scholarly journals Pathogenesis of Chronic Pancreatitis

1989 ◽  
Vol 3 (1) ◽  
pp. 15-20
Author(s):  
H Sarles ◽  
J.P. Bernard
Keyword(s):  
Chronic Pancreatitis ◽  
Alcohol Consumption ◽  
Pancreatic Juice ◽  
Secretory Protein ◽  
Pancreatic Acinar Cell ◽  
Pancreatic Ducts ◽  
Obstructive Pancreatitis ◽  
Chronic Calcifying Pancreatitis ◽  
Salt Crystals ◽  
Calcifying Pancreatitis

Studies from the Marseille group allowed differentiation of acute pancreatitis (a group of lesions secondary to either extrapancreatic causes such as gallstones or to pancreatic diseases such as cancer and chronic pancreatitis), from chronic pancreatitis. Two forms of chronic pancreatitis arc easily distinguished: obstructive pancreatitis secondary to pre-existing obstruction on pancreatic ducts (tumours, scars, etc); and the most frequent disease, chronic calcifying pancreatitis, which is a pancreatic lithiasis due to a double phenomenon. This double phenomenon is the precipitation of insoluble calcium salts and the precipitation of degraded fragments of a newly discovered secretory protein known as pancreatic stone protein (PSP). This family of glycoproteins, the amino acid sequence of which has been established, is synthesized by the pancreatic acinar cell and its biosynthesis is decreased in patients presenting with chronic calcifying pancreatitis. The secretory form of PSP prevents the formation of calcium salt crystals in the pancreatic juice which is normally supersaturated in calcium. Though the lesions and the secretory modifications of PSP are common to all forms of chronic calcifying pancreatitis, there are different etiological forms of the disease; alcoholic, tropical, hypercalcemic, hereditary and idiopathic. Alcohol consumption acts on pancreatic secretion by different mechanisms and is responsible for an increased secretion of secretory protein (enzymes) due to cholinergic, vagal reflexes sensitive to ethanol. Alcohol consumption is generally associated with protein rich and either fat rich or fat poor diets, both of which are risk factors. Hypercalcemia also increases the secretion of protein and the viscosity of pancreatic juice. The tropical form is not due, as previously suggested, to cassava (manioc) consumption or kwashiorkor, but it is endemic in populations submitted to fat poor, protein poor diets. These etiological factors are only acting on predisposed patients. This suggests chat a low or abnormal biosynthesis of PSP is responsible for the predisposition.

scholarly journals Protein Content of Precipitates Present in Pancreatic Juice of Alcoholic Subjects and Patients With Chronic Calcifying Pancreatitis

1983 ◽  
Vol 84 (1) ◽  
pp. 102-107 ◽  
Author(s):  
Odette Guy ◽  
Guillermo Robles-Diaz ◽  
Zygmunt Adrich ◽  
José Sahel ◽  
Henri Sarles
Keyword(s):  
Protein Content ◽  
Pancreatic Juice ◽  
Chronic Calcifying Pancreatitis ◽  
Calcifying Pancreatitis

scholarly journals Two SPINK1 Mutations Induce Early-Onset Severe Chronic Pancreatitis

2017 ◽  
Vol 11 (1) ◽  
pp. 85-88 ◽  
Author(s):  
Jean Louis Frossard ◽  
Michael A. Morris
Keyword(s):  
Abdominal Pain ◽  
Chronic Pancreatitis ◽  
Family History ◽  
Early Onset ◽  
Recurrent Abdominal Pain ◽  
Trypsin Activity ◽  
Chronic Calcifying Pancreatitis ◽  
History Of ◽  
Calcifying Pancreatitis

The SPINK1 protein is a potent antiprotease that can inactivate any intrapancreatic trypsin activity that would otherwise induce autodigestion of the pancreas. SPINK1 mutations have been recognized to be associated with chronic pancreatitis in patients without a family history of pancreatitis. We here describe the case of a 24-year-old woman referred to our service for recurrent abdominal pain and search for the cause of chronic calcifying pancreatitis, who was found to carry 2 SPINK1 mutations.

scholarly journals Differential diagnosis of pancreatic diseases: new approaches in laboratory and radiologic diagnosis

2020 ◽  
Vol 46 (1) ◽  
pp. 36-42
Author(s):  
L. V. Vinokurova ◽  
K. A. Lesko ◽  
D. S. Bordin ◽  
E. A. Dubtsova ◽  
E. Yu. Tyulyaeva ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Differential Diagnosis ◽  
Chronic Pancreatitis ◽  
Multislice Computed Tomography ◽  
Region Of Interest ◽  
Informative Marker ◽  
Intravenous Contrast ◽  
New Approaches ◽  
Chronic Calcifying Pancreatitis ◽  
Calcifying Pancreatitis

Aim. To assess significance of serum fibronectin (FN) and new approaches of processing computed tomography (CT) results for pancreatic cancer (PC) and chronic pancreatitis (CP) differential diagnosis. Materials and methods. Data of 49 patients with pancreatic lesions who underwent multislice computed tomography (MSCT) with intravenous contrast enhancement and FN evaluation in 2018 were analyzed. There were 29 (59.2%) males and 20 (40.8%) females, mean age 51.9±13.9 (30–82). All patients were divided in 3 groups: 1 — PC (17 patients, 34.6%) — morphologically verified, 2 — chronic pancreatitis with previous pancreonecrosis (CPPN) — 16 patients, 32.7%, 3 — chronic calcifying pancreatitis (CCP) — 16 patients, 32.7%. We calculated median of enhancement gradient between region of interest and intact parenchyma (Мgrad) based on MSCT results. Pearson’s correlation coefficient (rp) was calculated for correlation assessment. Results. We assessed mean Мgrad and mean serum FN rate in all three groups: PC — 28.1±2.6, р=0.0001, CPPN — 14.9±2.4, р=0.07, CCP — 13.3±0.7, р=0.08 for Мgrad, and 239.8±30.1, p=0.8, 243.5±33.8, p=0.7, 227.2±34.3, p=0.8 for serum FN rate, respectively. There was statistically significant strong correlation of Мgrad in patients with PC (rp=0.63, p=0.0001). We revealed cut-off point of Мgrad value for PC that was 20 (p=0.001). There were no statistically significant correlations of serum FN rate in all groups (PC rp=0.04, p=0.8; CPPN rp=0.06, p=0.7; CCP rp=-0.03, p=0.8). Conclusions. Mgrad evaluation based on MSCT is an informative marker for differential diagnosis between PC and chronic pancreatitis, high rates of Мgrad positively correlate with PC existence. There was no correlation between serum FN rate and existence of PC, CPPN or CCP.

Data Screening Methods – Application to Differential Diagnosis in Pancreatic Pathology from Radiological Signs

1978 ◽  
Vol 17 (01) ◽  
pp. 36-40 ◽  
Author(s):  
J.-P. Durbec ◽  
Jaqueline Cornée ◽  
P. Berthezene
Keyword(s):  
Differential Diagnosis ◽  
Mutual Information ◽  
Data Processing ◽  
Screening Methods ◽  
Automatic Data ◽  
Chronic Calcifying Pancreatitis ◽  
Number Of Patients ◽  
Calcifying Pancreatitis ◽  
Pancreatic Pathology ◽  
Data Screening

The practice of systematic examinations in hospitals and the increasing development of automatic data processing permits the storing of a great deal of information about a large number of patients belonging to different diagnosis groups.To predict or to characterize these diagnosis groups some descriptors are particularly useful, others carry no information. Data screening based on the properties of mutual information and on the log cross products ratios in contingency tables is developed. The most useful descriptors are selected. For each one the characterized groups are specified.This approach has been performed on a set of binary (presence—absence) radiological variables. Four diagnoses groups are concerned: cancer of pancreas, chronic calcifying pancreatitis, non-calcifying pancreatitis and probable pancreatitis. Only twenty of the three hundred and forty initial radiological variables are selected. The presence of each corresponding sign is associated with one or more diagnosis groups.

scholarly journals Gallstone disease, diabetes, calcium, triglycerides, smoking and alcohol consumption and pancreatitis risk: Mendelian randomization study

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Shuai Yuan ◽  
Edward L. Giovannucci ◽  
Susanna C. Larsson
Keyword(s):  
Type 2 Diabetes ◽  
Chronic Pancreatitis ◽  
Alcohol Consumption ◽  
Mendelian Randomization ◽  
Gallstone Disease ◽  
Smoking Initiation ◽  
Disease Type ◽  
Uk Biobank ◽  
Increased Risk

AbstractWe conducted a Mendelian randomization study to determine the potential causal associations of gallstone disease, diabetes, serum calcium, triglyceride levels, smoking and alcohol consumption with acute and chronic pancreatitis. Genetic variants associated with the exposures at p < 5 × 10−8 were selected from corresponding genome-wide association studies. Summary-level data for pancreatitis were obtained from the FinnGen consortium and UK Biobank. Univariable and multivariable Mendelian randomization analyses were performed and results from FinnGen and UK Biobank were combined using the fixed-effects meta-analysis method. Genetic predisposition to gallstone disease, type 2 diabetes and smoking initiation was associated with an increased risk of acute pancreatitis. The combined odds ratios (ORs) were 1.74 (95% confidence interval (CI), 1.57, 1.93) for gallstone disease, 1.14 (95% CI, 1.06, 1.21) for type 2 diabetes and 1.56 (95% CI, 1.32, 1.83) for smoking initiation. The association for type 2 diabetes attenuated after adjustment for gallstone disease. Genetic predisposition to gallstone disease and smoking initiation as well as higher genetically predicted serum calcium and triglyceride levels were associated with an increased risk of chronic pancreatitis. The combined ORs of chronic pancreatitis were 1.27 (95% CI, 1.08, 1.50) for gallstone disease, 1.86 (95% CI, 1.43, 2.43) for smoking initiation, 2.20 (95% CI, 1.30, 3.72) for calcium and 1.47 (95% CI, 1.23, 1.76) for triglycerides. This study provides evidence in support that gallstone disease, type 2 diabetes, smoking and elevated calcium and triglyceride levels are causally associated with the risk of acute or chronic pancreatitis.

Idiopathic chronic calcifying pancreatitis with diabetes mellitus

1993 ◽  
Vol 38 (5) ◽  
pp. 963-967 ◽  
Author(s):  
Takashi Matozaki ◽  
Choitsu Sakamoto ◽  
Toshiya Suzuki ◽  
Seiko Chujo ◽  
Kohei Matsuda ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Chronic Calcifying Pancreatitis ◽  
Calcifying Pancreatitis
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