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.

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

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.

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.

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.

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.

Effects of Helicobacter pylori infection and long-term proton pump inhibitor use on enterochromaffin-like cells.

BACKGROUND: Excessive release of gastrin leads to hypertrophy and hyperplasia of enterochromaffin-like cells (ECL) and prolonged stimulation of these cells causes functional impairment. The purpose of this study was to investigate the effect of Helicobacter pylori (H. pylori) infection and long-term proton pump inhibitors (PPI) use on ECL cells. METHODS: Fifteen patients who underwent endoscopy because of dyspeptic symptoms were enrolled in the present study. Biopsies were taken from corpus and antrum and existence of H. pylori was investigated with culture, cytology and CLOtest. The patients were divided into 3 groups. Group-A: H. pylori-negative, never treated previously with PPI; Group-B: H. pylori-positive, never treated previously with PPI; and group-C: H. pylori-negative and continuously treated with PPI for more than 6 months before the subject recruitment period. The features of ECL cell in oxyntic glands were examined with electron microscopy on biopsy specimens. RESULTS: ECL cells were completely normal in Group A. In group B, moderate hyperplasia and vacuolization was seen in ECL cells. In group C, ECL cell hyperplasia was observed and vacuoles with greater amounts of granules in enlarged vesicles were found more intensely in cytoplasm. CONCLUSION: The use of PPI for a long period of time and presence of H. pylori infection are risk factors for ECL hyperplasia.

The efficacy and safety of colonoscopy preparation with oral sodium phosphate in elderly patients.

BACKGROUND/AIMS: Oral sodium phosphate is an agent used commonly in our country for cleaning the intestines before colonoscopy. Our aim was to compare the safety, tolerability and efficiency of oral sodium phosphate solution used in colonoscopy preparation in patients over 70 years of age. METHODS: This study was carried out in Ankara University School of Medicine Cebeci Hospital Endoscopy Center between August 2008 and March 2009. The extent of colon cleanliness was scored in the colonoscopy procedure. The data from the two groups were compared. RESULTS: In our study, 55 patients were divided into two groups according to their age, as over 70 years (n: 25) and under 70 years (n: 30). The average age of the group under 70 years was 49.4±9.8 and of the group over 70 years was 71.4±1.2 (p=0.04). Among the patients included in this study, 59.1% were female (n: 28) and 50.9% were male (n: 27). In the over 70 years group, the intestinal cleanliness was poor-fair in 2 patients, acceptable in 7 patients and excellent in 16 patients. In the below 70 years group, the intestinal cleanliness was poor in 2 patients, acceptable in 9 patients, good in 13 patients, and excellent in 6 patients. In the statistical evaluation, it was determined that there was no statistical difference between the over- and below 70 years of age groups regarding good-excellent intestinal cleanliness and poor-medium intestinal cleanliness (p=0.109). There was no statistical difference between the groups with regard to the adverse effects. The sodium, potassium and creatinine levels were assessed on the procedure day in 5 patients with clinical side effects (abdominal pain, nausea, vomiting, dizziness, hypotension) in the elderly group. No electrolyte imbalance or renal function impairment was observed in these patients. CONCLUSIONS: In the group of patients over 70 years old, a special patient group without comorbid diseases, oral sodium phosphate solution used for colon preparation was effective and well-tolerated with a low adverse effect rate. In spite of this safe profile, since serum creatinine levels and electrolyte imbalance were assessed in only a limited number of patients, the relationship reported in the literature between oral sodium phosphate and electrolyte imbalance and renal function impairment should be kept in mind.

The prevalence of celiac disease in patients fulfilling Rome III criteria for irritable bowel syndrome.

BACKGROUND AND AIMS: Celiac disease shares several symptoms which constitute some of the ROME criteria used for the diagnosis of irritable bowel syndrome (IBS), and as such many patients with underlying Celiac disease may be mistakenly diagnosed as having IBS. The aim of the present study was to determine the prevalence of Celiac disease in patients with IBS fulfilling ROME III criteria. MATERIALS AND METHODS: Patients who fulfilled ROME III criteria for irritable bowel syndrome were screened for Celiac disease using the Biocard(TM) Celiac Disease Stick test, and patients who tested positive had their serum samples analyzed for antigliadin IgA and IgG, and anti-tissue transglutaminase IgA antibodies. Patients with detectable antibody levels underwent endoscopic duodenal biopsy to confirm a diagnosis of Celiac disease. RESULTS: Two of 100 patients who were diagnosed as having irritable bowel syndrome as per the Roma III criteria were found to have elevated levels of serum antigliadin IgA and IgG, and anti-tissue transglutaminase IgA antibodies, with histological evidence of Celiac disease on examination of duodenal biopsy. Both patients were started on a gluten-free diet, showing significant improvement in their symptoms on follow-up. CONCLUSIONS: Celiac disease is a common finding among patients labeled as IBS. Celiac disease must be considered in differential diagnosis of IBS especially in the therapy refractory group.

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.

The role of fecal calprotectin in investigating inflammatory bowel diseases

INTRODUCTION: Invasive and non-invasive tests can be used to evaluate the activity of inflammatory bowel diseases. OBJECTIVE: The aim of the present study was to investigate the role of fecal calprotectin in evaluating inflammatory bowel disease activity and the correlation of fecal calprotectin with the erythrocyte sedimentation rate and C reactive protein values in inflammatory bowel disease. METHOD: Sixty-five patients affected with inflammatory bowel disease were enrolled. Twenty outpatients diagnosed with inflammatory bowel disease comprised the control group. RESULTS: In the present study, all patients in the control group had an fecal calprotectin value lower than the cut-off point (50 mg/kg). CONCLUSION: In conclusion, fecal calprotectin was found to be strongly associated with colorectal inflammation indicating organic disease. Fecal calprotectin is a simple and non-invasive method for assessing excretion of macrophages into the gut lumen. Fecal calprotectin values can be used to evaluate the response to treatment, to screen asymptomatic patients, and to predict inflammatory bowel disease relapses.

A rare cause of ascites: Familial Mediterranean fever.

Familial Mediterranean fever is an autosomal recessive disorder characterized by sporadic, paroxysmal attacks of fever and serosal inflammation. In Familial Mediterranean fever, peritoneal effusion during abdominal attacks is usually mild, is not detected by clinical evaluation, and disappears during clinical remission. Chronic ascites has rarely been described in patients with Familial Mediterranean fever. Genetic analysis is highly specific and sensitive for diagnosis of Familial Mediterranean fever. All of the four cases discussed in our study had no benign or malignant pathology that could explain the ascites. They had suffered from repetitive periods of fever and ascites since childhood. Genetic analysis of these four cases revealed that one was M694V/M694V homozygote, one was M694V/? heterozygote, and the other two were M694V/V726A compound heterozygote. Ascites regressed with colchicine therapy. Since Familial Mediterranean fever is common our country, it should be kept in mind in the differential diagnosis in patients with ascites of unknown etiology.

An unusual presentation of Tangier disease with gallbladder involvement.

Tangier disease is a rare, autosomally inherited disorder of lipoprotein metabolism characterized by absence or marked deficiency of normal high density lipoprotein (HDL) cholesterol in plasma resulting in the accumulation of cholesterol esters in various organs. A 57-year old male with a past medical history of hypertension, coronary artery disease and splenectomy admitted to our hospital for rectal bleeding. In routine laboratory tests thrombocytopenia, hypocholesterolemia and low HDL levels were detected. Colonoscopy revealed 1-3 mm sized, brownish, spotty lesions spread throughout the colonic mucosa. Histopathologically accumulation of foam cells which showed lipid vacuoles and myeline figures on electron microscopy were observed. Bone marrow biopsy was also suggestive of lipid storage disease. The laparoscopic operation performed for acute cholecystitis showed similar appearances in the gall bladder and liver. The case was diagnosed as rare presentation of Tangier disease with gallbladder involvement in view of the low HDL cholesterol level and systemic lipid deposition.

Mucins in the colorectal neoplastic spectrum with reference to conventional and serrated adenomas.

BACKGROUND/AIMS: Alterations in expression of mucins and aberrant expression of various types of mucin genes were observed in colorectal adenomas and carcinomas, though their significance in neoplastic transformation of colorectal epithelium is yet to be determined. The aim of this study was to determine expression of MUC1, MUC2, MUC5AC, and MUC6 through conventional adenoma-carcinoma sequence and polyps involved in the "serrated" pathway of the colorectum using tissue array technique. METHODS: In this study, a total of 172 cases including 100 colorectal polyps [8 hyperplastic polyps, 10 sessile serrated adenomas, 19 tubular, 37 tubulovillous, and 26 villous adenomas], 16 adenomas with intramucosal carcinoma, 28 conventional colorectal cancers, and 28 normal mucosae were examined. Tissue array blocks were prepared and sections were stained immunohistochemically for MUC1, MUC2, MUC5AC, and MUC6. RESULTS: Expression of MUC1 significantly increased in close correlation with the neoplastic process and reached its highest values in intramucosal carcinomas and conventional colorectal cancers (p<0.001). In contrast, MUC2 expression showed a significant decrease in intramucosal carcinoma and conventional colorectal cancer groups (p<0.001). Sessile serrated adenomas exhibited the highest MUC5AC expression while adenomatous polyps showed an increase in MUC5AC expression in parallel with neoplastic progression (p<0.001). Hyperplastic polyps seemed to lie between normal mucosa and sessile serrated adenomas in terms of mucin expression, suggesting that they are morphologically and histogenetically linked. CONCLUSIONS: Upregulation of MUC1 and MUC6 through the adenoma-carcinoma sequence together with downregulation of MUC2 and MUC5AC at the neoplastic end of the spectrum seem to follow the steps of malignant transformation.

The significance of beta-catenin, E-cadherin, and P-cadherin expressions in neoplastic progression of colorectal mucosa: an immunohistochemical study.

BACKGROUND AND STUDY AIMS: The purpose of the current study was to investigate the role of beta-catenin, E-cadherin and P-cadherin in colorectal carcinogenesis using tissue array method. PATIENTS AND METHODS: Core tissue biopsies were taken from paraffin-embedded tissue blocks of 167 cases including 26 normal mucosae (NM), 99 colorectal polyps (10 hyperplastic polyps (HP), 8 traditional serrated (TSA), 17 tubular (TA), 37 tubulovillous (TVA), and 27 villous adenomas (VA)), 14 adenomas with intramucosal carcinoma (ACA), and 28 colorectal cancers (CCA). Immunohistochemistry was performed using antibodies to beta-catenin, E-cadherin, and P-cadherin. Distribution of positivity was assessed using percentage expression while an arbitrary grading scale was used for staining intensity. RESULTS: beta-catenin expression was cytoplasmic, membranous, and nuclear. Both E-cadherin and P-cadherin expressions were confined to cytoplasmic-membranous compartments. Membranous expression of beta-catenin significantly decreased in CCA (p < 0.01). Nuclear beta-catenin expression significantly increased in close correlation with neoplastic sequence reaching its highest expression in ACA and CCA (p < 0.001). Polyps with intraepithelial neoplasia (IEN) showed significantly higher nuclear beta-catenin expression in parallel with increasing grades of IEN (p < 0.001). E-cadherin and P-cadherin expression increased in polyps, whereas a significant decrease in their expression was observed in CCA (p < 0.001) while E-cadherin expression significantly increased in CCA compared to NM (p < 0.001), no such difference was observed in P-cadherin expression. CONCLUSIONS: Nuclear beta-catenin expression correlating with the grade of IEN in polyps and carcinomas supports its role in colorectal carcinogenesis. E-cadherin and P-cadherin expressions in adenomas suggest that these molecules might have role in adenoma formation though not necessarily be involved in neoplastic progression.

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.

Cytokine gene polymorphisms in Turkish patients with inflammatory bowel disease.

OBJECTIVE: Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory diseases of the bowel, the causes of which are not fully known. Ethnic differences in disease prevalence, familial aggregation of the disease and studies of twins provide the most important evidence to suggest that genetic factors play a role in the pathogenesis of inflammatory bowel disease (IBD). The aim of this study was to examine the allelic polymorphisms that can determine the immune response levels in tumor necrosis factor alpha (TNFalpha), interleukin-1beta (IL-1B), interleukin-1 receptor antagonist ( IL-1RN) and interleukin-10 (IL-10) genes and to investigate their roles in the inflammatory pathway in IBD. MATERIAL AND METHODS: The study included 120 patients with UC and 70 patients with CD who were diagnosed either endoscopically or histopathologically. The control group comprised 105 healthy individuals who stated that they had never had any bowel disease during their life span. The polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method for polymorphisms in the TNFalpha gene at positions -308 and -238, the IL-10 gene at positions -1082 and -627, the IL-1B gene at -511 regions and the variable number of tandem repeat (VNTR) method for polymorphism in the intron 2 of the IL-1RN gene were performed. The results were analyzed on agarose gel electrophoresis. RESULTS: No significant differences were found in the allele and genotype frequencies of the polymorphisms in the IL-1B, IL10, TNFalpha and IL-1RN genes between the patients with UC and CD and controls. CONCLUSIONS: The results suggest that these polymorphisms were not important risk factors in the susceptibility to IBD in Turkish patients.

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.

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.