Effects of a kefir supplement on symptoms, colonic transit, and bowel satisfaction score in patients with chronic constipation: a pilot study.

BACKGROUND/AIMS: Although probiotics have been extensively studied in irritable bowel syndrome, data on the impact of probiotics on chronic constipation are scarce. We aimed to evaluate the effects of kefir, which is a probiotic fermented milk product, on the symptoms, colonic transit, and bowel satisfaction scores of patients with chronic constipation. MATERIALS AND METHODS: Twenty consecutive patients with functional constipation according to the Rome II criteria were divided into two groups based on their colon transit studies: 1. The normal transit (NT) group (n=10); and 2. The slow transit (ST) group (n=10). After a baseline period, 500 mL/day of a probiotic kefir beverage was administered to all patients for 4 weeks. Defecation parameters (stool frequency, stool consistency, degree of straining, laxative consumption) were recorded in diaries daily by the patients. Bowel satisfaction scores were assessed using a visual analog scale. The colon transit study was repeated in the ST group at the end of the study. RESULTS: At the end of the study, the patients showed an increased stool frequency (p<0.001), improved stool consistency (p=0.014), and decreased laxative consumption (p=0.031). The degree of straining during evacuation showed a tendency to improve after kefir administration; however, this was not statistically significant (p=0.18). A repeat transit study showed an acceleration of colonic transit in the ST group (p=0.013). Bowel satisfaction scores also improved (p<0.001). CONCLUSION: This pilot study shows that kefir has positive effects on the symptoms of constipation. Our results also suggest that kefir improves bowel satisfaction scores and accelerates colonic transit. Controlled trials are warranted to confirm these findings.

Xanthogranulomatous pancreatitis treated by duodenum-preserving pancreatic head resection.

BACKGROUND: Xanthogranulomatosis is an idiopathic, rare process in which lipid-laden histiocytes are deposited at various locations in the body. We present two cases who were treated by duodenum-preserving pancreatic head resection and eventually diagnosed as having xanthogranulomatous pancreatitis. METHODS: A 30-year-old caucasian man was admitted to our clinic for vague abdominal pain and epigastric dullness. Magnetic resonance cholangiopancreatography and endoscopic retrograde pancreatography suggested the existence of chronic pancreatitis. Another 34-year-old caucasian woman was admitted to our clinic because of right upper quadrant pain. Magnetic resonance cholangiopancreatography demonstrated a dilatation and stone of the main pancreatic duct. Based on a diagnosis of chronic pancreatitis, pancreatic head resection was planned and a laparotomy was performed in both of cases. RESULTS: In both cases, duodenum-preserving pancreatic head resection was performed. Macroscopic and microscopic findings revealed xanthogranulomatous inflammation, which led to a diagnosis of xanthogranulomatous pancreatitis. CONCLUSION: Although this type of pancreatitis is extremely rare, it is important to keep it in mind for a differential diagnosis because it may simulate chronic pancreatitis or a malignant tumor on imaging.

Macrophage migration inhibitory factor expression and MIF gene -173 G/C polymorphism in nonalcoholic fatty liver disease.

AIM: To investigate the macrophage migration inhibitory factor (MIF) expression and -173 G/C polymorphism of the MIF gene in nonalcoholic fatty liver disease (NAFLD). METHOD: Ninety-one patients with diagnosis of NAFLD and 104 healthy controls were included in the study. MIF -173 G/C polymorphism was detected using the PCR-restriction fragment length polymorphism based method. NAFLD was stratified as nonalcoholic steatohepatitis (NASH), probable NASH and steatosis, respectively in groups 1, 2 and 3, according to NAFLD Activity Score. MIF expression was detected by immunohistochemistry staining. RESULTS: Mean age of the patients was 50.1+/-9.6 years, and 54 of them were male. Serum alanine aminotransferase and aspartate aminotransferase were 50/83, 42/63 and 31/32, respectively in groups 1, 2 and 3, (P<0.05). Both the MIF expression of hepatocytes and mononuclear cells were more prominent in groups 1 and 2 than group 3. There was no correlation between MIF expression of hepatocytes and fibrosis stage. However, MIF expression of mononuclear cells significantly increased according to fibrosis stage (P<0.05, R : 0.2). There was no significant correlation between MIF genotype and MIF expression in the liver. CONCLUSION: MIF expression is significantly increased especially by mononuclear cells in liver tissue of patients with NASH secondary to inflammation. Thus, it should be considered as a consequence not a causal factor.

Inhibition of renin-angiotensin system in experimental acute pancreatitis in rats: a new therapeutic target?

OBJECTIVE: Pancreatic renin-angiotensin system has been implied to play a role in the regulation of pancreatic functions and could be a new therapeutic target in acute pancreatitis. The aim of this study was to evaluate the therapeutic potential of angiotensin-converting-enzyme inhibition by captopril and angiotensin II type 1 receptor inhibition by L-158809 and losartan experimentally in acute pancreatitis. DESIGN: Rats were randomly divided into 15 groups. Acute edematous pancreatitis was induced by injection of cerulein 20microg/kg SC four times at hourly intervals. Severe necrotizing pancreatitis was induced by retrograde injection of 3% taurocholate into the biliary-pancreatic duct. INTERVENTIONS: Captopril, L-158809 and losartan were given intraperitoneally. Main outcome features: pancreatic pathology, pancreatic myeloperoxidase activity and serum amylase activity were assessed. RESULTS: Captopril decreased serum amylase (10,809+/-1867 vs. 4085+/-1028U/L, p<0.01), myeloperoxidase activity (3.5+/-0.5 vs. 1.5+/-0.1, p<0.05) and histopathological score (5.0+/-0.4 vs. 1.1+/-0.5, p<0.01) in acute edematous pancreatitis. In taurocholate induced severe necrotizing pancreatitis captopril ameliorated histopathological score (10.1+/-1.2 vs. 3.4+/-0.5, p<0.01), pancreatic parenchymal necrosis (4.5+/-0.6 vs. 0.0+/-0.0, p<0.001), fatty necrosis (2.8+/-0.9 vs. 0.1+/-0.1, p<0.01) and edema (2.1+/-0.3 vs. 1.4+/-0.3, p<0.05). However, L-158809 did not have similar beneficial effects on acute pancreatitis in rats while losartan decreased pancreatic parenchymal necrosis and neutrophil infiltration. CONCLUSIONS: This study not only demonstrated the differential effects of captopril, losartan and L-158809 in acute pancreatitis but also showed that there is still much to investigate about pancreatic renin-angiotensin system. Inhibition of angiotensin-converting enzyme should be evaluated carefully as a potential new therapeutic target in acute pancreatitis.

Common SPINK-1 mutations do not predispose to the development of non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is common in obese and diabetics. Serine protease inhibitor Kazal-1 (SPINK-1) protein is highly expressed in the liver and adipose tissue of diabetic and obese suggesting its role in NAFLD. SPINK-1 also behaves as an acute phase reactant protein. Some genetic factors including the genetic variations in SPINK-1 protein have been linked to chronic pancreatitis and diabetes. We therefore hypothesized that SPINK-1 mutations might be a risk factor for the development of NAFLD. METHODS: Liver biopsy proven fifty NAFLD cases (20 steatohepatitis, 30 diffuse fatty liver disease and 44 healthy controls were included to the study. Liver function tests were measured. Body mass index was calculated. Insulin resistance was determined by using a homeostasis model assessment (HOMA-IR). Ultrasound evaluation was performed for each subject. Common genetic mutations in the third exon of SPINK-1 gene were analyzed by direct sequencing method. RESULTS: We found two cases with a SNP at N34S location in NAFLD group (allele frequency %4). One subject with diffuse fatty liver disease and other with liver cirrhosis due to NAFLD had N34S mutation. No SNPs were detected in healthy controls. In conclusions, in limited number of patients SPINK-1 mutations were not considered as a risk factor alone for NAFLD development.

Diagnostic value of serum procalcitonin in determining the activity of inflammatory bowel disease.

BACKGROUND/AIMS: Procalcitonin and C-reactive protein are two acute-phase reactant proteins, although procalcitonin is a more specific marker for bacterial infections. Procalcitonin level might also be helpful to predict the disease activity of inflammatory bowel disease. This study aimed to compare the diagnostic value of serum procalcitonin and C-reactive protein as indicators of disease activity in inflammatory bowel disease. METHODS: Patients admitted to the inflammatory bowel disease inpatient clinic with suspected inflammatory bowel disease who had not yet been treated with immunosuppressive treatments were included. Disease activity, white blood cell count, sedimentation rate, serum procalcitonin and C-reactive protein levels were evaluated in 45 newly diagnosed inflammatory bowel disease patients (9 Crohn's disease and 36 ulcerative colitis). Fifty healthy volunteers were analyzed as a control group. RESULTS: Crohn's disease patients had higher procalcitonin and C-reactive protein levels than healthy controls (Procalcitonin: 0.143+/-0.081 vs. 0.065+/-0.008 ng/ml, p<0.05; C-reactive protein: 29+/-7.5 vs. 2.9+/-0.5 mg/dl, p<0.001, respectively). Ulcerative colitis patients also had slightly higher procalcitonin levels and significantly higher C-reactive protein levels than controls (Procalcitonin: 0.107+/-0.042 ng/ml; C-reactive protein: 23+/-5.5 mg/dl). Two Crohn's disease patients had procalcitonin value above 1 ng/ml. Receiver operating characteristic curve analysis demonstrated that C-reactive protein is the best marker of disease activity in inflammatory bowel disease while procalcitonin has low sensitivity and specificity. Serum procalcitonin levels were highly correlated with serum C-reactive protein but no other disease activity parameters. CONCLUSIONS: Although still within normal ranges, procalcitonin levels were slightly elevated in Crohn's disease but not in ulcerative colitis patients compared to healthy controls. Serum C-reactive protein is a reliable marker for disease activity in inflammatory bowel disease. Procalcitonin has no diagnostic value in determining disease activity.

Living donor liver transplantation for hepatitis B cirrhosis.

BACKGROUND AND AIM: Living donor liver transplantation (LDLT) has particular advantages for Turkey where hepatitis B virus (HBV) infection is the most common cause of cirrhosis, both because LDLT circumvents the difficulties encountered in the emerging world in providing deceased donor organs, and because it allows preemptive antiviral therapy. The aim of this study was to review one institution's experience with LDLT in patients with chronic HBV infection. METHODS: A total of 109 patients with chronic HBV infection underwent LDLT between September 1999 and June 2005, of whom 40 were coinfected with hepatitis D virus and 23 had hepatocellular carcinoma. Antiviral prophylaxis was attempted in all, beginning prior to transplantation with lamivudine or adefovir, and continuing after transplantation with low dose intramuscular hyperimmune B immunoglobulin (HBIg) plus lamivudine or adefovir. RESULTS: In a median follow up of 20 months (range 1-66 months), there was no donor mortality. One-year recipient survival was 90%, and in total 16 recipients died. None of the deaths was related to HBV. Recurrence of HBV infection was detected by reappearance of serum hepatitis B surface antigen in six patients (5.5%) at 5, 8, 12, 17, 34 and 46 months after transplantation, respectively. There was no influence of donor hepatitis B core antibody status on the likelihood of recurrence of HBV in the allograft. CONCLUSION: The results indicate that LDLT with antiviral treatment and low dose HBIg provides excellent results for donors and recipients.

Comparison of 1- and 2-week pantoprazole-based triple therapies in clarithromycin-sensitive and resistant cases.

BACKGROUND: The objectives of this prospective study were: (i) to compare the efficacy of 1-week with 2-week pantoprazole-based triple therapy and (ii) to evaluate the impact of clarithromycin resistance on Helicobacter pylori (H. pylori) eradication rates. METHODS: Eighty dyspeptic patients were randomly allocated to two groups. The first group (PAC-1, n=40) received pantoprazole 40 mg, amoxicillin 1000 mg, and clarithromycin 500 mg twice a day for one week, and the second group (PAC-2, n=40) received the same regimen for two weeks. Endoscopy was repeated one month after the end of the treatment. RESULTS: DNA extraction for clarithromycin resistance could not be performed in seven cases. Five cases were lost to follow-up. Clarithromycin resistance was found to be 44.1% (15/34) in the PAC-1 group and 58.8% (20/34) in the PAC-2 group (p>0.05). Eradication was achieved in 16 (PP: 47.1%, ITT: 44.4%) and 25 (PP:73.5%, ITT: 67.6%) patients in the PAC-1 and PAC-2 groups, respectively (p>0.05). H. pylori was eradicated in 4 of 15 (PP: 26.7%, ITT: 26.7%) clarithromycin-resistant patients in the PAC-1 group and in 12 of 20 (PP: 60%, ITT: 60%) clarithromycin-resistant patients in the PAC-2 group (p>0.05). Among the clarithromycin-sensitive ones, eradication was achieved in 12 of 19 (PP: 63.2%, ITT: 57.1%) patients in the PAC-1 group and in 13 of 14 (PP: 92.8%, ITT: 76.5%) patients in the PAC-2 group (p>0.05). CONCLUSION: Although the 2-week regimen of pantoprazole-based triple therapy was effective for H. pylori eradication in clarithromycin-sensitive cases, highly effective H. pylori eradication protocols are needed for clarithromycin-resistant ones.

High Helicobacter pylori resistance rate to clarithromycin in Turkey.

GOALS: To assess the resistance of Helicobacter pylori to clarithromycin in Turkey. BACKGROUND: Recent studies have emphasized the remarkable reduction in H. pylori eradication rates. Resistance to clarithromycin is the most important factor affecting the success of H. pylori eradication therapies. STUDY: The study involved 110 consecutive adult dyspeptic patients infected with H. pylori. Resistance to clarithromycin was studied by real-time polymerase chain reaction method on gastric biopsy specimens. RESULTS: Of the 110 patients, 56 (50.9%) were male and mean age (+/-SD) was 45.1+/-13.1 years. Overall, 53 (48.2%) patients were found to be resistant to clarithromycin. Resistance to clarithromycin was not statistically associated with age, sex, previous macrolide use, residence (urban/rural), education status, and presence of peptic ulcer. CONCLUSIONS: The rate of resistance to clarithromycin was found to be markedly high. This result may explain the recently reported low success rates of H. pylori eradication therapies with clarithromycin.

Adefovir dipivoxil alone or in combination with lamivudine for three months in patients with lamivudine resistant compensated chronic hepatitis B.

We studied clinical and laboratory effects of 3 months of lamivudine with adefovir combination and adefovir dipivoxil (AD) alone in the treatment of patients with lamivudine-resistant hepatitis B virus (HBV) infection. Eligible patients were hepatitis B surface antigen-positive men and women with compensated liver disease who were given lamivudine at least more than 6 months and had HBV polymerase gene mutation. Patients were assigned to receive adefovir 10 mg/day (Group 1) or adefovir 10 mg once daily and lamivudine 100 mg once daily combination during first 3 months, and then stopped lamivudine and continued adefovir (Group 2). Median age was 48 years (34 males and 20 females, and 35 were HBeAg-negative). Baseline median ALT, AST, and HBV DNA levels were 66 IU/l, 49 IU/l, and 6.7 log(10) copy/ml, respectively. Median adefovir therapy time and ALT normalization time were 9 and 3.5 months, respectively. There was no significant difference between groups according to the baseline HBV DNA, ALT, HBe Ag status, age, gender, and lamivudine resistance time. Virological and biochemical responses were similar in both groups during therapy. Two patients (8%) had ALT flare more than five times upper limit of normal without any clinical decompensation in Group 1. Mild ALT elevation according to baseline levels were found in 8 (27.6%) and 4 (17.4%) patients, respectively, in Group 2 and Group 1, and no statistically significance between two groups. In conclusion, this study showed that it is not necessary to continue lamivudine therapy while switching to AD therapy. Adefovir alone is effective in the treatment of patients with lamivudine resistant HBV infection and compensated liver disease, without significant clinical and laboratory flares. However, it is not easy to say that switching to AD with cessation of lamivudine is safe, because the study population is not enough for precise conclusion and resistance may be a considerable problem against AD in patients using long-term treatment.

Liver fibrosis is associated with decreased peripheral platelet count in patients with chronic hepatitis B and C.

Thrombocytopenia is a common complication of chronic liver diseases, but its pathogenesis is not clear. Although generally attributed to hypersplenism, other factors should also be considered. We investigated the relationship between the peripheral platelet count and the degree of fibrosis in patients with chronic viral hepatitis. In an effort to avoid the effects of hypersplenism, we excluded patients with splenomegaly and/or bi- or pan-cytopenia. Seven hundred eighty-four patients (265 chronic viral hepatitis C and 519 chronic viral hepatitis B) were included in the study. Univariate analysis showed that the peripheral platelet count had a negative correlation with fibrosis score, necroinflammatory activity, and age in both groups. In multivariate analysis, the peripheral platelet count had a similar correlation with the fibrosis score and age, but not with necroinflammatory activity, in both groups. The peripheral platelet count decreased more significantly in females with chronic hepatitis C but not in the chronic hepatitis B group. In conclusion, a decrease in peripheral platelet count may be a sign of an increase in the degree of fibrosis during the course of chronic viral hepatitis B and C and factors other than hypersplenism may play a role in this decrease in the peripheral platelet count.

Liver biopsy: is the pain for real or is it only the fear of it?

Although percutaneous liver biopsy (PLB) has very low mortality and morbidity rates, it often is considered painful and frightening by the patients. This study was designed to grade the intensity of pain expected before the procedure and experienced during the procedure, and whether there is any correlation between pain and the emotional state of the patient. A total of 118 consecutive patients (aged 19-68 (mean, 44) years), who were undergoing PLB for the first time, were included in the study. Visual Analogue Scale (VAS) was used before the procedure, after the procedure to grade the degree of pain expected, and the degree of the pain experienced respectively. All the patients were evaluated by a questionnaire for their personality and emotional situation by using the Minnesota Multiphasic Personality Inventory Somatization Sub-scale (MMPI-SS). Mean VAS score for expected pain before the procedure was 60+/-20 and for the pain experienced during the procedure was 22+/-16 (P < 0.0001). Although the expected pain scores of female patients were significantly higher than males (66+/-22 vs. 55+/-17; P=0.003), there was no difference between female and male patients in the experienced pain scores. The procedure of PLB is expected to be more painful than it really is by the patients, especially by females. Calming the patients by informing them about the procedure and their diseases will probably diminish the expected pain.

A cerebrovascular event after single-dose administration of recombinant factor VIIa in a patient with esophageal variceal bleeding.

Upper gastrointestinal bleeding (UGIB) is a life-threatening complication of cirrhosis that develops from esophageal varices in almost 70% of patients. The mortality rate from the bleeding episodes is reported to be 30% [1-4]. Standard management of UGIB of cirrhotic patients is vasoactive therapy combined with endoscopic procedures such as endoscopic sclerotherapy and band ligation [5]. Currently, it is reported that recombinant activated fVIIa (Novoseven, NovoNordisc) can correct the prothrombin time in decompensated cirrhotic patients and also can be used safely in Child's B and C cirrhotic patients with UGIB [6-8]. Herein, we describe the first case report in the literature of a cerebrovascular event after the administration of a single dose of fVIIa in a cirrhotic patient with esophageal variceal bleeding.

Results of endoscopic management of anastomotic biliary strictures after orthotopic liver transplantation.

BACKGROUND/AIMS: Anastomotic biliary strictures are common biliary complications after orthotopic liver transplantation. We assessed the success of endoscopic retrograde cholangio-pancreaticography (ERCP) in the treatment and outcome of post-liver transplantation anastomotic biliary strictures in a university hospital, retrospectively. METHODS: Thirty-three ERCPs were performed in 20 of 162 adult liver transplant recipients with duct to duct anastomosis. RESULTS: In five patients, ERCP failed because the stricture could not be passed with guidewire. Four patients were treated with balloon dilatation only; two of them are recurrence-free with a follow-up of 24 and 8 months. Eleven patients had balloon dilatation and plastic stent placement as their primary treatment modality. In six of them, the anastomosis remained patent for the rest of the follow-up (22+/-13 months). Five patients had stricture recurrence after first stenting which necessitated re-stenting; four of them required a third, and three had a fourth stenting. CONCLUSIONS: Endoscopic balloon dilatation and stenting are safe and effective means of treatment of anastomotic biliary strictures following liver transplantation.

Fulminant Budd-Chiari syndrome associated with polycythemia rubra vera and factor V Leiden mutation.

Budd-Chiari syndrome (BCS) is a severe disorder characterized by hepatic venous outflow obstruction. Hypercoagulable states are the major etiological factors for the development of BCS and can be identified in about 75% of patients. Multiple etiological factors can be found in the same patient. Hematologic abnormalities, especially myeloproliferative disorders, are the most common causes of BCS. Furthermore, the prevalence of factor V Leiden mutation is three times greater in patients with BCS. Although the clinical course tends to be chronic, BCS may, on rare occasions, cause acute liver failure. Herein, we report a patient who had factor V Leiden mutation and polycythemia rubra vera, presented as fulminant BCS.

Esophageal tuberculosis mimicking esophageal carcinoma.

Esophageal tuberculosis is rare. In some cases, the clinical presentation of this infection may mimic esophageal carcinoma. Differential diagnosis may be difficult and may result in an unnecessary surgical therapy such as esophagectomy. In this report we document the endoscopical, radiological, histological and bacteriological features of esophageal tuberculosis in a 62-year-old woman. She was admitted to our hospital complaining of dysphagia and odynophagia. Upper gastrointestinal endoscopy revealed an ulcerovegetant lesion in the right wall of the esophagus suggesting esophageal carcinoma. Further investigation resulted in a diagnosis of esophageal tuberculosis. She was successfully treated by antituberculous chemotherapy. We suggest that esophageal tuberculosis has to be kept in mind in the differential diagnosis of esophageal ulcerovegetant lesions.

Two-year interferon therapy with or without ribavirin in chronic delta hepatitis.

UNLABELLED: The only beneficial agent for the treatment of chronic delta hepatitis (CDH) is interferon (IFN). However, there is no consensus on the best dosage or duration of IFN therapy. As ribavirin (RBV) increases the sustained response when added to IFN in chronic hepatitis C, probably because of its immunomodulatory effect, we aimed to investigate the efficacy of 2-year IFN treatment and whether RBV had any additive effect to IFN in CDH. METHODS: Patients (n = 31) with CDH were randomized with a 1:2 ratio as 10 patients (3 females/7 males, age 39 +/- 9) receiving IFN monotherapy (9 MU IFN-alpha2a three times weekly) and 21 patients (8 females/13 males, age 38 +/- 11) receiving IFN plus RBV for 2 years (IFN at the same dosage and RBV at 1000-1200 mg/day). Alanine transferase normalization and hepatitis delta virus (HDV) RNA negativity at the end of treatment and at the end of the follow-up period (at least 6 months following 2-year treatment) were primary endpoints of the study. In addition, virological response and biochemical response were determined separately. RESULTS: Eight of 31 patients (25%) had cirrhosis in liver biopsies. Six patients from the IFN monotherapy group and 12 patients from the combination group had biochemical response. Five patients from the IFN monotherapy group and 11 patients from the combination group had virological response at the end of therapy. Two patients from the IFN group and five patients from the combination group had sustained biochemical response at the end of the follow-up period. Hepatitis B virus (HBV) activations with HBV DNA positivity were observed in two patients (one from the IFN monotherapy group, one from the combination group). Two patients (20%) in the IFN group and five patients (23.5%) in IFN plus RBV group remained as virological responders at the end of the follow-up period (P > 0.05). None of the patients with liver cirrhosis were responsive at the end of the follow-up period. CONCLUSION: Almost 20% of the patients with CDH were responsive to 2-year IFN treatment at the end of the follow-up period and no additional effect of RBV was observed. Patients with advanced liver disease failed to respond to treatment.

Endoscopic injection therapy of bleeding Dieulafoy lesion of the stomach.

BACKGROUND/AIMS: Dieulafoy's lesion is a rare cause of upper gastrointestinal bleeding and is potentially life threatening. The aim of this study is to determine the clinical features of these lesions and the efficacy of the endoscopic injection sclerotherapy in patients with Dieulafoy's lesion. METHODOLOGY: Between January 1994 and December 2001, twenty-eight patients with upper gastrointestinal bleeding due to Dieulafoy's lesion were treated by endoscopic injection sclerotherapy. Efficacy of endoscopic therapy and clinical findings of these cases were analyzed. RESULTS: The study group consisted of 22 male (78.5%) and 6 female (21.5%) patients with a mean age of 57 years (range 22-82 years). Significant comorbidity was present in 22 (78.5%) patients. Hemoglobin values of the patients ranged from 5.4-10.3 g/dL at hospitalization. The median transfusion requirement was 5 (range 0-12) units. Dieulafoy's lesion was observed in the proximal half of stomach in 25 cases (89.3%), in the antrum in 2 cases (7.1%) and in the angulus in 1 case (3.5%). Endoscopic injection sclerotherapy was successful in stopping the bleeding in 26 out of 28 patients (92.8%). CONCLUSIONS: Dieulafoy's lesions mostly affect the proximal stomach and cause serious upper gastrointestinal bleeding. Endoscopic injection sclerotherapy is an effective and a safe therapeutic method for Dieulafoy's lesion.