In order to improve the colonoscopic diagnosis as to the depth of submucosal invasive cancer of the colorectum, we analized the clinicopathological and colonoscopic features of 42 cases of the NPG (non polypoid growth) type submucosal invasive cancer of the colorectum. The cases were categorized into 10 of sm₁ (minimal submucosal invasion), 21 of sm₂ (moderate submucosal invasion), and 11 of sm₃ (severe submucosal invasion) according to the degree of submucosal invasion. Fourteen lesions were located in the rectum, 17 in the sigmoid colon, 5 in the descending colon, 3 in the transverse colon, and 3 in the ascending colon and the cecum. The mean±SE size of the NPG type submucosal invasive cancers was 11.6±1.6 mm in sm₁, 11.9±0.8 mm in sm₂ and 21.7±1.7 mm in sm₃, respectively. The lesions of sm₃ were significantly larger than those of sm₁ and sm₂ (p< 0.01). Nineteen of 21 cases of sm₁ and sm₃ cancers showed flat elevated lesions or distinct depressed lesions surrounded by marginal elevation, but 7 of 21 sm₂ cancers showed dome-like protruded lesions in their cross-section view. Colonoscopically, the marginal elevation of the mucosa surrounding the depressed area was normal in 5 of 10 lesions of sm₁, 15 of 21 lesions of sm₂ and 7 of 9 lesions of sm₃. White spots were found in 3 of 10 lesions of sm₁, 8 of 21 lesions of sm₂ and 6 of 9 lesions of sm₃. Abnormal fine vessels on the cancerous mucosa were demonstrated in 4 of 10 lesions of sm₁, 15 of 21 lesions of sm₂ and 5 of 9 lesions of sm₃. In summary, total evaluation of the findings on the size, their cross-section view (depressed, flat elevated, or dome-like protruded lesions), the elevated marginal mucosa surrounding the depressed area, white spots, and abnormal fine vessels on the cancerous mucosa gives us the exact colonoscopic diagnosis as to the degree of submucosal cancerous invasion.

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Conventional ultrasonography (US), abdominal computed tomography (CT), endoscopic ultrasonography (EUS) and intraductal ultrasonography (IDUS) were performed for 23 cases of intraductal papillary tumor (IDT) of the pancreas. On the basis of the histopathological analysis of 28 cases of resected IDT, criterion for differential diagnosis by imaging modalities was defined as follows : hyperplasia lucking wall thickening or nodule, adenoma having a nodule or wall thickening under 3mm, intraductal cancer having a nodule or wall thickening over 4mm, or a cyst filled with tumor, intraductal cancer with pancreatic parenchymal invasion having a mass with a mixed patterns (high and low internal echo patterns) or interruption of the pancreatic duct wall by tumor invasion. With this criterion, US and CT showed high specificity, but low sensitivity in the differential diagnosis of IDT. However, EUS and IDUS revealed high sensitivity and diagnostic accuracy for the differential diagnosis of neoplastic and non-neoplastic lesions. They also showed high diagnostic accuracy for differential diagnosis of benign and malignant tumors, and invasive and non-invasive lesions. Thus EUS and IDUS are considered to contribute much to the choice of the treatment of the IDT.

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We evaluated color flow images of ten esophageal variceal patients and nine gastric variceal patients by endoscopic ultrasonography (EUS) using Power Doppler by comparison with endoscopic color Doppler ultrasonography (color Doppler). EUS using Power Doppler was better than color Doppler in the capability of depicting variceal blood flow. It was difficult to depict variceal color flow images having different velocities via color Doppler. On the other hand, we could detect variceal color flow images graphically via Power Doppler. However, it was impossible to visualize the direction of blood flow in varices and perforating veins. We conclude that EUS using Power Doppler is a useful modality to evaluate the hemodynamics of esophago-gastric varices.

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42-year-old female patient, who had been diagnosed to have giant rugae gastritis since the age of 35, was admitted to our hospital because of iron deficiency anemia (hemoglobin content of 1.9 g/dl, serum iron level 16, ug/dl) and hypoproteinemia (total protein 3.6 g/dl). Huge gastric folds were observed on radiography and endoscopy. Endoscopic ultrasonography demonstrated the huge folds conprizing the thickened second and third layers of the gasrric wall, accompanied by small cystic components. Protein loss from the stomach was confirmed by scintigram using 99mTc-DTPA-HSA. The histology obtained by endoscopic resection of the gastric folds revealed massive hyperplasia of the f oveolar epithelium with cystic dilation of the glands, consistent with Menetrier's disease. After oral administration of f amotidine 40mg daily, the levels of homoglobin and serum protein became normal, although there was no significant change on the giant folds.

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We report two cases of angina pectoris having appeared after the endoscopic resection of the gastric mucosa (ER). The first case is a 80-year-old man, who was performed ER for an early gastric cancer. He complained of chest pain 4 days after ER, and the chest pain was relieved by sublingual administration of nitroglycerin tablet. Standard deviation of all sinus RR intervals over 24 hours, which is thought to show the state of the cardiac autonomic nervous activity, decreased after ER. The second case is a 58-year-old man, who had a non-obstructive hypertrophic cardiomyopathy, was performed ER for gastric adenoma. Chest pain appeared 4 days after the ER and it was relieved by sublingual treatment of nitroglycerin. Standard deviation of all sinus RR intervals over 24 hours decreased, and both spectral analysis and circulating levels of free norepinephrine showed that the sympathetic nervous activity seemes to be activated by the treatment of ER, which might cause vasospastic angina pectoris particularly in the patients with cardiac diseases.

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A 25-year-old woman was consulted to our hospital complaining of epigastric pain. Laboratory data showed hypoproteinemia. Upper gastrointestinal endoscopic examination revealed enlarged gastric folds and multiple nodular lesions covered by white coat in the body and fornix of the stomach, consistent with diffuse varioliform gastritis. After administration of lansoprazole, epigastric pain was improved but hypoproteinemia continued. Helicobacter pylori was positive by culture of the gastric mucosa. We diagnosed hypertrophic lymphocytic gastritis associated with protein-losing gastropathy according to histological and endoscopic examination of the stomach. After getting the informed consent, eradication therapy of Helicobacter pylori was performed. Then, serum total protein was normalized and abnormal findings of endoscopic and histological examination of the stomach was improved. Lymphocytic gastritis is a histological entity characterized by diffuse infiltration of small lymphocytes into the surface and foveolar gastric epith-elium. There are a few case reports of lymphocytic gastritis in Japan.

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A 51-year-old female with idiopathic portal hypertention (IPH) was admitted to our hospital with complaints of hematemesis and tarry stool. Emergent esophagogas-troduodenoscopy revealed varices in the second portion of the duodenum, on the top of which a fibrin plug was demonstrated. From this finding, rupture of duodenal varices was confirmed. The varices were treated twice by endoscopic injection sclerotherapy (EIS) with N-butyl-2-cyanoacrylate (Histoacryl). After EIS, no further bleeding occurred. Her clinical course was uneventful without any significant complications related to this the-apy.

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A 22-year-old female, nurse, was introduced and admitted to our hospital complaining of abdominal pain, bloody diarrhea, and fever. The diagnosis was the first onset of severe pancolitis (ulcerative colitis : UC) by barium enema X-ray study and endoscopic examina-tion etc. Because she worried about side effects of medical drugs such as corticosteroids and salazosulfapyridine, she wanted to be treated by leukocytapheresis (LCAP) first. Thus she was treated by this new therapy "LCAP" alone after informed consent. LCAP was performed with the Plasauto 2500 apheresis unit equipped with a Cellsorba (Asahi Medical Co. Ltd., Tokyo, Japan) leukocyte removal filter. Three thousand milliliters of whole blood were processed at a blood flow rate of 50 ml/min. LCAP was performed once weekly for 5 weeks as intensive therapy and once every 2 to 4 weeks as maintenance therapy. After the first session of the therapy, abdominal pain and fever disappeared. Her diarrhea also disappeared and the frequency of bowel habit decreased to 1-2 times/day after 3 sessions of LCAP from more than 7 times/day before LCAP. Endoscopic evaluation revealed remission after 7 sessions of LCAP without any drugs throughout this therapy and no deterioration was noted after the initiation of oral feeding. This suggests that LCAP alone may be effective to treat patients with the first onset of UC.

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A 59-year-old woman who had persistent right abdominal pain and diarrhea for nine months was admitted to Higasisumiyoshi Morimoto Hospital in April, 1995. A plain abdominal x-ray film revealed tubular calcification in the vascular wall of the right hemi -colon. Barium enema examination showed sclerosis of the colonic wall and irregular thumb-printing sign of the right hemi-colon. Colonoscopic examination showed marked blue-purple colored mucosa and irregular ulcer of the right hemi-colon. The operation was done with a preoperative diagnosis of progressive and irreversible ischemic colitis. Histopathological examination of the obtained specimen disclosed ischenic intestinal lesion caused by phlebosclerosis.

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The patient is an 82-year-old man. He was referred to our hospital for colpnoscopic examination due topositive stool occult blood on periodic health examination. When the descending colon was being examined under direct visual control, the mucosa turned whitely in all of a sudden in a longitudinal axis and bubble formation was seen. At the same site numerous millet grain sized minute white elavations were appeared. Later the mucosa changed in color from white to red. On the third day, longitudinal erosions were noted. Based on these findings, a diagnosis of acute ischemic colitis was made. Not only decrease in blood flow but also reperf ution has important implications with respect to the occurrence of an ischemic lesion. It appears that ischemia occurred when the mucosa turned white in color during colonoscopic examination and that reperf ution occerred when the mucosa changed color from white to red later. A view of the literatures revealed few reference to rapid .mucosal color changes from white to red occurring during colonoscopic examination.

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We report a case of arteriovenous malformation of the lower rectum which is very rare in location and in age. A 13-year-old girl who had no genetic abnormality, was admitted to the First Department of Surgery of Yamanashi Medical University with the chief complaint of massive rectal bleeding. Colonoscopy was performed two days after admission, demon-strating a reddish elevated lesion with blood clot in the lower rectum. On 9 days after admission, colonoscopy showed that the elevated lesion was enlarged and entirely reddish. Endoscopic ultrasonography revealed a hypoechoic lesion which was 5mm in size in the mucosal to submucosal layer. It was diagnosed as arteriovenous malformation of the rectum, and endoscopic resection was performed. Histological examination of the resected specimen confirmed the collection of thick-walled, slightly ectatic veins in the mucosal and submucosal layer. Some arteries were shown to coexist. At the surface of the mucosal layer, the artery was ruptured with thrombosis. After endoscopic resection, she had an uneventful course, passing no more blood per rectum during the subsequent 3-year period.

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A 53-year-old female was admitted to our hospital for close examination of a gallblad-der tumor. On admission, a pedunculated lesion with a nodular surface was detected on the body of the gallbladder by US and EUS. During ERCP, detachment of some parts of the polypoid lesion by compression was observed. US performed the following day demonstrat-ed a few small, isoechoic lesions around the tumor. Surgery revealed a tumor detached into several pieces. Pathological study verified a tubular adenoma with mild atypia.

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We experienced 5 cases of superficial colorectal tumor that were defficult to perform EMR. Five cases include II a, II a+II c, and LST. All these tumors had been previously performed endoscopic biopsy. On the next endoscopic study to perform EMR, tumors accompanied converging folds or depression which formerly not seen. They all had non-lifting sign. Surgical resection was carried out in 1 case and EMR in 4 seses. Pathological-ly all 4 specimens of EMR cases contained proper muscle layer to some extent and perforated in 1 case. The tumors were intramucosal carcinoma in 1 case, adenoma in 4 cases. Hawever all 5 tumors were intramural lesions, they all had remarkable fibrous change in the submucosal layer. That change made EMR defficult and might have been the result of former biopsy procedure. We conclude that biopsy should not be carried out before EMR if the colorectal tumor is superficial and submucosal invasion is unlikely on endoscopic finding.

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Recently in diagnosing of pancreatic cancer, endoscopical pancreatic biopsy and brushing cytology have been performed. We developed an originally deviced cytology brush which has 2.4 mm in diameter and 220cm in effective length allows to insert into the cannula for peroral micropancreatoscopy. This brushing can be carried out through the cannula after peroral micropancreatoscopy. We compared the rate of positive diagnosis of pancreatic cancer in 15 patients for the endoscopical pancreatic biopsy (43%), the ordinary cytology brush (60%) and our cytology brush (80%). It is suggested that our cytology brush is very useful for the diagnosis of pancreatic cancer.

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