The incidence of esophageal cancer arising from Barrett's esophagus is relatively highand a relationship between adenocarcinoma of the esophagus and Barrett's metaplasia isgenerally accepted. However, there are many things unknown about the genesis ofBarrett's esophagus. In this study, the genesis of Barrett's esophagus is examined by usingarat model. Also biological character of Barrett's esophagus is examined through theDNA analysis of some clinical cases. In a rat model, a total gastrectomy is performed andan esophagojejunostomy is made, then the esophagus is removed every one month after theoperation to be examined histologically. As a result, Barrett's epithelium arising fromesophagitis is observed at the area apart from the anastomosis in cases more than 4 monthsafter the operation. The DNA analysis of Barrett's esophagus in clinical cases is made by a microfluorophotometric method. The histogram of DNA content is classified into three ploidypatterns, and the DNA pattern of Barrett's esophagus is compared with that of a normaIgastric mucosa, a normal esophagus and a regenerative epithelium of a gastric ulcer andalso with that of a gastric cancer and an esophageal cancer. In Barrett's there are somecases with an aneuploidy or a mosaic pattern which are never observed in a normal mucosaand a regenerative epithelium of a gastric ulcer, and the incident of these abnormalpatterns in Barren's esophagus is Tower than that in cancer. The width of the spread ofDNA content and the ratio of cells with more than 6C of DNA content in Barrett'sesophagus are higher than those in a normal mucosa and a regenerative epithelium of agastric ulcer and lower than thane in cancer. Through these facts it is suggested that the biological character of Barrett's esophagusin malignancy may be between that of a normal mucosa and that of cancer.

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To investigate the clinical safety of glucagon for premeditation of upper gastrointestinal endoscopy, effccts of rntramuscural injection of l mg glucagon on blood glucose, ketoneand gastric peristalsis were evaluated in patierlts(n=33)with NIDDM. Patients subjectedto this study were classified into three groups=diet therapy group(n=6)("D"), oralhypoglycemic agent therapy group(n=19)("S")and insulin therapy grou.p(n=8)("I"). Blood glucose(BG)reached its peak value at 60-120minutes after injection ofglucagon. The peak value of BG and increment from FBG to the peak value of BG afterthe injection of glucagon were in order of"1", "S"and"D"groups. Maximum of the peakvalues of BG was 34amg/dl and maximum of the increments was 138mg/dl among the threegroups. An increase of BG after injection of glucagon in patients with FBG aver 150mg/dl ranged from 134 to 178%. Blood ketone at 120minutes after injection of glucagon tendedto decrease in"S"and"I". Gastric peristalsis was inhibited in 69.7%(23/33)of patients at 10 minutes afterinjection of glucagon. These results indicated that there was little possibility of risk of acute diabeticcomplication by glucagon administration in diabetic patients with"good"or"fair"control.Therefore glucagan can be used in safety far the premedicatian of upper gastrointestinalendoscopy in patients with diabetes mellitus.

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Colonic vascular lesions were studied endoscopically in 49 patients with liver cirrhosiscompared with 50 controls. The characteristic findings of colonoscopy in cirrhotic patientsand their incidence rates were:tree like-dilated vessels, 87.8%; coil like-fine vessels, 34.7%; vascular ectasia-like lesions, 44.9%; rectal varices, 20.4%. The prevalence ofeach finding was significantly higher in cirrhotic patients than controls. There was anassociation between the prevalence of vascular ectasia-like lesions and the presence ofesophageal varices, the degree of esophageal varices, and the presence of portal hypertensive gastropathy. From these findings, it is suggested that a patient having tree like-dilated vessels andat least one of three other findings, coil-like fine vessels, vascular ectasia-like lesions andrectal varices, should be diagnosed as portal hypertensive colopathy. To investigatewhether portal hypertensive colopathy that we defined has a relation to portal hypertension, clinical study was performed prospectively in 71 patients with chronic liver disease.Portal hypertensive colopathy was present in 35 patients, we found that an associationbetween the presence Qf portal hypertensive colopathy and the presence and form ofesophageal varices, and the presence of portal hypertensive gastropathy. These resultssuggest that this colopathy is related with portal hyperten, sion, which could support ourproposal of definition of portal hypertensive colopathy.

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We studied four PBC patients who were positive for HCV antibody and HCV-RNAand compared them with 350rdinary PBC patients, using their laparoscopic and clinicalfindings. The four subjects were all females;their average age of 62 was higher than thatfor HCV-negative subjects, which was 54.6. Laparoscopically, reddish patch and protuberance formation, which are regarded as characteristic of PBC, were noted in 51%and 29%of HCV-negative patients respectively, but in none of the positive sublects. While theincidence of reddish marking was 14%in the negative group, it was present in two of thefour positive patients(50%). The subjects were medically treated with UDCA, which wasexpected to improve hepatic function with no serious side effects. Though interferon didnot disturb the biochemical profile in our present series, the histological evidence suggestedapossible exacerbation of the biliary disorder. Utmost care should thus be taken in theadministration of the agent. The possible complication of hepatic cancer should also bekept in mind in the course on observation.

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A77-year-old male admitted to Kobe National Hospital because of severe dysphagiaand aspiration plleulnonia. He had partial gasrectomy at 620f age and after gasrectomyreflux esophagitis repeated for 15 years. On endoscopic examination, variform mucosalbridges were seen in the esophagus, a membranous mucosai bridge in the middle esophagusand a string-iike shaped mucosal bridge in the lower esophagus. The esophageal lumenwas separated by the mucosal bridge near the EG-lunction. He could not eat, so weremoved the mucQsal bridge with papillotomy k:nife and high fequency current. Soon afterthat he could eat solid foods.

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A 52-year-old female visited to a private clirlic because of fever, sore throat, andodynophagia. As the symptoms were not improved arld she complain.ed of retrosternalpain, she was referred to our hospital to undergo upper gastrointestinal endoscopy. Itshowed vesicle formation and small pounched-out, superficial ulcers and some of the ulcerscoalesced, forming IQngtudinal ulcers. Biopsy specimens taken from the margine of theulcers showed Cowdry type A incusion bodies in the epithelial cells. Although staining ofanti HSV-1 antibody was negative, we diagnosed herpes simplex esophagitis because ofclinical symptornes, endoscopic findings, and raising of viral titer. She was treated withaIltacid and endoscopically the lesions of herpes esophagitis and symptoms were improved.Only 4 cases of herpes esophagitis in otherwise healthy patients including this case, havebeen reported in Japan.

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Two cases of spontaneous intramural hematoma of the esophagus are reported. Caselwas a 67-year-01d female who was admitted to Qur hospital complaining of epigastricpain and hematemesis. Esophageal hematoma was recognized on the posterior wall of theentire esophagus. Case 2-was a 49-year-old female who was admitted to our hospitalbecause of hematernesis. Esophageal hematoma was observed on the right lateral walk ofthe upper esophagus. Both cases had no hemorrhagic tendency and were cured byconservative treatment. Esophageal hematema has been rarefy reperted. In Japan, including our cases, only g cases have been reported.

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The case is a 63-year-old man(at the first examination)who had been suffering fromrheumatoid arthritis from age 28. In 1981, he was hospitalized for melena, but detailedexamination revealed no bleeding source. Thereafter, he repeated hospitalization formelena and in 1985(age 67), colonoscopy revealed multiple irregular ulcers in the terminalileum. Analgesic anti-inflammatory suppository, Diclofenac, which was administratedsince three years ago, was discontinued, and the ulcers were disappeared. In 1991 (age 73), pyrexia and watery diarrhea occurred and colonoscopy revealed small psoudomembranesin the rectum and mutiple maculosus aphthoid lesions having red halo at their circumferances in the sigmoid colon. Gold preparation(aurothiomalate), which was given for the past5years(total 3730mg), was discontinued and subsequently the symptoms disappeared. This patient's colorectal mucous membrane recovered to the normal after administratingVancomycin for two weeks.

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A 63-year-01d female patient was found to be positive with fecal occult blood test.Endoscopic examillation. revealed right-sided ulcerative colitis. She has been treated with3g salazosulfapyridine and her condition has been in remission for approximately threeyears. fight-sided ulcerative colitis is uncommon and there have been only five reports inJapan. This case shows the presence of asymptomatic ulcerative colitis. However, itsincidence, disease history and Position among ulcerative colitis lesions should be furtherstudied.

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To evaluate the efficacy of endoscopic findings after submucosal 20%glucose infectionin diagnosing the depth of invasion of colorectal cancer, 77 cases were analyzed, and thedepth of invasion of the lesion lifted after injection was defined as M'or 5M1', and that ofnot lifted was SM2'and more. The depth of invasion of 62 cases of 681ifted lesions wereSM1'and less(91.2%). The endoscopic features of 4 cases of the other(6)lesions weresubpedunculated polyps. The depth of invasion of g cases of g not lifted lesions were SM2'and more (100%). Sensitivity was 91.2%, specificity 100%, and overall accuracy was 92.2%.Therefore it was concluded that endoscopic findings after submucosal injectionwas practical and useful method far diagnosing the depth of invasion.

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A 43-year-old rnale was introduced to our hospital due to cholecystolithiasis. DIC-CTrevealed a stone of 5mm ill diameter irl the end of the common bile duct. ERCP wasperformed and the papilla vater was shown with redness and swelling. Though wesuspected an illcarcerated stone, carlrlulation into the common bile duct was done verysmoothly and no stolle was detected. However, as soon as we finished the examination, severe epigastric pain and back pain occured, suddenly. We noticed the films showing astone incarcerated into the main pancreatic duct. So, we performed emergent EST alldremoved the stone. Clinical course aftr EST was good, then laparoscopic cholecystectomywas underwent. alld the both were cholesterol stones.

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A 20MHz ultrasonic miniature probe has been proved to be useful in diagnosing thedepth of invasion of superficial esophageal carcinQma. However, as this miniature proberequired adequate amount of water in the lumen, the study was limited on conventional leftlateral decubitus position. In order to fill up the esQphageal lumen with de-aerated water, the llew method with endoscopic balloon on right lateral decubitus position have beenperformed III patiellts who were consisted of forty-five superficial esophageal carcillomacases. As a result, fitip e:ndosonography including entire circumference of the esophagealwall structure was obtailled in 44 of 45 patients(97.8%). This facilitated precise diagnQsison depth of carcinomatous invasion. The results suggested that our simple method wasfound to be useful to obtain total circumferential ultrasound view of esophagus in goodquality. This method also enabled us to perform common endoscopic procedures such aschromoscopy o.r bicapsy without changing or pulling up the initial endoscope once insertedto the esophagus.

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