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Hitoshi OKANO, Tadashi KODAMA, Hideharu TSUJI, Masahiko TAKAMASU, Shoj ...
1986 Volume 83 Issue 12 Pages
2509-2513
Published: 1986
Released on J-STAGE: December 26, 2007
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Endoscopic injection sclerotherapy (EIS) of esophageal varices is now an effective and reconized procedure. But post-EIS esophageal ulcers are frequently seen and paralleled the trial times of EIS. It is suspected that these esophageal ulcers may cause some symptoms such as heart burn and dysphagia. These symptoms did not persist for more than three months. The purpose of our study was to determine whether esophageal motility and lower esophageal sphinctor (LES) pressure which due to ulcers cause symptoms. The change of resting LES pressure and esophageal peristaltic wave pressure were evaluated using the perfused open tip method before and after EIS. In the cases with esophageal ulcers, decreased resting LES pressure and peristaltic wave pressure were obtained. But these abnormalities returned to normal within six month. On the bases of our study, post-EIS esophageal ulcers should not be considered an avoidable complication from the point of manometric examination.
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Tadahisa MIYAMOTO, Makoto ITO, Kei MATSUSAKO, Kazuo IKEDA, Takasi JOH, ...
1986 Volume 83 Issue 12 Pages
2514-2519
Published: 1986
Released on J-STAGE: December 26, 2007
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The role of intracellular and extracellular calcium ion of gastric chief cells for pepsinogen secretion stimulated by carbachol and CCK-8 was evaluated using nicorandil (intracellular calcium antagonist) and verapamil (calcium channel blocker) in organ culture of rabbit gastric mucosa. The pepsinogen secretion stimulated by carbachol (10
-4M) was significantly inhibited by 10
-5 and 10
-4M nicorandil and CCK-8 (10
-8M) stimulated pepsinogen secretion was also significantly inhibited by 10
-6, 10
-5 and 10
-4M nicorandil. On the other hand, verapamil (10
-6-10
-4M) did not inhibit the pepsinogen secretion induced by carbachol and CCK-8. We conclude that a mobilization of the intracellular calcium ion of chief cell, not extracellular one, plays an important role in the mechnisms of pepsinogen secretion stimulated by carbachol and CCK-8.
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Takeshi YOSHIDA
1986 Volume 83 Issue 12 Pages
2520-2528
Published: 1986
Released on J-STAGE: December 26, 2007
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T cell subsets of peripheral blood lymphocytes (PBL) were examined in 30 patients with ulcerative colitis (UC) by a fluorescence activated cell sorter (FACS), using monoclonal antibodies to suppressor/cytotoxic (anti-Leu-2a) and helper/inducer (anti-Leu-3a) T cells. Leu-2a positive T cells were decreased in PBL from patients with active UC (9.1±5.6%, p<0.001) compared with normal controls (24.6±3.7%). Con A-induced suppressor T cell activity was decreased in patients with active UC whose Leu-2a positive cells in PBL were decreased. We examined the ability of PBL from patients with UC to produce and respond to exogenous interleukin 2 (IL2). IL2-production was normal in patients with active UC, while they had a decreased response to exogenous IL2. Moreover it was proven that the hyporesponsiveness was due to inadequate expression of IL2-receptors on the surface of Leu-2a positive T cells. These results suggest that decrease in the number and function of suppressor T cells demonstrated in patients with UC is caused by a disturbance in differentiation and prolieferation of suppressor T cells. The abnormality of suppressor T cell may play a role in the immunological disorders of patients with UC.
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Yousuke TANAKA, Tadao MANABE, Takayoshi TOBE
1986 Volume 83 Issue 12 Pages
2529-2537
Published: 1986
Released on J-STAGE: December 26, 2007
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To investigate the changes of fasting plasma secretin and gastrin levels associated with obstructive jaundice and its mechanism, ligation of the common bile duct (CBD) was performed in dogs, followed by external cholecystostomy to release obstructive jaundice and cimetidine administration to inhibit gastric acid secretion. Plasma secretin was measured with a new enzyme immunoassay method. Both the plasma secretin and gastrin levels rose significantly 2 days after CBD ligation, and thereafter remained significantly high. One day after the external cholecystostomy on the 8th post-ligation day, the secretin level fell significantly, and thereafter remained significantly low. Despite the administration of cimetidine after CBD ligation, the rise of secretin level was not inhibited. From 2 to 4 weeks after the CBD ligation the plasma secretin level was markedly elevated, but gastrin level tended to fall. These results suggests that the main mechanism of elevated plasma secretin levels in the early stage after CBD ligation is hepatic injury, probably due to impaired extraction of secretin.
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Tomio SUDA, Hiroshi KAMIO, Tsuneo MATSUIKE, Makoto MIKAMI, Yutaka BUN, ...
1986 Volume 83 Issue 12 Pages
2538-2544
Published: 1986
Released on J-STAGE: December 26, 2007
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Incidences of hepatic encephalopathy and mortality were surveyed in patients with liver cirrhosis for about two years after 75g oral glucose tolerance tests. Among four groups classified by glucose tolerance pattern, a group with diabetic pattern under 140mg/dl of fasting plasma glucose and high value of 2 hours plasma glucose (over 2.5 fold fasting value), was shown to have the highest incidence of hepatic encephalopathy and the highest mortality, and revealed the worst value in various tests of liver function. The high-risk group was explained to have a marked trend to induce hepatic encephalopathy due to low value of blood ketone body ratio (acetacetate/β-hydroxybutyrate) and serum amino acid imbalance. Thus, the glucose tolerance test was suggested to be an useful parameter for prediction of hepatic encephalopaty and mortality in patients with liver cirrhosis.
Severe disturbances of glucose metabolism were considered to be involved with hepatic encephalopathy in patients with liver cirrhosis.
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Shuichi SEKI, Yasuhiro MIZOGUCHI, Shinobu SAITO, Susumu SHIOMI, Yoshih ...
1986 Volume 83 Issue 12 Pages
2545-2549
Published: 1986
Released on J-STAGE: December 26, 2007
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At our department, 11 patients with drug-induced acute hepatic failure have been clinicopathologically studied during the past 17 years. The incidence of drug-induced acute hepatic failure was about 3% of hepatic injury due to drugs and about 26% of fulminant hepatic failure due to various agents including drugs, alcohol and viruses. The prognosis was poor in the patients with hepatic coma due to drugs, and most of these patients died within 10 days after the disturbance of consciousness.
Therefore, when administering drugs for long periods of time, liver function tests must be performed regularly, taking the mechanism of drug-induced hepatic injury into consideration.
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Yoshiro WATANABE, Masaaki EBARA, Masao OHTO, Masaharu YOSHIKAWA, Nobuy ...
1986 Volume 83 Issue 12 Pages
2550-2562
Published: 1986
Released on J-STAGE: December 26, 2007
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Twenty one cases of hemangioma of the liver were studied with Magnetic Resonance Imaging (MRI) and its diagnostic capability, with emphasis on differential diagnosis from hepatocellular carcinoma. The characteristic MRI findings of hemangioma were as follows: 1) well-circumbscribed, and homogenous signal intensity of the lesion. 2) On inversion recovery images, the intensity of the lesion is the same as or higher than that of the spleen. 3) On T2-weighted spin echo images, the intensity of the lesion is the same as or lower than that of the spleen.
The diagnostic capability of MRI for hemangioma was such that all lesions over 1.5cm in diameter were detected and the accuracy of differential diagnosis between hemangioma and hepatocellular carcinoma was 97.5%. Moreover, MRI made it possible to discriminate hemangioma from other hepatic mass lesions with great accuracy. In the future, MRI and sonography, both non-invasive diagnostic modalities, would play a major role in the diagnosis of hemangioma of the liver.
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Kenji IKEDA, Hiromitsu KUMADA, Ikuo NAKAMURA, Yasuji ARASE, Yasumi NOZ ...
1986 Volume 83 Issue 12 Pages
2563-2570
Published: 1986
Released on J-STAGE: December 26, 2007
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Repeated transcatheter arterial embolization (TAE) therapy was done for 98 patients with hepatocellular carcinoma. TAE was performed by Seldinger method using gelatin sponge particles as emboli. When viable tumor was suspected on computerized tomography (CT) after therapy, next TAE therapy was planned within three months as a rule.
Cumulative one-year survival rate after therapy was 71.6%, and two-year 44.1%, three-year 30.5%. Complete dissappearance of cancer on CT and angiogram was achieved in thirteen patients (13.3%). Adverse symptoms and sings were minimal as a whole.
"Every three-months TAE" therapy was done in 86 patients, but it was not attained in other 12 patients whose hepatoma required additional TAE therapy. In former group, out of 30 dead cases only 8 cases (26.7%) died from primary focus of the tumor, and 8 died from lung or brain metastasis of the tumor, 12 from hepatic failure or other etiology. In other hand, out of 12 patients who had insufficient "every three-months" therapy, 10 (83.3%) died from primary site of the tumor.
Although almost of hepatocellular carcinoma were successfully managed by repeated TAE therapy, certain kinds of tumors were difficult to treat which include infiltrative type of hepatocellular carcinoma and cases with HBe antigen positive liver cancer.
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Yutaka SASAGAWA
1986 Volume 83 Issue 12 Pages
2571-2579
Published: 1986
Released on J-STAGE: December 26, 2007
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We have often acquired low values on the BT-PABA tests for liver cirrhosis. The percentage of abnormality was even higher by the PABA absorption tests in order to exclude from abilities of intestinal absorption, liver and renal function. In these patients, the three factors of Pancreozymin-Secretin tests (PST) were almost within normal range and endoscopic retrograde pancreatography of them were nearly normal. Therefore, there was a dissociation between the BT-PABA tests and PST. On the BT-PABA tests the accumulated area of plasma PABA values from start to 90 minutes (Area PABA) was correlated with the total chymotrypsin output on the PST and it was significantly lower (p<0.01) in chronic pancreatitis than in normal controls. It is thought that serum PABA is reflected on a part of exocrine pancreatic function. In the patients of liver cirrhosis, showing low values of 6 hours' PABA excretion rates. Area PABA were almost within normal range. 6 hours' PABA excretion rates for liver cirrhosis was correlated with creatinin clearance rates, not with liver function. So it is suggested that low values on the BT-PABA tests for liver cirrhosis were due to renal dysfunction than exocrine pancreatic insufficiency.
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Harunobu MAEDA
1986 Volume 83 Issue 12 Pages
2580-2587
Published: 1986
Released on J-STAGE: December 26, 2007
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To demonstrate the progress of pathogenesis of pancreatic fibrosis and fat replacement, ductal and vascular obstructions were imposed on 5 groups of mongrel dogs.
When the pancreatic duct alone was obstructed in the first group of 10 dogs, mild acute pancreatitis, including pancreatic parenchymal edema associated with inflammatory cells, was found during the early stage. During the late stage, however, interlobular and intralobular fibrosis (also called pancreatic fibrosis) were seen.
In a second group of 14 dogs receiving obstructions to both the pancreatic duct and major pancreatic arteries, acute necrotizing pancreatitis, including pancreatic parenchymal necrosis and interlobular fibrosis, was apparent in the early stage. However, pancreatic fibrosis increased and sporadic or collected pancreatic fat replacement was seen in the later stage.
A third group of 10 dogs receiving obstructions to both the pancreatic duct and major pancreatic veins, and a fourth group of 7 dogs receiving obstructions to both the pancreatic duct and pancreatic lymph channels showed pathologic findings similar to the first group.
In a fifth group of 2 dogs with obstructions to the major pancreatic arteries imposed for 1 week after obstruction of the pancreatic ducts for 8 weeks, severe pancreatic fibrosis and fat replacement, similar to chronic pancreatitis in humans, were observed.
The foregoing results indicate that (1) pancreatic ischemia is an important factor influencing the induction of pancreatic fibrosis and fat replacement, and (2) pancreatic fat replacement is caused by chronic pancreatic ischemia.
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Kenji YAMAO, Saburo NAKAZAWA, Yasuo NAITO, [in Japanese], Eizo KIMOTO, ...
1986 Volume 83 Issue 12 Pages
2588-2597
Published: 1986
Released on J-STAGE: December 26, 2007
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Twelve cases of mucous producing pancreatic tumors including five benign tumors were analyzed clinically and histopathologically. They were different from usual pancreatic cancers in age, sex, chief complaint, and the clinical course. Mass survey by ultrasonography was useful for the detection of the dilated pancreatic duct and/or cystic lesion. ERCP was a very effective modality to make the final diagnoses of them. Enhanced CT and angiography were useful for the evaluation of extrapancreatic extension of these tumors and pancreatoscopy for intraductal growth. The pathological study revealed that histological types of these cases were variable. Papillary tumors were seen in the pancreatic duct of all these tumors. Adenoma and hyperplasia were thought to be as precancerous lesion of the mucous producing adenocarcinoma. It is suggested that the mucous producing adenoma and adenocarcinoma may closely relate to mucinous cystadenoma and cystadenocarcinomas from the view of the tumorgenesis. Mucous producing pancreatic tumor may be defined as a group of tumorous lesions which showed widened orifice of papilla of Vater and the dilated main pancreatic duct or cysticaly dilated branches containing mucous. It may not be defined from histopathological findings alone.
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Toru ITANO, Jun TOMODA, Hitoshi HARADA, Koichi UESAKA, Syunsuke KAGAWA ...
1986 Volume 83 Issue 12 Pages
2598-2601
Published: 1986
Released on J-STAGE: December 26, 2007
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Report of a case
Kenji TANEHIRO, Iwao TAKAGI, Kenzo YASUI, Toru KAKUTA, Ryoji SUZUKI
1986 Volume 83 Issue 12 Pages
2602-2605
Published: 1986
Released on J-STAGE: December 26, 2007
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Masayuki HIRAYAMA, Hideo ISHIZUKA, You KAWAMURA, Masahiko TOKORO, Yasu ...
1986 Volume 83 Issue 12 Pages
2606-2611
Published: 1986
Released on J-STAGE: December 26, 2007
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Yukitaka YAMASHITA, Kouzou KAJIMURA, Tooru KAJIYAMA, Takashi TAMADA, A ...
1986 Volume 83 Issue 12 Pages
2612-2615
Published: 1986
Released on J-STAGE: December 26, 2007
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Hiroko MATSUDA, Masahiro MATSUMOTO, Noriaki MIZUSHIMA, Katsutoshi TAMA ...
1986 Volume 83 Issue 12 Pages
2616-2620
Published: 1986
Released on J-STAGE: December 26, 2007
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Masafumi KOMATSU, Shuntaroh SUZUKI, Fumio TOBORI, Hitoshi YAGISAWA, Hi ...
1986 Volume 83 Issue 12 Pages
2621-2625
Published: 1986
Released on J-STAGE: December 26, 2007
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Report of the two Cases
Taketo KATSUKI, Hisashi TANIKAWA, Shingo SATO, Noboru NAKAGAWA
1986 Volume 83 Issue 12 Pages
2626-2629
Published: 1986
Released on J-STAGE: December 26, 2007
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Isao KATO, Hiroshi TSUJI, Eiji KAJIWARA, Takanobu SAKEMI, Koichiro MUR ...
1986 Volume 83 Issue 12 Pages
2630-2634
Published: 1986
Released on J-STAGE: December 26, 2007
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Takayuki MATSUMOTO, [in Japanese], [in Japanese], [in Japanese], [in J ...
1986 Volume 83 Issue 12 Pages
2635
Published: 1986
Released on J-STAGE: December 26, 2007
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Yutaka TAKAHASHI, [in Japanese], [in Japanese], [in Japanese]
1986 Volume 83 Issue 12 Pages
2636
Published: 1986
Released on J-STAGE: December 26, 2007
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Shunji YOSHIMURA, [in Japanese], [in Japanese], [in Japanese], [in Jap ...
1986 Volume 83 Issue 12 Pages
2637
Published: 1986
Released on J-STAGE: December 26, 2007
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Yoshihide SAKAGAMI, [in Japanese], [in Japanese], [in Japanese], [in J ...
1986 Volume 83 Issue 12 Pages
2638
Published: 1986
Released on J-STAGE: December 26, 2007
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Koichi SUDA, [in Japanese], [in Japanese], [in Japanese], [in Japanese ...
1986 Volume 83 Issue 12 Pages
2639
Published: 1986
Released on J-STAGE: December 26, 2007
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Masao ICHINOSE, [in Japanese], [in Japanese], [in Japanese], [in Japan ...
1986 Volume 83 Issue 12 Pages
2640
Published: 1986
Released on J-STAGE: December 26, 2007
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