灶邻近的主要血管均未受侵。全部病例胰周及腹膜后淋巴结未见18F-FDG局灶性摄取增高,未见远处脏器或（和）组织转移。结论 18 F-FDG PET/CT对诊断慢性肿块型胰腺炎具有一定价值。     

Pseudotumors due to IgG4 immune-complex tubulointerstitial nephritis associated with autoimmune pancreatocentric disease

Autoimmune pancreatitis (AIP) is a mass-forming chronic fibroinflammatory condition centered on the pancreatobiliary system and characterized by predominant immunoglobulin G4 (IgG4)-positive plasma cells. Recent reports have brought to light the multiorgan involvement of this disease. We describe a series of 5 cases of tubulointerstitial nephritis (TIN) associated with AIP and characterize the clinical, pathologic, ultrastructural, and immunopathologic features of TIN. The specimens consisted of 4 biopsies and 1 nephrectomy. The average patient age was 64 years (range 45 to 78) and the male to female ratio was 4:1. All had histologic and/or clinical and radiographic evidence of AIP, mass-forming sclerosing cholangitis, or both. The clinical impression in 4 patients was a renal mass or vasculitis. Two patients had renal insufficiency. Histologic preparations revealed a dense tubulointerstitial lymphoplasmacytic infiltrate. Eosinophils were often numerous. Tubulitis and tubular injury were present, along with tubular atrophy with focally thickened tubular basement membranes (TBMs). The histologic appearance ranged from a cellular, inflammatory pattern without tubular atrophy to a striking expansive interstitial fibrosis with tubular destruction. The nephrectomy specimen demonstrated a masslike nodular pattern of inflammation with normal renal tissue elsewhere. Glomeruli were uninvolved. By immunohistochemistry or immunofluorescence, numerous plasma cells in the infiltrate were positive for IgG4. TBM granular IgG deposits, predominantly of the IgG4 subclass, were detected in 4 of 5 cases by either immunofluorescence or immunohistochemistry. By electron microscopy, corresponding amorphous electron-dense deposits were present in the TBM in these cases. This type of TIN, typically characterized by a masslike lesion consisting of a lymphoplasmacytic infiltrate with eosinophils and prominent IgG4-positive plasma cells and immune-complex deposits in the TBM, may be part of a systemic IgG4-related disease, which we term "IgG4-associated immune complex Multiorgan Autoimmune Disease" (IMAD).     

自身免疫性胰腺炎的临床研究进展

自身免疫性胰腺炎是一种慢性的与自身免疫有关的胰腺炎.此病的特点为高球蛋白、IgG~4升高、抗碳酸酐酶抗体和抗乳铁蛋白抗体的存在,弥漫性肿大的胰腺、显著的淋巴细胞浸润伴随纤维化、临床表现多样、对激素治疗敏感.     

Mass-forming pancreatitis with positive fluoro-2-deoxy-<Emphasis Type="SmallCaps">d</Emphasis>-glucose positron emission tomography and positive diffusion-weighted imaging-magnetic resonance imaging: Report of a case

It is difficult to make an accurate radiological diagnosis of a pancreatic tumor because of its location and anatomical characteristics. Mass-forming pancreatitis and pancreatic cancer are particularly difficult to differentiate. New diagnostic technology, which includes diffusion-weighted imaging-magnetic resonance imaging (DWI-MRI) and 2-[¹⁸F]-fluoro-2-deoxy-Dglucose positron emission tomography (FDG-PET), offers hope for the detection of classical pancreatic cancer. Few studies have been conducted on FDG-PET and DWI-MRI as tools used to distinguish between mass-forming pancreatitis and pancreatic cancers. Furthermore, positive findings of mass-forming pancreatitis on DWI-MRI and FDG-PET have yet to be documented. We report a case of a pancreatic head tumor, present on FDG-PET and DWI-MRI which, on closer examination, revealed benign mass-forming pancreatitis. We discuss the utility of FDG-PET and DWI-MRI as preoperative diagnostic tools.     

Clinical evidence of pathogenesis in chronic pancreatitis

Chronic pancreatitis is a continuing inflammatory disease characterized by irreversible morphological change and, typically, by pain and permanent impairment of function. The pathogenesis of pancreatitis, either acute or chronic, is still controversial. There have been no widely accepted concepts to provide a reasonable explanation linking the known etiological factors and the pathophysiological aspects of the disease. Alcohol is undoubtedly the major etiological factor in most countries, and the relative importance of alcohol as a cause of chronic pancreatitis ranges from 40% to 90% in various countries. As fewer than 10% of alcoholics develop chronic pancreatitis, other nutritional or genetic influences are likely to be involved in the pathogenesis of alcoholic pancreatitis. Accessory pancreas incidentally found in patients with chronic alcoholic pancreatitis does not always have the pathological findings seen in the main pancreas. Integrity of the pancreatic duct seems to be another important factor for chronic alcoholic pancreatitis. Gene mutations of the cystic fibrosis transmembrane conductance regulator (CFTR), cationic trypsinogen, and pancreatic secretory trypsin inhibitor have been investigated in idiopathic chronic pancreatitis. Molecular and cell biology research during the past few years has elucidated pathophysiological factors that are involved in the pathogenesis of chronic pancreatitis, but cannot demonstrate a common pathway between etiological factors and the pathogenesis or development of the disease. Received: March 20, 2002 / Accepted: April 15, 2002 Offprint requests to: T. Hayakawa     

Idiopathic chronic pancreatitis with periductal lymphoplasmacytic infiltration: clinicopathologic features of 35 cases

To clarify clinicopathologic features of idiopathic chronic pancreatitis with lymphoplasmacytic infiltration, we carried out a study of 35 cases. There were two histologic groups, which we have designated lymphoplasmacytic sclerosing pancreatitis and idiopathic duct-centric chronic pancreatitis. Lymphoplasmacytic sclerosing pancreatitis (22 cases) was a fibrosing process with diffuse lymphoplasmacytic infiltrates involving pancreatic lobules and ducts, adipose tissue, blood vessels, and common bile duct. Obliterative phlebitis was found in every case except for one. The histologic features were similar to other idiopathic fibrosclerosing disorders, and one patient also had retroperitoneal fibrosis. Affected patients tended to be elderly men. Idiopathic duct-centric chronic pancreatitis (13 cases) was characterized by inflammatory infiltrates (including neutrophils) that were denser in the lobules than in interlobular fibrotic areas. Neutrophils were also prominent in the ducts, and destruction of the duct epithelium was commonly seen. Patient ages were more broadly distributed than in lymphoplasmacytic sclerosing pancreatitis. Two patients had inflammatory bowel disease. We conclude that idiopathic chronic pancreatitis with lymphoplasmacytic infiltration, sometimes called autoimmune pancreatitis, consists of at least two different processes. One of these, lymphoplasmacytic sclerosing pancreatitis, is a histologically unique lesion and could be a pancreatic manifestation of idiopathic fibrosclerosing disorders.