Symptoms Of Chronic Pancreatitis Research Articles

CYSTIC DEGENERATION OF THE DUODENUM ASSOCIATED WITH CHRONIC PANCREATITIS

Inflammatory cystic lesion of the descending part of the duodenum, mainly in the field of small duodenal papilla in chronic pancreatitis (CP) is described as “duodenal dystrophy” (DD). The pathogenesis of this condition has not been studied and treatment strategy is not defined. Purpose. Investigation of cystic inflammatory transformation of duodenal wall pathogenesis in patients with CP, described as a DD, and evaluate the clinical ef ficiency of surgical treatment. Material and methods . Eighty two patients with DD were retrospectively included over 12 years. The diagnosis of DD was established by transabdominal ultrasound, CT, MRI and endosonography. Initially, all patients were treated conservatively. 74 patients required surgical treatment subsequently after conservative treatment with a median duration of 2 years. 34 patients underwent pancreaticoduodenectomy (PD), 21 patients underwent duodenum resection, 15 – duodenum preserving pancreatic head resection of (DPPHR). 4 patients underwent palliative operations. Diagnosis of CP and DD was verified by histological study of surgical specimens. Not operated patients (8) are under observation. Long-term results of surgical treatment were evaluated in 47 patients with a median follow-up was 49.9 months. Results . Histological examination resulted that in 69.9% of DD was related with groove pancreatitis, with ectopic pancreatic tissue – in 30.1%. DD was associated with CP in 92.6% of cases. Clinical presentation of DD was not related with etiology and showed typical symptoms of CP: abdominal pain occurred in 98.8% of patients, body weight loss – 61.7%, duodenal obstruction – 35.8%, biliary hypertension – 34.1%. The overall morbidity was 35.1%. Overall postoperative mortality was 1.37% (1 patient). 66% of patients had no clinical symptoms postoperatively, a significant improvement – 32%, no effect – 2%. Conclusion. The most cases of DD is related with groove pancreatitis, less – with ectopic pancreatic tissue in the duodenal wall. Typically DD occurs in patients with CP. Treatment of patients with CP and DD should be started with conservative therapy. Surgery is indicated for persistent abdominal pain and presence of CP complications. Procedures of choice are PD and DPPHR.

Gremlin1 and chronic pancreatitis: a new clinical target and biomarker?

Chronic pancreatitis (CP) is a progressive inflammatory condition triggered by the loss of exocrine pancreatic acini and fibrosis or scarring of pancreas tissue [1]. The exocrine pancreas comprises about 90 % of total pancreas and releases digestive enzymes such as chymotrypsin, amylase and lipase in response to a meal. CP develops in 16 % of patients presenting with acute pancreatitis, a number which increases to 38 % upon second admission. The most common symptom of CP is abdominal pain, which can be both intermittent and persistent. Furthermore, 95 % of CP patients present with alcoholic or idiopathic disease [1]; however, excessive consumption of alcohol alone may not be the cause of CP. Additional causes of CP include gallstones, exposure to volatile hydrocarbons, viral infection and genetic mutations [2]. There are various genetic forms of CP including gain-of-function mutations in genes such as Prss1 which results in a form of trypsin that is resistant to degradation and can lead to an autosomal-dominant hereditary form of CP [1]. In contrast, loss-of-function mutations in genes such as Spink1 and Cftr, which is involved in the inactivation of pancreatic trypsin, are also associated with CP. The overall survival rate for CP patients is only 50 % at 20–25 years from diagnosis [3], and CP patients also have an increased risk of developing pancreatic cancer [4]. Current treatments for CP involve pain management with paracetamol and non-steroid anti-inflammatory drugs as first line, followed by mild opioids such as tramadol. An important clinical feature of CP is steatorrhea, caused by reduced absorption of fat in the intestine. Supplementation of pancreatic enzymes such as lipase, together with H2 histamine antagonists, is used to reduce this malabsorption of lipids [1]. Micronutrient therapy containing antioxidants such as Antox® (containing methyl and thiol moieties, as well as methionine and vitamin C) is now being tested, as it has been shown to control the pain and attacks associated with CP [1]. The pathogenesis of CP is believed to be associated with inappropriate pancreatic enzyme activation and clearance from the acinar cells. Increased pancreatic Ca levels as a result of excessive consumption of alcohol or other causes is common in CP, with calcifying protein deposits implicated in the blockage of the acinar ducts, leading to digestive enzyme accumulation and subsequent inflammation. Other evidence suggests that noxious agents such as alcohol are directly toxic to the acinar cells and may also trigger the activation of pancreatic stellate cells [5]. An important element of the pathogenesis of CP is fibrosis, which can occur via sustained activation of pancreatic stellate cells that migrate to sites of tissue damage and secrete excess extracellular matrix proteins, causing fibrosis or scarring [6]. Factors that drive this fibrotic response include lipid peroxidation products released by acinar cells and TGF-β1 release by reactive oxygen species (ROS)-activated mast cells that infiltrate the pancreas as part of the inflammatory response to CP [1]. Progression of fibrosis in CP is associated with the loss of acinar and islet cells, leading to both exocrine and endocrine pancreas dysfunction. There are currently no effective therapies to prevent or reverse CP [7]. Given the insidious nature of CP, together with the increased mortality rate and pancreas cancer risk, improved treatment options for reversing the progressive fibrosis associated with this disease are urgently needed. To this end, new molecular targets that are involved in the onset and progression of fibrosis associated with CP need to be identified. * Derek P. Brazil d.brazil@qub.ac.uk

Quality of life in patients with chronic pancreatitis – Possibilities of measurement of the phenomenon in research

ObjectiveTo discover which of the measurement tools were used for the assessment of quality of life (QoL) in patients with chronic pancreatitis (CP); to search for a specific tool that was validated and standardized directly for CP; to summarize the main areas of symptomatology that dominated the decrease overall in QoL in patients with CP. MethodsThe method of the overall conceptualization approach was the analysis, comparison, critical discussion and summarization of the available results of studies researched between 2000 and 2014 in relevant databases. The analyzed studies were included in the selective sample according to predefined criteria. This paper presents the results of a partial objective regarding a comprehensive research project. ResultsThe identified tools include the following questionnaires: SQUALA (1 study); SF-36 (4 studies); SF-12 (6 studies); EORTC QLQ-C30 in the form of QLQ-PAN26 (3 studies). A specific and new tool is PANQOLI (1 study). The most significant factor of decreased QoL included pain; other factors were: chronic diarrhoea, digestion issues, diabetes mellitus, severity and length of disease, number of relapses and comorbidities, loss of job, unemployment, early retirement, financial issues, sleeping issues, fatigue. On the contrary, the aetiology had no effect on QoL; the same applies to surgery or endoscopic therapies. ConclusionTo assess QoL the following questionnaires were used: subjective QoL questionnaires specific for chronic diseases, and a questionnaire originally intended for patients with tumour diseases. This shows a degree of interest in the area of QoL in CP patients. The sum of the findings can be used for a comparison between domestic results and to identify the dominant CP symptoms. A great challenge is the standardization and linguistic validation of the PANQOLI questionnaire in the Czech sociocultural environment.

Cochrane Corner: Antioxidants to reduce pain in chronic pancreatitis

The common symptoms of chronic pancreatitis (CP) include frequent or constant pain in the upper abdomen radiating to the back, and weight loss resulting from by malabsorption of food. Diabetes may also develop if the insulin-producing cells of the pancreas are damaged. It is a difficult to treat condition, usually involving a low-fat diet, medications for the pain and sometimes patients require pancreatic enzymes, insulin or surgery. CP occurs more frequently inmen than inwomen, often developing in people aged 30–40. Oxidative stress has been implicated in the pathophysiology of CP and there is evidence that the pain of CPmay be in part be due to oxygen free radical induced pancreatic damage [1]. Peoplewith the condition may also have a reduced intake of antioxidants as a result of eating less because of pain, and also as a result of malabsorption, and lower levels of antioxidants are often observed in patients with the disease [2]. It is thought that improving the status of antioxidants might be effective in slowing the disease process and reducing pain. This Cochrane review included 12 RCTs, with a total of 585 participants, which evaluated antioxidants for the treatment of pain in CP [3]. Six trials were double-blind, placebo-controlled studies, and the other six were of less robust methodology. The antioxidant treatments used in the studies varied widely, but in general consisted of a combination of several commonly used antioxidants, in particular, selenium, ascorbic acid, b-carotene, atocopherol, and methionine. As studies used different types, numbers of preparations and doses of antioxidants, and as there Cochrane review Pancreatitis Antioxidants

Total pancreatectomy with islet autologous transplantation: the cure for chronic pancreatitis?

Chronic pancreatitis (CP) is a debilitating disease that leads to varying degrees of pancreatic endocrine and exocrine dysfunction. One of the most difficult symptoms of CP is severe abdominal pain, which is often challenging to control with available analgesics and therapies. In the last decade, total pancreatectomy with autologous islet cell transplantation has emerged as a promising treatment for the refractory pain of CP and is currently performed at approximately a dozen centers in the United States. While total pancreatectomy is not a new procedure, the endocrine function-preserving autologous islet cell isolation and re-implantation have made the prospect of total pancreatectomy more acceptable to patients and clinicians. This review will focus on the current status of total pancreatectomy with autologous islet cell transplant including patient selection, technical considerations, and outcomes. As the procedure is performed at an increasing number of centers, this review will highlight opportunities for quality improvement and outcome optimization.

Antioxidants Are Not Useful in Reducing Both Pain and Inflammation in Chronic Pancreatitis

Pain is the main clinical symptom of chronic pancreatitis at its early stages; then the pain tends to disappear during the progression of the disease. Several options have been proposed to treat pain and inflammation in chronic pancreatitis; medical, endoscopic or surgical treatments have been considered, and the controversy surrounding their efficacy is ongoing. One medical option is to use antioxidants for both preventing and curing the flare-ups of chronic pancreatitis. The data regarding this treatment are highly debated; some authors have reported their efficacy in reducing pain and inflammation whereas others have not. We have reviewed the current knowledge and recent patents on this topic and, at present, we do not recommend this therapeutic approach and additional studies are required for reconsidering this interesting therapeutic option.

Electrophysiology as a tool to unravel the origin of pancreatic pain.

Intense abdominal pain is the most common symptom in chronic pancreatitis, but the underlying mechanisms are not completely understood and pain management remains a significant clinical challenge. The focus of pain origin in chronic pancreatitis traditionally has been on the pancreatic gland, assuming pain to originate in the pancreas or its surrounding organs. However, research in the last decade points to abnormal central nervous system pain processing. For this reason, electroencephalography has been receiving increasing attention. In contrast to imaging methods such as functional magnetic resonance imaging and positron emission tomography, electroencephalogram has excellent temporal resolution making it possible to investigate central processing of pain on a millisecond time scale. Moreover, continuously advancing methodology made it possible to explore brain sources responsible for generation of evoked potentials and hence to study brain reorganization due to pain in chronic pancreatitis. The aim of this review is to give an overview of the current methods and findings in electroencephalography as a tool to unravel the origin of pancreatic pain.

Management of Chronic Pancreatitis

Advances in our understanding of chronic pancreatitis have improved our care of patients with this disease. Although our therapies are imperfect and many patients remain symptomatic, appropriate medical care improves the quality of life in these patients. Proper management requires an accurate diagnosis, recognition of the modifiable causes of disease, assessment of symptoms and complications, treatment of these symptoms and complications utilizing a multidisciplinary team, and ongoing monitoring for the effect of therapy and the occurrence of complications.

Advances in Diagnosis and Treatment of Biliopancreatic Diseases

Management of biliopancreatic diseases has seen great progress in recent years. Innovations in endoscopy have allowed gastroenterologists to assist in the care of many conditions of the biliary tree and pancreas, which were previously only managed surgically. Outcomes for many of these endoscopic interventions are comparable to their surgical counterpart. However, endoscopists taking care of these patients should be well aware of the limitations of their procedures and the advantages of surgery for certain patients. This special issue will address some of the main challenges faced today by physicians taking care of patients with pancreatic and biliary diseases. Endosonography, or endoscopic ultrasound (EUS), which previously was only considered a diagnostic tool, has now emerged as a useful therapeutic technique. In contrast, endoscopic retrograde cholangiopancreatography, or ERCP, has now become mainly a therapeutic tool. Some ERCP techniques have been adopted by endosonographers and allowed interventions for draining bile ducts and peripancreatic fluid collections, previously considered outside the realm of endoscopy. Despite the advances in outcomes and minimal invasiveness of EUS and ERCP-guided interventions, several risks and complications still remain. Pancreatitis is a well-recognized complication of ERCP with a significant incidence that has not been reduced greatly throughout recent years. Numerous studies have looked at ways of decreasing the risk of this dreadful complication. This special issue will discuss and review the problem of post-ERCP pancreatitis, a topic that raises a high level of concern for many who do this procedure, and ways to reduce its risk, especially in patients considered at high risk for developing this complication. Incidental pancreatic cysts continue to pose a diagnostic dilemma for gastroenterologists and surgeons alike. Despite the ability of safely obtaining a tissue sample during EUS examination, the utility of cytopathology in determining the exact nature of these lesions remains limited. More recently, DNA analysis of fluid obtained during aspiration has shown promise in improving the diagnostic accuracy of EUS-FNA. However, the effect of these newer tests in terms of deciding when to observe versus surgically resect in many of these incidental cysts remains to be proven. Pancreatologists agree that a reliable method for determining the nature and prognosis of pancreatic cystic neoplasms is required for improving the management strategy in asymptomatic patients. Abdominal pain is a cardinal symptom of chronic pancreatitis. The effectiveness of medical therapy, in the form of pancreatic enzyme supplementation or octreotide injections, is dismal. Pain relief can certainly be obtained with the use of narcotic medications, but at the cost of significant side effects, such as constipation, sedation, and drug dependence. Endoscopic alternatives for improving pain in chronic pancreatitis include those guided by ERCP, such as intraductal stone removal, stricture dilation, or drainage procedures, and EUS-guided celiac plexus block. This special issue will review the ERCP-guided interventions and discuss the efficacy of EUS-guided celiac plexus neurolysis for the treatment of pain in patients with pancreatic cancer. As advances in endoscopy and surgical innovations are introduced into the field of biliary and pancreatic diseases, many diseases previously requiring complicated surgeries with prolonged recovery are now being managed by minimally invasive techniques. Many of these procedures have a reduced risk when compared to their surgical alternative. However, long-term efficacy and patient risk factors need close consideration when deciding between different management alternatives. Many, if not all, biliary and pancreatic disorders require a close interaction between gastroenterologist and surgeon. The phrase “No man is an island” by John Donne (1572–1631) emphasizes the importance of consensus between specialists and should always be in the minds of those managing patients with biliopancreatic diseases. Fauze Maluf-Filho Jose G. de la Mora Levy Carlos G. Micames

Chronic Pancreatitis and Its Effect on Employment and Health Care Experience

Symptoms of chronic pancreatitis (CP) frequently hinder patients' ability to work. The aim of our study was to evaluate the impact of CP on employment patterns and health care experience. Patients with CP at 4 US pancreas centers were evaluated. A survey was given to each patient during an office visit between July 1, 2006 and October 31, 2007. One hundred eleven patient surveys were returned. The median age was 52 years; the median duration of CP symptoms was 8.2 years. Seventy-four percent had their work lives altered by CP, 60% reported an effect on their social lives, and 46% reported an effect on their spouse/significant other relationship (P < 0.03). Only 37% were currently employed. During the week before completing the survey, the patients who were employed reported absences from their job due to CP symptoms, a median of 14 hours. On at least 1 visit to the ED, 80% of respondents reported that they had not been treated with respect and dignity, 45% had been labeled an alcoholic, and 29% had been labeled a drug seeker. Chronic pancreatitis had a profound impact on employment patterns. Comprehensive efforts are needed to improve the health care experience of patients with this disease.

Descending Inhibitory Pain Modulation Is Impaired in Patients With Chronic Pancreatitis

Pain is a prominent symptom in chronic pancreatitis (CP), but the underlying mechanisms are incompletely understood. We investigated the role of descending pain modulation from supraspinal structures as well as central nervous system sensitization in patients with pain from CP. Twenty-five patients with CP and 15 healthy volunteers were included. Descending pain modulation was investigated by diffuse noxious inhibitory control (a descending inhibitory response after conditioning stimulation). Central pain processing was investigated as the perceptual responses to multimodal (electrical, thermal, and mechanical) stimulations of the rectosigmoid and evoked brain potentials after electrical stimulation of the rectosigmoid. Compared with healthy volunteers, the efficacy of diffuse noxious inhibitory control was reduced in patients with CP (13% +/- 21% vs 39% +/- 22%, respectively; F = 3.8; P = .01); central sensitization was indicated by remote hyperalgesia in the rectosigmoid to electrical stimulation (21 +/- 15 mA vs 27 +/- 15 mA; F = 6.2; P = .02) and heat stimulation (51 degrees C +/- 5 degrees C vs 53 degrees C +/- 4 degrees C; F = 5.9; P = .02). Compared with controls, patients with CP had increased latency of the early P1 peak to rectosigmoid stimulation (85 +/- 21 ms vs 108 +/- 28 ms, respectively; P = .02), possibly reflecting reorganization of central pain pathways. Patients with CP have impairments in inhibitory pain modulation and evidence of central sensitization. Treatment of their pain therefore should focus not only on the pancreas, but also on descending pain modulation from supraspinal structures and central nervous system sensitization.

Differential methylation of cell‐free circulating DNA among patients with pancreatic cancer versus chronic pancreatitis

: Although patients with chronic pancreatitis (CP) have an increased risk of pancreatic cancer (PanCa), the timely detection of PanCa often is difficult, because the symptoms of CP and PanCa are very similar. Moreover, secondary inflammation may be identified in PanCa, further complicating diagnosis. To improve the survival of patients with PanCa, a reliable test to differentiate CP from PanCa is needed. In this article, the authors describe a methylation profile of cell-free plasma DNA that distinguished CP from PanCa with >90% accuracy. : Methylation in cell-free, plasma DNA was compared among 30 samples from patients with CP, 30 samples from patients with PanCa, and 30 samples from healthy controls (N) using a microarray-mediated methylation analysis of 56 fragments in each sample (MethDet56). Statistical analysis was done by using the Fisher exact test, a naive Bayes algorithm, and 25 rounds of 5-fold cross-validation. : The MethDet56 methylation analysis technique identified 17 gene promoters as informative (8 for distinguishing N from CP and 14 for distinguishing CP from PanCa). It achieved 81.7% sensitivity and 78% specificity (P<.01) in the detection of CP (N vs CP) and 91.2% sensitivity and 90.8% specificity (P<.01) in the differential detection of PanCa (PanCa vs CP). : The current data suggested that, among patients with pancreatic disease, the methylation profiles of inflammatory disease and cancer are different and open a new venue for the development of biomarkers for differential diagnosis. Further investigation of diagnostic biomarkers for pancreatic cancer based on methylation in cell-free, circulating DNA appears to be warranted. Cancer 2010. (c) 2010 American Cancer Society.

Chronic pancreatitis

We review important new clinical observations in chronic pancreatitis made in the last year. Cholecystokinin-stimulated endoscopic pancreatic function testing has low specificity for diagnosis of early chronic pancreatitis, likely because of correctable technical limitations or failure to exclude confounding diseases. Fecal elastase 1 is a poor test for diagnosing pancreatic malabsorption. A 2-week trial of corticosteroids may differentiate autoimmune pancreatitis (AIP) from pancreatic cancer in select patients. A genetic screen may help to predict relapse of AIP. Repeated, 6-month visits to counsel against alcohol use may reduce recurrent attacks of alcoholic pancreatitis. A five-component antioxidant cocktail may reduce the frequency of pain in chronic pancreatitis by 1.5 days per month. Researchers this last year have further characterized clinical aspects of chronic pancreatitis that may lead to improved detection of early chronic pancreatitis and AIP, risk stratification and application of risk-lowering strategies to prevent relapses in AIP or the development of recurrent (and possibly chronic) alcoholic pancreatitis and new evidence that antioxidants may have a modest effect on reducing the dominant symptom in chronic pancreatitis, abdominal pain.

The Effect of Chronic Pancreatitis on Employment

Purpose: Patients with chronic pancreatitis (CP) often suffer debilitating symptoms leading to interruptions in their ability to work. The aim of this study was to evaluate the effect of chronic pancreatitis on employment status in patients presenting for clinical evaluation. Methods: Patients with established CP presenting for clinical evaluation at four U.S. pancreas centers – Dartmouth-Hitchcock Medical Center (NH), the University of Cincinnati (OH), Brigham and Women's Hospital (MA) and Mayo Clinic Rochester (MN) – were included. The diagnosis of CP was based on the evaluation of the treating clinician at each center. Patients with chronic pancreatitis evaluated in each institution's pancreas clinic between July 1st 2006 and October 31st 2007 were asked to complete a 72 item survey at the conclusion of one of their office visits. Completed surveys were mailed to the coordinating center (Dartmouth) anonymously where all data analysis was completed. The study was approved by the IRB at each institution. Results: 111 patient surveys were returned. Patients had a mean age of 50 years; 50% were male; 59% were married; 82% had finished high school. Only 37% were presently employed (73% currently full-time); 56% earned less than $25,000 (U.S.) per year (median personal income in the U.S $32,140); only 30% earned more than $50,000 (U.S.) per year. Given the ability to choose from 9 domains in which CP could affect their lives, 74% reported that their work lives were altered by CP; 60% reported an effect on their social lives; 46% reported an effect on their spouse/significant other relationships. Given the ability then to choose which of the 9 domains was most affected by CP, 28% reported difficulty in completing daily activities while 26% had difficulty in employment. In the week prior to completing the survey, the 37% of patients who were employed reported working a mean of 28.5 hours and being absent from their job a mean of 16.9 hours due to CP symptoms. The most important patient concerns were that CP symptoms would interfere with their professional lives (34%); would shorten their lifespan (22%); would be passed on to their children (18%); or would develop into cancer (13%). Conclusion: In the United States, patients with CP have high unemployment rates, below median personal income, and miss significant time at work due to their illness. The deleterious effect of their disease on employment status and personal life is of significant concern to patients. It is important for physicians to be more aware of these concerns.

Diagnostik und Therapie der chronischen Pankreatitis

Chronic pancreatitis (CP) is characterized by progressive, chronic inflammation of the pancreas, resulting in loss of exocrine and endocrine function and chronic abdominal pain. In most cases, CP is induced by long-term alcoholism. The second most frequent diagnosis is idiopathic CP, in the absence of known causes of CP. However, the identification of genetic and immunological causes continuously reduces the number of cases classified as idiopathic pancreatitis. Common symptoms of CP comprise abdominal pain radiating to the back, diarrhea, steatorrhea and the development of diabetes. The diagnosis is mainly based on clinical features, typical morphological findings such as pancreatic calcifications, duct stenoses and dilatations, as well as pathologic pancreatic function tests. Treatment of CP includes watch and wait strategies in asymptomatic patients, symptomatic treatment of the clinical features such as pain, exocrine and endocrine insufficiency, as well as interventional or surgical therapy of complications such as pseudocysts, pancreatic duct stenosis, stones or biliary obstruction.

Screening for human cationic trypsinogen (PRSS1) and trypsinogen inhibitor gene (SPINK1) mutations in a Finnish family with hereditary pancreatitis

Objective. Mutations in the cationic trypsinogen gene (PRSS1) have been linked with hereditary pancreatitis (HP). A change in R122H in the third exon is one of the mutations most frequently associated with HP. A mutation N34S in the serine protease inhibitor Kazal type 1 gene has also been shown to be linked with HP. The purpose of this study was to report on the incidence of PRSS1 and SPINK1 mutations in a Finnish family with HP and to correlate the findings to the clinical symptoms. Material and methods. The study included 36 individuals from one Finnish family with HP (21 M, 15 F, median age 38 years). All individuals underwent abdominal ultrasound and laboratory tests (glucose, faecal elastase-1 test). Blood samples were taken for mutational analysis of PRSS1 (R122H, N29I and A16V) and SPINK1 (N34S). Results. Ten (28%) individuals were affected by mutations: the most frequent mutation was R122H, affecting 8 (22%) individuals; 2 (6%) individuals were affected by the N34S mutation and none by the other tested mutations (N29I and A16V). Four out of eight (50%) R122H-positive individuals had a diagnosis of chronic pancreatitis without other known aetiologies. Four out of five (80%) male individuals with the R122H mutation also had clinical pancreatitis, whereas none of the three mutation-positive females had any signs or symptoms of chronic pancreatitis. The two individuals with the N34S mutation did not have any signs of chronic pancreatitis. Conclusions. In the investigated Finnish pedigree with HP, the PRSS1 mutation R122H is linked with chronic disease. Although the SPINK1 mutation (N34S) was also observed in two individuals, it was not linked with the disease.

Estimation of the prevalence and incidence of chronic pancreatitis and its complications: A prospective survey in adults attending gastroenterologists in France

Incidence and prevalence of chronic pancreatitis (CP) are poorly known and prospective nationwide epidemiologic estimation has never been performed. To estimate prospectively national incidence and prevalence of patients attending gastroenterologists for CP in France. Study was proposed to all of the French gastroenterologists (N=3215) of whom 753 accepted to participate (24% private, 40% hospital and 36% both). Were included all patients suffering from proved or suspected CP, from 04-2003 to 07-2003. Certain diagnostic criteria were pancreatic calcifications, ductal or histological abnormalities. For all of non-responder gastroenterologists, a tracking system was used (mail or by phone). A total of 456 gastroenterologists returned at least 1 case on 1748 patients. Median patient age was 51 years; sex-ratio was 5.07. Median duration between the first CP sign and the inclusion was 41 months. CP cause was alcoholism (84%), hereditary (1%), cystic fibrosis (1%), idiopathic (9%), other (6%). CP diagnosis was certain in 77%: calcifications (85%), ductal abnormalities (57%), and histology (8%). CP symptoms were: chronic abdominal pain (53%), acute pancreatitis episodes (67%), pseudocysts (40%), bi-liary tract compression (21%), diabetes mellitus (32%), pancreatic exocrine insufficiency (36%). Maximal annual incidence was 4,646 (crude annual incidence: 7.7 per 100,000; 12.9 in male; 2.6 in female) and prevalence was 15,832 cases (crude prevalence: 26.4 per 100,000; 43.8 in male; 9.0 in female). New CP patients attending gastroenterologists are about 5,000 a year. CP prevalence is about 16,000 patients (in France: 60,400,000 inhabitants). Frequency of main complications is close to hospital series, confirming that results issued from these centers are not or a few biased.

The role of endoscopy in patients with chronic pancreatitis

Chronic pancreatitis (CP) is an inflammatory process characterized by destruction of pancreatic parenchyma and ductal structures with formation of fibrosis. Pain is the predominant symptom of CP and its origin is multifactorial. 1 Steer M.L. Waxman I. Freedman S. Chronic pancreatitis. N Engl J Med. 1995; 332: 1482-1490 Crossref PubMed Scopus (579) Google Scholar Treatment is directed toward control of symptoms and management of the structural complications. Medical therapies such as abstinence from alcohol, dietary alterations, analgesics, oral enzyme supplements, and somatostatin analogs are variably effective in relieving pain. In patients for whom medical management fails, surgical and endoscopic options are available.

Long-Term Outcomes after Post-ERCP Pancreatitis

Purpose: The long-term sequelae of a single episode of pancreatitis is not well defined. The dogma is that once the inciting event is removed, the pancreas should fully recover and not lead to any chronic parenchymal/ductal changes or symptoms of chronic pancreatitis. Aim: To assess the clinical long-term pancreatic sequelae in patients developing acute post-ERCP pancreatitis. Methods: Endoscopic and medical records of patients undergoing ERCP during a 12 year period were reviewed. Those with post-ERCP pancreatitis were selected and clinical, laboratory and radiological information suggestive of chronic pancreatitis was sought and retrieved. Severity of post-ERCP pancreatitis was defined by clinical (presence of end-organ failure), radiological criteria (CT severity index score) and/or length of stay in the hospital. Long-term sequelae of pancreatic dysfunction including chronic pancreatitis was defined: a) clinically by the presence of either chronic pancreatic-type of pain, malabsorption (weight loss; fat in stools; chronic diarrhea); b) radiographically by the presence of pancreatic calcifications, abnormal pancreatic duct anatomy, distal CBD stricture compatible with chronic pancreatitis; and/or c) EUS criteria, developing after the index episode. Results: Of 2104 ERCPs there were 48 where patients developed post-ERCP pancreatitis (2.2%) of which 4 patients (0.1%) had severe pancreatitis based on presence of organ failure and/or CT criteria, and/or length of stay. Ten patients had prior evidence of chronic pancreatitis and thus were excluded. The mean follow up for the remaining 38 patients was 57.5 months. Of the 4 patients with severe post-ERCP pancreatitis, 2 died, 1 developed recurrent pancreatitis secondary to a suspected sphincter of Oddi dysfunction and the other did not developed any clinical long-term sequelae. Of the remaining 34 patients with post-ERCP pancreatitis, 2 were diagnosed with pancreatic cancer (one primary and the other metastatic from renal cell carcinoma) shortly after the episode. Clinically, none of the 32 remaining patients had symptoms compatible with chronic pancreatitis; 22 had plain X rays and none showed pancreatic calcifications; and 15 had repeated CT scans and none had pancreato/biliary abnormalities. Conclusions: Similar to what is described in gallstone pancreatitis, the development of chronic pancreatic sequelae after an episode of post-ERCP pancreatitis seems to be rare (non-existing in our limited series). Larger studies are required to assess the true incidence of chronic pancreatic sequelae after post-ERCP pancreatitis.

Chronic pancreatitis of alcoholic and nonalcoholic origin

Fibroinflammatory changes to the pancreatic tissue characterize chronic pancreatitis. This article summarizes the current state of knowledge on the pathology and pathogenesis of chronic pancreatitis associated with alcohol, hereditary factors, metabolic conditions, and anatomical abnormalities. Specifically, the pathogenetic mechanisms that lead to chronic pancreatitis in patients with alcohol abuse will be discussed. In addition, brief descriptions of the features of chronic pancreatitis of nonalcoholic origin and of the pancreatic fibrosis that is not associated with symptoms of chronic pancreatitis will be given.