Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nineteen patients with pancreatitis and 40 with pancreatic carcinoma were examined for certain immunological characteristics (immunoglobulins, immune complexes, PHA-induced lymphocyte proliferation) and for the level of carcinoembryonic antigen (CEA) and CA 19-9 depending on blood bilirubin. Hyperbilirubinemia was identified in 21 patients with carcinoma and in 3 suffering from pancreatitis. Both patients' groups manifested an increase of the IgA level. Especially high characteristics were seen in hyperbilirubinemia. The level of other class immunoglobulins and immune complexes did not depend on blood bilirubin. The patients demonstrated suppression of PHA-induced lymphocyte response by autologous plasma, with more remarkable suppression being observable in hyperbilirubinemia. The level of CEA or CA 19-9 was increased in 89% of the patients with pancreatic carcinoma and in 30% of pancreatitis patients. No relationship was recorded between the level of oncofetal antigens and blood bilirubin.
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PMID:[The immunological indices in inflammatory and tumorous diseases of the pancreas]. 150 77

A case of multiple myeloma (Bence Jones, lambda) associated with alcoholic liver cirrhosis is reported. A 56-year-old Japanese male died of hepatic failure and hypercalcemia. Autopsy revealed alcoholic liver cirrhosis and plasma cell myeloma. Immunoelectrophoretic analysis of his reserved serum disclosed the presence of M component of lambda Bence Jones protein. IgA and lambda light chain were demonstrated in the cytoplasm of the myeloma cells. Complications such as generalized amyloidosis, metastatic calcification, myeloma kidney and hemorrhagic pancreatitis were noted. The coexistence of multiple myeloma and liver cirrhosis has rarely been reported. On the basis of a review of the reported cases, a possible association between both diseases was discussed.
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PMID:Multiple myeloma in alcoholic liver cirrhosis. 265 75

In 29 patients (twelve female, 17 male) the following immunologic parameters were examined before and between days 1 to 3, 6 to 8, 13 to 15 and 20 to 22 after open-heart surgery: T-lymphocytes; immunoglobulins IgG, IgM, IgA, IgE; complement factors C3, C4 and the autoantibodies (Anti-DNA, myocardial antibodies, SMA, ANA, AMA) to assess changes in these parameters and their relationship to postoperative complications, in particular post-cardiotomy-syndrome (PCS). PCS was found in five patients (17.2%), in three fully developed, in two in a partial form. In the very early (first to third day) postoperative course, significant suppression of most parameters was found, most likely due to tissue traumatization intraoperatively as well as to the extracorporeal circulation. There was suppression of T-lymphocytes, immunoglobulins IgG, IgM and IgA and the complement factors C3 and C4. The IgE rose slightly. The serum IgM level appears to be of prognostic relevance since the patients with IgM suppression had a higher incidence of postoperative complications (PCS, pancreatitis). In the later postoperative course IgM, C3 and C4 significantly exceeded the preoperative values. The rise in IgM can be explained as an immunologic answer to a subclinical infection or to an immunization by autoantigenic tissue. The rise in C3 and C4 was interpreted as an acute phase reaction. These changes, however, had no influence on the postoperative course of the autoantibodies, only subsarcolemmal myocardial antibodies were found preoperatively; in four of the five patients with PCS, these myocardial antibodies were present prior to surgery. Postoperative myocardial antibodies were found in 75% of the patients. In all probability they are only indicative of nonspecific myocardial lesions.
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PMID:[Changes in immunologic parameters following heart operations with special reference to the postcardiotomy syndrome]. 348 59

The proliferation of pancreatic extracellular matrix, which characterizes chronic pancreatitis, has been analysed using immunohistochemistry. The relationship of matrix components to intraductal precipitates and the presence of serum proteins in precipitates were also studied to investigate the suggestion that ductal permeability increases in chronic pancreatitis. Pancreatic tissue from organ donors was compared with that from patients with chronic calcifying or chronic obstructive pancreatitis. Frozen sections were labeled with monospecific antibodies to collagen types I, III, pro-III and IV, laminin, fibronectin, IgG, IgA, and IgM and then visualized by indirect immunofluorescence. In chronic pancreatitis, interstitial collagens and fibronectin appeared increased and disorganized in both fibrous tissue and areas that appeared histologically normal. Type IV collagen distribution was abnormal and in some sites was present with interstitial collagen. In addition, intraductal precipitates were shown to contain immunoglobulins, and defects were identified in the duct basal lamina associated with precipitates. These results demonstrate that in chronic pancreatitis interstitial collagens are extensively disorganized, the fibrosis possibly being relatively labile. The presence of serum proteins in intraductal precipitates confirms an increase in ductal permeability, and associated defects in the basal lamina appear to define a route via which serum proteins may enter the intraluminal compartment.
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PMID:Pancreatic extracellular matrix alterations in chronic pancreatitis. 357 15

Serum immunoglobulin concentrations were measured in 40 patients with calcific pancreatitis. A significant elevation of the mean serum IgA and IgG concentration when compared with a control group was found. The IgA was raised in 50% and the IgG in 27.5% when the individual results were assessed. The IgA did not appear to be of the secretory type. The possible significance of the raised IgA and IgG is discussed with reference to local pancreatic IgA production, autoimmune factors in chronic pancreatitis, and the ductal protein plugs in this disease.
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PMID:Serum immunoglobulins in calcific pancreatitis. 475 35

It was demonstrated by indirect immunofluorescence that Crohn's disease and ulcerative colitis are serologically distinct. In 59 patients with Crohn's disease, confirmed by endoscopy and histology, 23 (39%) had serum autoantibodies against exocrine pancreas; in 17 (29%) the titre was 1 : 100 or higher. In 46 patients with confirmed ulcerative colitis pancreas antibodies were demonstrated only twice, in 100 healthy control subjects only 3 times, with titres less than 1 : 100. Pancreas antibodies do not occur in high concentrations in pancreatitis; titres higher than 1 : 100 therefore suggest Crohn's disease. The pancreas antibodies of patients with Crohn's disease were predominantly immunoglobulins IgA and IgG, twice they were IgD and once IgM, never IgE. In 6 patients the pancreas antibodies fixed complement. Autoantibodies against intestinal goblet cells were found only in patients with ulcerative colitis (13 of 46 = 28%). The titres range was from 1 : 10 to 1 : 1000. The goblet-cell antibodies consisted only of IgA and IgG, never reacting with complement. These results indicate that determining pancreas and goblet-cell antibodies alone will make it possible to diagnose either Crohn's disease or ulcerative colitis in more than a quarter of patients with chronic inflammatory intestinal disease.
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PMID:[Autoantibodies against the exocrine pancreas and against intestinal goblet cells in the diagnosis of Crohn's disease and ulcerative colitis]. 615 Aug 41

alpha 2-macroglobulin is probably the most important of the antiproteases in plasma. In this study, the relationships of plasma alpha 2-macroglobulin to the clinical features of acute pancreatitis as well as to plasma levels of other antiproteases, immunoglobulins, and immunoreactive trypsin, were investigated in 55 patients with acute pancreatitis. The mean level of alpha 2-macroglobulin in 395 plasma samples from the patients was 2.12 g/liter compared with 2.41 g/liter in 29 healthy subjects and 2.93 g/liter in 17 patients with septicemia. Plasma levels were lower in 12 patients with severe pancreatitis than in 43 with mild attacks, and the lowest levels in three fatal attacks were less than half the mean of the normal range. Lowest levels were recorded at a mean time of 3 days after admission in the patients with mild attacks, at 5 days after admission in the patients with severe attacks, and 9 days after admission in those with fatal attacks. In contrast, plasma levels of the alpha 1-proteinase inhibitor antichymotrypsin and C-reactive protein increased to above normal levels during the attack, significantly more so in severe compared with mild attacks. Plasma levels of IgA, IgG, and IgM remained within the normal range or were increased. In patients with severe pancreatitis, plasma levels of immunoreactive trypsin remained elevated for longer than in those with mild attacks although there was little initial difference in the levels. These data suggest that decreasing levels of alpha 2-macroglobulin during the course of acute pancreatitis are due to a specific mechanism and unrelated, for the most part, to any generalized effect of pancreatitis on protein synthesis. The formation of rapidly cleared complexes between alpha 2-macroglobulin and active proteases is the most tenable explanation for the depletion of plasma levels, but the clinical significance of the changes remains unclear.
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PMID:Relation of alpha 2-macroglobulin and other antiproteases to the clinical features of acute pancreatitis. 619 93

The differential diagnosis between chronic pancreatitis and pancreatic cancer can be very difficult. In 60 patients with either of these conditions, who had satisfactory ERCP study, clinical features were correctly matched with the final diagnosis by discriminant analysis in 44 (73%). The sensitivity of ERCP radiographic findings in pancreatic cancer was 80% and sensitivity of cytology was 54%. To see if exocrine function was specific for cancer, fresh pancreatic secretions were aspirated in 27 patients at the time of ERCP. By isoelectric focusing, a pattern of extreme zymogen depletion was observed in chronic alcoholic pancreatitis (Group 1), pancreatic cancer (Group 2), and chronic nonalcoholic pancreatitis (Group 3). The three groups were not distinguishable. By contrast, significant changes in albumin, IgG and IgA concentrations were seen in Group 2. The albumin level was over ten-fold greater than in Groups 1 and 3 (p less than 0.02 and less than 0.05). The IgG was seven-fold and two-fold greater (p less than 0.01 and greater than 0.2) and the IgA was 15-fold and six-fold greater (p less than 0.002 and less than 0.05) than in Groups 1 and 3, respectively. The two groups of pancreatitis had similar concentrations of albumin and IgA. The ratio of albumin to IgG was also different in Group 2 from the other groups, suggesting different mechanisms for the appearance of proteins in pancreatic secretions. Nonzymogen protein levels can distinguish chronic pancreatitis from pancreatic cancer, and further study of them may identify useful tumor-specific markers.
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PMID:Clinical and secretory differences in pancreatic cancer and chronic pancreatitis. 725 47

Infectious complications are the leading cause of death in acute pancreatitis. Individual factors of immune defence could be of significance, whether or not a patient develops a severe course with infectious complications. In a prospective 5-year trial including 72 patients, we investigated 29 cellular and humoral markers of the body's defence system for their potential to indicate the severity and course of acute pancreatitis. Complement factors C3 and C4 as well as immunoglobulins IgG, IgM and IgA were normal, in general. Measurable levels of IL-1 alpha, IL-1 beta, IL-2 and sIL-2R could be detected only occasionally. Values of alpha 1-AT, TNF-alpha, TNF alpha-Rp75, neopterin, sICAM-1, IL-8, IL-1RA and sIL-6R did not correlate with a severe course. Due to the high magnitude of increase, CRP, IL-6 and granulocyte elastase were the best indicators of the inflammatory process. Delayed-type hypersensitivity response was the only early predictor of a severe course. It was superior over other cellular markers such as monocyte count or CD4+/CD8+ ratio. In vitro function of polymorphonuclear granulocytes (PMN) was not adequate to the severity of the disease already during the first week of illness. During further course, PMN motility and capacities to produce reactive oxygen species even worsened. The compromized PMN function could explain the frequent development of infectious complications in patients suffering from severe pancreatitis. These results should encourage new concepts of infection prophylaxis using stimulants of cellular defence.
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PMID:[Cellular and humoral functions in acute pancreatitis]. 913

Since PAP is a stress protein expressed in human pancreas during pancreatitis but also constitutively synthesized in the small intestine, we looked whether its expression would be altered in patients with celiac disease. Serum PAP concentrations were determined consecutively in 54 patients with celiac disease on a free diet (group A), in 47 patients with celiac disease on a gluten-free diet (group B), in 22 patients with other intestinal pathologies but with normal intestinal mucosa (group C), in 14 patients with retarded growth, no gastrointestinal disease and normal intestinal mucosa (group D), and in 17 controls (group E). Serum PAP levels (ng/ml) were significantly higher in group A (127.3 +/- 56.8) than in the other groups (B: 47.2 +/- 20.5; C: 51.5 +/- 32.2; D: 47 +/- 22.8; E: 27.6 +/- 9.0), which were not different from each other. In group A, a positive correlation was observed between serum PAP values and antigluten antibody levels (vs. AGA IgG r = 0.58, p < 0.001; vs. AGA IgA r = 0.66, p < 0.001). Furthermore, 12 patients from group A were evaluated after 10-12 months of gluten-free diet and in all of them PAP serum concentration had decreased (mean +/- SE before the diet 122.5 +/- 36.4, after the diet 48.7 +/- 13.7, p < 0.0001). In addition, we performed an immunocytochemical study to localize PAP in the intestinal mucosa of patients from all groups except E. PAP was localized to the Paneth cells and to some globet cells, in patients with mucosal atrophy as well as in those with normal mucosa with no obvious quantitative difference. We concluded that in patients with celiac disease the active phase of the disease was accompanied by an increased serum concentration of PAP. Further studies are necessary to understand the mechanism leading to PAP elevation in the serum of patients with celiac disease.
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PMID:Pancreatitis-associated protein in patients with celiac disease: serum levels and immunocytochemical localization in small intestine. 914 97


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