Pancreatic Tissue In Patients Research Articles

Phospholipase A2 activity in body fluids and pancreatic tissue in patients with acute necrotising pancreatitis

To measure pancreatic and non-pancreatic phospholipase A2 activity in human acute necrotising pancreatitis. Prospective study. University hospital, Finland. 20 patients with acute necrotising pancreatitis. Serum and urine samples were taken daily for a week and fluid from peritoneal lavage for six days after admission. Samples from the pleural cavity were taken from patients in whom pleural drainage was considered necessary. Pancreatic tissue was recovered from the patients who were operated on for acute pancreatitis or for pancreatic tumour. Serum phospholipase A2, amylase, and lipase activities. Serum phospholipase A2 activity increased up to eightfold, 25.0 (5.4) IU/L (n = 20, range 9.0-77 IU/L) (reference value <3 IU/L) and remained high during the first week, whereas serum amylase and lipase returned to the reference range during the first four days. The maximal phospholipase A2 activity in urine was 4.5 IU/L, in the fluid from peritoneal lavage 16.9 IU/L, and in the fluid from the pleural cavity 37.0 IU/L. Phospholipase A2 activity in necrotic pancreatic tissue ranged from 0.25 to 5.70 IU/g and in normal pancreatic tissue from 9.85 to 15.0 IU/g. Preincubation at 60 degrees C showed non-pancreatic phospholipase A2 activity predominated in serum, whereas part of the enzyme activity in the fluids from pleural cavity and peritoneal lavage proved to be of pancreatic derivation. The results suggest a role for both pancreatic and non-pancreatic phospholipase A2 in acute pancreatitis. Preincubation at 60 degrees C proved useful in the differentiation between pancreatic and non-pancreatic phospholipase A2 activity.

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

Background—The predominace 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,...

Expression of blood group-related antigens in normal and malignant pancreatic tissue correlated with genotype of the patient defined by saliva glycoprotein.

Seven murine monoclonal antibodies (MoAb) detecting blood group antigens of the Lewis system and their sialylated derivatives were used to define their immunohistochemical distribution in normal and malignant pancreatic tissues. The specific blood group antigens studied included Lewis(a) (Le(a)), Lewisb (Leb), Lewisx (Le(x)), Lewis(y) (Le(y)), sialyl-Lewis(a) (s-Le(a)), sialyl-lacto-N-tetraose (s-LNT), and sialyl-Lewisx (s-Le(x)). The expression of these antigens was analyzed by immunoperoxidase technique in pancreatic tissue of patients with (n = 27) and without (n = 19) pancreatic cancer. The genetic background of their secretor status and their Lewis phenotypes were determined by the enzyme-linked immunosorbent assay using purified salivary glycoprotein and MoAb against eight different blood group-related antigens (Le(a), Leb, Le(x), Le(y), H1, H2, A, B2), and the putative genotypes of the patients were classified as follows: SeLe, Sele, seLe, and sele. The following results were obtained: (1) In normal pancreas, Le(a), s-Le(a), s-LNT, and s-Le(x) were expressed in ducts, but their expression was restricted to the luminal side of the cytoplasm (cytoplasmic type with positive polarity). Leb and Le(y) showed similar patterns of expression in ducts and some parts of the acinus. In contrast, Le(x) was absent in most cases. (2) Expression of Leb was observed in normal pancreatic ducts in all 46 patients, regardless of their genotypes. Le(a) and s-Le(a) were not expressed in specimens from patients with the seLe and sele saliva phenotypes. (3) In pancreatic cancer, the following antigens were expressed cytoplasmically in the proportion of cases indicated: Le(a) (78%), Leb (85%), Le(x) (33%), Le(y) (44%), s-Le(a) (78%), s-LNT (89%), and s-Le(x) (85%). They also were detected in the surrounding stroma. This pattern of expression is distinct from that found in normal pancreatic tissue. Patients with Sele and sele genotypes did not express Le(a) or s-Le(a), except in one case. (4) Serum levels of carbohydrate antigen 19-9 (CA 19-9) were not elevated in patients with pancreatic cancer with the Sele and sele genotypes but were elevated in most patients with SeLe and seLe genotypes. The overall findings indicate that Lewis-related antigens act as pancreatic tissue-related antigens, depending in part on salivary phenotypes of the patient. With proper antigen selection and the determination of secretor status, these anti-blood group MoAb may be of clinical utility in the diagnosis of pancreatic cancer.

Amyloid protein in somatostatinoma differs from human islet amyloid polypeptide

Amyloid deposits in somatostatinomas are rare observations. To examine the characteristics of this amyloid, we compared amyloid deposits in a somatostatinoma to those found in pancreatic tissue in patients with Type II diabetes mellitus and in insulinomas, using immunohistochemical techniques and specific antibodies to islet amyloid polypeptide or other pancreatic hormones, as well as electron-microscopy. Antibodies to islet amyloid polypeptide regions 8-17 or 25-37 were confirmed to be specific. Amyloid deposits in patients with Type II diabetes mellitus and in insulinomas, but not those in the somatostatinoma strongly reacted with these antibodies, or to an antibody to amyloid P component. Amyloid deposits in the somatostatinoma were not reactive with antibodies to somatostatin or to other pancreatic hormones. Electron-microscopic examinations revealed that amyloid fibrils in the somatostatinoma were thinner and more randomly distributed than were those in islets from patients with Type II diabetes mellitus. As amyloid in somatostatinomas is unlike that consisting of islet amyloid polypeptide or other mature pancreatic hormones, it may be a novel type of local amyloid in pancreatic islets.