Pathology of Acute and Chronic Pancreatitis

Klöppel, Günter; Maillet, B.

doi:10.1097/00006676-199311000-00001

Cited by 254 publications

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“…C hronic pancreatitis is characterized by a progressive loss and fibrosis of exocrine parenchyma whereas the endocrine part of the organ remains structurally intact for a prolonged period of time (Bockman, 1997;Klöppel and Maillet, 1993;Sarles, 1991). The disease is often accompanied by duct ectasia and might be initiated by ductal obstruction or distortion (Klöppel and Maillet, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…The disease is often accompanied by duct ectasia and might be initiated by ductal obstruction or distortion (Klöppel and Maillet, 1993). Furthermore, foci of lymphohistiocytic infiltrates are commonly found and are also associated with regressing parenchyma (Bockman, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…In chronic pancreatitis the CD95 Ϫ /CD95L ϩ status is conserved in islet cells even in the vicinity of lymphohistiocytic infiltrates, whereas it is lost in acini coexpressing HLA-DR. As a potential consequence, and possibly triggered by local release of IFN␥, CD4 ϩ Th1 cells may cognately interact with and successfully attack exocrine cells by triggering CD95 on their target without being killed by epithelial, CD95L-mediated, counterattack. (Lab Invest 2001, 81:317-326).C hronic pancreatitis is characterized by a progressive loss and fibrosis of exocrine parenchyma whereas the endocrine part of the organ remains structurally intact for a prolonged period of time (Bockman, 1997;Klöppel and Maillet, 1993;Sarles, 1991). The disease is often accompanied by duct ectasia and might be initiated by ductal obstruction or distortion (Klöppel and Maillet, 1993).…”

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Differential and Mutually Exclusive Expression of CD95 and CD95 Ligand in Epithelia of Normal Pancreas and Chronic Pancreatitis

Hasel

Rau

Perner

et al. 2001

Laboratory Investigation

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SUMMARY:Acinar regression in chronic pancreatitis may be due to immune attack in parenchymal areas neoexpressing HLA-DR molecules. CD4 ϩ Th1 cytotoxic T cells induce apoptosis of their targets via oligomerizing CD95 (APO-1/Fas) death receptors on target cells by their CD95 ligand (CD95L). We determined the expression of CD95 and CD95L in epithelia of normal and chronically inflamed pancreatic tissues. We applied RT-PCR and Western blotting for CD95L expression profiles, serial frozen section immunohistochemistry to detect CD95, CD95L, and HLA-DR molecules, CD3, CD4, CD11c, and S-100 protein (S100p). Normal pancreases and chronic pancreatitis contain CD95L message and protein. Immunohistochemistry revealed a mutually exclusive expression of CD95 and CD95L. Physiologically, acini were CD95 Ϫ /CD95L ϩ , ducts were CD95 Ϫ /CD95L Ϫ , and islets were CD95 Ϫ /CD95L ϩ . In areas of lymphohistiocytic infiltration, mainly consisting of CD3 ϩ CD4 ϩ T cells and CD11c ϩ , CD4 ϩ/Ϫ , S100p ϩ interstitial dendritic cells, and in areas of initial fibrosis, acini and ducts were HLA-DR ϩ , acini CD95 ϩ /CD95L Ϫ , and ducts CD95 ϩ /CD95L Ϫ . Islet cells were CD95 Ϫ /CD95L ϩ in both conditions. IFN␥ levels in protein lysates, as measured by an immunoassay, were significantly higher in chronic pancreatitis than in normal pancreas (p Ͻ 0.0003). In vitro, IFN␥ downmodulated CD95L message and protein in ASPC1 and BxPc3 pancreatic carcinoma cells. In conclusion, pancreatic epithelia differentially express CD95 and CD95L in a mutually exclusive manner. In chronic pancreatitis the CD95 Ϫ /CD95L ϩ status is conserved in islet cells even in the vicinity of lymphohistiocytic infiltrates, whereas it is lost in acini coexpressing HLA-DR. As a potential consequence, and possibly triggered by local release of IFN␥, CD4 ϩ Th1 cells may cognately interact with and successfully attack exocrine cells by triggering CD95 on their target without being killed by epithelial, CD95L-mediated, counterattack. (Lab Invest 2001, 81:317-326).C hronic pancreatitis is characterized by a progressive loss and fibrosis of exocrine parenchyma whereas the endocrine part of the organ remains structurally intact for a prolonged period of time (Bockman, 1997;Klöppel and Maillet, 1993;Sarles, 1991). The disease is often accompanied by duct ectasia and might be initiated by ductal obstruction or distortion (Klöppel and Maillet, 1993). Furthermore, foci of lymphohistiocytic infiltrates are commonly found and are also associated with regressing parenchyma (Bockman, 1997). These infiltrates were shown to contain activated cytotoxic T cells (Hunger et al, 1997), suggesting a role of the immune system in the pathogenesis of acinar atrophy and local scarring. Induction of HLA-DR molecules was observed in parenchymal areas affected by chronic pancreatitis (Bedossa et al, 1990;Jalleh et al, 1993) and transcripts for MCP-1 chemokine have been detected in areas of early stage of chronic pancreatitis (Saurer et al, 2000). Local expression of T cell tropic chemokines may recruit T cell...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Differential and Mutually Exclusive Expression of CD95 and CD95 Ligand in Epithelia of Normal Pancreas and Chronic Pancreatitis

Hasel

Rau

Perner

et al. 2001

Laboratory Investigation

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“…55 Formation typically occurs as a result of limited pancreatic necrosis causing a pancreatic duct leak with subsequent organization, or from areas of necrosis that liquefy over time. 56 Both pancreatic pseudocysts and necrotic pancreatic tissue may become infected leading to abscess formation. 51 Pancreatic necrosis is defined as diffuse or focal areas of nonviable pancreatic parenchyma, and it is seen in approximately 20% of patients with acute pancreatitis.…”

Section: Natural History and Complicationsmentioning

confidence: 99%

Acute pancreatitis

Munsell

Buscaglia

2010

Journal of Hospital Medicine

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Acute pancreatitis is a common disease most frequently caused by gallstone disease or excess alcohol ingestion. Diagnosis is usually based on characteristic symptoms, often in conjunction with elevated serum pancreatic enzymes. Imaging is not always necessary, but may be performed for many reasons, such as to confirm a diagnosis of pancreatitis, rule out other causes of abdominal pain, elucidate the cause of pancreatitis, or to evaluate for complications such as necrosis or pseudocysts. Though the majority of patients will have mild, self‐limiting disease, some will develop severe disease associated with organ failure. These patients are at risk to develop complications from ongoing pancreatic inflammation such as pancreatic necrosis, fluid collections, pseudocysts, and pancreatic duct disruption. Validated scoring systems can help predict the severity of pancreatitis, and thus, guide monitoring and intervention.Treatment of acute pancreatitis involves supportive care with fluid replacement, pain control, and controlled initiation of regular food intake. Prophylactic antibiotics are not recommended in acute pancreatitis if there is no evidence of pancreatic infection. In patients who fail to improve, further evaluation is necessary to assess for complications that require intervention such as pseudocysts or pancreatic necrosis. Endoscopy, including ERCP and EUS, and/or cholecystectomy may be indicated in the appropriate clinical setting. Ultimately, the management of the patient with severe acute pancreatitis will require a multidisciplinary approach. Journal of Hospital Medicine 2010;5:241–250. © 2010 Society of Hospital Medicine.

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“…[1][2][3][4][5] This inflammation causes intractable abdominal pain. The purpose of surgical treatment for chronic pancreatitis is pain management.…”

Section: Introductionmentioning

confidence: 99%

Pancreatic islet autotransplantation with total pancreatectomy for chronic pancreatitis

et al. 2012

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Pain relief and improvement in quality of life are the main targets for treatment of chronic pancreatitis. The use of total pancreatectomy for chronic pancreatitis is a radical and in some ways ideal strategy. However, total pancreatectomy is associated with severe diabetic control problems. Total pancreatectomy with islet autotransplantation can relieve severe pain and prevent post-surgical diabetes. In islet autotransplantation, patients with chronic pancreatitis receive their own islet cells and therefore do not require immunosuppression. In the future, total pancreatectomy with islet autotransplantation may be considered a treatment option for chronic pancreatitis patients.

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Pathology of Acute and Chronic Pancreatitis

Cited by 254 publications

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Differential and Mutually Exclusive Expression of CD95 and CD95 Ligand in Epithelia of Normal Pancreas and Chronic Pancreatitis

Differential and Mutually Exclusive Expression of CD95 and CD95 Ligand in Epithelia of Normal Pancreas and Chronic Pancreatitis

Acute pancreatitis

Pancreatic islet autotransplantation with total pancreatectomy for chronic pancreatitis

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