Pancreatitis and the Risk of Pancreatic Cancer

Lowenfels, Albert B.; Maisonneuve, Patrick; Cavallini, Giorgio; Ammann, Rudolf W.; Lankisch, P. G.; Andersen, Jens Rikardt; DiMagno, Eugene P.; Andrén‐Sandberg, Åke; Domellöf, L

doi:10.1056/nejm199305203282001

Cited by 1,539 publications

(489 citation statements)

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“…The patients' mean age was 52.98 (±9.40) years; subtracting mean disease duration from mean age confirms data published by Lowenfels et al 21 , who found that the mean age of their patients at diagnosis of chronic pancreatitis was 44.6 years. Yet Mullhaupt et al 22 found a mean age at alcoholic chronic pancreatitis onset of 36 years in a sample of 265 patients.…”

Section: Discussionsupporting

confidence: 87%

Alcoholic chronic pancreatitis: A quality of life study

et al. 2016

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A B S T R A C T ObjectiveTo compare the quality of life between patients with alcoholic chronic pancreatitis and controls, and between diabetic and non-diabetic patients, correlating clinical, sociodemographic, and nutritional factors with their quality of life scores. MethodsForty-three outpatients of the pancreas and biliary tract clinic diagnosed with alcoholic chronic pancreatitis were assessed. Quality of life was measured by the Brazilian version of the Short Form-36. The control group consisted of 43 healthy companions. Nutritional status was classified according to body mass index and triceps, biceps, suprailiac, and subscapular skinfold thicknesses, using the appropriate methods. The percentage of body fat was given by adding the four skinfold thicknesses and by bioelectrical impedance analysis. The statistical tests included the Chi-square, Mann-Whitney, and Spearman's correlation tests, with the significance level set at p<0.05. ResultsThe sociodemographic variables of the case and control groups did not differ. Quality of life was lower in alcoholic chronic pancreatitis patients than in controls. The only quality of life domain that differed between diabetics and non-diabetics was functional capacity, lower in diabetics (p=0.022). Smoking duration, alcohol intake in grams, and time since pancreatic surgery correlated negatively with the quality of life of alcoholic chronic pancreatitis patients. Old age, skinfold thicknesses, and percentage of body fat correlated positively with quality of life.

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Section: Discussionsupporting

confidence: 87%

Alcoholic chronic pancreatitis: A quality of life study

et al. 2016

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“…The risk of pancreatic cancer is known to increase with the duration of CP [39], therefore follow up imaging in CP is recommended [40]. Two cases of pancreatic cancer were identified in our cohort, thus supporting routine pancreatic imaging when PEI is diagnosed.…”

Section: Imagingsupporting

confidence: 66%

Should we Investigate Gastroenterology Patients for Pancreatic Exocrine Insufficiency? A Dual Centre UK Study

Campbell

Sanders

Francis

et al. 2016

JGLD

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Background & Aims: Pancreatic exocrine insufficiency may be under recognised in gastroenterological practice. We aimed to identify the prevalence of pancreatic insufficiency in secondary care gastroenterology clinics and determine if co-morbidity or presenting symptoms could predict diagnosis. A secondary aim was to assess response to treatment. Methods: A dual centre retrospective analysis was conducted in secondary care gastroenterology clinics. Patients tested for pancreatic exocrine insufficiency with faecal elastase-1 (FEL-1) between 2009 and 2013 were identified in two centres. Demographics, indication and co-morbidities were recorded in addition to dose and response to pancreatic enzyme replacement therapy. Binary logistic regression was used to assess if symptoms or co-morbidities could predict pancreatic insufficiency. Results: 1821 patients were tested, 13.1% had low FEL-1 (<200μg/g). This prevalence was sub-analysed with 5.4% having FEL-1 100-200μg/g (mild insufficiency) and 7.6% having faecal elastase readings <100μg/g. Low FEL-1 was most significantly associated with weight loss or steatorrhoea. Co-morbidity analysis showed that low levels were significantly associated with excess alcohol intake, diabetes mellitus or human immunodeficiency virus; 80.0% treated with enzyme supplements reported symptomatic benefit with no difference in response between high and low dose supplementation (p=0.761). Conclusion: Targeting the use of FEL-1 in individuals with specific symptoms and associated conditions can lead to improved recognition of pancreatic exocrine insufficiency in a significant proportion of secondary care patients. Intervening with lifestyle advice such as smoking cessation and minimising alcohol intake could improve outcomes. In addition, up to 80% of patients with low faecal elastase respond to supplementation. Abbreviations: CFA: coefficient of fat absorption; CP: chronic pancreatitis; ELISA: enzyme-linked immune-absorbent assay; PEI: pancreatic exocrine insufficiency; FEL-1: faecal elastase-1; HIV: human immunodeficiency virus; IBD: inflammatory bowel disease; IBS: irritable bowel syndrome; PERT: pancreatic enzyme replacement therapy.

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“…The inherited basis of B10-20% of familial pancreatic cancers has been identified and is reflected largely in germline mutations in the BRCA2 gene (Goggins et al, 1996;Ozcelik et al, 1997;Hahn et al, 2003) (The Breast Cancer Linkage Consortium, 1999;Murphy et al, 2002). Germline mutations in the p16 (Goldstein et al, 1995;Lynch et al, 2000;Vasen et al, 2000;Bartsch et al, 2002), FANCC (van der Heijden et al, 2003;Rogers et al, 2004), FANCG (van der Heijden et al, 2003;Rogers et al, 2004), PRSS1 (Lowenfels et al, 1993(Lowenfels et al, , 1997, STK11 (Giardiello et al, 2000;Lim et al, 2004), and hMLH1 (Yamamoto et al, 2001) genes are infrequent causes of familial pancreatic cancer and are associated with a number of cancer syndromes, including familial multiple mole melanoma (FAMMM), hereditary pancreatitis, hereditary nonpolyposis colon cancer, and Peutz-Jeghers syndrome. In addition, germline BRCA2 mutations are observed in B5% of patients with apparently sporadic pancreatic cancer, that is, patients who do not appear to have an inherited predisposition to pancreatic or breast/ovarian cancer (Goggins et al, 1996;Ozcelik et al, 1997;The Breast Cancer Linkage Consortium, 1999;Figer et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Increased prevalence of the BRCA2 polymorphic stop codon K3326X among individuals with familial pancreatic cancer

et al. 2005

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Germline BRCA2 mutations predispose to the development of pancreatic cancer. A polymorphic stop codon in the coding region of BRCA2 (K3326X) has been described, and although an initial epidemiological study suggested it was not disease causing, subsequent studies have been inconclusive. To investigate the biological significance of the K3326X polymorphism, we determined its prevalence in patients with sporadic and familial pancreatic cancer. Using a case-control design, we studied 250 patients with resected sporadic pancreatic adenocarcinomas, 144 patients with familial pancreatic adenocarcinoma, 115 spouses of patients with pancreatic cancer, and a disease control group of 135 patients without a personal history of cancer who had undergone cholecystectomy for non-neoplastic disease. The K3326X polymorphism was detected using heteroduplex analysis and DNA sequencing. The BRCA2 K3326X polymorphism was significantly more prevalent in individuals with familial pancreatic cancer: 8/144 (5.6%) vs 3/250 controls (1.2%) (odds ratio, 4.84; 95% CI, 1.27-18.55, Po0.01). One K3326X carrier with familial pancreatic cancer carried an alteration (IVS 16-2A>G) suspected to be deleterious. Excluding this case did not alter the significance of the association (OR: 4.24, Po0.01). In contrast, there was no difference in prevalence among individuals with sporadic pancreatic cancer -7/250 (OR: 2.37, 95% CI: 0.61-9.27). The increased prevalence of the BRCA2 K3326X polymorphism in patients with familial pancreatic cancer suggests that this polymorphism is deleterious and contributes to pancreatic cancer risk.

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Pancreatitis and the Risk of Pancreatic Cancer

Abstract: The risk of pancreatic cancer is significantly elevated in subjects with chronic pancreatitis and appears to be independent of sex, country, and type of pancreatitis.

Cited by 1,539 publications

References 25 publications

Alcoholic chronic pancreatitis: A quality of life study

Alcoholic chronic pancreatitis: A quality of life study

Should we Investigate Gastroenterology Patients for Pancreatic Exocrine Insufficiency? A Dual Centre UK Study

Increased prevalence of the BRCA2 polymorphic stop codon K3326X among individuals with familial pancreatic cancer

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