Understanding Of Pancreatitis Research Articles

Global epidemiology and holistic prevention of pancreatitis.

Knowledge of pancreatitis in the 20th century was shaped predominantly by animal data and clinical trials. Several large general population-based cohort studies and comprehensive systematic literature reviews in the 21st century have had a major effect on our understanding of pancreatitis and its sequelae. This Review provides precise and up-to-date data on the burden ofacute pancreatitis, chronic pancreatitis and post-pancreatitis diabetes mellitus. Exocrine pancreatic insufficiency and altered bone metabolism following pancreatitis are also discussed. Furthermore, the article introduces a framework for the holistic prevention of pancreatitis with a view to providing guidance on strategies and intervention objectives at primary, secondary and tertiary levels. Concerted efforts by not only gastroenterologists and surgeons but also primary care physicians, endocrinologists, radiologists, pain specialists, dietitians, epidemiologists and public health specialists will be required to reduce meaningfully the burden of pancreatitis and its sequelae over the ensuing decades.

Risk factors for pancreatic cancer: underlying mechanisms and potential targets.

Purpose of the review: Pancreatic cancer is extremely aggressive, forming highly chemo-resistant tumors, and has one of the worst prognoses. The evolution of this cancer is multi-factorial. Repeated acute pancreatic injury and inflammation are important contributing factors in the development of pancreatic cancer. This article attempts to understand the common pathways linking pancreatitis to pancreatic cancer.Recent findings: Intracellular activation of both pancreatic enzymes and the transcription factor NF-κB are important mechanisms that induce acute pancreatitis (AP). Recurrent pancreatic injury due to genetic susceptibility, environmental factors such as smoking, alcohol intake, and conditions such as obesity lead to increases in oxidative stress, impaired autophagy and constitutive activation of inflammatory pathways. These processes can stimulate pancreatic stellate cells, thereby increasing fibrosis and encouraging chronic disease development. Activation of oncogenic Kras mutations through inflammation, coupled with altered levels of tumor suppressor proteins (p53 and p16) can ultimately lead to development of pancreatic cancer.Summary: Although our understanding of pancreatitis and pancreatic cancer has tremendously increased over many years, much remains to be elucidated in terms of common pathways linking these conditions.

Endotherapy for Organized Pancreatic Necrosis: Perspectives After 20 Years

It has been nearly 20 years since the first peroral endoscopic necrosectomy was performed for patients with pancreatitis. We have since increased our understanding of pancreatitis, and the nomenclature has changed to define disease in which necrosis becomes organized (called "walled-off"). Endoscopic approaches to evaluate and treat pancreatitis have progressed from making small transmural tracts for irrigation to making large tracts, which allow the endoscope to move directly into necrotic cavities and perform endoscopic necrosectomy. The purpose of endoscopic debridement is to irrigate and/or remove areas of necrosis. Collaboration between therapeutic endoscopists and interventional radiologists has led to a combined approach to organized pancreatic necrosis. We discuss the history of peroral endoscopic treatment of organized (walled-off) pancreatic necrosis and current endoscopic approaches to therapy.

A systems biology approach to genetic studies of pancreatitis and other complex diseases.

Pancreatitis is usually inflammation of the pancreas without infection. Our understanding of pancreatitis has been built on autopsy studies, surgical biopsies and surrogate markers of inflammation and fibroses, including abdominal imaging techniques and pancreatic functional studies. However, the discovery that a number of different environmental factors and various genetic abnormalities are seen in patients with similar appearing pancreatitis phenotypes teaches us that end-stage pathology is not the disorder. Understanding complex associations and interactions requires that the components and their interactions be organized, stratified and functionally defined. Systems biology, in the broad sense, provides the approach and tools to define the complex mechanisms driving pathology. As the mathematics behind these pathways and mechanisms are defined and calibrated, the potential pathology of patients with early signs of disease can be predicted, and a number of patient-specific targets for intervention can be defined.

Review of idiopathic pancreatitis

Recent advances in understanding of pancreatitis and advances in technology have uncovered the veils of idiopathic pancreatitis to a point where a thorough history and judicious use of diagnostic techniques elucidate the cause in over 80% of cases. This review examines the multitude of etiologies of what were once labeled idiopathic pancreatitis and provides the current evidence on each. This review begins with a background review of the current epidemiology of idiopathic pancreatitis prior to discussion of various etiologies. Etiologies of medications, infections, toxins, autoimmune disorders, vascular causes, and anatomic and functional causes are explored in detail. We conclude with management of true idiopathic pancreatitis and a summary of the various etiologic agents. Throughout this review, areas of controversies are highlighted.

Surgical management of acute pancreatitis.

A review of clinical experiences with 350 patients with acute pancreatitis and several hundred patients with other acute abdominal diseases revealed that the diagnosis of acute pancreatitis is primarily a bedside diagnosis. Laboratory aids are helpful here, yet unreliable. The mortality rate from acute pancreatitis has fallen to approximately eight per cent since the advent of better transfusion and antibacterial therapy. A recent development in the understanding of pancreatitis has been the realization that this term covers several diseases. Gallstone pancreatitis seldom leads to chronic pancreatitis and can be interrupted by definitive gallstone surgery. Alcoholic pancreatitis characteristically leads to chronic pancreatitis and responds poorly to biliary tract surgery.