Human pancreatic secretory protein profiles in pancreas cancer and chronic pancreatitis

1985 ◽  
Vol 30 (3) ◽  
pp. 200-203 ◽  
Author(s):  
Thomas Taylor White ◽  
Barbara J. Allan ◽  
John J. Schilling ◽  
Hiroshi Miyashita
2001 ◽  
Vol 15 (24) ◽  
pp. 2420-2425 ◽  
Author(s):  
A. Valerio ◽  
D. Basso ◽  
S. Mazza ◽  
G. Baldo ◽  
A. Tiengo ◽  
...  

2000 ◽  
Vol 118 (4) ◽  
pp. A422
Author(s):  
Patrick Maisonneuve ◽  
Albert B. Lowenfels ◽  
Giorgio Cavallini ◽  
Rudolf W. Ammann ◽  
Paul G. Lankisch ◽  
...  

1989 ◽  
Vol 3 (1) ◽  
pp. 15-20
Author(s):  
H Sarles ◽  
J.P. Bernard

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.


1983 ◽  
Vol 28 (9) ◽  
pp. 792-800 ◽  
Author(s):  
Thomas Taylor White ◽  
Barbara J. Allan ◽  
John J. Schilling ◽  
Hiroshi Miyashita

2004 ◽  
Vol 59 (5) ◽  
pp. P236 ◽  
Author(s):  
Julia K. LeBlanc ◽  
John Dewitt ◽  
Lee McHenry ◽  
Stuart Sherman ◽  
Thomas Imperiale ◽  
...  

Doctor Ru ◽  
2020 ◽  
Vol 19 (7) ◽  
pp. 15-20
Author(s):  
I.N. Grigoryeva ◽  
◽  
O.V. Efimova ◽  
T.I. Romanova ◽  
◽  
...  

Study Objective: to determine blood lipids and incidence of dyslipidemia in patients with acute pancreatitis (AP), chronic pancreatitis (CP) and pancreas cancer (PC), and to compare them. Study Design: observational multicentral single-arm cross section clinical case series. Materials and Methods. The study enrolled 44 patients with AP, 97 patients with CP, 45 with PC; age and sex composition of groups was comparable. Blood lipids were measured using standard methods. Study Results. Hypercholesterolemia was more common in CP (58.8%), whereas in AP it was (40.9%, p = 0.049) or PC (15.6%, p = 0.000). The rate of hypertriglyceridemia was comparable. Hypoalphacholesterolemia was more common in PC (80.0%), whereas in AP it was (45.5%, p = 0.001) or CP (27.8%, p = 0.000). There is direct association between increased high density lipoprotein cholesterol (HDLP-C) per 1 mmol/L with CP risk (Exp (B) = 21.618; 95% CI: 4.741–98.582, p = 0.000) and invert association with PC risk (Exp (B) = 0.015; 95% CI: 0.002–0.092, p = 0.000). There is also a correlation between total cholesterol and pancreonecrosis and “specific” CP: increase of 1 mmol/L in total cholesterol results in pancreonecrosis risk reduction of 37.7% (Exp (B) = 0.623; 95% CI: 0.389–0.996, p = 0.048), “specific” CP — of 47.4% (Exp (B) = 0.526; 95% CI: 0.305–0.908, p = 0.021). Conclusion. Hypercholesterolemia was more often diagnosed in CP, hypoalphacholesterolemia — in PC; hypertriglyceridemia was comparable. There is a direct correlation between HDLP-C and PC and inverse correlation — with risk of pancreac cancer. Total cholesterol was reversely associated with the risk of pancreonecrosis and specific CP. The evidence determines the need in additional study of association between pancreatic diseases and blood lipids. Keywords: acute pancreatitis, chronic pancreatitis, pancreatic cancer, dyslipidemia, blood lipids.


2020 ◽  
Vol 158 (6) ◽  
pp. S-337-S-338
Author(s):  
Sridevi K. Pokala ◽  
Fady Youssef ◽  
Lin Liu ◽  
Ranier Bustamante ◽  
Mythri Catari ◽  
...  

2021 ◽  
Vol Volume 14 ◽  
pp. 7381-7392
Author(s):  
Chaochao Tan ◽  
Yan Xiao ◽  
Xiangping Huang ◽  
Ling Wu ◽  
Ying Huang

Pancreatology ◽  
2017 ◽  
Vol 17 (3) ◽  
pp. S102
Author(s):  
Anu Aronen ◽  
Janne Aittoniemi ◽  
Reetta Huttunen ◽  
Anssi Nikkola ◽  
Jussi Nikkola ◽  
...  

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