Evaluation of Early Atherosclerosis Markers in Patients with Inflammatory Bowel Disease.

BACKGROUND The aim of this study was to investigate relationships between early atherosclerosis and inflammatory bowel disease (IBD) using laboratory, functional, and morphological markers of atherosclerosis. MATERIAL AND METHODS In the present prospective single-center study, 96 patients with IBD (58 patients with ulcerative colitis and 36 patients with Crohn's disease) and 65 healthy control subjects were included. The demographic data of each patient and control subject were recorded. The patients with IBD and healthy controls were compared in terms of the carotid intima-media thickness (CIMT), the values of flow-mediated dilatation (FMD) and nitroglycerine-mediated dilatation (NMD), and the levels of von Willebrand factor antigen (VWF-Ag), D-dimer, and lipoprotein (a). RESULTS There were no significant differences between the IBD patients and controls in terms of age, sex, BMI, systolic and diastolic BPs, serum levels of total cholesterol, low-density lipoprotein, or triglycerides. IBD patients had significantly higher levels of VWF-Ag (156.6±58.9 vs. 104.2±43.3, P<0.001) and D-dimer (337.2±710.8 vs. 175.9±110.9, P<0.001) as compared to the controls. No significant differences were determined between the 2 groups in terms of FMD and NMD values. Although statistically not significant, the CIMT values were higher in the IBD patients than in the controls (0.517±0.141 mm vs. 0.467±0.099 mm, P=0.073). In the correlation analysis, the CIMT was found to be correlated negatively with FMD and positively with high sensitive C-reactive protein, VWF-Ag, and D-dimer. CONCLUSIONS These findings suggest that VWF-Ag and D-dimer can be beneficial early atherosclerosis markers in IBD patients.

Patterns and Grading of Gastrointestinal Graft-Versus-Host Disease: A Clinicopathologic Correlation Study.

BACKGROUND: The present study investigated gastrointestinal involvement patterns of acute graft-versus-host disease and assessed the correlation of pathologic severity with clinical grading. METHODS: Pathology reports of gastrointestinal (GI) endoscopic biopsies taken from 164 post-hematopoietic stem cell transplant patients with at least 1 endoscopic gastrointestinal biopsy diagnosed as "consistent with acute graft-versus-host disease" between 2005 and 2019 were retrieved from the automated hospital database. Endoscopic, pathologic and clinical gradings were performed using Freiburg criteria, Lerner and modified Seattle-Glucksberg grading systems, respectively. RESULTS: The majority of the patients (n = 140, 85.4%) were investigated with more than one biopsy from various gastrointestinal sites with a total of 479 biopsies: 44 (9.2%) esophagus, 90 (18.8%) stomach, 91 (19.0%) duodenum, 20 (4.2%) terminal ileum, 32 (6.7%) right colon, 87 (18.2%) left colon and, 115 (23.9%) rectum. Overall, lower gastrointestinal (n = 118/126, 93.6%) and upper gastrointestinal (n = 91/97, 93.8%) involvements were similar (P = .3). While the most severely affected site was duodenum (P = .021) in upper gastrointestinal, pathologic grades were similar in lower gastrointestinal sites, though more severe than upper gastrointestinal (P = .003). Pathologic grading had a low positive correlation with both clinical (r = 0.308, P = .001) and endoscopic grading (coefficient: 0.261, P = .003). CONCLUSION: Considering the similar graft-versus-host disease frequency of upper and lower gastrointestinal tract, distal colon evaluation with rectosigmoidoscopy seems to be a practical approach in patients with suspected gastrointestinal graft-versus-host disease. As it was positively correlated with both endoscopic and clinical grade, pathologic grading should be performed in these patients to assess gastrointestinal involvement patterns.

The effect of endogenous hypergastrinemia on lower esophageal sphincter pressure and esophageal motility.

BACKGROUND/AIMS: The effect of exogenous hypergastrinemia on esophageal motor function has been well documented. However, it is not known whether chronic endogenous hypergastrinemia influences esophageal motility and lower esophageal sphincter pressure. The purpose of this study was to investigate the effect of chronic hypergastrinemia on lower esophageal sphincter pressure and esophageal motility in patients with significantly elevated serum gastrin levels. METHODOLOGY: 37 patients (28 women; mean age, 53.7 years) with autoimmune gastritis and 35 functional dyspepsia patients participated in this study. Esophageal motility testing was performed by using an eight-lumen water-perfused catheter. Ten wet swallows were given and each contraction was analysed for lower esophageal sphincter pressure, lower esophageal sphincter relaxation, contraction amplitude and peak velocity. RESULTS: Mean serum fasting gastrin level was 1382.8±731.9pg/mL in patients with autoimmune gastritis and 107±83.9pg/mL in the control group (p=0.000). Mean lower esophageal sphincter pressure (31.6±14.42mmHg vs. 20.5±8.05mmHg, p=0.000) and mean contraction amplitude (82.48±35.0mmHg vs. 58.11±21.75mmHg, p=0.001), in hypergastrinemic patients were significantly higher than in the control group. CONCLUSIONS: These results suggest that in patients with autoimmune gastritis, prolonged and significant elevation of serum gastrin levels, increases lower esophageal sphincter pressure and esophageal body contraction amplitude. However, this increase in lower esophageal sphincter pressure does not cause upper gastrointestinal symptoms in patients with autoimmune gastritis.

The association of anti-CD74 antibody with spondyloarthropathies.

OBJECTIVE: The etiopathogenesis of spondyloarthropathies (SpA) is still unclear. Recently, anti-CD74 antibody has been suspected to play a role in SpA etiopathogenesis. This study aimed to examine the levels of anti-CD74 antibody in patients with SpA and investigate their association with disease activity. METHODS: This study was conducted using data from patients who were treated at the departments of rheumatology and gastroenterology between June 2013 and November 2013. The demographic and clinical characteristics of the participants and their serum IgG-type antibodies against anti-CD74 were analyzed. RESULTS: We analyzed 111 patients with ankylosing spondylitis (AS), 108 patients with inflammatory bowel disease (IBD), and 101 healthy controls. The rate of human leukocyte antigen-B27 positivity was 86.5% in patients with AS and 21.3% in patients with IBD. The mean levels of anti-CD74 antibodies in the AS, IBD, and control groups were 6.99±3.24 ng/mL, 6.25±3.34 ng/mL, and 7.83±4.72 ng/mL, respectively. Anti-CD74 levels were higher in healthy controls than in patients with IBD (p=0.009). There was no significant difference in anti-CD74 levels between the AS and IBD groups and the AS and control groups. In addition, there was no correlation between anti-CD74 levels and disease activity. CONCLUSION: This study could not find an association between anti-CD74 levels and SpA in Turkish patients.

The characteristics and clinical outcome of drug-induced liver injury: a single-center experience.

BACKGROUND AND GOALS: The aim of this cohort study was to determine the characteristics and clinical outcome of 170 patients with drug-induced liver injury (DILI) in a single center. STUDY: Between January 2001 and June 2007, a total of 170 individuals who were diagnosed with DILI were retrospectively analyzed. The median follow-up period was 110.0 days. RESULTS: During the study period, a total of 5471 new patients were assessed for liver test abnormalities. Of those, 170 patients (3.1%) fulfilled the criteria of DILI. A total of 83 different drugs were considered to be related to the hepatotoxicity; a single drug was suspected in 57.6% of individuals. The median interval between the suspicious drug intake and DILI recognition was 15.0 days. Hepatocellular pattern was observed in 50.0% of patients with a mean alanine aminotransferase level of 952.2+/-907.0 U/L. The main causative group of drugs was antibiotics. Sixty-two patients required hospitalization; acute liver failure developed in 14 (8.2%), chronicity was observed in 19 (11.2%), and 7 died (4.1%). Overall, complete recovery occurred in 82% of patients. The presence of jaundice on admission and shorter interval period between drug intake and DILI recognition were identified as risk factors for the development of acute liver failure. CONCLUSIONS: DILI is an important cause of liver test abnormalities in outpatient clinics, and antibiotics represent the most common drug group. Overall, complete recovery after the withdrawal of the suspicious drug occurred in the majority of patients, but DILI may progress to acute liver failure, chronicity, and death.

A rare case of malignant syphilis after adalimumab therapy due to Crohn's disease associated with bariatric surgery.

Malignant syphilis (also known lues maligna) is a rare and severe variant of secondary syphilis. It is most commonly seen in patients who are infected with human immunodeficiency virus (HIV), and rarely, it can occur in immunocompetent individuals. The exact mechanism of the development of malignant syphilis is not clear. It could probably be associated with immunosuppression, inappropriate immune response of the host, or virulent strain of Treponema pallidum. Coexistence of immunosuppression and inappropriate immune response may predispose to develop malignant syphilis in HIV-infected patients with immune reconstitution inflammatory syndrome. Herein, we report the first case of malignant syphilis after adalimumab therapy for Crohn's disease due to bariatric surgery and discuss the underlying possible pathogenic mechanisms.

Vascular endothelial growth factor, endostatin levels and clinical features among patients with ulcerative colitis and irritable bowel syndrome and among healthy controls: a cross-sectional analytical study.

BACKGROUND: Increased angiogenetic activity in inflammatory bowel disease (IBD) has been shown in previous studies. The aim of this study was to evaluate the relationship of serum vascular endothelial growth factor (VEGF) and endostatin levels with clinical features and mucosal expression in patients with ulcerative colitis (UC). DESIGN AND SETTING: Cross-sectional analytical study conducted in a tertiary-level public hospital. METHODS: Serum VEGF and endostatin levels were determined in 82 individuals: 39 with UC, 28 with irritable bowel syndrome (IBS) and 15 healthy controls (HCs), using enzyme-linked immunosorbent assays (ELISA). VEGF and endostatin expressions were studied using immunohistochemistry (IHC). RESULTS: Mean serum VEGF and endostatin levels were significantly higher in patients with UC than in patients with IBS and in HCs (511.9 ± 377.5 pg/ml, 305.0 ± 121.42 pg/ml and 36.1 ± 40.6 pg/ml; P = 0.001 for VEGF; and 155.50 ± 59.8 ng/ml, 116.9 ± 23.8 ng/ml and 102.2 ± 22.4 ng/ml; P < 0.001 for endostatin, respectively). There was a positive correlation between serum VEGF and endostatin levels (r = 0.422; P < 0.01). Mean H-scores for VEGF expression were higher in the active UC group than in the inactive UC and IBS groups, in the stroma, endothelium and epithelium. Mean H-scores for endostatin expression were higher in the active UC group than in the inactive UC and IBS groups, in the stroma and endothelium. There was no endostatin expression in the epithelium. CONCLUSION: Increased endostatin appears to be a defensive reaction to increased VEGF in patients with UC.

Discriminant value of IEL counts and distribution pattern through the spectrum of gluten sensitivity: a simple diagnostic approach.

Intraepithelial lymphocytosis (IELosis) with or without villous abnormality is a characteristic feature of gluten sensitivity (GS) including celiac disease (CD) and non-celiac-GS, although various conditions may also be associated with IELosis. In order to distinguish GS from the other causes of IELosis, a threshold for IEL counts is necessary. We aimed to determine a cut-off value for IELs and monitor its value in the spectrum of GS in a large cohort. For this purpose, the duodenal biopsies from four groups of individuals including Types 1 (n = 88) and 3 (n = 92) CD, non-CD IELosis (n = 112), and control (n = 82) cases, all strictly defined by their clinical, laboratory, and serologic features, were evaluated. The number of IELs/100 enterocytes and their distribution pattern on H&E- and CD3-immunostained sections were assessed for each group. Kruskal-Wallis test and ROC curve analysis for discriminant value were employed for statistics. The IEL counts showed an increasing trend through the spectrum of mucosal pathology including controls (12.06; 21.40), non-CD IELosis (28.62; 39.46), Type 1 CD (49.27; 60.15), and Type 3 CD (58.53; 71.74) both on H&E- and CD3-immunostained sections, respectively (p < 0.001). ROC analysis revealed 20.5 on H&E and 28.5 on CD3 as the IEL cut-off values with a sensitivity of 95.9 and 87.7% and a specificity of 98.8% and 93.9%, respectively, for controls. IELs showed a diffuse distribution pattern per biopsy piece and per villus (90.9%, 100%, respectively) in nearly all of Type 1 CD cases (p < 0.001). An IEL cut-off value of 20.5 on H&E together with a diffuse distribution pattern seem to be the most discriminant features for the diagnosis of CD, even for the milder forms of the disease.

NOD2/CARD15, NOD1/CARD4, and ICAM-1 gene polymorphisms in Turkish patients with inflammatory bowel disease.

PURPOSE: The genetic susceptibility of people with certain NOD2/CARD15, NOD1/CARD4, and ICAM-1 gene variants to inflammatory bowel disease is still under investigation. The aim of this study was to investigate polymorphisms in the NOD2/CARD15 (R702W, G908R, and 3020insC), NOD1/CARD4 (E266K, D372N), and ICAM-1 (G241R, K469E) genes, which are known to be associated with inflammation, in Turkish patients with inflammatory bowel disease and healthy control groups. METHODS: The genotypes of 70 patients with endoscopically and histopathologically diagnosed Crohn's disease (38 men, 32 women; mean age, 38.8 +/- 1.3), 120 patients with ulcerative colitis (67 men, 53 women; mean age, 41.7 +/- 1.3) and 106 healthy control subjects (37 men, 69 women; mean age, 35.7 +/- 1.4), who stated that they had never had any prior bowel disease history, were compared. A polymerase chain reaction-restriction fragment length polymorphism analysis was performed for two variants of the ICAM-1 gene, the three main variants of the NOD2/CARD15 gene, and the E266K variant of the NOD1/CARD4 gene, and DNA sequencing was used for the D372N polymorphism of the NOD1/CARD4 gene. RESULTS: In this study, the three previously described Crohn's disease-predisposing variants of the NOD2/CARD15 gene and the polymorphisms examined in the NOD1/CARD4 and ICAM-1 genes were not found to be associated with ulcerative colitis or Crohn's disease. CONCLUSIONS: These findings suggest that the polymorphisms observed in the NOD2/CARD15, NOD1/CARD4, and ICAM-1 genes are not genetic susceptibility factors for Crohn's disease or ulcerative colitis in Turkey.

Classification chaos in coeliac disease: Does it really matter?

The spectrum of mucosal pathology in coeliac disease (CD), initially defined by Marsh in 1992 has been subjected to several modifications in the following years by Oberhuber, then by Corazza and Villanaci, and finally by Ensari. The present study, aimed to end the ongoing confusion regarding the classification of mucosal pathology in CD by applying all the classifications proposed so far on a large series of cases. A total of 270 duodenal biopsies taken from the distal duodenum of patients with a diagnosis of CD were included in the study. All biopsies were classified according to Marsh, Oberhuber, Corazza Villanaci, and Ensari classification schemes. For statistical analyses cases were divided into three groups: Group 1 included type 1 lesions in Marsh, Ensari, and Oberhuber and grade A in Corazza Villanaci classifications. Group 2 comprised of type 2 lesions in Marsh and Ensari classifications together with type2, type 3a and 3b lesions in Oberhuber classification and grade B1 lesions in Corazza Villanaci classification. Group 3 included type 3 lesions in Marsh and Ensari classifications, and type 3c lesions in Oberhuber, and grade B2 lesions in Corazza Villanaci classifications. The kappa value was 1.00 (excellent) for group 1, 0.53 (fair) for group 2 and 0.78 (excellent) for group 3 (p<0.0001). These results suggest that any of the above classification system would serve similar purposes in the diagnosis of CD. Therefore, it is advisable that the pathologist should use the simplest reliable scheme.

Lamivudine treatment in HBeAg-negative chronic hepatitis B patients with low level viraemia.

BACKGROUND: Our aim was to determine the short-term natural course of viraemia and the response to lamivudine treatment in HBeAg-negative chronic hepatitis B patients with a persistently low hepatitis B virus (HBV)-DNA level. METHODS: A total of 55 patients were included. Group 1 consisted of 37 patients with low-level viraemia and high serum alanine aminotransferase (ALT) levels and further randomized to two groups: group 1a (n=19) patients received 1 year of lamivudine therapy and group 1b (n=18) patients were untreated controls. Group 2 consisted of 18 inactive carriers who were followed as controls of untreated low viraemic chronic hepatitis B patients. HBV DNA was longitudinally determined by real-time polymerase chain reaction assay. RESULTS: A female predominance in group 2 was observed while males were predominant in group 1. Mean age and baseline HBV-DNA levels did not differ between group 1 and 2 patients while group 1 patients had a higher histological score (P<0.01). Of group 1a patients, 44% had complete ALT normalization at end of treatment, whereas 21% untreated group 1b patients had normal ALT at the end of the follow-up. No change in histological activity was observed in group 1a patients at the end of treatment. HBV-DNA levels did not significantly change from baseline to end-of-treatment/observation period in patient groups. The viraemia course was not different across the groups. CONCLUSIONS: Low viraemic HBeAg-negative patients with high ALT present with minimal/mild histological activity. Inactive carriers cannot be differentiated from low viraemic patients with high ALT based on HBV DNA determination. Although lamivudine treatment can be effective in some cases, observation rather than a prompt treatment attempt seems to be more logical because of mild histological changes and low response rate to treatment in these patients.

Dual benefit from intramuscular interferon-beta treatment in a patient with multiple sclerosis and chronic hepatitis-C virus infection.

In patients with hepatitis C virus infection interferon-beta therapy is most effective when administered by the intravenous route. However we would like to present a patient with multiple sclerosis and chronic hepatitis C virus infection who obtained dual benefit from intramuscular interferon-beta therapy. Intramuscular interferon-beta 1a (Avonex) 6 million U/week was started for prevention of attacks in a 32-year-old woman with multiple sclerosis. She had acquired hepatitis C virus infection from blood transfusion during a Caesarean section. Although serum transaminases were within normal limits anti-hepatitis C virus test by ELISA and hepatitis C virus RNA by polymerase chain reaction were positive. Liver biopsy revealed chronic persistent hepatitis. Considering the use of interferon-beta 1a for multiple sclerosis prophylaxis and the stage of hepatitis the patient was not offered any additional treatment. Repeat liver biopsy performed after one year showed the absence of previous findings. The patient has also cleared the hepatitis-C virus RNA.

The effect of rabeprazole alone or in combination with H2 receptor blocker on intragastric pH: a pilot study.

BACKGROUND/AIMS: Proton pump inhibitors have been widely used in recent years. However, there are studies suggesting that proton pump inhibitors may not control the gastric acidity effectively during the night, especially in gastroesophageal reflux disease. It has therefore been suggested that H2 receptor blockers should be added to the therapy. The aim of our study was to evaluate the effects of proton pump inhibitors alone or in combination with H2 receptor blockers on gastric acidity with 24-hour gastric pH monitoring. METHODS: Esophagogastroscopy and 24-hour gastric pH monitoring were performed on 10 patients with dyspeptic symptoms. No patient had antacidity. All patients had erosive antral gastritis. Patients were randomized to two groups as either proton pump inhibitor therapy group (rabeprazole 20 mg/day, p.o.) or proton pump inhibitor + H2 receptor blocker therapy group (rabeprazole 20 mg/day, p.o. + famotidine 40 mg/day, p.o). After one month of treatment, 24-hour gastric pH monitoring was re-performed. RESULTS: Seven female and three male patients were enrolled into the study. The mean age was 51.1+/-11.56 years. All patients had antral erosive gastritis. Gastric pH was measured as less than 4 in 81.4% of the 24-hour period prior to rabeprazole treatment. With rabeprazole treatment this ratio decreased to 27.6% (p<0.05). These ratios were 86.3% and 4.55%, respectively, in the group that received combination therapy (p<0.05). CONCLUSIONS: Combination therapy with H2 receptor blockers and proton pump inhibitors seemed to control intra-gastric pH better than proton pump inhibitors alone. Use of H2 receptor blockers and proton pump inhibitors in combination to control intra-gastric pH is more beneficial.

Factor V Leiden, prothrombin G20210A and MTHFR gene mutations in inflammatory bowel disease.

BACKGROUND/AIMS: Thromboembolic events are more common in patients with inflammatory bowel disease than in the normal population; however, the reason for the increased prevalence is not clear. The aim of this study was to evaluate the prevalence of factor V Leiden, prothrombin G20210A and methylene tetrahydrofolate reductase (MTHFR) gene mutations in IBD patients followed in our outpatient clinic. METHODS: Thirty-four patients with ulcerative colitis and 28 patients with Crohn's disease and 80 healthy controls were included in the study. No patient had a history of previous thromboembolism. Factor V Leiden, prothrombin G20210A and MTHFR gene mutations were studied. RESULTS: Heterozygote factor V Leiden mutation was found in five (6.25%) control patients and in two (3.2%) IBD patients. Heterozygote MTHFR mutation was obtained in seven (11.3%) IBD patients and in five (6.25%) controls. Heterozygote prothrombin G20210A mutation was found in two (2.5%) and homozygote MTHFR mutation in one (1.25%) control patient. There was no statistical difference between the IBD group and healthy controls. CONCLUSIONS: Genetic mutations that could increase the thrombosis risk were not found to be different in IBD versus the normal population in our study.

Upper gastrointestinal findings in oral lichen planus.

BACKGROUND/AIMS: Lichen planus is an inflammatory disease of the skin and mucous membranes. Oral mucosa is known to be frequently affected by the disease, but it has also been observed that gastrointestinal mucosas are sometimes involved. METHODS: In this study, the upper gastrointestinal tract was investigated endoscopically and histopathologically in 20 patients with oral lichen planus. RESULTS: Endoscopy determined antral gastritis in seven patients, esophagitis in four, bulbitis in three, chronic duodenal ulcer in one and esophageal sphincter dysfunction in one patient. Lichen planus-like changes on the esophageal mucosa at histopathological examination were found in one patient. Findings in the other patients were as follows: chronic atrophic gastritis (nine), helicobacter pylori infection (nine), esophagitis (two), bulbitis (two) and erosive gastritis (one). CONCLUSION: Patients with Lichen planus should be evaluated for possible gastro-intestinal involvement with endoscop.

Percutaneous transhepatic venoplasty: an alternative treatment for Budd-Chiari syndrome.

BACKGROUND/AIMS: In patients with Budd-Chiari syndrome due to short segment hepatic vein stenosis where percutaenous transluminal venoplasty is not successful, percutaneous transhepatic balloon venoplasty may be a valid treatment option. The aim of this prospective study was to evaluate the effects of this procedure for the treatment of patients with Budd-Chiari syndrome, in whom transluminal cannulation was unsuccessful. METHODS: Ten patients with short segment occlusion of the hepatic veins were treated by percutaneous transhepatic balloon venoplasty between January 1997 and January 2000. The median follow-up period of these patients was 20 months (2-33 months). RESULTS: The procedure was unsuccessful in two patients. Eight patients (five men, three women) with a median age of 28 (range, 15-61) years were treated by percutaneous transhepatic balloon venoplasty and in seven of them, clinical symptoms including abdominal distension and ascites, resolved completely. Long term anticoagulation therapy was not given to the patients. One patient with advanced stage liver disease died of variceal bleeding two months after the procedure. During follow-up, symptomatic reocclusion requiring dilatation occurred in three patients. CONCLUSIONS: Percutaneous transhepatic balloon venoplasty is an alternative treatment option for selected patients with Budd-Chiari syndrome when transluminal cannulation of the hepatic veins is not possible. Long term anticoagulation therapy seems to be necessary in these patients.

The mutations in ISDR of NS5A gene are not associated with response to interferon treatment in Turkish patients with chronic hepatitis C virus genotype 1b infection.

BACKGROUND/AIMS: A significant association between variations in amino acid sequences resides between 2209-2248 nucleotides of HCV non-structural 5A (NS5A) gene, and response to interferon treatment has been proposed. The aim of this study was to determine whether the amino acid sequence changes in ISDR could be correlated to response to alpha interferon treatment in Turkish patients infected with HCV genotypes 1b and 1a. METHODS: Thirty-nine patients with chronic C virus infection (35 and 4 patients with genotype 1b and 1a, respectively), receiving 3x3-5 MU of interferon a-2b for six months were included in the study. Following PCR amplification of the region from pre-treatment serum samples, the products were directly sequenced. The amino acid sequence of NS5A was compared with the published sequence for HCV-J (AA 2209-2248). Mutant type was defined as three or more amino acid mutations, and intermediate type as 1-3 amino acids in this region. Otherwise, they were defined as the wild type (no amino acid mutations). HCV RNA serum viremia levels were analyzed by branched DNA assay. RESULTS: Eighteen patients were responders (R; 46%), whereas 21 patients were non-responders (NR; 54%). Amino acid changes in both R and NR groups did not show significant difference. Intermediate or wild type strains were detected in both groups. CONCLUSIONS: In this study, we could not determine a significant association between number of amino acid changes in NS5A2209-2248 and response to interferon treatment. In the majority of the patients, it seems that amino acid sequences in this region are well conserved.

Manometric assessment of esophageal motor function in patients with primary biliary cirrhosis.

INTRODUCTION/AIM: Primary biliary cirrhosis is associated with other autoimmune diseases including Sjögren's syndrome, and scleroderma. Esophageal dysmotility is well known in scleroderma, and Sjögren's syndrome. The aim of this study is to investigate whether any esophageal motor dysfunction exists in patients with primary biliary cirrhosis. METHOD: The study was performed in 37 patients (36 women, mean age: 56.29 ± 10.01 years) who met diagnostic criteria for primary biliary cirrhosis. Thirty-seven functional dyspepsia patients, were also included as a control group. Patients entering the study were asked to complete a symptom questionnaire. Distal esophageal contraction amplitude, and lower esophageal sphincter resting pressure were assessed. RESULTS: Manometric findings in primary biliary cirrhosis patients vs. controls were as follows: Median lower esophageal sphincter resting pressure (mmHg): (24 vs 20, p=0.033); median esophageal contraction amplitude (mmHg): (71 vs 56, p=0.050); mean lower esophageal sphincter relaxation duration (sc, x ± SD): (6.10 ± 1.18 vs 8.29 ± 1.92, p<0.001); and median lower esophageal sphincter relaxation (%) (96 vs 98, p=0.019); respectively. No significant differences were evident in median peak velocity (sc) (3.20 vs 3.02, p=0.778) between patients with primary biliary cirrhosis and the functional dyspepsia patients. Esophageal dysmotility was found in 17 (45.9%) primary biliary cirrhosis patients (non-specific esophageal motor disorder in ten patients, hypomotility of esophagus in five patients, nutcracker esophagus in one patient and hypertensive lower esophageal sphincter in one patient). CONCLUSION: Esophageal dysmotility was detected in 45.9% of patients. The study suggests that subclinic esophageal dysmotility is frequent in patients with primary biliary cirrhosis.

Vascular endothelial growth factor, endostatin levels and clinical features among patients with ulcerative colitis and irritable bowel syndrome and among healthy controls: a cross-sectional analytical study

ABSTRACT BACKGROUND: Increased angiogenetic activity in inflammatory bowel disease (IBD) has been shown in previous studies. The aim of this study was to evaluate the relationship of serum vascular endothelial growth factor (VEGF) and endostatin levels with clinical features and mucosal expression in patients with ulcerative colitis (UC). DESIGN AND SETTING: Cross-sectional analytical study conducted in a tertiary-level public hospital. METHODS: Serum VEGF and endostatin levels were determined in 82 individuals: 39 with UC, 28 with irritable bowel syndrome (IBS) and 15 healthy controls (HCs), using enzyme-linked immunosorbent assays (ELISA). VEGF and endostatin expressions were studied using immunohistochemistry (IHC). RESULTS: Mean serum VEGF and endostatin levels were significantly higher in patients with UC than in patients with IBS and in HCs (511.9 ± 377.5 pg/ml, 305.0 ± 121.42 pg/ml and 36.1 ± 40.6 pg/ml; P = 0.001 for VEGF; and 155.50 ± 59.8 ng/ml, 116.9 ± 23.8 ng/ml and 102.2 ± 22.4 ng/ml; P < 0.001 for endostatin, respectively). There was a positive correlation between serum VEGF and endostatin levels (r = 0.422; P < 0.01). Mean H-scores for VEGF expression were higher in the active UC group than in the inactive UC and IBS groups, in the stroma, endothelium and epithelium. Mean H-scores for endostatin expression were higher in the active UC group than in the inactive UC and IBS groups, in the stroma and endothelium. There was no endostatin expression in the epithelium. CONCLUSION: Increased endostatin appears to be a defensive reaction to increased VEGF in patients with UC.