Biomedical subjects
Publications and source records attributed to H Oguchi.
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Pancreatic oncofetal antigen (POA) was purified from fetal pancreas and migrated in beta-region electrophoretically. Its molecular weight was 80 X 10(4) daltons. Enzyme immunoassay for serum POA revealed that elevated levels of POA were found in sera of patients with pancreatic cancer. By a serological screening of 440 out-patients with combined assay of tumor markers including POA, 4 cases of pancreatic cancer were found. POA was demonstrated in the ductal cells of fetal pancreas and cancer cells of duct cell type pancreatic adenocarcinoma immunohistochemically. Elevated levels of serum POA of patients with pancreatic cancer was probably derived from cancer tissue. These findings indicate that serum POA assay is clinically useful.
We investigated the usefulness of enzyme immunoassay (EIA) for pancreatic oncofetal antigen (POA). The crude POA isolated from POA-positive ascitic fluid of patients with pancreatic cancer was injected into rabbits to raise anti-POA serum. The adsorbed antiserum was used for EIA as anti-POA serum. For the establishment of EIA system for POA, anti-POA-Fab' fragment was conjugated to beta-D-galactosidase from Escherichia Coli. Normal subjects (205 controls) and 132 patients (47 with pancreatic cancer, 22 with chronic pancreatitis, and 63 with other malignant disease) were surveyed. The standard serum from patient M with pancreatic cancer was used in quantitatively determining serum POA levels; value was expressed arbitrarily as 1000U/ml. Normal upper limit of POA was defined as less than 400U/ml (mean + 2SD of normal subjects). POA level higher than normal was observed in 72% of patients with pancreatic cancer, 23-44% of patients with other malignant diseases, and 18% of patients with chronic pancreatitis. The susceptibility of the isolated POA to several enzymes and chemical reagents was also studied. These results suggest the usefulness of EIA for POA in diagnosis of pancreatic cancer.
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Humoral hypercalcemia associated with malignancy has rarely been reported in exocrine pancreatic cancer. We report a patient with cancer of the exocrine pancreas who presented with hypercalcemia which did not respond to indomethacin. Her serum levels of parathyroid hormone and vitamin D derivatives were low. Technetium diphosphonate bone scan revealed no evidence of bone metastasis, a finding which was confirmed at autopsy. On light microscopy, histological classification of the tumor was moderately differentiated tubular adenocarcinoma. The electron microscopic study, however, revealed a few zymogen-like granules containing cancer cells lying between ductal-type cancer cells. A review of humoral hypercalcemia in cancer of the exocrine pancreas is presented. A humoral factor(s) other than parathyroid hormone, prostaglandin E, and vitamin D derivatives is considered responsible for hypercalcemia in this patient.
Screening for pancreatic cancer was carried out by serum pancreatic oncofetal antigen (POA) tests in 440 out-patients with abdominal complaints, with concomitant assay of carcinoembryonic antigen, alpha-fetoprotein and ferritin. POA was positive in 13 patients, of whom 3 cases of pancreatic cancer, and 4 of other malignant diseases were diagnosed while the remaining 6 were non-malignant. Of these out-patients, 5 cases were finally diagnosed as having pancreatic cancer by further examinations. Of these 5 patients, POA was negative in 2, of whom one was positive for CEA and AFP. Accordingly, when POA test was applied concomitantly with the other 3 marker tests, the detection rate of pancreatic cancer was elevated to 4/5. Twenty-three patients were found to have malignant diseases and 20 of them were positive for at least one of the 4 markers tested. These results suggest that serum POA assay is useful for screening the pancreatic cancer, especially when the other tumor markers are assayed concomitantly.
Renal biopsies from 10 patients who had residual symptoms of toxemia of pregnancy were examined by light, electron and immunofluorescent microscopy. The biopsies were performed 1 month to 3 months postpartum. The glomeruli showed a similar lesion, even though to a lesser degree, to that found in toxemia of pregnancy. Subepithelial swellings and endothelial cytoplasmic microtubular structures were also observed. Mesangial and monocyte-like cells contained lysosomes, cholesterol clefts and lipid-containing vacuoles with or without myelin figures, suggesting reparative process in the glomeruli. The present study indicates that the glomerular injury persists for a few months after delivery, together with the concurrent reparative process.
Pancreatic oncofetal antigen (POA) purified by us has been detected in sera of patients with carcinoma of the pancreas by the micro-Ouchterlony method. In an attempt to improve the sensitivity and clinical usefulness of the serum POA assay, we established an enzyme immunoassay for POA and reported the results with this method. In this study, we investigated serum POA levels in pancreatic cancer and other diseases. The tissue localization of this POA in the pancreas was also studied. For the establishment of the enzyme immunoassay, an anti-POA-F(ab')2 fragment prepared from absorbed antiserum was conjugated with beta-D-galactosidase. The solid-phase "sandwich" principle was used. The normal upper limit of the serum POA level was defined as 400 units/ml. Among 60 patients with pancreatic cancer, 44 had elevated levels (73.3%). Of 22 cases with chronic pancreatitis, 4 had elevated levels (18.2%). In malignant diseases other than pancreatic cancer, elevated levels of serum POA were seen in 17.6% to 48.5% of the patients, most of whom had only slightly elevated levels. These results indicate that enzyme immunoassay for POA is clinically useful for making a diagnosis of pancreatic cancer. Immunoperoxidase staining showed POA to be found at the apical surface of ductular cells in fetal pancreas, at the luminal surface of glandular structures in pancreatic cancer tissue, and also at the luminal surface of the small duct in normal pancreas. Thus it is suggested that a high level of serum POA in patients with pancreatic cancer is derived from pancreatic cancer tissue.
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Sixteen years follow-up was performed in a male of long-standing alcohol indulgence who had an alcoholic liver disease at the outset, followed by alcoholic pancreatitis which progressed finally to pancreatic calcification. During this course, the abnormalities of endoscopic pancreatogram were unremittingly progressive, whereas exocrine and endocrine pancreatic dysfunction remained fluctuating, but ultimately deteriorated. In contrast functional and histological abnormalities of the liver were not progressive but returned toward normal. The follow-up observations in this case suggest that some cases of typical alcoholic pancreatitis may have unremittingly progressive morphologic changes with fairly well reserved capacity of exocrine and endocrine pancreatic functions and their hepatic lesions may not be in parallel with pancreatic lesions.
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HLA A and B antigens in 46 patients with chronic pancreatitis were studied in Japan. Patients were divided into the two groups according to the etiology of the disease: one was chronic idiopathic pancreatitis (18 cases) and the other was chronic alcoholic pancreatitis (28 cases). One hundred twenty unrelated subjects were also examined as control. HLA B5 was detected in 14 of 18 cases of chronic idiopathic pancreatitis, which was significantly higher statistically than in control (P less than 0.001, corrected P less than 0.05). In contrast, no HLA antigens of locus A and B were found which had a relationship to chronic alcoholic pancreatitis. These results suggest that some genetic factors may be implicated in the development of chronic idiopathic pancreatitis and differing from that of alcoholic pancreatitis.
Studies on the purification, characterization and clinical application of pancreatic oncofetal antigen were reported. This antigen was purified from fetal pancreas, and migrated in the beta-region on electrophoresis. Its molecular weight was about 80 x 10(4) daltons on gel filtration with a Sephacryl S-300. This antigen is clearly different from other oncofetal antigens such as alfafetoprotein, carcinoembryonic antigen or ferritin. Clinically, this pancreatic oncofetal antigen was positive in sera of 68.4% of the patients with pancreatic cancer. However, elevated level of this antigen was also observed in the sera of some patients with biliary tract cancer, colon cancer or gastric cancer. The antigen was also found in pancreatic juice obtained from patients with pancreatic cancer in almost the same incidence as in their sera. It is suggested that a pancreatic oncofetal antigen assay of sera and pancreatic juice in combination with other oncofetal antigens is valuable for the diagnosis and monitoring the clinical course of pancreatic cancer.
A peptide containing 59 amino acid residues with a stoichiometric amount of dihydroxylysinonorleucine (0.7 mole) and hydroxylysinonorleucine (0.2 mole) was isolated from reduced 3H labelled bovine bone collagen sequentially cleaved with CNBr and trypsin. Further cleavage of the isolated crosslinked peptide with periodate yielded a radioactive peptide of 45 residues and a non-radioactive peptide of 16 residues. From the characteristic amino acid composition of these peptides it was deduced that the peptide was derived from an intermolecularly crosslinked region between lysyl or hydroxylysl residues in the carboxy-terminal extension of alpha 1-CB6 (17C residue) and alpha 1-CB5 (87th residue). This finding supports the observation that the alpha 1-CB6 peak was prominent on carboxymethyl cellulose chromatography of the CNBr digest of bone collagen only after limited pepsin digestion, and is consistent with the results obtained from a smaller crosslinked peptide previously isolated from calf bone collagen.
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The pancreatic duct system was studied with repeated endoscopic retrograde pancreatography in 31 patients with chronic pancreatitis, 32 patients with suspected chronic pancreatitis, and 16 controls without pancreatic disease. In chronic alcoholic pancreatitis the pancreatograms showed marked changes during the initial examination with progression even after abstinence or reduction of drinking. In the alcoholics with suspected chronic pancreatitis, progressive lesions in branch ducts with almost intact main ducts were recognized. In contrast, no remarkable alterations on serial pancreatograms were observed in nonalcoholic cases with definite or suspected chronic pancreatitis. These results suggest that pancreatic duct lesions play an important role in the development and progression of chronic alcoholic pancreatitis in contrast to chronic nonalcoholic pancreatitis.
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