The 2016 HaPanEU/United European Gastroenterology guidelines provide evidence-based recommendations concerning key aspects of the medical and surgical management of chronic pancreatitis based on current available evidence. These recommendations should serve as a reference standard for existing management of the disease and as a guide for future clinical research.
Chronic pancreatitis is defined as a pathological fibro-inflammatory syndrome of the pancreas in individuals with genetic, environmental and/or other risk factors who develop persistent pathological responses to parenchymal injury or stress. Potential causes can include toxic factors (such as alcohol or smoking), metabolic abnormalities, idiopathic mechanisms, genetics, autoimmune responses and obstructive mechanisms. The pathophysiology of chronic pancreatitis is fairly complex and includes acinar cell injury, acinar stress responses, duct dysfunction, persistent or altered inflammation, and/or neuro-immune crosstalk, but these mechanisms are not completely understood. Chronic pancreatitis is characterized by ongoing inflammation of the pancreas that results in progressive loss of the endocrine and exocrine compartment owing to atrophy and/or replacement with fibrotic tissue. Functional consequences include recurrent or constant abdominal pain, diabetes mellitus (endocrine insufficiency) and maldigestion (exocrine insufficiency). Diagnosing early-stage chronic pancreatitis is challenging as changes are subtle, ill-defined and overlap those of other disorders. Later stages are characterized by variable fibrosis and calcification of the pancreatic parenchyma; dilatation, distortion and stricturing of the pancreatic ducts; pseudocysts; intrapancreatic bile duct stricturing; narrowing of the duodenum; and superior mesenteric, portal and/or splenic vein thrombosis. Treatment options comprise medical, radiological, endoscopic and surgical interventions, but evidence-based approaches are limited. This Primer highlights the major progress that has been made in understanding the pathophysiology, presentation, prevalence and management of chronic pancreatitis and its complications.
There has been a proliferation and divergence of imaging-based tumor-specific response criteria over the past 3 decades whose purpose is to achieve objective assessment of treatment response in oncologic clinical trials. The World Health Organization (WHO) criteria, published in 1981, were the first response criteria and made use of bidimensional measurements of tumors. The Response Evaluation Criteria in Solid Tumors (RECIST) were created in 2000 and revised in 2009. The RECIST criteria made use of unidimensional measurements and addressed several pitfalls and limitations of the original WHO criteria. Both the WHO and RECIST criteria were developed during the era of cytotoxic chemotherapeutic agents and are still widely used. However, treatment strategies changed over the past decade, and the limitations of using tumor size alone in patients undergoing targeted therapy (including arbitrarily determined cutoff values to categorize tumor response and progression, lack of information about changes in tumor attenuation, inability to help distinguish viable tumor from nonviable components, and inconsistency of size measurements) necessitated revision of these criteria. More recent criteria that are used for targeted therapies include the Choi response criteria for gastrointestinal stromal tumor, modified RECIST criteria for hepatocellular carcinoma, and Immune-related Response Criteria for melanoma. The Cheson criteria and Positron Emission Tomography Response Criteria in Solid Tumors make use of positron emission tomography to provide functional information and thereby help determine tumor viability. As newer therapeutic agents and approaches become available, it may be necessary to further modify existing anatomy-based response-assessment methodologies, verify promising functional imaging methods in large prospective trials, and investigate new quantitative imaging technologies.
The ADCs in cirrhotic livers are significantly lower than those in nonfibrotic livers. However, ADC values measured using the current generation of scanners are not reliable enough to replace liver biopsy for staging hepatic fibrosis.
ADC measurements may aid in differentiating among the various subgroups of renal masses, particularly benign cystic lesions from cystic renal cell cancers.
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