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PubMed1976

Comparison of pancreatic dysfunction in chronic alcoholic pancreatitis and chronic gallstone pancreatitis.

Comparative assessments of the endocrine and exocrine functions of the pancreas associated with gallstone pancreatitis or alcoholic pancreatitis were performed in a series of 86 patients, 20 with cholelithiasis, 12 with chronic alcoholism, 24 with chronic gallstone pancreatitis and 30 with chronic alcoholic pancreatitis and 32 healthy subjects were served as controls. The patients with cholelithiasis showed exocrine hypersecretion of the pancreas. In the patients with gallstone pancreatitis, all the assessed parameters of exocrine function were depressed. On the other hand, no pancreatic exocrine dysfunction was dispalyed in cases with chronic alcoholism. In the non-calcifying alcoholic pancreatitis, both the volume output and the the maximum concentration and output of bicarbonate were diminished but depression in amylase output was not seen. All these parameters were lowered in patients with calcifying pancreatitis. Elevation of hexosamine concentration in the pancreatic juice was evident in alcoholic pancreatitis as compared with gallstone pancreatitis, being particularly prominent in cases of non-calcifying pancreatitis. Patients with alcoholic pancreatitis were observed to secrete viscous pancreatic juice richer in amylase and hexosamine content, than those in the patients with gallstone pancreatitis. Endocrine dysfunction of the pancreas is more frequent and intense in alcoholic pancreatitis than in gallstone pancreatitis.

Alcoholism↗
PubMed2003

Chromosomal instability in pancreatic ductal cells from patients with chronic pancreatitis and pancreatic adenocarcinoma.

Pancreatic adenocarcinoma is a disease with high mortality for which chronic pancreatitis confers a markedly increased risk. We hypothesize that chromosome instability and genomic damage occur in pre-neoplastic pancreatic ductal epithelium, and that this damage may be related to oxidative stress. We used dual-color fluorescence in situ hybridization with centromere probes and locus-specific arm probes for chromosome arms 11q, 17p, and 18q to identify genomic instability in cultures of normal-appearing human pancreatic ductal epithelium from normal organ donor controls compared to patients with chronic pancreatitis or pancreatic adenocarcinoma. To examine early pancreatic tumorigenesis, we studied only normal-appearing pancreatic ductal cells adjacent to pancreatitis or carcinoma. We found that, compared to the finding in normal controls, chromosomal abnormalities are present in normal-appearing human pancreatic ductal epithelia obtained from patients with chronic pancreatitis or pancreatic adenocarcinoma. Furthermore, these chromosomal abnormalities could be induced in cultured pancreatic ductal epithelium from normal organ donors by chronic exposure to dilute hydrogen peroxide, suggesting that oxidative stress may contribute to the development of chromosomal instability in the pancreas. These results elucidate a potential mechanism linking chronic pancreatitis to pancreatic cancer and suggest that chromosomal instability may be an early event in the pathogenesis of pancreatic cancer.

Adenocarcinoma↗
PubMed1995

Pancreatic juice 90K and serum CA 19-9 combined determination can discriminate between pancreatic cancer and chronic pancreatitis.

OBJECTIVES: Differential diagnosis of pancreatic cancer versus chronic pancreatitis may be difficult. The aim of this study is to determine whether a group of tumor-associated antigens could differentiate between the two pathologies. METHODS: CA 19-9, TAG-72, CAR-3, and a newly discovered antigen termed "90K" were determined in the serum and in the pancreatic juice of 19 patients with pancreatic cancer, 20 patients with chronic pancreatitis, and seven controls with lithiasis of extrapancreatic bile ducts. RESULTS: The serum antigen levels of all three markers except 90K were significantly higher in pancreatic cancer than in chronic pancreatitis. High correlations were found between serum CA 19-9 and both TAG-72 and CAR-3. 90K did not correlate with other markers. In pancreatic juice, only 90K values were significantly higher in chronic pancreatitis than in pancreatic cancer, and only 90K and CA 19-9 were significantly correlated. At the stepwise discriminant analysis, serum CA 19-9 and pancreatic juice 90K had independent diagnostic roles. Used in combination, they correctly identified 84.2% of pancreatic cancer and 90% of chronic pancreatitis. CONCLUSIONS: These data suggest that pancreatic juice 90K and serum CA 19-9 can discriminate between chronic pancreatitis and pancreatic cancer. The data further support the complementary use of tumor-associated antigens along with other diagnostic tools.

Antigens, Neoplasm↗
PubMed2002

Pancreatic stone protein of pancreatic calculi in chronic calcified pancreatitis in man.

CONTEXT: The role of protein components of pancreatic secretions has been controversial in pancreatic stone formation. OBJECTIVE: To study the lithogenic role of pancreatic stone protein and lactoferrin in stone formation in chronic pancreatitis. PATIENTS: Pancreatic stones were collected from 13 patients with alcoholic (n=6) and nonalcoholic (n=7) chronic calcified pancreatitis. MAIN OUTCOME MEASURES: Pancreatic stone extracts were analyzed for pancreatic stone protein and lactoferrin using enzyme immunoassay. The localization of pancreatic stone protein immunoreactivity in the stone was observed using immunogold staining and scanning electron microscopy. RESULTS: Immunoreactivities for pancreatic stone protein were detected in the stones from all 13 patients with chronic calcified pancreatitis and for lactoferrin in the stones from five of the 13 patients. Pancreatic stone protein immunoreactivity distributed diffusely from the center to the periphery of the pancreatic stones. CONCLUSIONS: Involvement of pancreatic stone protein seems to be constant from the initial step of the stone formation to subsequent steps of the stone growth. However, pancreatic stone protein is only one of the precipitating proteins in pancreatic secretions such as lactoferrin, trypsinogen, etc.

Adult↗
PubMed2006

Influence of glutamine on pancreatic blood flow and apoptosis of pancreatic acinar in rats with severe acute pancreatitis.

OBJECTIVE: To investigate the role of glutamine on splanchnic blood flow, apoptosis of pancreatic acinar and the underlying mechanism in rats with severe acute pancreatitis. METHODS: Forty-eight rats were randomized into two groups: the glutamine group (n = 24) and the severe acute pancreatitis group (n = 24). Jejunotomy was performed in all rats: the glutamine group also received glutamine, and the severe acute pancreatitis group received normal saline. Each group was then subdivided into three subgroups of eight rats each, with the rats be killed at 12, 24 and 36 h after the operation, respectively. A control group underwent sham operation (n = 8). The regional pancreatic microvascular blood flow was measured by Doppler ultrasound. The blood flow of the portal vein, splenic artery and superior mesenteric artery were also recorded. Apoptosis of pancreatic acinar cells was evaluated by TUNEL method. RESULTS: The regional pancreatic microvascular blood flow (KHz) decreased significantly in the severe acute pancreatitis group (P < 0.01), and continued to decrease after 24 h (vs. 12 h, P < 0.01). The blood flow of the portal vein, splenic artery and superior mesenteric artery also decreased in the severe acute pancreatitis group. The glutamine group showed increased regional pancreatic microvascular blood flows, as well as increased blood flow of the portal vein, splenic artery and superior mesenteric artery (vs. the severe acute pancreatitis group, P < 0.01). The apoptotic index of pancreatic acinar in the glutamine group was higher than in the severe acute pancreatitis group (P < 0.01), and both were much higher than that in the control group (P < 0.01). CONCLUSIONS: Enteral administration of glutamine increased the splanchnic blood flow in severe acute pancreatitis rats. The apoptotic index of pancreatic acinar was negatively correlated with the severity of the disease. The interrelation between glutamine and apoptosis in severe acute pancreatitis is worthy of further investigation.

Animals↗
PubMedDate not supplied

Endoscopically placed pancreatic stent in a patient with concomitant two locations of main pancreatic duct disruption following pancreatic trauma.

Severe pancreatic trauma involving disruption of the main pancreatic duct usually requires operative management. Recently, the successful non-operative treatment of proximal main pancreatic duct injuries by pancreatic stent has been described as having good results. Computed tomography of a 36-year-old man who sustained a blunt abdominal trauma in a motor vehicle accident disclosed a large amount of fluid in the cavity of the lesser sac, as well as a laceration of the pancreatic parenchyma at the pancreatic neck. Without definite evidence of pancreatic duct injury during laparotomy, no pancreatic resection was performed. However, postoperative endoscopic retrograde cholangiopancreatography showed 2 sites of main pancreatic duct disruption at the pancreatic neck and body, respectively. The first attempt for endoscopic pancreatic drainage failed with the endoscopic nasopancreatic drainage tube penetrating into the peritoneal cavity through the distal disruption site. A 5-French pancreatic stent was used for another attempt and successfully passed through the proximal disruption site with its tip located just proximal to distal disruption site. The patient improved steadily and was discharged uneventfully. The presenting case demonstrated that the endoscopically placed pancreatic stent was highly effective for the management of severe pancreatic trauma even though there were 2 sites of main pancreatic duct disruption, and pancreatic resection could be avoided.

Adult↗
PubMed1987

Determination of CA 19-9 antigen in serum and pancreatic juice for differential diagnosis of pancreatic adenocarcinoma from chronic pancreatitis.

Serum CA 19-9 levels were measured in 63 patients with ductal pancreatic adenocarcinoma and in 49 patients with chronic pancreatitis. Concentrations were abnormally high (greater than 40 U/ml) in 57 (90%) patients with cancer and only in 5 (10%) patients with chronic pancreatitis. All patients with falsely normal serum values had poorly differentiated carcinomas. Median CA 19-9 concentrations were progressively higher in patients with more advanced cancer. Fifteen of 16 (93%) patients with localized cancer has abnormal serum levels but only 5 (31%) of them had values greater than 120 U/ml, which was the highest score observed in patients with chronic pancreatitis. Pure pancreatic juice was obtained endoscopically from 23 patients with pancreatic cancer and from 20 with chronic pancreatitis. CA 19-9 concentrations in pancreatic juice were significantly higher in patients with cancer than in non-neoplastic patients. All 11 patients with resectable cancer investigated had a ratio of CA 19-9 to secretory protein concentration in pancreatic juice above the range of patients with chronic pancreatitis. We conclude that serum CA 19-9 determination is highly sensitive and specific for the differential diagnosis of pancreatic cancer versus chronic pancreatitis. However, moderately increased values (less than 120 U/ml), as seen in patients with localized pancreatic adenocarcinoma, are not conclusive for malignancy. The measurement of CA 19-9 to total protein ratio in pure pancreatic juice is proposed as an adjunctive, accurate diagnostic marker for early stages of pancreatic adenocarcinoma.

Adenocarcinoma↗
PubMed2004

Pancreatic duct strictures are a common cause of recurrent pancreatitis after successful management of pancreatic necrosis.

BACKGROUND: Successful surgical management of pancreatic necrosis can result in structural changes that cause recurrent pancreatitis. The purpose of this study is to review our clinical experience managing recurrent pancreatitis in patients after successful pancreatic debridement. METHODS: We retrospectively reviewed 98 patients with pancreatic necrosis treated by debridement who made a complete recovery at our institution over an 8-year period (January 1995 to January 2003). RESULTS: Fourteen patients (14%) developed recurrent pancreatitis 5 to 39 months (median, 15 months) after recovery. Five patients (36%) had pancreatic pseudocysts and 9 (64%) had radiologic evidence of obstructive pancreatitis. All patients had either a high-grade pancreatic duct stricture (N=7) or complete duct cutoff (N=7), localized to the pancreatic neck (N=10) or proximal pancreatic body (N=4) identified by either endoscopic retrograde cholangiopancreatography or magnetic resonance cholangiopancreatography. Two patients failed endoscopic stent therapy. All patients required re-operative treatment: 6 distal pancreatectomy, 6 pancreatico-jejunostomy Roux-en-Y, and 2 cystojejunostomy Roux-en-Y with no recurrence of pancreatitis after a median follow-up of 22 months. CONCLUSIONS: Recurrent pancreatitis occurs in 14% of patients after successful pancreatic debridement. Pancreatic duct obstruction in the neck or proximal body is the primary etiologic factor. Re-operation directed at alleviating this ductal obstruction by resection or drainage is effective.

Adult↗
PubMed2003

A prospective evaluation of pancreatic exocrine function in patients with acute pancreatitis: correlation with extent of necrosis and pancreatic endocrine insufficiency.

AIMS: The aim of this prospective study was to assess pancreatic exocrine function in patients recovering from a first attack of acute pancreatitis, and to evaluate its relationship to severity of attack, extent of pancreatic necrosis and severity of pancreatic endocrine insufficiency. METHODS: Between December 2000 and November 2001, 23 patients were prospectively evaluated. Pancreatic exocrine function was measured by the faecal elastase-1 test and insufficiency was classified as moderately impaired or severely impaired. Pancreatic necrosis was determined by contrast-enhanced CT scan, and its extent was categorised according to Balthazar's classification. The severity of pancreatic endocrine insufficiency was categorised according to insulin dependence. Attacks were classified as mild (n = 16) or severe (n = 7) according to the Atlanta criteria. RESULTS: Pancreatic exocrine insufficiency was significantly more frequent in patients recovering from severe attacks than mild (n = 6, 86% vs. n = 2, 13%; p = 0.002), and in those who developed pancreatic necrosis or pseudocyst than those who did not (6 of 7 patients vs. 2 of 16 patients, and 5 of 5 patients vs. 3 of 18 patients respectively; p = 0.002). The development of exocrine insufficiency correlated strongly with the extent of pancreatic necrosis (r = -0.754, p < 0.001), and the severity of pancreatic endocrine insufficiency (n = 4, r = -0.453, p = 0.03). CONCLUSION: Pancreatic exocrine insufficiency is a common occurrence in patients recovering from severe acute pancreatitis, and its severity correlates with the extent of pancreatic necrosis and the severity of concomitant pancreatic endocrine insufficiency.

Adult↗
PubMed2001

Pancreatitis-associated protein levels in pancreatic juice from patients with pancreatic diseases.

BACKGROUND: Pancreatitis-associated protein (PAP), the acute-phase protein of the pancreas, is overexpressed in acute pancreatitis. Serum PAP levels were reported to be useful as an indicator of the severity, prognosis and healing of acute pancreatitis. Although PAP was originally identified in pancreatic juice, there has been no clinical report on PAP levels in pancreatic juice. This study was conducted to determine levels of PAP in pancreatic juice (PJ-PAP) in various human pancreatic diseases. METHODS: PAP levels in endoscopically aspirated PJ were measured by enzyme-linked immunosorbent assay in 86 patients with pancreatic diseases. RESULTS: 55% of 22 patients with pancreatic cancer (PC) and 25% of 49 patients with chronic pancreatitis (CP) were positive (> 350 ng/ml) for PJ-PAP. PJ-PAP levels were significantly higher in PC than in CP, in which PJ-PAP was also significantly higher than in 15 control subjects. There was no significant correlation between PJ-PAP and serum PAP, and combination assay of serum PAP and/or PJ-PAP detected 80% of PC cases and 44% of CP cases. CONCLUSIONS: We have demonstrated that human PAP could be detected in pancreatic juice from patients with pancreatic diseases. Determination of PAP in pancreatic juice might be helpful for early detection of pancreatic injury.

Acute-Phase Proteins↗
PubMed1998

Secretory immunoglobulin A in pancreatic juice and pancreatic tissue of patients with chronic pancreatitis.

BACKGROUND: The predominance of secretory IgA (S-IgA) in intestinal secretions compared with blood is well established, but concentrations of this protein in pancreatic juice and its origin, especially in chronic pancreatitis, are unknown. AIMS: To investigate the role of S-IgA in chronic pancreatitis. PATIENTS: Twenty one patients with chronic pancreatitis (group I), three patients with proven malignancies (group II), and 12 patients without pancreatic disease (group III). METHODS: Pure human pancreatic juice was collected endoscopically in four fractions after consecutive stimulation with secretin and cholecystokinin (CCK). Samples were analysed for S-IgA, protein, trypsinogen, and proteolytic activity. RESULTS: The S-IgA level was significant increased in fraction 1 of pancreatic juice of group I (1210 (1411) ng/ml) compared with controls (33 (70) ng/ml). Protein concentrations and trypsinogen content were lower in group I than in the other groups. Proteolytic activity could be observed in 53% of all 133 pancreatic juice samples, but in 87% of fraction 1. In pancreatic tissue of three patients with chronic pancreatitis both IgA and secretory component were detected by immunohistology. Expression of the secretory component by human pancreatic epithelial cells was increased in patients with chronic pancreatitis compared with normal controls. The concentration of S-IgA in pancreatic juice did not correlate with the serum S-IgA level. In contrast, serum levels of S-IgA were decreased in patients with chronic pancreatitis. CONCLUSION: There are high levels of S-IgA in human pancreatic juice following chronic inflammation and a protective role is suggested for this immunoglobulin.

Adult↗
PubMed2006

Acute suppuration of the pancreatic duct associated with pancreatic ductal obstruction due to pancreas carcinoma.

Acute obstructive suppurative cholangitis is a well-known clinical entity; however, acute suppuration of the pancreatic duct in the setting of pancreatic ductal obstruction is an uncommon pancreatic disorder. We report a case of acute suppuration of the pancreatic duct without either a concomitant pancreatic abscess or an infected pseudocyst, presenting as acute relapsing pancreatitis. In this case, the underlying cause of suppuration of the pancreatic duct was pancreatic ductal obstruction and chronic pancreatitis secondary to pancreas head carcinoma along with infection of Escherichia coli. Endoscopic placement of a pancreatic stent resulted in an evacuation of grayish thick pus from the distal pancreatic duct with a dramatic improvement of the disease. This case proposes the concept that acute suppuration of the pancreatic duct is a complex process involving the chronically damaged pancreas, pancreatic outflow obstruction, and subsequent bacterial infection. Antibiotic treatment is effective but temporary; therefore, the immediate drainage of the infected pancreatic duct is mandatory.

Aged↗
PubMed1999

Increased angiogenin expression in obstructive chronic pancreatitis surrounding pancreatic cancer but not in pure chronic pancreatitis.

We previously demonstrated the increased expression of angiogenin (ANG) in pancreatic cancer and its relation to cancer aggressiveness; however, the expression patterns and the roles of angiogenin in chronic pancreatitis are still unknown. We investigated the expression of ANG both in the tissues and in the sera of chronic pancreatitis patients (pure chronic pancreatitis) by using in situ hybridization, Western blot analysis, and enzyme-linked immunosorbent assay. In situ hybridization revealed no detectable ANG messenger RNA (mRNA) signals in all tissues of pure chronic pancreatitis and normal pancreas. Only a small amount of protein band expression was obtained in all of the protein lysates of pure chronic pancreatitis and normal pancreas. Accordingly, there was no significant difference between the mean serum ANG concentration of chronic pancreatitis patients (352.1+/-72.5 ng/ml) and that of healthy volunteers (357.6+/-45.2 ng/ml). By contrast, acinar cells and interstitial fibroblasts in the tissues surrounding pancreatic cancer showed increased ANG mRNA expression. Strong protein band expression was obtained in the protein lysates of pancreatic cancer surrounding tissue, and mean serum ANG concentration was increased in pancreatic cancer patients. These findings suggest that ANG expression is increased in pancreatic cancer surrounding tissue but is not increased in pure chronic pancreatitis, and that ANG is potentially involved in the pancreatic cancer microenvironment rather than the establishment of pure chronic pancreatitis.

Blotting, Western↗
PubMed2003

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.

Adolescent↗
PubMedDate not supplied

Postoperative pancreatic fistula following distal pancreatectomy for pancreatic neoplasm; can pancreatic fistula be prevented?

BACKGROUND/AIMS: Pancreatic fistula is a potentially fatal complication in pancreatic surgery. The objective of this study was to analyze the incidence of pancreatic fistula in patients who underwent distal pancreatectomy for pancreatic neoplasm. METHODOLOGY: Forty-seven patients who underwent distal pancreatectomy for neoplasm of the pancreas at Kochi Medical School between October 1981 and December 2002 were studied. Comparative analysis was carried out to identify the correlations between the incidence of pancreatic fistula and parameters of preoperative evaluation, intraoperative procedure, and postoperative laboratory investigation. RESULTS: The incidence of pancreatic fistula in patients who underwent distal pancreatectomy for pancreatic neoplasm was 27.7%. Intraoperatively, the frequency of pancreatic fistula was significantly high in patients who underwent distal pancreatectomy without lymph node dissection and ligation of the splenic artery. No significant difference was recognized between the conventional surgical division and auto suture staple groups, however, in the ultrasonically activated scalpel (USAS) group, no pancreatic fistula was observed. A multivariate analysis revealed that independent high incidence of pancreatic fistula were 1) the situation of the tumor at pancreatic body, 2) the procedure of D2 lymph node dissection, and 3) the ligation of the root of splenic artery. In the group with the presence of pancreatic fistula, the serum amylase level on the first postoperative day was significantly higher than that in the group without fistula. CONCLUSIONS: Our findings supported that pancreatic fistula may be preventable by use of the USAS and treatment of acute pancreatitis in the early postoperative stage.

Adult↗
PubMed2001

Pancreatic intraductal sampling during ERCP in patients with chronic pancreatitis and pancreatic cancer: cytologic studies and k-ras-2 codon 12 molecular analysis in 47 cases.

BACKGROUND: A preoperative tissue diagnosis of pancreatic cancer is desirable but difficult to obtain. METHODS: Pancreatic brush cytology, salvage cytology, and collection of pancreatic juice were attempted prospectively during ERCP in 34 patients with pancreatic cancer and 11 with chronic pancreatitis. K-ras-2 codon 12 was analyzed for presence and type of point mutations. RESULTS: Brush cytology coupled with salvage cytology had a sensitivity of 74%. The addition of cytologic analysis of pancreatic juice did not substantially improve sensitivity (76%). K-ras-2 was mutated in both cancer (87%) and pancreatitis (40%). The specificity for cytology was 100% and for K-ras-2 mutations 60%. Combining cytology with mutation analysis increased sensitivity to 93% but reduced the positive predictive value. The negative predictive value never exceeded 75%. None of the patients with chronic pancreatitis had cancer develop (median follow-up 60 months). CONCLUSIONS: Pancreatic ductal brushing with salvage cytology is useful in the diagnosis of cancer, whereas cytologic analysis of pancreatic juice can be abandoned. At present, K-ras-2 mutation is not useful for differentiating pancreatic cancer from chronic pancreatitis or the identification of patients with chronic pancreatitis at risk for malignant transformation.

Adult↗
PubMed1976

Carcinoembryonic antigen (CEA) activity in pancreatic juice of patients with pancreatic carcinoma and pancreatitis.

Carcinoembryonic antigen (CEA) activity was assayed in plasma and in pure pancreatic juice from eight patients with carcinoma of the pancreas, 28 patients with pancreatitis, and 13 controls with no demonstrable pancreatic disease. Juice specimens were obtained via direct transduodenal cannulation of the pancreatic duct. The mean pancreatic juice CEA activities in controls, pancreatitis, and pancreatic carcinoma were 8.1 ng/ml, 18.6 ng/ml, and 309 ng/ml, respectively. Pancreatic juice CEA activity in patients with cancer of that organ was significantly higher than in those with pancreatitis or in controls. None of the 32 subjects with both pancreatic juice CEA activity less than 30 ng/ml and plasma CEA less than 2.5 ng/ml had pancreatic cancer. Three of the four patients with CEA elevations in both fluids above these levels harbored this malignancy. These findings suggest that combined measurement of CEA activity in plasma and pancreatic juice may help in diagnosing pancreatic disease.

Carcinoembryonic Antigen↗
PubMed2003

p8 improves pancreatic response to acute pancreatitis by enhancing the expression of the anti-inflammatory protein pancreatitis-associated protein I.

p8 is a transcription cofactor whose expression is strongly and rapidly activated in pancreatic acinar cells during the acute phase of pancreatitis. A p8-deficient mouse strain was generated as a tool to investigate its function. Upon induction of acute pancreatitis, myeloperoxidase activity in pancreas and serum concentrations of amylase and lipase were much higher and pancreatic lesions more severe in p8-deficient mice than in wild-type, indicating that p8 expression decreased pancreatic sensitivity to pancreatitis induction. The protective mechanism might involve the pancreatitis-associated protein (PAP I), whose strong induction during pancreatitis is p8-dependent, because administration of anti-PAP I antibodies to rats increased pancreatic inflammation during pancreatitis. In addition, 100 ng/ml PAP I in the culture medium of macrophages prevented their activation by tumor necrosis factor alpha, strongly suggesting that PAP I was an anti-inflammatory factor. Finally, PAP I was able to inhibit NFkappaB activation by tumor necrosis factor alpha, in macrophages and in the AR42J pancreatic acinar cell line. In conclusion, p8 improves pancreatic resistance to inducers of acute pancreatitis by a mechanism implicating the expression of the anti-inflammatory protein PAP I.

Alleles↗