We studied arterial oxygen desaturation, using a pulse oximeter, in 132 patients undergoing diagnostic upper gastrointestinal endoscopy to obtain predictive factors of the change. The baseline arterial oxygen saturation (SaO2) level was 98.8+/- 1.2%. During the procedure, oxygen desaturation (SaO2>95%) was found in 90.2% of the patients, Mild oxygen desaturation (95>SaO2>90%) was found in 9.8% of the patients, and there was no severe oxygen desaturation(SaO2<90%). Age(P=0.52), gender(P =0.48), smoking(P =0.71), body mass index(P =0.32), and endoscopy time(P = 0.68) was not related to the degree of oxygen desaturation. These results suggest that oxygen desaturation, which may rarely induce serious cardiopulmonary events, is not frequently observed during non-sedated diagnostic upper endoscopy.
Endoscopy ; Endoscopy, Gastrointestinal* ; Humans ; Oxygen*

Retrospective studies of duodenal polyps have shown a prevalence of 0.3-4.6% in patients referred to upper gastrointestinal endoscopy, and histologic classification have been inconsistent. A prospective consecutive study was carried out in 3,871 patients referred to diagnostic endoscopy, Sixteen patients had polyps in the first part of duodenum, for a prevalence 0.41%(0.28-0.53%, 95% confidence interval). Fourteen polyps were either inflammatory(thirteen polyps) or ectopic gastric mucosa(one polyp). Two hyperplasitc polyps were founded. All polyps were benign and sessile, and most of polyps(75%) were solitary.
Classification ; Duodenum ; Endoscopy* ; Endoscopy, Gastrointestinal ; Humans ; Polyps* ; Prevalence* ; Prospective Studies

Background/Aims: Pancreatitis is one of the major complications of ERCP. The purpose of this study is to evaluate the incidence rate and risk factors of ERCP- induced pancreatitis. Method: We analysed 99 consecutive patients(45 males and 44 females) undergoing ERCP from March to September, 1994. The level of serum amylase was measured and clinical assessment of pancreatitis was performed before, 24 hour, 48 hour, and 72 hour after ERCP. We defined clidical pancreatitis as combination of elevated amylase level over 2 days with abdomial pain and tenderness.(continue..)
Amylases ; Cholangiopancreatography, Endoscopic Retrograde* ; Humans ; Incidence ; Male ; Pancreatitis* ; Risk Factors

Leiomyosarcoma of small intestine is an uncommon tumor, comprising less than 20 percent of all primary malignant tumors of small intestine. Duodenal leiomyosarcoma is rare disease which amount to about 20 percent of all small bowel malignancy but potentially curable tumors often diagnosed at an advanced age, so its five-year survival following resection approximates 50% in reported series. Recently, several cases of leiomyosarcomas of duodenum were diagnosed by hypotonic duodenograhy in Korea. We experienced a woman with duodenal leiomyosarcoma that was diagnosed by endoscopic duodenal biopsy and received currative resection of the tumor(Whipple's operation). We report the case with review of the literatures.
Biopsy ; Duodenum ; Endoscopy ; Female ; Humans ; Intestine, Small ; Korea ; Leiomyosarcoma* ; Rare Diseases

Primary sclerosing cholangitis is a chronic disease of unknown cause, characterized by inflammation and fibrosis of the biliary tree with diffuse multifocal stricture formation. With increasing knowledge of primary sclerosing cholangitis, it is now recognized that in the setting of inflammatory bowel disease, cholangiocarcinoma is a complication of primary sclerosing cholangitis. We recently experienced a case of 41 year old female patient who had Crohns disease associated with primary sclerosing cholangitis and cholangioearcinoma. We report a case of primary sclerosing cholangitis with cholangiocarcinoma with literature review.
Adult ; Biliary Tract* ; Cholangiocarcinoma* ; Cholangitis, Sclerosing* ; Chronic Disease ; Constriction, Pathologic ; Crohn Disease ; Female ; Fibrosis ; Humans ; Inflammation ; Inflammatory Bowel Diseases ; Pancreas*

Intraluminal duodenal diverticulum (IDD) is a rare congenital abnormality, consisting of a sac-like mucosal lesion in the duodenum. Cases of IDD can present with gastrointestinal bleeding, duodenal obstruction, or pancreatitis. Here, we report a rare case of a 25-year-old female presenting with IDD complicated by duodeno-duodenal intussusception and recurrent pancreatitis. The diagnosis was based on findings from radiologic examinations (CT and MRI), upper gastrointestinal series (barium swallow), and gastroduodenofiberscopy. Laparoscopic excision of the presumed duodenal duplication was performed. The subsequent histopathologic evaluation of the excised sac revealed normal mucosa on both sides, but the absence of a proper muscle layer confirmed the diagnosis of IDD. Radiologic detection of a saccular structure in the second portion of the duodenum can indicate IDD with duodeno-duodenal intussusception as the lead point

A choledochocele is a benign cyst-like herniation of the intramural segment of the distal common bile duct protruding into the duodenal lumen. Cholangiography is essential to demonstrate a choledochocele. Because choledochoceles are often associated with characteristic structual alterations of the papilla of Vater and the peripapillary area, ERCP is helpful in demonstrating a choledochocele. We present the clinical, endoscopic and radiographic (ERCP) findings in a patient with choledochocele.
Cholangiography ; Cholangiopancreatography, Endoscopic Retrograde ; Choledochal Cyst* ; Common Bile Duct ; Humans

A choledochocele is a benign cyst-like herniation of the intramural segment of the distal common bile duct protruding into the duodenal lumen. Cholangiography is essential to demonstrate a choledochocele. Because choledochoceles are often associated with characteristic structual alterations of the papilla of Vater and the peripapillary area, ERCP is helpful in demonstrating a choledochocele. We present the clinical, endoscopic and radiographic (ERCP) findings in a patient with choledochocele.
Cholangiography ; Cholangiopancreatography, Endoscopic Retrograde ; Choledochal Cyst* ; Common Bile Duct ; Humans

BACKGROUND: There is an increased prevalence of peptic ulcer disease in patients with liver cirrhosis, but the role of Helicobacter pylori is unclear. METHOD: IgG antibodies against H. pylori were measured in 30 patients with compensated liver cirrhosis, in 30 sex- and age-matched patients with decompensated liver cirrhosis, and 30 normal controls. All patients underwent a panendosocpic examination in order to search for the evidence of esophageal varices, congestive gastropathy, and peptic ulcers. RESULTS: Duodenal ulcers were more common in compensated and decompensated cirrhotic patients (13.3% and 13.3%, respectively) than in the normal controlled group (6.7%, p<0.05). The prevalence of H. pylori was not statistically different among the three groups (normal 63.3%, compenstated 63.3%, and decompensated, 70.0%; p > 0,05). The prevalence of H. pylori also showed no statistical differences in respect to duodenal ulcers (100%, 75%, and 75%, repectively, p>0.05) or gastric ulcers (100%, 100%, and 60%, respectively, p >0.05). The prevalence of an H. pylori infection did not differ significantly in relation to the presence or absence of esophageal varices or of congestive gastropathy. In cirrhotic patients with peptic ulcers, the prevalence of H. pylori was lower in the presence of esopahgeal varices (60.0% vs 100% if without varices, p=0.04) and in the presence of congestive gastropathy (50.0% vs 88.9% p=0.03). CONCLUSIONS: The prevalence of peptic ulcer was increased in cirrhotic patients, but the prevalence of H. pylori was similar in compensated cirrhotic patients, decompensated cirrhotic patinets, and in the normal controlled group. The frequency of non-H. pylori associated with peptic ulccrs in cirrhotic patients was increased in the presence of an esophageal varix or a congestive gastropathy.
Antibodies ; Duodenal Ulcer ; Esophageal and Gastric Varices ; Estrogens, Conjugated (USP) ; Helicobacter pylori* ; Helicobacter* ; Humans ; Immunoglobulin G ; Liver Cirrhosis ; Peptic Ulcer* ; Prevalence ; Prospective Studies* ; Stomach Ulcer ; Varicose Veins

BACKGROUND: Impairment of relaxing response and augmentation of contractile response to vasoactive substances have been reported in atherosclerotic arteries. These alterations in vascular reactivity are considered as an underlying mechanism for the development of acute vasospasm in atherosclerotic coronary artery. Recently, it has been reported that lysophophatidylcholine (LPC), an oxidative metabolite of low density lipoprotein causes this functional abnormality. However, the precise mechanism of LPC induced change of vascular reactivity is still uncertain. METHOD: In this study, to elucidate the underlying mechanisms of abnormal vascular reactivity in atherosclerotic coronary artery, we examined the effect of LPC on whole cell K+current using patch clamping technique in rabbit coronary smooth muscle cells. RESULTS: Application of LPC(1microM) showed dual effect on whole cell outward current which depends on the magnitude of test potentials. At relatively high depolarizing test potentials (> 10 mV), LPC increased amplitude of outward current which was blocked by Gd3+ not by iberiotoxin (100 nM) and TEA (1 mM). Reversal potential of this Gd3+sensitive, LPC-induced current was -9.7 +/- 0.6 mV. At less depolarizing test potentials (< 10 mV), LPC decreased whole cell K+currents in a dose dependent manner (from 0.01 to 10 microM) in the range of -30 mV to +0 mV. Half maximal inhibition of K+current was 1.509 microM at 0 mV test potential (n =5). Depolarizing holding potential (0 mV) prevented this LPC-induced inhibition of K+current. Steady state activation and inactivation parameters of K+current were significantly shifted to the positive direction by application of LPC (p < 0.01, n =8). Pretreatment of staurosporine (100 nM), a blocker of protein kinase C partially blocked LPC-induced decrease of K+currents. CONCLUSION: LPC-induced inhibition of voltage dependent K+current may explain abnormal vascular reactivity in atherosclerotic coronary artery.
Arteries ; Constriction ; Coronary Vessels ; Lipoproteins ; Lysophosphatidylcholines* ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Protein Kinase C ; Staurosporine ; Tea