Measurement of serum PSP/reg-protein concentration in various diseases with a newly developed enzyme-linked immunosorbent assay

An enzyme-linked immunosorbent assay, based on two monoclonal antibodies (Hreg1-1 and Hreg101-1) specific for pancreatic stone protein (PSP)/reg-protein, was developed to determine the concentration of this protein in serum from individuals with various diseases. The serum concentration of PSP/reg-protein was significantly higher in patients with various pancreatic diseases than in normal controls, and was also significantly higher in patients with acute pancreatitis or chronic relapsing pancreatitis than in patients with chronic pancreatitis. Furthermore, the serum PSP/reg-protein concentration was also significantly increased in liver cirrhosis, choledocholithiasis, and various cancers of the digestive system, and was extremely high in all patients tested with chronic renal failure. A significant correlation was apparent between the serum concentration of PSP/reg-protein and elastase-I in 68 patients with chronic pancreatitis or pancreatic cancer. Whereas only 7 of these patients showed a normal serum PSP/reg-protein concentration and a significantly increased elastase-I concentration, 15 of these patients showed a significantly increased serum PSP/reg-protein coecentration and a normal serum elastase-1 concentration. These results indicate that the serum PSP/reg-protein concentration may reflect pancreatic damage, especially in acute pancreatitis, and may be as sensitive a marker for such damage as elastase-I, although false positivity was apparent in renal failure and in some patients with hepatic dysfunction or digestive system malignancies.     

Overexpression of pancreatitis-associated protein (PAP) in human pancreatic ductal adenocarcinoma

Pancreatitis-associated protein (PAP) is almost absent in normal pancreas, but is strongly induced in acute pancreatitis. PAP mRNA is also expressed in cancer cells, including pancreatic ductal adenocarcinoma. However, the clinicopathological significance of PAP in human pancreatic cancer is not clear. We examined PAP expression in pancreatic tissues from individuals with pancreatic ductal adenocarcinoma using immunohistochemistry. PAP was overexpressed in 79% (30 of 38) of pancreatic ductal adenocarcinoma, 19% (7 of 36) of chronic pancreatitis, and 29% (2 of 7) of mucinous cystadenoma. PAP was found in malignant ductular structures in pancreatic carcinomas as well as in benign proliferating ductules and acinar cells in chronic pancreatitis. It was not expressed in normal pancreas. The incidence of PAP overexpression was significantly higher in pancreatic cancer than in the other pancreatic diseases (P < 0.01). PAP overexpression was significantly correlated with nodal involvement, distant metastasis (P < 0.05), and short survival (P < 0.01) in pancreatic cancer. These results suggest that overexpression of PAP in human pancreatic ductal adenocarcinoma indicates tumor aggressiveness.     

Serum pancreatic stone protein in pancreatic diseases

Summary Serum pancreatic stone protein (PSP) was determined in sera of pancreatic and nonpancreatic diseases using enzyme immunoassay specific to human PSP to study the diagnostic and pathophysiological significance of PSP. Serum PSP in acute pancreatitis (mean±SD=1075.4±2849.1 ng/mL,n=33) was significantly higher than that in controls (78.6±31.8 ng/mL,n=37,p<0.01), chronic pancreatitis (156.8±82.8 ng/mL,n=32,p<0.05), and pancreatic cancer (148.468.8 ng/mL,n=26,p<0.05). No significant difference was found between noncalcified and calcified chronic pancreatitis. Serum PSP levels were significantly higher in chronic renal failure under hemodialysis (1796.0±1492.9 ng/mL) than in other diseases such as peptic ulcer, liver cirrhosis, gallstone, and diabetes mellitus. Low but significant correlation was obtained between serum PSP and serum immunoreactive trypsin (r=0.22,p<0.05). Increased serum PSP levels in acute pancreatitis and chronic renal failure suggest that serum PSP levels reflect reflux from pancreatic secretion, release from damaged pancreatic acinar cells, or retention in circulation, and can be useful for diagnosis of acute pancreatitis, but not chronic calcified pancreatitis.     

Pharmacological treatment of non-alcoholic steatohepatitis: The current evidence

¹²⁵I-protein-radioiodinated pure pancreatic juice samples from patients with adenocarcinoma of the pancreas, chronic pancreatitis, or intact pancreas were analysed by high-resolution SDS-polyacrylamide gel electrophoresis and subsequent autoradiography. Experiments resulted in the detection of a 180K protein, probably a glycoprotein, in the pure pancreatic juice from pancreatic carcinoma (93%) and chronic pancreatitis (73%) patients, which was completely absent from pancreatic juice from intact pancreas. Sephadex G-200-isolated 18UK protein was found to be different from carcinoembryonic antigen (CEA) when traced by a commercial CEA radioimmunoassay, but it seemed identical in pancreatic juice samples from patients with pancreatic carcinoma and chronic pancreatitis, at least with regard to isoelectric point. In brief, the present results suggest that 180K protein identification in pancreatic juice permits adenocarcinoma of the pancreas and chronic pancreatitis to be differentiated from normal conditions but that distinction between pancreatic carcinoma and chronic pancreatitis is unlikely.     

Immunolocalization of pS2, a putative growth factor, in pancreatic carcinoma

pS2 is a 60 amino acid secretory polypeptide which belongs to a newly described family of trefoil-shaped growth factors. It is widely distributed throughout the gastrointestinal tract, particularly adjacent to damaged mucosa, and is also expressed by some epithelial tumours such as breast carcinoma. The aim of this study was to examine the expression of pS2 in pancreatic cancer. The presence of pS2 was analysed immunohistochemically using two antibodies, a polyclonal (pNR-2) and a monoclonal (pS2^TM) in 42 cases of pancreatic adenocarcinoma and 10 cases of ampullary carcinoma. The findings were compared with chronic pancreatitis and normal pancreas. No immunostaining was seen in normal pancreas, with the exception of one area of ductular proliferation, and although 8/10 cases of chronic pancreatitis expressed pS2, it was focal and confined to the occasional duct. In contrast, a significant proportion of malignant cells in 23/42 (55%) of pancreatic adenocarcinoma and 8/10 (80%) of ampullary tumours expressed immunoreactive pS2. The finding of pS2 expression in more than 50% of pancreatic and ampullary carcinomas in contrast to the findings seen in chronic pancreatitis and normal pancreas suggests that pS2 may play an important role in the growth of these highly malignant tumours.     

Argyrophilic Nucleolar Organizer Regions May Help the Differential Diagnostic Distinction between Chronic Pancreatitis and Pancreatic Ductal Adenocarcinoma

Mäkinen K, Eskelinen M, Lipponen P, Pasanen P, Nuutinen P, Alhava E. Argyrophilic nucleolar organizer regions may help the differential diagnostic distinction between chronic pancreatitis and pancreatic ductal adenocarcinoma. Scand J Gastroenterol 1994;29:1029-1033.

Background: The aim of this study was to determine whether the number of argyrophilic nucleolar organizer regions (AgNORs) could be of diagnostic significance in differentiating between chronic pancreatitis and pancreatic ductal adenocarcinoma.

Methods: The number of AgNORs was enumerated in biopsy specimens of normal pancreas, chronic pancreatitis, and pancreatic ductal adenocarcinoma.

Results: The number of AgNORs was lower in patients with normal pancreas than in patients with chronic pancreatitis or pancreatic adenocarcinoma. In addition, the number of AgNORs was significantly lower in chronic pancreatitis than in pancreatic ductal adenocarcinoma (p < 0.001).

Conclusions: The diagnosis of pancreatic adenocarcinoma is usually clear. Difficulties can be encountered, however, in cases of chronic pancreatitis, specially when biopsy material is small. Our results suggest that the number of AgNORs may help in distinguishing between chronic pancreatitis and pancreatic ductal adenocarcinoma, especially in diagnostically difficult specimens.     

Determination of Plasma Trypsin-Like Activity in Healthy Subjects, Patients With Mild to Moderate Alcoholic Chronic Pancreatitis, and Patients With Nonjaundice Pancreatic Cancer

Trypsin-like activity is released after stimulation of the exocrine pancreas. We investigated under basal conditions and after stimulation by a meal whether patients suffering from pancreatic disorders differ with respect to plasma trypsin-like activity (PTLA). In 45 subjects (healthy volunteers: n = 18, mild/moderate alcoholic chronic pancreatitis: n = 16, nonjaundice pancreatic cancer n = 7, and calcifying chronic pancreatitis: n = 4), basal and postprandial levels of PTLA were measured over a period of 2 hours. Basal plasma levels were similar in the first 3 groups. After stimulation, healthy volunteers and patients with pancreatic cancer showed significant decreases in trypsin-like activity; however, plasma levels did not decrease in patients with mild/moderate chronic pancreatitis (P < .001). Healthy individuals demonstrate a consistent decrease in postprandial trypsin-like plasma activity. This response is not altered in patients with pancreatic cancer, and it is not seen in patients with mild/moderate alcoholic chronic pancreatitis.     

Role of Osteopontin in Calcification in Autoimmune Pancreatitis

Objectives The aim of the present study was to determine the potential for pancreatic calcification in autoimmune pancreatitis by investigating osteopontin and CD44 expression. Methods Human pancreatic tissues in normal pancreas, chronic pancreatitis, and autoimmune pancreatitis were obtained from the surgical specimens of 42 patients. Pancreatic tissues from male Wistar Bonn/Kobori rats were also used as an animal autoimmune pancreatitis model. Results The incidences of osteopontin expression in centroacinar cells in chronic pancreatitis with calcification and in autoimmune pancreatitis were significantly greater than that in normal pancreas (P < 0.05). Some cases of chronic pancreatitis and autoimmune pancreatitis expressed CD44 in centroacinar cells and ductal cells. In male Wistar Bonn/Kobori rats, the inflammatory area and percentage of osteopontin-CD44-positive cells increased with advancing age (P < 0.01 or 0.05). Conclusions These results suggest that autoimmune pancreatitis has the potential for pancreatic calcification over a long-term clinical course.     

Pancreatic Sphincterotomy and Pure Pancreatic Juice Collection for Treatment of Chronic Pancreatitis

Abstract: After our introduction of endoscopic pancreatic sphincterotomy for treatment of chronic pancreatitis in 1985, our interest has been focused to the value of pure pancreatic juice collection with or without pancreatic sphincterotomy for management of chronic pancreatitis. Through pancreatic sphincterotomy, pain relief was obtained in 13 out of 16 cases with moderate and marked chronic pancreatitis. After pancreatic sphincterotomy extraction of pancreatic calculi using basket forceps was done successfully in 2 of these cases, Spontaneous stone passage occured in the other 2. In pure pancreatic juice collection without pancreatic sphincterotomy, pain relief was seen in 6 out of 13 cases with mild and moderate chronic pancreatitis. The protein plug was simultaneously aspirated during the procedure in 3 cases. Recently, we have indicated in these patients both pancreatic sphincterotomy and pure pancreatic juice collection and noted pain relief was obtained in all of the 8 cases with this approach. With an improvement in the technology of pancreatic drainage, these endoscopic treatment modalities may be possibly useful to stop the progression of chronic pancreatitis.     

Immunohistochemical demonstration of the p53 tumour suppressor gene product in cancer of the pancreas and chronic pancreatitis

The p53 tumour suppressor gene and its protein products after point mutations are currently attracting wide attention in the investigation of human tumours. In this study we present the findings on percutaneous pancreatic biopsies of 82 cases after routine processing and immunostaining for the polyclonal p53 antibody CM1, an antibody directed against both wild and mutant forms of p53 protein. There were 51 carcinomas, 5 islet cell tumours, 16 cases of chronic pancreatitis (including one with atypical ductal epithelium) and seven histologically normal pancreatic biopsy specimens. None of the seven normal cases showed any definite nuclear immunostaining for p53. Thirty-two (63%) of the pancreatic adenocarcinomas showed moderate to intense immunoreactivity. Of the 16 cases of chronic pancreatitis, 11 were negative and three showed equivocal immunostaining. The one case with ductal epithelial atypia showed mild to moderate immunoreactivity. All islet cell tumours were negative. The expression of the p53 gene, therefore, appears increased in the majority of pancreatic adenocarcinomas while this is not observed in chronic pancreatitis or normal pancreatic tissue. Nuclear immunoreactivity for p53 protein may represent mutant forms because of the short half-life of the wild-type protein. The lack of p53 expression in some cases of pancreatic adenocarcinoma may be due to different types of mutant proteins not detectable by the CM1 antibody. Nuclear immunoreactivity to the p53 protein in pancreatic biopsy is more suggestive of a malignant tumour than chronic pancreatitis.     

COMP is Selectively Up-regulated in Degenerating Acinar Cells in Chronic Pancreatitis and in Chronic-Pancreatitis-like Lesions in Pancreatic Cancer

Background: Chronic pancreatitis (CP) is an inflammatory disease of the pancreas characterized histomorphologically by progressive development of fibrosis and atrophy of the pancreatic parenchyma. Cartilage oligomeric matrix protein (COMP) is a member of the thrombospondin (TSP) family of extracellular glycoproteins that is expressed in CP tissues. In the present study, we characterized COMP mRNA and protein expression in the normal pancreas, chronic pancreatitis, and pancreatic cancer tissues. Methods: 15 normal pancreatic tissues, 14 CP tissues and 14 pancreatic cancer tissues were analyzed by Northern blotting, Western blotting, in situ hybridization and immunohistochemistry. Results: COMP mRNA and protein were detected at moderate to high levels in chronic pancreatitis tissues, at moderate levels in pancreatic cancer tissues, but at low levels in normal pancreatic tissues and in four pancreatic cancer cell lines. COMP mRNA signals and immunoreactivity were strongly present in the cytoplasm of degenerating acinar cells in CP tissues as well as in CP-like lesions in pancreatic cancer tissues. COMP protein was also present in the fibrotic tissue in CP. In contrast, COMP expression was weak to absent in the cytoplasm of cancer cells in pancreatic cancer tissues, and in ductal cells and islet cells in normal pancreatic tissues. Conclusion: COMP is preferentially expressed in degenerating acinar cells in CP and in CP-like areas in pancreatic cancer, suggesting a potential role of this gene in the course of acinar cell degeneration and dedifferentiation. COMP might thus serve as a marker for tissue destruction and disease activity in CP.     

No evidence of helicobacter pylori sequences in pancreatic juices of patients affected by chronic pancreatitis

Summary Background: The course of chronic pancreatitis is often unpredictable and many factors are likely to be involved in the progression of the disease. In physiological condition, pancreatic juice exerts significant antibacterial activity, which is impaired in patients with chronic pancreatitis. Aim: Hypothesizing that Helicobacter pylori could, in these conditions, lead to an ascending infection, we aimed to assess the presence of H. pylori sequences in pancreatic juices of patients with chronic pancreatitis. Methods: 40 patients (mean age 52±3 yr) with alcoholic chronic pancreatitis and H. pylori infection were examined. Pancreatic juices were collected during endoscopic retrograde cholangiopancreatography. Using polymerase chain reaction (PCR) with two primers homologous to a portion of urease-C gene, H. pylori DNA was detected. Gastric biopsies, microscopically positive to H. pylori were used as positive controls. Results: All gastric biopsies produced H. pylori-specific DNA products. Conversely, no H. pylori urease-C gene sequences have been detected in any of the pancreatic juices. Conclusion: Our data suggest that the impaired antibacterial activity of pancreatic juices in patients affected by chronic pancreatitis does not have a permissive role for a superimposing H. pylori infection in the pancreas. The possibility that Helicobacter species other than pylori may be involved in a superimposing infection requires further investigation.     

Idiopathic chronic calcifying pancreatitis with diabetes mellitus

Summary We present a case of a 27-year-old female suffering from chronic calcifying pancreatitis with diabetes mellitus. Radiographic examinations and exocrine pancreatic function tests revealed considerable dilatation of pancreatic ducts with large intraductal calculi and exocrine pancreatic insufficiency, respectively. Recent literature indicates that a decrease in the activity of pancreatic stone protein (PSP), which inhibits CaCO₃ crystal formation in pancreatic juice, is closely related to the development of chronic calcifying pancreatitis. The patient had no apparent cause or family history of pancreatitis. We therefore investigated the possibility that alterations in the PSP gene might explain the chronic pancreatitis seen in this patient. Six exons of the PSP gene amplified by polymerase chain reaction were directly sequenced, but there was no apparent base mutation observed. Furthermore, Southern blot analysis revealed neither rearrangement nor deletion of the PSP gene in the genomic DNA of this case. However, this genetic approach will be useful for future study of the etiology of hereditary pancreatitis.     

Differentiation between pancreatic carcinoma and mass-forming chronic pancreatitis: usefulness of high b value diffusion-weighted imaging

OBJECTIVE: To investigate the value of high b value diffusion‐weighted (DW) imaging in differentiating between pancreatic carcinoma and mass‐forming chronic pancreatitis (MFCP). METHODS: Fifty‐one consecutive patients with pathology‐proven pancreatic carcinoma (n = 37) or MFCP (n = 14) were evaluated with DW imaging (b value, 0 and 1000 s/mm²) at a 3‐T MR system. Overall 20 healthy volunteers were evaluated as the control group. The apparent diffusion coefficient (ADC) values of normal pancreas, pancreatic carcinoma, MFCP, and mass‐associated obstructive pancreatitis were measured. RESULTS: On high b value (1000 s/mm²) DW images, both pancreatic carcinoma and MFCP were hyperintense focal lesions; mass‐associated obstructive pancreatitis occurred in 17 of 37 (45.9%) pancreatic carcinoma and 8 of 14 (57.1%) MFCP. The ADC (×10^?3 mm²/s) of the pancreatic carcinomas (1.06 ± 0.15) was significantly lower than that of normal pancreas (1.47 ± 0.18; P < 0.01), MFCP (1.35 ± 0.14; P < 0.01) and mass‐associated chronic pancreatitis (1.44 ± 0.17; P < 0.01). The ADC of MFCP was also lower than that in the normal pancreas (P = 0.025), whereas the ADC of mass‐associated obstructive pancreatitis was not different from those of the MFCP (P = 0.113) and normal pancreas (P = 0.544). When 1.195 was used as the optimal cut‐off value, ADC quantification obtained a sensitivity of 85.7% and a specificity of 86.5% for differentiating pancreatic carcinomas from MFCP. CONCLUSION: High b value DW imaging in combination with ADC quantification at a 3‐T MR system is useful in differentiating between pancreatic carcinoma and MFCP.     

Angiopathies in pancreatic diabetes resulting from chronic pancreatitis

Summary Conclusions. Marked diabetic micro- and macroangiopathies were recognized in three autopsy cases with pancreatic diabetes resulting from chronic pancreatitis. Background. Recent reports have suggested that diabetic retinopathy occurs as one of the microangiopathies in patients with secondary diabetes following chronic pancreatitis. Methods. We report three autopsy cases with pancreatic diabetes. Cases 1 and 2 showed alcoholic chronic pancreatitis. Case 3 was a patient with chronic pancreatitis resulting from hyperparathyroidism. All three cases had pancreatic calcification and markedly decreased exocrine pancreatic function. There was no family history of diabetes in these patients. The HbA₁ values were elevated, with diminished secretion of both insulin and glucagon. Results. The common features of the clinical courses were poor glycemic control, including insulin-induced hypoglycemic attacks in the early stage and microangiopathy, followed by difficulties in treatment for hypertension in the late stage of pancreatic diabetes. Autopsies, performed after 12–18 yr of diabetes, revealed fibrosis of the pancreas, disappearance of acinar cells in the exocrine pancreas, atrophy, a diminished number of islets of Langerhans, and diabetic glomerulosclerosis, with arteriosclerosis in the brain, heart, and kidneys. Cerebral hemorrhage, heart failure, and myocardial infarction were suggested to be the main causes of death. Although the serum lipid levels were rather low in cases 1 and 2, arteriosclerosis was marked by the age of 60, and serum protein levels were also low in all three cases.     

Analysis of pancreatic stone protein gene of hereditary pancreatitis]

To investigate the pathogenesis of hereditary pancreatitis we determined whether pancreatic stone protein (PSP) gene was structurally altered in two independent families diagnosed as hereditary pancreatitis. Because, it has been shown that a decrease in the activity of PSP which inhibits CaCO3 crystal formation in pancreatic juice is closely related to the development of chronic calcifying pancreatitis. Southern blot analysis revealed neither a rearrangement nor a gross deletion of PSP gene in genomic DNA of affected members of both families. Furthermore, six exons of PSP gene amplified by polymerase chain reaction from genomic DNA was directly sequenced, while no apparent base mutation was observed. The immunohistochemical study utilizing monoclonal antibody to PSP showed the presence of immunoreactive PSP in the section of pancreatic tissue obtained from a patient affected with hereditary pancreatitis. However, the level of immunoreactive PSP in the remaining acinar cells of the patient pancreas was not reduced when compared with that of normal pancreas. Results, therefore, indicate that genetic alteration of PSP gene may not be responsible for the pathogenesis of hereditary pancreatitis.     

Fecal pancreatic elastase: a reproducible marker for severe exocrine pancreatic insufficiency

Background In order to apply fecal pancreatic elastase for follow-up of exocrine pancreatic function in chronic pancreatitis and cystic fibrosis, we examined the sensitivity, specificity, and long-term variability of a new polyclonal antibody-based enzyme-linked immunosorbent assay (ELISA). Methods Patients with definite chronic pancreatitis (n = 23), probable or possible chronic pancreatitis (n = 14), autoimmune pancreatitis (n = 7), or acute pancreatitis (n = 11), and 51 healthy subjects and 11 healthy infants participated in this study. Pancreatic function was graded as normal (n = 3), mild (n = 18), moderate (n = 9), or severe (n = 18) exocrine insufficiency on the basis of secretin tests. Fecal pancreatic elastase was measured by a new ELISA. Results Fecal pancreatic elastase concentration in control subjects varied widely, with a median of 478 μg/g. The specificity of this test was 90.2% with a cutoff value of >200 μg/g. The sensitivities were 60.9% for detecting definite chronic pancreatitis, 76.5% for calcifying pancreatitis, 71.4% for autoimmune pancreatitis, and 7.1% for probable or possible chronic pancreatitis. The sensitivities were 16.7% for mild, 12.5% for moderate, and 72.2% for severe exocrine pancreatic insufficiency. Forty patients were reexamined after a median interval of 347 days. The fecal pancreatic elastase levels between the first and second tests were not significantly different. Two infants, 4.5 and 5 months old, had abnormally low values, but after a median of 304 days all infants showed normal levels (median, 444 μg/g). Conclusions Fecal pancreatic elastase is a reproducible marker for severe exocrine pancreatic insufficiency. This test is valuable for longitudinal follow-up of exocrine pancreatic function.     

Diagnosis of Chronic Pancreatitis by Endoscopic Ultrasonography

Abstract: This study evaluates the usefulness of endoscopic ultrasonography in the diagnosis of chronic pancreatitis. 52 patients with chronic pancreatitis, which included 15 cases of mild pancreatitis, 19 cases of moderate pancreatitis and 18 cases of advanced pancreatitis, were diagnosed by endoscopic retrograde cholangiopancreatography and further investigated by endoscopic ultrasonography. The 4 main findings of 1) dilatation of the main pancreatic duct, 2) irregularity of the main pancreatic duct, 3) inhomogeneity of the pancreatic parenchyma and, 4) irregular configuration of the pancreas were reviewed. In all of the 18 cases of advanced pancreatitis, irregularity of the main pancreatic duct, inhomogeneity of the pancreatic parenchyma and irregular configuration of the pancreas were seen. 89% of these patients had dilatation of the main pancreatic duct. In the patients with moderate pancreatitis, on the other hand, all 4 findings occurred with a frequency of between 58% to 95%. In the patients with mild pancreatitis, irregularity of the main pancreatic duct, inhomogeneity of the pancreatic parenchyma and irregular configuration of the pancreas occurred at a rate of 40% to 93%, and dilatation of the main pancreatic duct occurred rarely in only 13% of the patients. We were able to detect abnormalties in the pancreatic parenchyma by endoscopic ultrasonography even in the early stages of chronic pancreatitis, and this suggests that this technique may be useful in the diagnosis of mild pancreatitis, which usually causes quite minor abnormal changes in the main pancreatic duct.     

Pancreatic cysts and pseudocysts associated with acute and chronic pancreatitis

We reviewed 106 consecutive patients with cysts or pseudocysts of the pancreas associated with pancreatitis. A pancreatic fluid collection (PFC) was defined as a limited collection containing pancreatic juice either pure or with pus or blood. Seventy-seven patients presented with chronic pancreatitis (CP) and 29 patients presented with acute pancreatitis (AP). CP-associated PFC was observed in young alcoholic men (mean age 40.8 years) on a high fat, protein, and carbohydrate diet. None of this group had gallstones. In this population, PFC was located in the head of the pancreas in 68% of the cases, was partly extrapancreatic in 22% of the cases, and resolved spontaneously in 9%. AP- associated PFC was as frequent in nonalcoholic men as in nonalcoholic women and presented with gallstones in 48%. They developed later (mean age 53.0 years), resolved spontaneously in 20%, and were located in the body or tail of the gland in 69%. CP-PFC may be designated retention cysts or retention pseudocysts (extrapancreatic); AP-PFC may be designated necrotic pseudocysts.     

P8 expression is induced in acinar cells during chronic pancreatitis

The p8 gene is barely expressed in the normal pancreas, but is overexpressed in acute pancreatitis. To elucidate the dynamic expression of p8 mRNA and its significance in the course of chronic pancreatitis, we investigated the p8 expression in spontaneous chronic pancreatitis in the WBN/Kob rat as well as in humans and arginine-treated rat pancreatic acinar AR4-2J cells. p8 mRNA was significantly increased at 12 weeks when chronic pancreatitis first appeared in the WBN/Kob rats. p8 was immunolocalized in the acinar cell nuclei. Acinar cell apoptosis was significantly increased at 12 and 20 weeks in the WBN/Kob rats. In AR4-2J cells, p8 mRNA was significantly induced at 4 hr after arginine addition. Apoptosis of AR4-2J cells was not increased during the strong expression of p8 mRNA. These results suggest that p8 is induced in the acinar cells during chronic pancreatitis as the self-defence mechanism against proapoptotic insults.