Chronic Pancreatitis and the Differential Diagnosis Versus Pancreatic Cancer

2009 ◽  
Vol 133 (3) ◽  
pp. 382-387 ◽  
Author(s):  
Günter Klöppel ◽  
N. Volkan Adsay

Abstract Context.—Distinguishing chronic pancreatitis from pancreatic ductal adenocarcinoma (PDAC) is a well-known challenge, at both the clinical and the morphologic level. Objective.—To focus on the histopathologic findings that are diagnostic or suggestive of PDAC. Data Sources.—Findings that are specific to PDAC are the presence of duct structures in perineural and vascular spaces and (“naked”) ducts in fatty tissue. However, these findings are only observed in specimens containing extrapancreatic tissue. The features that are suggestive of PDAC in specimens from the pancreas include haphazard distribution of ductlike structures (ie, loss of a lobular pattern), markedly irregular ductal contours, ruptured ducts, nuclear enlargement, pleomorphism and hyperchromatism, and mitotic figures. Immunohistologic markers that are helpful are carcinoembryonic antigen, MUC1, p53, and Ki-67/ MIB1. Conclusions.—There are a few features that are diagnostic and a number that are suggestive of PDAC. Therefore, a combination of several features may be required to clearly distinguish chronic pancreatitis from invasive PDAC.

2020 ◽  
Vol 25 (2) ◽  
pp. 65-71
Author(s):  
Jae Hyuck Chang

More than 80% of patients with pancreatic ductal adenocarcinoma (PDA) present with symptomatic, surgically unresectable disease. If a “stage shift” from the current 20% resectable proportion to greater by early detection can be achieved, it will unequivocally lead to improved survival in this otherwise dismal disease. Although the goal of early detection of PDA is laudable, the relatively low prevalence PDA renders general population screening infeasible. To avoid the perils of overdiagnosis and to focus early detection efforts on individuals deemed to be at higher-than-average risk, we need to define those subsets of individuals, such as familial kindred and patients with precursor cystic lesions, chronic pancreatitis, and new-onset diabetes. The next step is to determine when and how often to conduct surveillance in the atrisk individuals and the modalities (biomarkers and imaging) that will be used in the surveillance and diagnostic settings, respectively. Nonetheless, vast challenges still remain in terms of validated blood-based biomarkers, imaging modality, and when and how often the surveillance.


EBioMedicine ◽  
2022 ◽  
Vol 75 ◽  
pp. 103797
Author(s):  
Neus Martínez-Bosch ◽  
Helena Cristóbal ◽  
Mar Iglesias ◽  
Meritxell Gironella ◽  
Luis Barranco ◽  
...  

Pancreas ◽  
2018 ◽  
Vol 47 (4) ◽  
pp. 459-465
Author(s):  
Huimin Zhang ◽  
Wei Han ◽  
Meng Jin ◽  
Yamin Lai ◽  
Xi Wang ◽  
...  

HPB Surgery ◽  
1989 ◽  
Vol 1 (4) ◽  
pp. 309-317 ◽  
Author(s):  
Michele Carlucci ◽  
Alessandro Zerbi ◽  
Danilo Parolini ◽  
Sandro Sironi ◽  
Angelo Vanzulli ◽  
...  

Differential diagnosis between pancreatic cancer and chronic pancreatitis is still difficult to establish. In 63 patients with suspected pancreatic neoplasm we performed: serum CA 19-9 assessment, abdominal ultrasound, CT scan and CT-guided pancreatic percutaneous fine-needle biopsy. The conclusive diagnosis was pancreatic cancer in 40 patients and chronic pancreatitis in 23 patients. With regard to the differential diagnosis, sensitivity and specificity were respectively 80% and 78% for serum CA 19-9, 75% and 65% for abdominal US, 85% and 70% for CT scan, 00% and 87% for percutaneous fine-needle biopsy. We conclude that CT-guided percutaneous fine-needle biopsy is the most reliable method for differential diagnosis between pancreatic cancer and chronic pancreatitis.


2016 ◽  
Vol 34 (5) ◽  
pp. 525-531 ◽  
Author(s):  
Markus M. Lerch ◽  
Julia Mayerle ◽  
Ujjwal Mahajan ◽  
Matthias Sendler ◽  
F. Ulrich Weiss ◽  
...  

Background: Pancreatic ductal adenocarcinoma (PDAC) is the 4th leading cause of cancer death worldwide and compared to other malignancies its share in cancer mortality is expected to rise further. This is due to a lack of sensitive diagnostic tools that would permit earlier detection in a potentially curable stage and the very slow progress in finding effective drug treatments for pancreatic cancer. Key Messages: Aside from genetic predispositions and environmental agents, chronic pancreatitis is by far the greatest risk factor for PDAC. It also shares several etiological factors with pancreatic cancer and represents its most challenging differential diagnosis. Biomarkers that can distinguish between chronic pancreatitis and PDAC may therefore be suitable for the latter's early detection. Moreover, targeting the natural history of chronic pancreatitis would be one approach to prevent PDAC. Targeting tumor-cell signaling directly by interfering with receptor tyrosine kinases has shown some efficacy, although the results in clinical trials were less encouraging than for other cancers. Other compounds developed have targeted the formation of extracellular matrix around the tumor, the proteolytic activity in the tumor environment, histone deacetylases, hedgehog signaling and heat shock proteins, but none has yet found its way into routine patient care. Attempts to individualize treatment according to the tumor's somatic mutation profile are novel but so far impractical. Conclusions: Progress in the treatment of pancreatic cancer has been exceedingly slow and mostly dependent on improved pharmaceutical preparations or combinations of established chemotherapeutic agents. The promise of major breakthroughs implied in targeting tumor signal transduction events has so far not materialized.


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