Diagnosing Chronic Pancreatitis

Diagnosing CP can range from routine in those with severe disease and obvious calcifications on CT imaging to elusive in those patients with early changes in CP. The workup of suspected CP should follow a progressively noninvasive to more invasive STEP-wise approach in a patient with a suspicious clinical presentation and risk factors that raise their pretest probability of disease. After a thorough history and physical examination, basic laboratories should be obtained such as lipase, amylase, metabolic panel, and indirect PFTs (fecal elastase-1, serum trypsin). Computed tomography remains the best initial imaging modality to obtain as it has good sensitivity for severe CP and may obviate the need for other diagnostic tests. When equivocal, an MRCP should be obtained for a more detailed evaluation of the both the pancreatic parenchyma and ducts. If the diagnosis remains in doubt, EUS should be performed with or without pancreas function testing. ERCP remains a last-line diagnostic test and seldom should be used outside of therapeutic purposes. Future advances should target optimizing current diagnostic tools to more accurately diagnose early CP, as it is in this population where the benefits of delaying progression of CP may have the most profound effect. Likely the best way at establishing a diagnosis in these patients is via pancreatic function testing in the setting of indeterminate EUS results. Biomarker studies of pancreas fluid may supplement diagnosis.     

Guidelines for the Diagnostic Cross Sectional Imaging and Severity Scoring of Chronic Pancreatitis

The paper presents the international guidelines for imaging evaluation of chronic pancreatitis. The following consensus was obtained: Computed tomography (CT) is often the most appropriate initial imaging modality for evaluation of patients with suspected chronic pancreatitis (CP) depicting most changes in pancreatic morphology. CT is also indicated to exclude other potential intraabdominal pathologies presenting with symptoms similar to CP. However, CT cannot exclude a diagnosis of CP nor can it be used to exclusively diagnose early or mild disease. Here magnetic resonance imaging (MRI) and MR cholangiopancreatography (MRCP) is superior and is indicated especially in patients where no specific pathological changes are seen on CT. Secretin-stimulated MRCP is more accurate than standard MRCP in the depiction of subtle ductal changes. It should be performed after a negative MRCP, when there is still clinical suspicion of CP. Endoscopic ultrasound (EUS) can also be used to diagnose parenchymal and ductal changes mainly during the early stage of the disease.No validated radiological severity scoring systems for CP are available, although a modified Cambridge Classification has been used for MRCP. There is an unmet need for development of a new and validated radiological CP severity scoring system based on imaging criteria including glandular volume loss, ductal changes, parenchymal calcifications and parenchymal fibrosis based on CT and/or MRI. Secretin-stimulated MRCP in addition, can provide assessment of exocrine function and ductal compliance. An algorithm is presented, where these imaging parameters can be incorporated together with clinical findings in the classification and severity grading of CP.     

慢性胰腺炎的并发症

目的：探讨慢性胰腺炎（Chronic pancreatitis,CP）并发症的发生率、临床表现及诊断,旨在提高对于CP并发症的认识。方法：回顾性分析北京协和医院1982年－2001年确诊CP的236例住院患者。所有病例均符合1983年日本胰腺病协会关于CP的诊断标准,其中经病理证实者82例。结果：236例CP患者中156例出现并发症,占66．1％。其中,胆道梗阻、狭窄41例,占236例CP的17．4％;胰腺假性囊肿40例,占16．9％,脾静脉狭窄32例,占13．6％;胰源性浆膜腔积液19例,占8．1％; 上消化道不全梗阻17例,占7．2％;消化性溃疡14例,占5．9％;邻近血管病变13例,占5．5％;合并症还涉及胰腺癌（占4．2％）、结核及胰外肿瘤。结论：CP并发症相当常见,临床表现丰富多彩,有些患者以 并发症首诊,应提高对CP并发症的认识。     

Complications of Chronic Pancreatitis

Chronic pancreatitis is a disease that leads to irreversible changes in the pancreatic morphology and function. The loss of function can lead to diabetes mellitus and exocrine pancreatic insufficiency. The inflammation and fibrosis can also lead to other complications including a chronic abdominal pain syndrome, metabolic bone disease, and pancretic cancer. This article reviews our current understanding of the mechanisms and management of these complications of chronic pancreatitis.     

Complications of Chronic Pancreatitis

Summary: Alcohol-induced chronic pancreatitis has many complications. This man, since chronic pancreatitis first became clinically apparent, has developed diabetes mellitus, steatorrhoea, ascites (pancreatic) with a possible pseudocyst and a peripancreatic abscess, gallstones, partial common bile duct obstruction, gastric and duodenal deformities (due to adjacent pancreatitis, or peptic duodenal ulceration) and hepatic portal cirrhosis. Pulmonary tuberculosis was present at the time of onset of his pancreatitis. The course of his disease is followed illustrating the spectrum of complications which may develop during the course of chronic pancreatitis.     

Autoantibodies in Chronic Pancreatitis

In 60 consecutive patients clinically suspected of having chronic pancreatitis the serum concentration of the immunoglobulins (IgA, IgG, IgM), the IgG- and IgA-type non-organ-specific autoantibodies against nuclear material (ANA), smooth and striated muscle, mitochondria, basal membrane, and reticulin, and the IgG- and IgA-type pancreas-specific antibodies against islet cells, acinus cells, and ductal cells (DA) were estimated blindly. In 23 of the patients chronic pancreatitis was verified, whereas chronic pancreatitis was rejected in 37 patients (control group). IgG and IgA were found in significantly higher concentrations in the patients with chronic pancreatitis than in the control group but within the normal range. ANA and DA occurred very frequently in both groups but with no statistical difference. Other autoantibodies only occurred sporadically. The findings of this study do not support the view of an immunological pathogenesis in chronic pancreatitis.     

Eosinophilia Associated with Chronic Pancreatitis: An Analysis of 122 Patients with Definite Chronic Pancreatitis

Among 122 patients with chronic pancreatitis, marked eosinophilia (greater than 500 eosinophils/mm3 in the peripheral blood) was observed in 21 cases (17.2%). All of the affected patients were males, and there was no significant difference in the incidence of eosinophilia between patients with alcoholic and nonalcoholic pancreatitis. In the patients with eosinophilia, endocrine pancreatic function was maintained comparatively well, despite marked exocrine pancreatic dysfunction. The eosinophilia of chronic pancreatitis frequently developed in association with severe damage to neighboring organs (pleural effusion, pericarditis, and ascites), as well as in association with pancreatic pseudocyst. Our findings suggest that there is a close correlation between marked eosinophilia and severe tissue injury during acute exacerbations of chronic pancreatitis.     

Serum Gastrin in Chronic Pancreatitis

Fasting serum gastrin and gastrin response to a protein meal were measured in a group of patients with chronic pancreatitis and in controls. No significant differences were found between the two groups of subjects. In patients with chronic pancreatitis no relation was found between gastrin release and the severity of pancreatic exocrine insufficiency.     

Gastrinoma Presenting as Chronic Pancreatitis

We present here an unusual case of a pancreatic gastrinoma that caused recurrent episodes of clinical pancreatitis secondary to complete obstruction of the main pancreatic duct. The patient did not manifest signs or symptoms of peptic ulcer disease.     

Endoscopic Therapies for Chronic Pancreatitis

Chronic pancreatitis is a fibroinflammatory disease of the pancreas leading to varying degrees of endocrine and exocrine dysfunction. Treatment options are generally designed to control the pain of chronic pancreatitis, and endoscopic therapy is one of the main treatment modalities. Herein, we describe the endoscopic management of pancreatic duct calculi and strictures, entrapment of the intrapancreatic bile duct, celiac plexus interventions, and drainage of pancreatic pseudocysts.     

Immunological Changes of Mild Acute Pancreatitis in Late-Stage Alcoholic Chronic Pancreatitis

The exact immunological mechanisms underlyingalcoholic chronic pancreatitis are unclear. Toinvestigate the role of the tumor necrosis factor (TNF)receptor pathway the serum levels of TNF-,soluble TNF receptors-p55/-p75, and CRP were determinedby ELISA in 34 patients with late-stage alcoholicchronic pancreatitis and 28 controls. The diseaseactivity (Balthazar scoring system) of acutepancreatitis on the background of late-stage chronicpancreatitis correlated with an increase of functionallyactive TNF receptor-p55/-p75 serum levels. Unstimulatedperipheral blood mononuclear cells are one source of soluble TNF receptors and demonstrated asystemic leukocyte activation. The marked enhancement ofsoluble TNF receptors suggests that alcoholic chronicpancreatitis may be characterized by transient peaks of in situ TNF- productionpreceding a long-lasting release of soluble TNFreceptors. The data demonstrate immunological changescharacteristic of acute pancreatitis in late-stagealcoholic chronic pancreatitis.