胰头肿块型慢性胰腺炎的治疗

胰头肿块型慢性胰腺炎已被视为胰腺癌的癌前病变,并且可以导致胰管、胆管及十二指肠梗阻,其与胰头癌的鉴别诊断困难,然而二者的预后截然不同。因此,胰头肿块型慢性胰腺炎一旦诊断明确即应积极手术治疗,以切除病变,缓解疼痛症状,改善病人的生活质量。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）和保留十二指肠的胰头切除术（Beger手术及其改良术式）。手术方式尽可能采用胰十二指肠切除术,不仅切除了胰头部肿块、解除了胆道、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,行胰十二指肠切除术有极大风险,可考虑行保留十二指肠的胰头切除术。     

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??Treatment of Chronic pancreatitis(CP) with an inflammatory mass ZHANG Zhong-tao,YIN Jie. Beijing Friendship Hospital,Capital Medical University,Beijing100050,China
Corresponding author: ZHANG Zhong-tao,E-mail: zhangzht@medmail.com.cn
Abstract Chronic pancreatitis(CP) with an inflammatory mass has been thought of as a precancerous lesion of pancreatic cancer, and it can lead to obstruction of the pancreatic duct, bile duct and duodenum. The CP with mass and pancreatic cancer are difficult to identify from clinical performance, and their prognosis are very different. Once CP with mass has been diagnosed it should be clear that surgical treatment is necessary in order to remove the focus, ease pain, and improve the patient's quality of life. Surgical strategy in CP with mass has been directed at the pancreatic head with a variety of tactics including pancreatoduodenectomy (Whipple procedure with or without pylorus preservation) and duodenum-preserving resection of the pancreatic head (Beger operation and other operations). Pancreatoduodenectomy is preformed in the treatment of CP with mass, not only resection of the pancreatic head mass, lifting the obstruction of the pancreatic duct, bile duct and duodenum, but also removing the potential causes of pancreatic cancer. Pancreatoduodenectomy is a great risk When the pancreatic head mass is large, but the partial head resection can be accomplished with relative safety.     

Pancreatic stellate cell activation and MMP production in experimental pancreatic fibrosis

BACKGROUND: The early events in pancreatic fibrosis are poorly understood. We examined the production of collagen and matrix metalloproteinases as well as the activation of pancreatic stellate cells in a rodent model of pancreatic fibrosis. MATERIALS AND METHODS: Pancreatitis was induced in rats by hyperstimulation with cerulein (50 microg/kg/day ip) and concurrent pancreatic duct obstruction (SHOP model) for 96 h (n = 48). Sham animals were injected with saline and underwent laparotomy and manipulation of the pancreas with no duct obstruction (n = 28). Rats were sacrificed daily for 18 days. Serial pancreatic sections were stained with H&E [histology], trichrome [collagen], and alpha smooth muscle actin (alpha-SMA) antibodies [activated stellate cells]. Total pancreatic matrix metalloproteinase (MMP)-2 and 9 were determined by gelatin zymography. MMP-1 production was examined using Western blotting. RESULTS: There were occasional alpha-SMA-positive cells in the pancreatic parenchyma of normal and sham animals. Within 48 h of pancreatitis induction in SHOP animals, histologic evidence of pancreatic inflammation was present, and stellate cells (alpha-SMA-positive cells) appeared surrounding pancreatic acini. The appearance of these cells was followed by collagen deposition in the same area. MMP-1 and 2 proteins increased significantly during pancreatitis while MMP-9 did not. The pancreatic architecture returned to normal by 18 days after the induction of pancreatitis. CONCLUSION: Acute pancreatic inflammation results in stellate cell activation and collagen deposition in the same area. Collagen is then resorbed at a time when MMP-1 and 2 peak. The fibrosis of acute pancreatic inflammation in this model completely resolves with restoration of normal architecture.     

Molecular mechanisms in chronic pancreatitis.

The pathogenesis of chronic pancreatitis (CP) is still controversial. None of the proposed models has been able to provide a convincing link between the known etiological factors - alcohol abuse, metabolic disturbances, congenital or acquired obstruction of the duct system - and the complex morphological and pathophysiological aspects of the disease. Molecular and cell biology research during the last years, however, has elucidated that a dysregulated immune response, together with an active involvement of pancreatic parenchymal cells, contributes to tissue destruction, fibrosis and remodeling in CP. Infiltration of the pancreas by particular subsets of immune effector cells, aberrant and enhanced expression of MHC molecules, and overexpression of growth factors and their receptors have all recently been found to play a role in CP. In addition, genetic analysis has led to the discovery of genes that predispose their carriers to the development of the disease, and has shed new light on the relation between CP and pancreatic cancer.     

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。     

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??Diagnosis and treatment of chronic pancreatitis with mass in the head of the pancreas ZHANG Zhong-tao, YIN Jie.Department of General Surgery, Beijing Friendship Hospital Affiliated to Capital University of Medical Sciences, Beijing 100050, China Corresponding author: ZHANG Zhong-tao, E-mail: zhangzht@medmail. com.cn Abstract Chronic pancreatitis (CP) with mass and pancreatic cancer are difficult to identify from the Clinical performance. At present, we have the CP with mass as a precancerous lesion of pancreatic cancer. Imaging methods in the diagnosis of the CP with mass plays an important role, which is very helpful for the Indications for surgery of the hands, of resectable pancreatic head tumor, and surgical options, as well as estimates of the difficulty of the surgery. Surgical strategy in CP with mass has been directed at the pancreatic head with a variety of tactics including pancreatoduodenectomy(Whipple procedure with or without pylorus preservation) and partial resection of the pancreatic duct drainage(Frey operation, Beger operation ). Once the diagnosis of the CP with mass should be clear that the surgical treatment, pancreatoduodenectomy is preformed in the treatment of CP with mass, not only resection of the pancreatic head mass, the lifting of the bile duct and pancreatic duct and obstruction of the duodenum, but also in addition to the potential causes of pancreatic cancer. Pancreatoduodenectomy is great risk When the great mass of pancreatic head, but the partial head resection can be accomplished with relative safety.     

Early versus late surgical drainage for obstructive pancreatitis in an experimental model

BACKGROUND: Chronic pancreatitis (CP) is characterized by intractable abdominal pain, and pancreatic exocrine and endocrine dysfunction. This study investigated whether early surgical drainage of pancreatic duct obstruction leads to improved recovery of pancreatic function compared with late surgical drainage in an experimental model of chronic obstructive pancreatitis. METHODS: Twenty-one piglets underwent pancreatic duct ligation and subsequent longitudinal pancreaticojejunostomy after 3 weeks (early drainage) or 6 weeks (late drainage), and drainage continued for 6 weeks. In controls with CP pancreatic duct ligation was continued for 12 weeks without a drainage procedure. RESULTS: Histological pancreatitis scores decreased with early drainage (P = 0.005), but not with late drainage. Pancreatic secretion of amylase and lipase was restored after early but not late drainage (P = 0.003 and P = 0.048 respectively). Excretion levels of lipase were restored to near-baseline preligation levels after early drainage. Pancreatic endocrine function (glucose tolerance test) showed no insufficiency in either group. CONCLUSION: In this model of early versus late surgical drainage of obstructive pancreatitis, histology grades and pancreatic exocrine function showed improvement in the early drainage group but no recovery in the late drainage group.     

Surgical treatment of pancreas divisum causing chronic pancreatitis: The outcome benefits of duodenum-preserving pancreatic head resection

Pancreas divisum (PD) represents a duct anomaly in the pancreatic head ducts, leading frequently leading to recurrent acute pancreatitis (rAP) or chronic pancreatitis (CP). Based on endoscopic retrograde cholangiopancreatography, pancreas divisum can be found in 1% to 6% of patients with pancreatitis. The correlation of this abnormality with pancreatic disease is an issue of continuing controversy. Because of the underlying duct anomalies and major pathomorphological changes in the pancreatic head, duodenumpreserving pancreatic head resection (DPPHR) offers an option for causal treatment. Thirty-six patients with pancreatitis caused by PD were treated surgically. Thirty patients suffered from CP, 6 from rAP. The mean duration of the disease was 47.5 and 49.8 months, respectively. The age at the time of surgery was 39.2 years in the CPgroup, and 27.6 years in the rAP group. Median hospitalization since diagnosis was 18.8 weeks for CP patients and 24.6 weeks for rAP patients. Previous procedures performed in these patients included endoscopic papillotomy (30%), duct stenting (14%), and surgical treatment (17%). The median preoperative pain score was 8 on a visual analog scale. According to the classification of pancreas divisum, 10 patients demonstrated a complete PD, 25 had a functionally incomplete PD, and 1 had a dorsal duct type. The pain status as well as the endocrine (oral glucose tolerance test) and exocrine (pancreolauryl test) function were evaluated preoperatively and early and late postoperatively with a median follow-up time of 39.3 months. There was no operative-related mortality. The follow-up was 100%; 4 patients died (1 from suicide, 1 from cardiac arrest, and 2 from cancer of the esophagus). Fifty percent of the patients were completely pain-free,31%hada significant reduction of pain with a median pain score of 2 (P < 0.001). Six patients (5 CP, 1 rAP) had further attacks of acute pancreatitis with a need for hospitalization. DPPHR reduced pain and preserved the endocrine function in the majority of patients with pancreas divisum. Therefore, DPPHR is an alternative to other resective or drainage procedures after failure of interventional treatment.     

Effects of heparin in experimental models of acute pancreatitis and post-ERCP pancreatitis

BACKGROUND: Acute pancreatitis (AP) is a complication of diagnostic or therapeutic endoscopic retrograde cholangiopancreatography (ERCP). In a recent clinical trial, a decreased rate of post-ERCP pancreatitis was shown after prophylactic heparin treatment. The aim of this study was to evaluate the effects of prophylactic heparin application in various experimental models of AP and pancreatic duct obstruction and to assess the underlying mechanisms. METHODS: In various experimental models, pancreatic injury of graded severity was induced in Wistar rats: (1) mild pancreatitis by IV cerulein infusion over 6 hours; (2) severe pancreatitis by infusion of glycodeoxycholic acid into the pancreatic duct plus IV cerulein application over 6 hours. The clinical ERCP situation was imitated in groups (3) obstruction of the pancreatic duct and (4) infusion of contrast medium into the pancreatic duct plus obstruction. In every group the animals received either no heparin (n=six per group) or continuous IV heparin (n=six per group) starting before pancreatic injury. Histologic changes, amylase, and lipase in plasma were evaluated 12 hours after induction of pancreatic injury. Additional animals were treated to investigate pancreatic microcirculation by intravital microscopy (n=six per group). RESULTS: In groups 1, 3, and 4 (mild AP/duct obstruction/duct obstruction plus contrast medium), IV heparin-treated animals showed reduced edema, inflammation, and peak amylase values compared with the corresponding non-heparin-treated animals (P<.05). Moreover, mean erythrocyte velocity was significantly higher and leukocyte-endothelium interaction was reduced in these groups after prophylactic administration of heparin. In contrast, group 2 (severe AP) did not show any difference between control animals and animals that received heparin as assessed by histology and intravital microscopy. CONCLUSIONS: Prophylactic systemic application of heparin provides a protective effect in mild AP and in experimental post-ERCP pancreatitis. The mechanism of the protective effects of heparin seems to be the reduction of leukocyte-endothelium interaction and the normalization of pancreatic microcirculation.     

软骨寡聚基质蛋白在慢性胰腺炎损伤中退变腺泡细胞内的表达

目的 研究正常胰腺、慢性胰腺炎与胰腺癌组织中软骨寡聚基质蛋白(cartilage oligomeric matrix protein,COMP)mRNA和蛋白表达水平的差异,揭示COMP在慢性胰腺炎样损伤中的意义。方法 采用Northern印迹法、Western印迹法、原位杂交法与免疫组化方法对14例慢性胰腺炎、14例胰腺癌及15例正常胰腺组织进行分析。结果 在慢性胰腺炎组织中和胰腺癌组织中类似慢性胰腺炎损伤的退变腺泡细胞胞浆内,存在高水平的COMP mRNA信号与免疫反应;而在胰腺癌细胞、正常胰腺组织的导管细胞与胰岛细胞的胞浆内,COMP mRNA信号与免疫反应微弱或缺如。结论 COMP在慢性胰腺炎及胰腺癌中类似慢性胰腺炎损伤的退变腺泡细胞内高表达,可能与慢性胰腺炎中腺泡细胞功能异常有关。     

Bile and pancreatic juice exclusion activates acinar stress kinases and exacerbates gallstone pancreatitis

HYPOTHESIS: Bile and pancreatic juice exclusion from gut activates acinar stress kinases and exacerbates gallstone pancreatitis as evidenced by the ameliorating effects of replacement therapy in an experimental model of duct ligation-induced acute pancreatitis. In the early stages of gallstone pancreatitis, bile-pancreatic juice cannot enter the gut. Enteral exclusion worsens pancreatitis by causing feedback hyperstimulation of the exocrine pancreas that activates acinar cell stress kinases. Investigations using a unique surgical model, the Donor Rat Model, showed that duodenal replacement of bile-pancreatic juice in rats with duct ligation attenuates pancreatic stress kinase activation, reduces pancreatic cytokine production, and ameliorates pancreatic morphologic changes. These findings suggest that exclusion-induced acinar hyperstimulation, in the presence of duct obstruction, exacerbates acute pancreatitis via stress kinase activation. Although acinar hyperstimulation has often been implicated in the pathogenesis of acute pancreatitis, the lack of supporting evidence remains a conspicuous void. The proposed hypothesis draws on fresh evidence to present a new paradigm that reexamines the role of exocrine pancreatic hyperstimulation in gallstone pancreatitis pathogenesis.     

Characterization of a Novel Model of Pancreatic Fibrosis and Acinar Atrophy

Significant fibrosis and acinar atrophy are characteristics of chronic pancreatitis; however, because of the lack of a reproducible model, early phases of these changes are poorly understood. We have developed a model of severe hyperstimulation and obstruction pancreatitis (SHOP) to better define the mechanisms of early pancreatic fibrogenesis. Sprague-Dawley rats were used and SHOP was induced by complete pancreatic duct obstruction and daily cerulein hyperstimulation (50 (μg/kg intraperitoneally). Animals were killed at 24, 48, 72, and 96 hours. Control animals underwent sham operation and received no cerulein. Pancreata were prepared for hematoxylin and eosin and sirius red (collagen-specific) staining and for hydroxyproline assay (measure of total collagen content). We found moderate amounts of edema and inflammation but minimal parenchymal necrosis. Significant loss of acinar cell mass was noted by 48 hours, and normal acinar cells were essentially absent by 96 hours. Tissue collagen content increased with time and large amounts of interstitial collagen were detected by 72 hours. In conclusion, SHOP is a novel model of early pancreatic fibrosis associated with minimal necrosis and a significant decrease in acinar cell mass, making it an ideal model to study the early cellular mechanisms of pancreatic fibrogenesis. Presented at the Thirty-Ninth Annual Meeting of The Society for Surgery of the Alimentary Tract, New Orleans, La., May 17–20,1998.     

胰头部肿块鉴别诊断和临床对策

胰头部肿块的鉴别诊断中最为困难的是胰头肿块型胰腺炎与胰腺癌的鉴别。近年来,血清肿瘤标记物检查、多排螺旋CT和内镜超声引导穿刺活检等技术的发展为临床鉴别诊断提供了很多帮助,但仍有部分病人不能通过非手术方法获得确诊。对于这些病人,在与病人及家属进行充分沟通后,可以考虑行剖腹探查,建议术中对胰头部肿块行细针多点穿刺细胞学检查,并由专业人员及时处理标本。慢性胰腺炎是胰腺癌的癌前病变,并且可以导致胰管、胆管及十二指肠梗阻,行胰十二指肠切除术或保留十二指肠的胰头切除术能切除病变,缓解疼痛症状,改善病人的生活质量。但由于该手术创伤大,术后并发症发生率较高,应严格掌握手术适应证,加强围手术期处理,由经验丰富的医师实施手术,将并发症的发生率降到最低。     

Segmental occlusion of the pancreatic duct with prolamine to prevent fistula formation after distal pancreatectomy.

OBJECTIVE: The authors used prolamine (Ethibloc, Ethicon GmBH, Norderstedt, Germany) for segmental obstruction of the pancreatic duct to prevent pancreatic fistula development after distal pancreatectomy combined with total gastrectomy for gastric malignancies. SUMMARY BACKGROUND DATA: Although the initial clinical application of prolamine was pancreatic duct obstruction for patients with pancreatitis and undergoing pancreatic transplantation and pancreaticoduodenectomy for pancreatic cancer, there are no reports on prevention of pancreatic fistula formation after distal pancreatectomy. METHODS: Prolamine (0.2 mL) was injected into the distal segment of the main duct in the remaining pancreata of 51 patients. Small pancreatic ducts on the cut surface, from which prolamine extravasates, were closed by ligation, the main duct was ligated doubly, and the transected pancreatic margin was closed 15 minutes after phenylpropanolamine hydrochloride injection. RESULTS: No patient developed a pancreatic fistula or the complication of arterial bleeding due to prolonged infection. CONCLUSION: Segmental obstruction of the pancreatic duct with prolamine is useful for preventing pancreatic fistula development after distal pancreatectomy.     

Decreased type IV collagenase activity in experimental pancreatic fibrosis

BACKGROUND: Severe hyperstimulation and duct obstruction pancreatitis (SHOP) is characterized by pancreatic fibrosis and loss of acinar cell mass. MMP-2 and MMP-9 are type IV collagenases and gelatinases. We hypothesized that fibrosis results from disruption of the normal collagen homeostasis and that altered activity of the type IV collagenases may contribute to pancreatic fibrosis in SHOP. METHODS: SHOP rats (n = 15) were prepared with pancreatic duct obstruction and cerulein (50 microg/kg/d, ip) hyperstimulation. Pancreas from unoperated control (n = 8), 48 h SHOP (n = 8), and 96 h SHOP (n = 7) rats was harvested, homogenized, and assayed for protein concentration (BCA method). Type IV collagenase (MMP-2 and MMP-9) expression was measured by zymography using gelatin as substrate. Type IV collagenase activity was quantified with a fluorescence assay. RESULTS: Expression of the active form of MMP-9 decreased while latent MMP-9 and active and latent MMP-2 increased on gelatin zymography. Activity of type IV collagenases (MMP-2 and MMP-9) progressively decreases with SHOP injury. The differences between expression and activity are likely due to posttranslational regulators such as MT-MMPs and TIMPs. CONCLUSIONS: Collagenase expression and activity are decreased in the SHOP model of pancreatitis, suggesting a decrease in the homeostatic mechanisms for type IV collagen in the extracellular matrix. Therefore, early fibrosis in the SHOP model is, at least in part, due to alterations in collagen homeostasis and not simply increased collagen production.     

Palliation of pancreatic cancer using electrolytic ablation

Background: Inoperable pancreatic cancer has a dismal prognosis. Palliation involves either stenting or surgical bypass. Stenting does not relieve gastric outlet obstruction, and surgical bypass is a major procedure. A minimally invasive procedure is needed that relieves both gastric outlet and biliary obstruction, with the potential for relieving pain. Methods: In an experimental model, pancreatic electrolysis was investigated. The pancreatic duct was cannulated via a transduodenal approach with an electrode catheter. In 6 animals an electrolytic "lesion" was created using a direct current generator. Six animals were controls. The local and systemic effects of electrolysis were assessed using histological and biochemical parameters. Results: The pancreatic duct was cannulated in all animals and treatment was uneventful. Electrolytic lesions comprised a central area of necrosis with a sharp demarcation between necrotic and viable pancreas. All animals developed transient hyperamylasemia after electrolysis. There was no significant difference between treatment and controls. Importantly, no animal had clinical, biochemical, or histological evidence of pancreatitis. Conclusions: This experimental study suggested that electrolytic palliation of inoperable pancreatic cancer via the gastrointestinal tract is potentially safe. In patients, this treatment could be performed during endoscopic retrograde cholangiopancreatography and may have therapeutic advantages when compared to stenting or biliary bypass.     

胰头肿块型慢性胰腺炎的诊断与治疗

目的：探讨胰头肿块型慢性胰腺炎的诊治方法。方法：对近15年行胰十二指肠切除术并经病理证实的17例胰头肿块型慢性胰腺炎的临床资料进行回顾性分析。结果：本组术前均不能排除胰头癌。17例均行胰十二指肠切除术，术后发生胰漏1例，其余恢复顺利，效果良好。结论：胰头肿块型慢性胰腺炎早期诊断困难，尤其应与胰头癌相鉴别。对不能排除胰头癌或出现顽固性疼痛，胆管、胰管及十二指肠梗阻时，应行胰十二指肠切除术。     

Myofibroblasts are responsible for the desmoplastic reaction surrounding human pancreatic carcinomas

BACKGROUND: The cell type responsible for the desmoplastic reaction surrounding human pancreatic carcinoma is unknown. Hepatic stellate cells, which activate to a myofibroblast-like form, are responsible for collagen deposition in cirrhosis and around hepatocellular carcinomas. Recently, pancreatic stellate cells have been described and implicated in the fibrosis of chronic pancreatitis. We sought to determine whether these cells are responsible for the scirrhous reaction surrounding pancreatic adenocarcinomas. METHODS: Archival formalin-fixed, paraffin-embedded pancreatic tissues from 10 patients undergoing pancreaticoduodenectomy for ductal adenocarcinoma and from 2 patients with pancreatic islet cell tumors were examined immunohistochemically for alpha-smooth muscle actin (alpha-SMA), smooth muscle myosin heavy chain (SMMHC), procollagen I, collagen IV, and endothelial cell markers, von Willebrand factor and cluster of differentiation 31. RESULTS: In non-neoplastic areas, staining for alpha-SMA and SMMHC was confined to interlobular septal regions. In contrast, the desmoplastic reaction surrounding all 10 pancreatic adenocarcinoma specimens displayed intense interstitial staining for alpha-SMA, SMMHC, and collagen IV but no staining for von Willebrand factor and cluster of differentiation 31. Procollagen I staining localized intracellularly to fibroblast-shaped cells within this alpha-SMA/SMMHC-positive scirrhous region. Islet cell tumors demonstrated an increase in alpha-SMA staining, although this was not as marked as in ductal adenocarcinomas. CONCLUSIONS: A massive increase in myofibroblast activity, compatible with the activation of stellate cells, is associated with the deposition of collagen types I and IV in the desmoplastic reaction around pancreatic adenocarcinomas.     

Identification of Disease-specific Genes in Chronic Pancreatitis Using DNA Array Technology

OBJECTIVE: To use DNA arrays to analyze the differential gene expression patterns in the normal pancreas and in pancreatic diseases. SUMMARY BACKGROUND DATA: Genome-wide gene expression analysis will provide new insights into gene function and cause of disease. METHODS: RNA was extracted from eight normal pancreatic specimens, eight specimens with chronic pancreatitis (CP), and eight pancreatic cancer (PCa) tissues. Poly A(+) RNA was purified, reverse-transcribed, and converted into cRNA using biotinylated nucleotides. The HuGeneFL DNA array containing 5,600 full-length human genes was used for analysis. RESULTS: First, normal pancreatic tissues were analyzed in comparison with a panel of other normal tissues (colon, liver, prostate, lung, lymph node). This analysis revealed 11 signature genes that were selectively expressed in the pancreas (e.g., pancreatic elastase-IIA). Comparison of the expression of 5,600 genes between the normal pancreas, CP, and PCa specimens showed that the expression of 34 genes was decreased in CP tissues compared with normal pancreatic tissues, and that the expression of all of these genes was simultaneously decreased in PCa. In addition, the expression of 157 genes was increased in CP tissues compared with the normal pancreas. Of those, 152 genes were simultaneously increased in PCa. Thus, only 5 of 5,600 genes were significantly overexpressed in CP compared with both normal pancreas and PCa. CONCLUSIONS: The majority of alterations observed in CP are present in PCa, and the number of genes whose expression is selectively deregulated in CP is surprisingly small. These results may provide new insight into the pathobiology of CP and help identify certain molecular alterations that might serve as targets for new diagnostic tools and disease-specific therapy.     

Clinical and experimental studies on serum and urine amylase levels in carcinoma of the pancreas and periampullary region

Serum and urinary amylase level are different between in cases with carcinoma of the pancreas head and in those with carcinoma of body or tail of the pancreas. In this study the relationship between elevation in serum and urinary amylase level and the portion of obstructed pancreatic duct by tumor was analysed in cases with pancreatic carcinoma was analysed and also this was investigated in experimental model of pancreatic duct ligated dog. In patients with carcinoma of the pancreas and periampullary region, the site of obstruction of the main pancreatic duct was estimated by ERP and serum and urinary amylase level were measured. The values of serum amylase level were different according to the site of obstruction of the pancreatic duct by the tumor and in cases with highly elevated serum amylase levels the main pancreatic duct was obstructed within 5cm from the duodenal papilla. Pathology of these cases revealed pancreatic fibrosis derived from pancreatitis accompanied by tumor was closely related to serum and urinary amylase level. In pancreatic ligated dogs similar findings were observed. These data suggested that elevated serum amylase level is due to the pancreatic duct obstruction in cases with carcinoma of the periampullary duodenum.