Upper socioeconomic status is associated with lower Helicobacter pylori infection rate among patients undergoing gastroscopy.

INTRODUCTION: Socioeconomic factors play an important role in the prevalence of Helicobacter pylori (HP) infection. The aim of this study is to investigate HP prevalence among symptomatic patients in the upper socioeconomic segment of the population undergoing gastroscopy in an endemic urban region. METHODOLOGY: Over a 12-month period, data were collected from the first consecutive 1000 patients (500 from university hospital, 500 from community hospital) who had gastroscopy and HP evaluation. RESULTS: Overall, 211/1000 patients (21.1 %) were found to have HP in gastric biopsies. The specificity, sensitivity, positive predictive value, negative predictive value and diagnostic accuracy of rapid urease test were 87.5%, 99.7%, 99%, 96.5%, and 96.9% respectively. Atrophic gastritis, gastric and duodenal ulcers were significantly more common in HP positive patients. Age based distribution of HP prevalence: > 6 decades (15.5%), 3rd-5th decades (26.1%), < 3rd decades (10.4%). CONCLUSION: In an HP endemic country, the prevalence of HP infection among symptomatic patients belonging to the upper socioeconomic segment of the population appears to be markedly lower. The lowest prevalence in young patients is expected to result in future decrease in HP prevalence.

Gastroesophageal reflux disease and the relationship with Helicobacter pylori.

After Helicobacter pylori was identified, and its relationship with peptic ulcer disease was exactly shown, the relationship of this bacterium with gastroesophageal reflux disease (GERD) gained momentum and discussions continue to this day. We reviewed the literature for the relationship between H. pylori and GERD. According to the existing data, there is no relationship between GERD and H. pylori presence. Successful eradication therapy does not have an impact on the emergence or exacerbation of GERD. However Barrett's esophagus and esophageal adenocarcinoma are less frequent, especially in the presence of CagA positive H. pylori infections. Long-term use of proton pump inhibitor (PPI) may have an impact on the development of atrophy and/or intestinal metaplasia in H. pylori positive patients; therefore, H. pylori eradication is recommended in patients that should use long-term PPI. As a conclusion, H. pylori screening and the eradication decision should be independent of GERD, except for patients that will use long-term PPI.

Mutations in RAD21 disrupt regulation of APOB in patients with chronic intestinal pseudo-obstruction.

BACKGROUND & AIMS: Chronic intestinal pseudo-obstruction (CIPO) is characterized by severe intestinal dysmotility that mimics a mechanical subocclusion with no evidence of gut obstruction. We searched for genetic variants associated with CIPO to increase our understanding of its pathogenesis and to identify potential biomarkers. METHODS: We performed whole-exome sequencing of genomic DNA from patients with familial CIPO syndrome. Blood and lymphoblastoid cells were collected from patients and controls (individuals without CIPO); levels of messenger RNA (mRNA) and proteins were analyzed by quantitative reverse-transcription polymerase chain reaction, immunoblot, and mobility shift assays. Complementary DNAs were transfected into HEK293 cells. Expression of rad21 was suppressed in zebrafish embryos using a splice-blocking morpholino (rad21a). Gut tissues were collected and analyzed. RESULTS: We identified a homozygous mutation (p.622, encodes Ala>Thr) in RAD21 in patients from a consanguineous family with CIPO. Expression of RUNX1, a target of RAD21, was reduced in cells from patients with CIPO compared with controls. In zebrafish, suppression of rad21a reduced expression of runx1; this phenotype was corrected by injection of human RAD21 mRNA, but not with the mRNA from the mutated p.622 allele. rad21a Morpholino zebrafish had delayed intestinal transit and greatly reduced numbers of enteric neurons, similar to patients with CIPO. This defect was greater in zebrafish with suppressed expression of ret and rad21, indicating their interaction in the regulation of gut neurogenesis. The promoter region of APOB bound RAD21 but not RAD21 p.622 Ala>Thr; expression of wild-type RAD21 in HEK293 cells repressed expression of APOB, compared with control vector. The gut-specific isoform of APOB (APOB48) is overexpressed in sera from patients with CIPO who carry the RAD21 mutation. APOB48 also is overexpressed in sporadic CIPO in sera and gut biopsy specimens. CONCLUSIONS: Some patients with CIPO carry mutations in RAD21 that disrupt the ability of its product to regulate genes such as RUNX1 and APOB. Reduced expression of rad21 in zebrafish, and dysregulation of these target genes, disrupts intestinal transit and the development of enteric neurons.

Is It Barrett's Esophagus or Gastric Heterotopia?

Columnar epithelium in the distal part of the esophagus is generally related to Barrett's esophagus. Barrett's esophagus is a well-known premalignant lesion for adenocarcinoma of the esophagus. Therefore, its diagnosis and surveillance are important. Columnar epithelium in the esophagus other than Barrett's esophagus can be gastric heterotopia, which generally takes place in the upper part of the esophagus and is named inlet patch. The presence of gastric metaplasia in the distal part of the esophagus is rare and can cause misdiagnosis. Therefore, its differentiation from Barrett's esophagus is important. Here we present a case of gastric heterotopia located in the distal part of the esophagus that caused reflux-like symptoms and needed differentiation from Barrett's esophagus.

Eosinophilic jejunitis presenting as intractable abdominal pain.

Eosinophilic gastroenteritis is an uncommon disease characterized by eosinophilic infiltration of the gastrointestinal tract. The clinical manifestations are related to the layer(s) and extent of the bowel involved. In this paper, we present a case of intractable abdominal pain caused by jejunal submucosal eosinophilic infiltration without mucosal involvement, diagnosed by deep endoscopic biopsies. The patient was successfully treated with steroids without need for surgery for diagnosis or therapy.

Association of the MEFV gene variations with inflammatory bowel disease in Turkey.

BACKGROUND: Association of NOD2 (CARD15) gene mutations with inflammatory bowel diseases (IBD) is well known. We herein aimed to investigate the role of familial Mediterranean fever-associated MEFV variations in IBD patients as additional regional-specific risk factor. STUDY: One hundred thirty-seven (78 female, 56.9%) IBD patients [62 Crohn's disease (CD), 75 ulcerative colitis (UC)] were enrolled into the study. The diagnosis of all patients was confirmed by colonoscopy, histopathology, and the clinical findings. One hundred one healthy donors' samples were used as healthy controls. All patients were genotyped for the most common E148Q, M608I, M694V, and V726A variations of the MEFV and R702W, G908R, and 1007fs of the NOD2. RESULTS: The overall MEFV variation frequency was found to be higher in the IBD (25.5%) patients (28% in UC, 22.6% in CD) compared with controls (9.9%, P=0.006). This association was stronger with the penetrant exon 10 variations (M694V, M680I, V726A; odds ratio =4.5, P=0.001). Contribution of M694V was higher compared with the other variations (14.5% in CD, 17.3% in UC and 3% in controls, odds ratio =6.039, 95% confidence intervals, 1.7-20.7, P=0.002). The overall frequency of 3 NOD2 variants in the IBD group was not different from that of controls. CONCLUSIONS: The results of this study suggest that the MEFV variations may be an additional susceptibility factor for IBD in certain parts of the world where the carrier rate is high, and the genetic background of the IBD patients may show regional changes.

An observational European study on clinical outcomes associated with current management strategies for non-variceal upper gastrointestinal bleeding (ENERGIB-Turkey).

BACKGROUND/AIMS: This observational, retrospective cohort study assessed outcomes of the current management strategies for nonvariceal upper gastrointestinal bleeding in several European countries (Belgium, Greece, Italy, Norway, Portugal, Spain, and Turkey) (NCT00797641; ENERGIB). MATERIALS AND METHODS: Turkey contributed 23 sites to this study. Adult patients (≥18 years old) consecutively admitted to hospital and who underwent endoscopy for overt non-variceal upper gastrointestinal bleeding (hematemesis, melena or hematochezia, with other clinical/laboratory evidence of acute upper GI blood loss) were included in the study. Data were collected from patient medical records regarding bleeding continuation, re-bleeding, pharmacological treatment, surgery, and mortality during a 30-day follow-up period. RESULTS: A total of 423 patients (67.4% men; mean age: 57.8 ± 18.9 years) were enrolled in the Turkish study centers, of whom 96.2% were admitted to hospital with acute non-variceal upper gastrointestinal bleeding. At admission, the most common symptom was melena (76.1%); 28.6% of patients were taking aspirin, 19.9% were on non-steroidal anti-inflammatory drugs, and 7.3% were on proton pump inhibitors. The most common diagnoses were duodenal (45.2%) and gastric (27.7%) ulcers and gastritis/gastric erosions (26.2%). Patients were most often managed in general medical wards (45.4%). A gastrointestinal team was in charge of treatment in 64.8% of cases. Therapeutic procedures were performed in 32.4% of patients during endoscopy. After the endoscopy, most patients (94.6%) received proton pump inhibitors. Mean (SD) hospital stay was 5.36 ± 4.91 days. The cumulative proportions of continued bleeding/re-bleeding, complications and mortality within 30 days of the non-variceal upper gastrointestinal bleeding episode were 9.0%, 5.7% and 2.8%, respectively. In the Turkish sub-group of patients, the significant risk factors for bleeding continuation or re-bleeding were age >65 years, presentation with hematemesis or shock/syncope, and the diagnosis of duodenal ulcer. The risk of clinical complications after non-variceal upper gastrointestinal bleeding was higher in female patients older than 65 years, in patients with comorbidities, and in patients presenting with shock/syncope, and also according to time to endoscopy. The use of aspirin, non-steroidal anti-inflammatory drugs or warfarin at baseline was negatively associated with the development of bleeding or clinical complications. The risk of death within 30 days after non-variceal upper gastrointestinal bleeding was significantly higher in patients older than 65 years and in those receiving transfusions other than intravenous fluid or red blood cells within 12 hours of presentation. CONCLUSIONS: According to the survey results, non-variceal upper gastrointestinal bleeding in Turkey varies from that in other European countries in a number of aspects. These differences could be associated with a younger population and Helicobacter pylori incidence. Despite the diminishing need for surgical intervention and mortality rates for non-variceal upper gastrointestinal bleeding, as is the case in other European countries, non-variceal upper gastrointestinal bleeding remains a serious problem.

Etiological factors of duodenal and gastric ulcers.

BACKGROUND/AIMS: We aimed to determine the etiology of patients with duodenal and gastric ulcers. METHODS: 140 patients diagnosed with peptic ulcer between April 2002-2009 were enrolled in this prospective study. Two biopsy specimens were collected from the antrum and corpus for histology and one for rapid urease testing, and stool samples were analyzed for Helicobacter pylori antigen. Serum calcium and gastrin levels were also analyzed. RESULTS: 82 (58%) patients were male, with a median age of 47.70±15.03 years (range: 16-92). The ulcer was located in the duodenum in 96 patients, stomach in 40, and both duodenum and stomach in 4. The rates of patients positive for Helicobacter pylori antigen in stool, positive in urease testing and positive for Helicobacter pylori presence in antral and corpus samples were 48%, 52%, 67%, and 60%, respectively. 107 (76%) patients were positive for Helicobacter pylori in one of the test methods. 64 (46%) patients had a history of nonsteroidal antiinflammatory drug use within the last month. Mean levels of calcium and gastrin were 9.29±0.40 (7.90-10.20) and 73.96±89.88 (12.86-562.50), respectively. Gastrin level was correlated to inflammatory activity (p<0.05). 19 (13.6%) of the patients were negative for Helicobacter pylori, nonsteroidal anti- inflammatory drug use and hypersecretory illness, and were classified as idiopathic. CONCLUSIONS: The most common cause of duodenal and gastric ulcer was Helicobacter pylori, and it was responsible for three-fourths of the cases. About half of the patients had a history of nonsteroidal antiinflammatory drug use, and nonsteroidal antiinflammatory drug and Helicobacter pylori were both responsible for the ulcer in three-fourths of these patients. In about one-tenth of the patients, nonsteroidal antiinflammatory drug use was the cause of ulcer alone, and about one-tenth of the ulcers were classified as idiopathic.

Effect of proton pump inhibitor (PPI) treatment in obstructive sleep apnea syndrome: an esophageal impedance-pHmetry study.

BACKGROUND/AIMS: There is an increasing interest for a link between gastroesophageal reflux (GER) and obstructive sleep apnea syndrome (OSAS). There is no study in the literature which examines the relationship between OSAS and esophageal functions in adults with impedance. We first evaluated the role of reflux in OSAS with simultaneous polysomnography and impedance-pHmetry and then investigated whether the effect of proton pump inhibitor (PPI) treatment changes in these parameters. METHODOLOGY: Twenty two OSAS patients who had applied to sleep laboratory between September 2007 and May 2008 were consecutively enrolled to the study. Twenty four hours esophageal impedance study was performed during polysomnographic recording. At least 50% of all apneas in patients must proceed with a reflux event in 2 minute intervals in order to be considered reflux related apnea patient. RESULTS: Pathologic reflux episodes were determined in 20 patients (8 were weakly acidic, 12 were acidic). Reflux dependent apnea was found in 6 patients. There was endoscopically esophagitis in all reflux related apnea patients. There was a negative correlation between initial mean SaO2 and gas reflux events at night (p=0.004, r =-0.588) and mixed reflux events at night (p=0.02, r=0.493). There was a statistically significant regression of AHI (apnea hypopnea index) after 3-months PPI treatment (p=0.012). CONCLUSIONS: Reflux may trigger apnea in some of the OSAS patients. Therefore, each OSAS patient must be inquired about esophageal and extraesophageal symptoms of reflux.

Anticoagulant therapy and Budd-Chiari syndrome: is it successful?

BACKGROUND/AIMS: Anticoagulant therapy is an accepted treatment for Budd-Chiari syndrome (BCS). However, the natural course of untreated patients is unclear. We aimed to evaluate the efficacy of anticoagulant therapy on survival in BCS. METHODOLOGY: Between 1995 and 2007, 45 patients diagnosed with BCS based on the clinical, biochemical, radiological and histological findings were retrospectively evaluated with respect to underlying disease, therapeutic interventions, complications and overall outcome. Complications and survival during the follow-up period were compared in between anticoagulant treated and untreated cases. RESULTS: Mean patient age was 34.4 +/- 11.8 years and 46.7% (21) of them were male. Median followup time was 24 months (6-132); 8.9% of patients were diagnosed as acute, 31.1% as subacute and 60% as chronic BCS according to disease duration. Centrilobular necrosis was found in 16 of 36 biopsy performed patients. Etiological factors were detected in 60% of patients and 40% of them were cryptogenic. Twenty four of them received anticoagulant therapy, the remaining 21 were followed-up with supportive medical therapy. Five patients who had shunt operation were excluded for survival analyses. Complications were similar between treated and untreated cases (p>0.05). There was a positive correlation between survival and centrilobular necrosis (r=0.376, p=0.037). The mean survival periods were 95.5 months (%95 CI 73-117 months) and 72.5 months (%95 CI 42-103 months) in anticoagulant treated and untreated patients, respectively (p>0.246). CONCLUSION: Most patients with BCS are admitted to hospital at the chronic stage and more than half of them have underlying thrombotic risk factor. In our study, no beneficial effects of anticoagulant therapy were observed on the survival and complications of liver disease.

Is portal hypertensive enteropathy an important additional cause of blood loss in portal hypertensive patients?

OBJECTIVE: Recently, mucosal changes of small bowel were defined by developing new imaging techniques including capsule endoscopy (CE) in portal hypertensive patients. However, the clinical impact of these changes is unknown. In this study, we aimed to determine the additional cause of blood loss in portal hypertensive patients. MATERIAL AND METHODS: A total of 444 portal hypertensive patients, hospitalized in our clinic between 2005 and 2007, were evaluated. Patients with obscure bleeding were enrolled to this prospective case-control study. CE was performed in 21 patients who met inclusion criteria. Gastroscopy, colonoscopy and computerized tomography/small bowel enema were performed in all patients. RESULTS: Fourteen cirrhotic and seven noncirrhotic portal hypertensive patients were enrolled to this study. Mean age of patients was 47.9±15.6 years, and 13 of 21 were male. Small bowel varices were found in 7 patients (1 active bleeding) and other mucosal abnormalities in 10 patients (vascular ectasia, erosion and edema, 1 active bleeding). Although two of them were normal, jejunal malignant mass was found in two patients (1 active bleeding). Of 21 patients, 19 (90.5%) patients had portal hypertensive abnormalities (including varices). However, ileal varices rate was 57.1% (4 patients) in noncirrhotic portal hypertensive patients and 21.4% (3 patients) in cirrhotics. CONCLUSION: Ninety percent of patients had portal hypertensive abnormalities in small bowel and one-third of them had small bowel varices. Small bowel varices and vascular ectasia were the main causes of obscure bleeding in portal hypertensive patients.

Electron microscopic findings in non-alcoholic fatty liver disease: is there a difference between hepatosteatosis and steatohepatitis?

BACKGROUND AND AIMS: Non-alcoholic fatty liver disease has long been accepted as benign; however, recent evidence suggests that the disease may progress to cirrhosis and hepatocellular carcinoma, although the natural course of the disease is still unclear. This study was designed to comparatively evaluate electron microscopic features of non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH). METHODS: Quantitative and semi-quantitative ultrastructural evaluations were performed on liver biopsies from 23 patients, 10 with NAFL and 13 with NASH. RESULTS: No statistically significant difference was noted between NAFL and NASH patients in ultrastructural features of hepatocytes including megamitochondria, intramitochondrial crystalline inclusions, mitochondrial matrix granules, foamy cytoplasmic appearance, electron-lucent and glycogen-containing nuclear regions, lipofuscin granules, or an increased frequency of vesicles containing electron-dense material in peribiliary Golgi zone; however, the mitochondrial diameter was significantly higher in the NASH patients. Intercellular distance and microvilli between hepatocytes, collagen and electron-dense material accumulation in the space of Disse, electron-dense material accumulation and microvillus density in bile canaliculi did not differ significantly between the groups. CONCLUSIONS: Our data show that, although NAFL and NASH can be distinguished by their distinct light microscopic features, ultrastructural characteristics are similar, which suggests that NAFL may also have the potential to progress to fibrosis and cirrhosis like NASH.

A new agent for tumour necrosis factor-alpha inhibition: In vitro effects of dipyridamole in Crohn's disease.

BACKGROUND: Tumour necrosis factor-alpha (TNF-alpha) plays a central role in inflammatory cascade in Crohn's disease (CD). Our study aims to investigate the in vitro effects of dipyridamole (DP) on the TNF-alpha and interleukin-10 (IL-10) production in the intestinal mononuclear cells of CD patients. MATERIAL AND METHODS: Thirteen patients with CD and in 17 healthy individuals underwent colonoscopy and biopsy samples were taken. Cultured mononuclear cells were preincubated with DP1 (0.7 microg/ml), DP2 (1.25 microg/ml), methotrexate (MTX)1 (0.5 nmol/L) and MTX2 (1.5 nmol/L). These cells were then stimulated with lipopolysaccaride (LPS) and phytohemagglutinin (PHA). The levels of TNF-alpha and IL-10 in supernatants were measured with standard immunoassay monoclonal antibody method. RESULTS: An appropriate cell culture could be obtained in 10 patients with CD and 12 healthy individuals. In LPS stimulated cells, MTX1 and MTX2 were superior to DP1 and DP2 in suppressing TNF-alpha in both groups. In PHA stimulated cells, while MTX1 was superior to DP1, MTX2 and DP2 had an equivalent effect in CD patients (p<0.05, p>0.05, respectively). In LPS-stimulated cells DP2 was significantly superior to MTX2 in increasing IL-10 levels in both groups (p<0.05). In PHA stimulated cells, DP1 and DP2 caused a higher increase in IL-10 levels compared with MTX1 and MTX2 in CD group (p<0.05). CONCLUSIONS: Dipyridamole suppresses TNF-alpha similar with MTX. It seems to be superior to MTX in increasing IL-10 levels. Addition of DP to anti-TNF medications may create a synergy in cytokine modulation.

Diagnostic Capability of Capsule Endoscopy in Small Bowel Diseases.

Capsule Endoscopy (CE) is a recently developed noninvasive technique for imaging of small bowel pathologies. It is a swallowable wireless mini-camera for getting images of the gastrointestinal (GI) mucosa. General indications of CE are obscure bleeding, iron deficiency anemia, Crohn disease, abdominal pain, polyposis coli, celiac disease and small bowel tumors. Obstruction must be excluded with small bowel radiography before using CE. Bowel preparation can be recommended for good visualization. The main indication is obscure GI bleeding. Even though useful for the other indications in selected cases, large polypoid lesions may be missed. Diagnostic capability of CE and double balloon enteroscopy (DBE) are similar and CE is a good complemantary method for DBE.

Utility of esophageal manometry and pH-metry in gastroesophageal reflux disease before surgery.

BACKGROUND/AIMS: The necessity of manometric evaluation before fundoplication in patients with gastroesophageal reflux disease is still a matter of debate. However, misdiagnosis can be responsible for postoperative problems. We aimed to evaluate the necessities of manometry and pH-metry before fundoplication in order to prevent possible complications after surgery. METHODS: Between 1997 and 2004, 259 consecutive patients who referred to our laboratory with a diagnosis of gastroesophageal reflux disease and request for manometric test before surgery were evaluated retrospectively. Manometric analysis was performed in all patients and 24-hour ambulatory pH-metry in 91 of them. RESULTS: The mean age of the patients was 42.6+/-13 years and 51% were female. While 102 (39.4%) of the patients had normal esophageal motility, 122 (47.1%) had gastroesophageal reflux-related dysmotility (22% with ineffective esophageal motility, 25.1% with hypotensive lower esophageal sphincter). Primary esophageal motility disorders were detected in 29 (11.2%) patients (4 achalasia, 24 uncoordinated contractions and 1 nutcracker esophagus). Six patients had secondary dysmotility caused by scleroderma. Pathologic reflux was detected in 54 (59.3%) patients in whom pH-metry was performed. CONCLUSIONS: Our results support that manometry and pH-metry must be performed before surgery in gastroesophageal reflux disease.

Intestinal metaplasia in portal hypertensive gastropathy: a frequent pathology.

OBJECTIVE: To compare the frequency of intestinal metaplasia (IM) in patients with portal hypertensive gastropathy (PHG) to the control group with functional dyspepsia. METHODS: Two-hundred and eighty-nine cases were prospectively evaluated in three groups (controls:group I--123 patients; cirrhotics: group II--135 patients; noncirrhotic portal hypertensives: group III--31 patients). Mucosal biopsies (three antrum, one angulus, two corpus) were taken and examined for atrophy, IM, dysplasia, Helicobacter pylori (Hp) and histologic PHG. RESULTS: Frequencies of IM in groups I, II and III were 17.1% (type I, 3.3%; type II, 10.6%; type III, 3.3%), 34.3% (type I, 9.6%; type II, 17%; type III, 6.7%) and 33.3% (type I, 9.7%; type II, 12.9%; type III, 9.7%), respectively. In patients with PHG, frequency of IM was significantly higher than in control group (P<0.05) and correlated with the severity of PHG (P<0.05). The frequency of type III IM was not statistically different among the three groups. Frequency of atrophy in cirrhotic patients was higher than in control group (17.9% in group I, 32.6% in group II, 25.8% in group III; P<0.05). In the control group, Hp prevalence was significantly higher than in patients with PHG (P<0.05) and there was a positive correlation between Hp and atrophy (P<0.05). In multivariate analysis, PHG and age were found as independent predictors for IM; PHG, age and Hp for atrophy. CONCLUSION: Frequencies of atrophy and IM are higher in patients with PHG. PHG is a reliable marker for IM and atrophy in gastric mucosa.

A rare cause of hemosuccus pancreaticus: primary splenic artery aneurysm ruptured into pancreatic serous cystadenoma.

Hemosuccus pancreaticus is a rare clinical condition defined as bleeding into the pancreatic duct from a peripancreatic artery. We present here a 57-year-old woman admitted to our clinic with abdominal pain, tar-colored stool and confusion. Further investigations were done because of severe anemia. Abdominal computerized tomography revealed intraabdominal hematoma. Laparotomy was performed, which confirmed that intraabdominal haemorrhagia had occurred with the rupture of a splenic artery aneurysm into a pancreatic serous cystadenoma, which ruptured into the abdomen because of high pressure. This is an interesting case diagnosed with multidisciplinary approaches.

Rapidly progressive HCV cirrhosis in a hypogammaglobulinemic patient.

Contrary to the widely known view of the insidious, slowly progressive pattern of hepatitis C, a rapidly progressive cirrhotic form can develop in immunodeficient conditions. Hepatitis C leads to cirrhosis in immunocompetent hosts after 20 years of infection however in hypogammaglobulinemic patients disease progresses faster, leading to cirrhosis and death within 10 years of diagnosis and frequently earlier. Here we present a 57-year-old woman with common variable immunodeficiency infected with hepatitis C after antral and duodenal resection and gastrojejunostomy operation in another hospital for lymphoma mimicking duodenal nodular hyperplasia which then rapidly progressed to decompensated cirrhosis in less than two years.

Eosinophilic esophagitis: case report.

Eosinophilic esophagitis is an inflammatory condition of the esophagus characterized by eosinophilic infiltration. It is a condition mainly affecting children; the adult form has only recently gained recognition as a distinct entity. The major symptom among adults with eosinophilic esophagitis is dysphagia. It is often misdiagnosed as gastroesophageal reflux disease because of the similarity in symptoms. An endoscopic biopsy is required to distinguish between the conditions. The cause of eosinophilic esophagitis is poorly understood, but food allergy has been implicated. Topical steroids are the most effective and convenient method for the treatment of eosinophilic esophagitis in adults. The long-term prognosis of eosinophilic esophagitis is uncertain; however, data suggests a benign course. We herein present two eosinophilic esophagitis cases that were the first to be diagnosed in our clinic.

What is the reason of elevated alanine aminotransferase level in HBeAg negative patients with low viremia: NAFLD or chronic hepatitis?

BACKGROUND AND STUDY AIMS: Increased alanine aminotransferase (ALT) levels with negative hepatitis B virus (HBV) DNA by hybridization is a common problem in Turkey where is a mild endemic region. We aimed to evaluate the causes of elevated ALT levels in patients who are negative for hepatitis B e antigen (HBeAg) and HBV DNA (by hybridization) for at least 6 months. PATIENTS-METHODS: Forty-nine patients were enrolled in this study. Histological changes [histological activity index (HAI), and the extent of fibrosis] were assessed according to the Knodell scoring system and steatosis were graded by Brunt's classification for NAFLD in all patients. RESULTS: A mean age of the patients was 34.9 +/- 12.1 years (16-70). 43 (87.8%) of them were male. Mean ALT level was 95 +/- 39.7 IU/L (50- 258). Hyperglycemia (>100 mg/dL) and hyperlipidemia were found in 12 and 24 patients, respectively. Hepatic steatosis (7 patients grade 1; 5 patients grade 2; and 7 patients grade 3), ground-glass hepatocyte, chronic hepatitis, and Wilson disease were found in liver biopsy in 38.8%, 32.6%, 26.6%, 2%, respectively. Mean HAI was 6.5 +/- 3.6 (4-12) in chronic hepatitis. Seven patients (53.9%) were in stage 1 and 2 while 6 patients (46.1%) were in stage 3 and 4. CONCLUSIONS: Nonalcoholic fatty liver disease is the most common cause of elevated ALT levels in HBeAg negative/HBV DNA negative patients. Chronic hepatitis B was found in 26.6% of these patients.