Role of Environmental Risk Factors in the Etiology of Inflammatory Bowel Diseases: A Multicenter Study.

BACKGROUND: The increasing global incidence and prevalence of inflammatory bowel disease (IBD) necessitates an investigation into the potential influence of environmental risk factors on its origin. AIM: This multicenter case-control study aimed to investigate potential environmental risk factors contributing to IBD development in Turkey. METHODS: The study included 156 Crohn's disease (CD), 277 ulcerative colitis (UC) patients, and 468 controls (matched for age and gender) from six hospitals' gastroenterology departments. Data collection relied on the International Organization of IBD's questionnaire on environmental factors. Each environmental factor was initially analyzed using univariate and subsequently multivariate logistic regression models. RESULTS: In the multivariate model, regular coffee consumption was associated with decreased odds for both CD (OR 0.28; 95% CI 0.14-0.55) and UC (OR 0.25; 95% CI 0.15-0.42). Stress was associated with UC (OR 3.27; 95% CI 1.76-6.10) and CD (OR 4.40; 95% CI 2.12-9.10) development. A history of childhood infectious diseases (gastroenteritis, upper respiratory tract infections, etc.) raised the odds for both CD (OR 9.45; 95% CI 2.51-35.6) and UC (OR 7.56; 95% CI 1.57-36.4). Conversely, consuming well/spring water (OR 0.22; 95% CI 0.10-0.50) and childhood antibiotic use (OR 0.41; 95% CI 0.18-0.93) showed a positive association against UC. Increased consumption of refined sugar and industrial food products emerged as risk factors for IBD. Smoking increased the risk for CD (OR 2.38; 95% CI 1.16-4.91), while ex-smoking increased the risk for UC (OR 3.16; 95% CI 1.19-8.37). CONCLUSIONS: This study represents the first multicenter case-control study in Turkey examining the effects of environmental factors on IBD. It revealed that coffee consumption is positively associated, while stress and childhood infection-related diseases are risk factors. These findings, which are not supported by other studies, provide insight into the relationships between these factors and IBD.

Management of traumatic bile duct injuries in children.

PURPOSE: Pediatric experience with biliary tract injuries (BTI) is limited and mostly consists of case presentations. The purpose of this study is to evaluate clinical and radiological findings of possible BTI, treatment strategies, and results. METHODS: The records of nine patients with the diagnosis of BTI between July 2009 and November 2017 were reviewed retrospectively. RESULTS: There were seven boys and two girls (mean 8.05 ± 4.39 years). The mechanisms were motor vehicle occupant, fall, crush and gunshot wound. Hepatic laceration routes that extended into the porta hepatis and contracted the gall bladder were demonstrated on computerized tomography (CT). Bile duct injury was diagnosed with bile leakage from the thoracic tube (n = 2), from the abdominal drain (n = 2) and by paracentesis (n = 5). Extrahepatic (n = 8) and intrahepatic (n = 1) bile duct injuries were diagnosed by cholangiography. Endoscopic retrograde cholangiography, sphincterotomy, and stent placement were successfully completed in five patients. Peritoneal drainage stopped after 3-17 days of procedure in four patients. The fifth patient was operated with the diagnosis of cystic duct avulsion. Cholecystectomies, primary repair of laceration, cystic duct ligation, and Roux-en-Y hepatoportoenterostomy were performed in the remaining four patients. All patients presented with clinically normal findings, normal liver functions, and normal ultrasonographic findings in the follow-up period. CONCLUSIONS: The presentation of the parenchymal injury extending to the porta hepatis with contracted gall bladder on CT and diffuse homogenous abdominal fluid should be considered as signs of BTI. We suggest a multi-disciplinary approach for the diagnosis and treatment of BTIs. Surgery may be indicated according to the patient's clinical condition, radiological findings and failure of non-operative treatment.

High Dose Oral Furosemide with Salt Ingestion in the Treatment of Refractory Ascites of Liver Cirrhosis.

PURPOSE: We aimed to evaluate and compare the efficacy and safety of high-dose furosemide+salt orally by comparing HSS+ furosemide (i.v.) and repeated paracentesis in patients with RA. METHODS: This was a prospective study of 78 cirrhotic patients with RA, randomized into three groups: Group A (n= 25) i.v. furosemide (200-300 mg bid) and 3% hypotonic saline solution (HSS) (once or twice a day); Group B (n= 26) oral furosemide tablets (360-520 mg bid) and salt (2.5 g bid); and, Group C (n= 27) repeated large-volume-paracentesis (RLVP) with albumin infusion. Patients without hyperkalemia were administrated 100 mg of spironolactone/day. During the follow-up; INR, creatinine, and total bilirubin levels were measured to determine the change in MELD (model of end stage liver disease) score. RESULTS: Hepatic encephalopathy (HE), severe episodes of spontaneous bacterial peritonitis (SBP) and pleural effusions (PE) occurred more frequently in Group C. Improvement in Child-Pugh and MELD score was better in Group A and B than Group C. In Group B, improvements were seen in the Child-Pugh and MELD score, reduction in body weight, duration and number of hospitalization. In Groups A and B, remarkable increases in diuresis were observed (706±116 to 2425±633 mL and 691±111 to 2405±772 mL) and serum sodium levels also improved. HE and SBP were occurred more often in group C (p<0.002). Hospitalization decreased significantly in Group B (p<0.001). There was no significant difference in survival among groups. CONCLUSION: High dose oral furosemide with salt ingestion may be an alternative, effective, safe and well-tolerated method of therapy for RA.

Nasobiliary Drainage for Benign Recurrent Intrahepatic Cholestasis in Patients Refractory to Standard Therapy.

PURPOSE: Benign recurrent intrahepatic cholestasis (BRIC) is characterized by episodic cholestasis and pruritus without anatomical obstruction. The aim of this study was to evaluate the safety and efficacy of nasobiliary drainage (NBD) in patients with BRIC refractory to medical therapy and to determine whether the use of NBD prolongs the episode duration. METHODS: This was a multicenter retrospective study consisting of 33 patients suffering from BRIC. All patients were administrated medical treatment and 16 patients who were refractory to standard medical therapies improved on treatment with temporary endoscopic NBD. Duration of treatment response and associated complications were analyzed. RESULTS: Sixteen patients (43% females) underwent 25 NBD procedures. The median duration of NBD was 17 days. There were significant improvements in total and direct bilirubin and alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase on the 3rd day of NBD. Longer clinical remission was monitored in the NBD group. Post-endoscopic retrograde cholangiopancreatography pancreatitis was observed in one of 16 cases. CONCLUSION: NBD effectively eliminates BRIC in all patients and improves biomarkers of cholestasis. It can be suggested that patients with attacks of BRIC can be treated with temporary endoscopic NBD; however, the results of this study should be confirmed by prospective studies in the future.

Impact of Helicobacter pylori on the clinical course of recurrent aphthous stomatitis.

BACKGROUND: Recurrent aphthous stomatitis is one of the most common lesions of oral mucosa. Helicobacter pylori is suggested as one of the etiological agents of recurrent aphthous stomatitis. Here, we conduct a study for evaluating the impact of H. pylori eradication on clinical course of recurrent aphthous stomatitis. METHODS: Forty-six patients with minor aphthous lesions were enrolled. The number of RAS lesions at last 6 months and vitamin B(12) levels were recorded. All patients were detected for H. pylori with endoscopic biopsy. H. pylori was positive in 30 patients and negative in 16 patients. H. pylori-positive 30 patients received eradication therapy. Three months after therapy, patients were re-evaluated with urea breath test; 18 patients were negative (eradicated), and the remainders (12 patients) were positive (non-eradicated) for H. pylori. 6 months after eradication, vitamin B(12) levels and number of aphthous lesions at 6 months were recorded. RESULTS: Vitamin B(12) levels were significantly increased in H. pylori-eradicated group (P = 0.001), whereas no significant change was found in non-eradicated group (P = 0.638). Mean number of aphthous lesions (per 6 months) of H. pylori-eradicated group was significantly decreased after eradication (P = 0.0001); in the non-eradicated group, no significant change was found (P = 0.677). In Hp-positive group, number of RAS lesions and vitamin B(12) levels were negatively correlated when evaluated both before and after eradication. CONCLUSIONS: This study provides evidence to support the beneficial effect of H. pylori eradication in patients with recurrent aphthous stomatitis. The underlying mechanism might be the increase in vitamin B(12) levels after eradication.

Early effect of peginterferon alpha-2b plus ribavirin treatment on blood pressure and insulin resistance in patients with chronic hepatitis C.

BACKGROUND/AIM: To investigate the early effects of peginterferon alpha-2b plus ribavirin therapy on blood pressure and related cardiovascular risk parameters, and also insulin resistance in patients with chronic hepatitis C virus (HCV) infection. METHODOLOGY: Twenty-nine patients with chronic hepatitis C (CHC) were enrolled in the study. Twenty-four hour ambulatory blood pressure monitoring (ABPM) of all patients was recorded in the pre-treatment period, and after the 1st and 8th weeks of treatment. Lipid profile, insulin resistance (IR), body mass index (BMI), complete blood counts and transaminase levels were also recorded at the same time periods. RESULTS: Fifteen of the 29 patients studied were hypertensive before treatment. The baseline, 1st week and 8th week recordings of ABPM (daytime, nighttime, mean systolic and diastolic measurements) did not show any significant change. Among hypertensive patients, differences in pretreatment, 1st and 8th week of treatment values of median systolic and diastolic blood pressures were not statistically significant. After the 8th week, total cholesterol, LDL, HDL, hemoglobin, white blood cell, platelet and AST/ALT were significantly decreased (p<0.05). Serum triglyceride levels increased significantly (p<0.0001) and HOMA-IR decreased (p=0.07). CONCLUSION: Peginterferon alpha-2b plus ribavirin therapy did not cause any increase in blood pressure in hypertensive and normotensive CHC patients in the early period of treatment. This treatment resulted in early but not significant changes in the IR status of CHC patients.

Bismuth-based first-line therapy for Helicobacter pylori eradication in type 2 diabetes mellitus patients.

BACKGROUND/AIM: The primary aim of this study was to assess the efficacy of a bismuth-based quadruple regimen as first-line therapy for Helicobacter pylori (HP) eradication in diabetes mellitus (DM) patients. The secondary aim was to study the effect of HP eradication on dyspeptic symptoms in DM patients. METHOD: Eighty-nine consecutive type 2 DM and 48 non-diabetic age- and sex-matched patients were enrolled in this study. Diabetic patients were randomized to receive either pantoprazole (40 mg b.i.d.), clarithromycin (500 mg b.i.d.), and amoxicillin (1 g b.i.d., PCA-DM group) for 14 days, or pantoprazole (40 mg b.i.d.), bismuth citrate (400 mg b.i.d.), tetracycline (500 mg q.i.d.), and metronidazole (500 mg b.i.d., PBTM-DM group) for 14 days as the eradication regimen. All non-diabetic patients were treated by quadruple therapy (PBTM-non-DM group) for 14 days. We used the validated Leeds Dyspepsia Questionnaire (LDQ) to assess dyspeptic symptoms at baseline and 6 weeks after the end of treatment. RESULTS: The HP eradication rates with intention-to-treat (ITT) and per-protocol (PP) analyses were 51% (for both) in the PCA-DM group; 81 and 85% in the PBTM-DM group, and 85 and 87% in the PBTM-non-DM group. The eradication rates are not different between the PBTM-DM and PBTM-non-DM groups (p > 0.05). The eradication rate was significantly lower in the PCA-DM group with both ITT and PP analysis than in the PBTM-DM and PBTM-non-DM groups (p < 0.05). LDQ score was 4.53 +/- 7.7 in DM patients with successful eradication and 14.68 +/- 5.9 in DM patients without successful eradication (p < 0.05). CONCLUSION: The bismuth-based quadruple eradication regimen as first-line therapy is safe, tolerable and achieves a high cure rate in patients with DM, and successful eradication may be beneficial on dyspeptic symptoms.

A recent evaluation of empirical cephalosporin treatment and antibiotic resistance of changing bacterial profiles in spontaneous bacterial peritonitis.

The aim of this research is to evaluate the recent changes in microorganisms causing spontaneous bacterial peritonitis in cirrhotic patients, antibiotic resistance, and response to empirical cephalosporin therapy. A total of 218 patients with ascites secondary to cirrhosis were enrolled. Parenteral cefotaxime or cefepime was given to patients who had a neutrophil count of 250/mm(3) or more or a positive bacterial culture of ascitic fluid. Antibiotic failure was defined by an absence of clinical improvement and an insufficient decrease in neutrophil count of ascites (<25% of initial value) by the third day of therapy. Of all the patients, 44.6% had culture-negative neutrocytic ascites, 24.8% had spontaneous bacterial peritonitis, and 10.1% had monomicrobial nonneutrocytic bacterascites. Growth in culture was observed in 76 patients (34.9%). The two most common isolated bacteria were Escherichia coli (33.8%) and coagulase-negative Staphylococcus (CoNS; 19.7%). The two cephalosporins were effective against E. coli (82%) and but not against CoNS (44%), while levofloxacin showed reasonable activity against both E. coli (71%) and CoNS (90%) in vitro. We confirmed a recent increased incidence of spontaneous bacterial peritonitis caused by Gram-positive bacteria. Levofloxacin seems to be a good alternative treatment for patients with uncomplicated spontaneous ascites infections.

The role of ascitic fluid viscosity in the differential diagnosis of ascites.

BACKGROUND: Ascites is defined as the pathological accumulation of fluid in the peritoneal cavity. It is the most common complication of cirrhosis, which is also the most common cause of ascites. Viscosity is a measure of the resistance of a fluid to deform under shear stress. Plasma viscosity is influenced by the concentration of plasma proteins and lipoproteins, with the major contribution from fibrinogen. To our knowledge, the viscosity of ascitic fluid has not yet been studied. OBJECTIVE: To evaluate the role of ascitic fluid viscosity in discriminating between ascites due to portal hypertension-related and nonportal hypertension-related causes, and to compare results with the serum-ascites albumin gradient (SAAG). METHODS: The present study involved 142 patients with ascites presenting with diverse medical problems. Serum total protein, albumin, glucose, lactate dehydrogenase (LDH) levels and complete blood count were obtained for all subjects. Paracentesis was performed routinely on admission and all ascitic fluid samples were evaluated by manual cell count with differential, ascitic fluid culture and biochemistry (total protein, albumin, glucose and LDH). Cultures of ascitic fluid were performed at bedside in all patients using blood culture bottles. Ascitic fluid viscosity was measured in a commercially available cone and plate viscometer. RESULTS: Of the 142 patients studied, 34 (24%) had an SAAG of 11 gL or less, whereas 108 (76%) had an SAAG of greater than 11 gL. Sex and mean age did not differ significantly between the two groups (P>0.05). Serum total protein, albumin, glucose, LDH levels, leukocyte count, ascitic fluid glucose levels and ascitic fluid leukocyte counts were similar in both groups, with no statistically significant relationship detected (P>0.05). However, the mean (+/-SD) ascitic fluid total protein (0.0172+/-0.1104 gL versus 0.043+/-0.011 gL), albumin (0.0104+/-0.0064 gL versus 0.0276+/-0.0069 gL) and LDH (102.76+/-80.95 UL versus 885.71+/-199.93 UL) were found to be higher in patients with an SAAG of 11 gL or less than in those with an SAAG of greater than 11 gL (P<0.001). The mean ascitic fluid viscosities were 0.86+/-0.12 centipoise (cP) and 1.22+/-0.25 cP in patients with an SAAG greater than 11 gL and an SAAG of 11 gL or less, respectively (P<0.001). Although ascitic fluid infection was detected in 35 patients (24.6%) (19 patients with spontaneous bacterial peritonitis, seven patients with culture-negative neutrocytic ascites, three patients with monobacterial non-neutrocytic bacterascites and six patients with secondary bacterial peritonitis), no significant effect on ascitic fluid viscosity was detected. Multiple linear regression analysis revealed that ascitic fluid total protein, albumin and LDH levels were independent predictors of ascitic fluid viscosity (P<0.001). The sensitivity, specificity, and positive and negative predictive values of ascitic fluid viscosity for the discrimination between ascites due to portal hypertension-related and nonportal hypertension-related causes according to the SAAG were determined by receiver operating characteristic analysis. Regarding the cut-off value of 1.03 cP, ascitic fluid viscosity measurement had a high sensitivity, specificity (98% and 80%, respectively), and positive and negative predictive value (79% and 94%, respectively) for the etiological discrimination of ascites. CONCLUSION: The measurement of ascitic fluid viscosity correlates significantly with SAAG values. In view of its simplicity, low cost, small sample volume requirement and allowance for measurement in previously frozen samples, measurement of ascites viscosity could be useful for the accurate and rapid classification of ascites.

Clarithromycin resistance and efficacy of clarithromycin-containing triple eradication therapy for Helicobacter pylori infection in type 2 diabetes mellitus patients.

BACKGROUND: Antimicrobial resistance in Helicobacter pylori infection is an important factor leading to failure of therapy. The aim of this study was to determine the eradication rate of H pylori in type 2 diabetes mellitus and to assess the effect of clarithromycin resistance on H pylori eradication. METHOD: Fifty-six consecutive patients with type 2 diabetes mellitus and 58 age- and sex-matched control patients were included in the study. H pylori infection was assessed by a rapid urease test and histopathological examination of biopsy specimens. Biopsies were also taken for antibiotic susceptibility testing. All enrolled patients were treated with triple therapy consisting of clarithromycin, amoxicillin, and pantoprazole for 14 days. C-13 urea breath test was performed 6 weeks after completing the triple therapy to assess eradication and associated point mutations using real-time polymerase chain reaction (PCR). RESULTS: H pylori was eradicated in 42.9% of diabetic patients and 79.3% of control patients, (P < 0.05). In type 2 diabetes mellitus patients, clarithromycin resistance was 64.3% (36/56), while in the control group, clarithromycin resistance was 35.7% (20/58) (P < 0.05). H pylori was eradicated in 14 (70%) of the 20 clarithromycin-susceptible diabetic patients and in only 10 (27.8%) of the 36 clarithromycin-resistant diabetic patients. CONCLUSION: The H pylori eradication rate was significantly lower and clarithromycin resistance was significantly higher in type 2 diabetics. Alternative and new treatment protocols and antibiotic susceptibility testing are needed to achieve successful eradication rates.

Plasma viscosity changes in patients with liver cirrhosis.

OBJECTIVES: Plasma viscosity (PV) is a major determinant of capillary blood flow through the microcirculation, which, if impaired, can result in potentially important clinical sequelae. The objectives of this study were to investigate the alterations of PV values in different stages of cirrhosis, and to determine if any change in PV correlates with Child score or Model for End-Stage Liver Disease (MELD) score or has any prognostic significance. METHOD: The study included 92 patients with cirrhosis and 28 healthy volunteers. Upper endoscopic and ultrasonographic examinations of the patients were obtained. Serum biochemistry fibrinogen, complete blood count, C-reactive protein (CRP), and lipid profile were performed. PV was determined using a rotational viscosimeter. RESULTS: PV decreased with the progression in Child scores (Child A: 1.46 +/- 0.20 mPa-s, Child B: 1.33 +/- 0.21 mPa-s, Child C: 1.12 +/- 0.15 mPa-s), (P < 0.001). A similar change was detected between the MELD score and PV (P < 0.001). There was a positive correlation between the total protein, albumin and plasma viscosity in the control group, but a similar relationship was not found in cirrhotic patients. History of hepatic encephalopathy (30 of 92 patients) was independently associated with decreased PV (P = 0.003). CONCLUSION: We observed that increasing Child and MELD scores were significantly associated with lower PV levels irrespective of biochemical and hematologic values. These observations support the concept that hemorheologic changes in cirrhotic patients might be either the cause or the result of a pathophysiological process, and it may not be easy to distinguish between these two possibilities.

The relationship between fibrosis and nodule structure and esophageal varices.

BACKGROUND/AIMS: The aim of the present study was to evaluate the histopathological findings of cirrhosis together with clinical and laboratory parameters, and to investigate their relationship with esophageal varices that are portal hypertension findings. MATERIALS AND METHODS: A total of 67 (42 male and 25 female) patients who were diagnosed with cirrhosis were included in the study. The mean age of the patients was 51.6±19.0 (1-81) years. The biopsy specimens of the patients were graded in terms of fibrosis, nodularity, loss of portal area, central venous loss, inflammation, and steatosis. The spleen sizes were graded ultrasonographically, and the esophageal varices were graded endoscopically. RESULTS: In the multivariate regression analysis, there was a correlation between the advanced disease stage (Child-Pugh score odds ratio (OR): 1.47, 95% confidence interval (CI): 1.018-2.121, p=0.040), presence of micronodularity (OR: 0.318, 95% CI: 0.120-0.842, p=0.021), grade of central venous loss (OR: 5.231, 95% CI: 1.132-24.176, p=0.034), and presence of esophageal varicose veins. CONCLUSION: Although thrombocytopenia and splenomegaly may predict the presence of large esophageal varices, cirrhosis histopathology is the main factor in the presence of varices.

The prevalence of occult hepatitis B virus infection in type 2 diabetes mellitus patients.

AIM: The prevalence of occult hepatitis B virus (HBV) infection is relatively frequent among patients with immune suppression. The impairment of the immune system is well demonstrated in diabetics. We aimed to investigate the prevalence of occult HBV infection among hepatitis B core antibody (HbcAb)+/- hepatitis B surface antibody (anti-HBs) positive type 2 diabetes mellitus patients. MATERIALS AND METHODS: The study involved 100 HBcAb+/-anti-HBs type 2 diabetes mellitus patients and 100 age and sex matched, HBcAb+/-anti-HBs healthy blood donors. Exclusion criteria were positive serology for HBsAg, hepatitis C virus or HIV, diagnosis of malignancy or earlier organ transplantation history, use of immunosuppressive therapy. All patients were questioned about their past medical history and were tested for serum alanine aminotransferase and HBV DNA level. RESULTS: The diabetic patients did not differ significantly from healthy controls in terms of sex and age. HBV DNA was detected in 11% of the diabetic patients (1 x 10-5 x 10 copies/ml) and in 3% of the controls (4 x 10-1 x 10 copies/ml). The difference between groups was statistically significant (P<0.05). The history of blood transfusion, surgery, and vaccination for HBV and alcohol use were similar in both groups (P>0.05). The serum alanine aminotransferase levels in diabetic patients were close to those of controls (26.2+/-16.4 IU/l vs. 23.9+/-9.7 IU/l; P>0.05). CONCLUSION: These data suggest that the prevalence of occult HBV infection is higher in diabetics compared with healthy controls and this may contribute to the increased prevalence of primary hepatocellular carcinoma in diabetics.

Thrombopoietin or interleukin-6 has no effect on thrombocytopenia of cirrhosis.

BACKGROUND/AIMS: We aimed to compare the level of thrombocytopenia in cirrhotic patients with HBV and those with HCV, and to investigate whether the reduced serum level of IL-6 in patients with HCV is responsible for the lower platelet count compared to those with HBV through the effect on serum thrombopoietin level. METHODOLOGY: Fifty-three patients with liver cirrhosis, 28 of who were HBV- seropositive (Group A), 25 of who were HCV- seropositive (Group B) and 15 healthy controls were enrolled in this study. RESULTS: Platelet count in group B [75 (1.5-99) K/microL] were lower than those of group A [140 (62-374) K/microL] (p < 0.001). The median levels of serum thrombopoietin in patients [group A: 31.9 (31-113) pg/mL and group B: 38.0 (31.2-102) pg/mL] and controls [31.3 (31-153) pg/mL] did not show statistically significant difference. The patients compared to controls, had higher serum IL-6 levels [3.6 (2-1150) vs. 2.0 (2-9.9) pg/mL], (p < 0.01), which showed similarity in group A and B patients [3.65 (2-1150) vs. 3.3 (2-45) pg/mL], (p=NS). Serum thrombopoietin level was not correlated with serum IL-6 levels in any group. Serum thrombopoietin and IL-6 levels had no relationship with platelet count and with Child-Pugh score. CONCLUSIONS: Our study showed that cirrhotic patients with HCV had lower platelet count than those with HBV and controls, and this difference does not appear to be related with either serum thrombopoietin or IL-6 level.

The importance of salivary cortisol in the diagnosis of adrenal insufficiency in cirrhosis.

BACKGROUND/AIMS: Reports on adrenal insufficiency (AI) are unexpectedly high in cirrhosis, and the diagnosis of this condition remains a challenge. We aimed to define the prevalence rate of AI in stable cirrhotic patients and determine the correlations of free cortisol and salivary cortisol with total cortisol. MATERIALS AND METHODS: Between January 2011 and September 2011, 110 consecutive cirrhotic patients without any infection or hemodynamic instability were enrolled. Baseline total and salivary cortisol levels were measured. The free cortisol level was calculated according to the Coolens' formula. Post-stimulation total and salivary cortisol levels were measured, and the free cortisol level was recalculated. RESULTS: The mean age of the patients was 62.1±11.4 years. There were 54 males (49.1%). The mean Child-Turcotte-Pugh (CTP) score was 7.2±2.3. Twenty-two (20%) patients were at the CTP-C level. AI was present in 23 (20.9%) and 17 (15.5%) of all patients according to the total and free cortisol criteria, respectively. For basal and stimulated levels, salivary cortisol rather than total cortisol correlates well with free cortisol. CONCLUSION: The diagnosis of AI on the basis of total cortisol measurement overestimates the prevalence of AI in cirrhosis. Salivary cortisol, which correlates well with free cortisol, is a promising alternative for the diagnosis of AI in cirrhotic patients.

Plasma viscosity: a potential predictor of both medical treatment response and clinical stage of ulcerative colitis.

AIM: Ulcerative colitis (UC) is one of the major forms of chronic relapsing inflammatory bowel diseases. The ability to identify type, severity and responsiveness to therapy of UC using laboratory parameters has long been the aim of clinical studies. The aim of this study was to assess the relation betweenplasma viscosity (PV) and disease activity and response to medical treatment in patients with UC. MATERIAL AND METHODS: The study included 105 patients with UC and 42 healthy volunteers. Blood samples were assessed for PV, erythrocyte sedimentation rate (ESR), high sensitive C-reactive protein (hs-CRP), D-dimer, and fibrinogen. RESULTS: Patients with UC were grouped according to disease activity, i.e. active (n= 59) and remission (n= 46). PV was higher in those with active UC compared with those with UC in remission or healthy subjects. It was significantly higher in both UC refractory to steroid compared to UC responsive to steroid (p< 0.001) and UC refractory to cyclosporine compared to UC responsive cyclosporine (p= 0.003). IncreasedSimple Clinical Colitis Activity Index (SCCAI), Endoscopic Grading Scale (EGS), and Histological Disease Activity (HAD) scores were significantly associated with higher PV in patients with UC. CONCLUSION: PV is a useful marker in predicting response to steroid or cyclosporine treatment in patients with active UC. It could be replaced by ESR or hs-CRP as a measure of the acute phase response in UC since it is sufficiently sensitive. These findings may help identify patients with active UC who will require colectomy. KEY WORDS: Biomarkers, Disease activity, Medical treatment, Steroid-refractory ulcerative colitis, Ulcerative colitis.

Helicobacter pylori eradication lowers serum homocysteine level in patients without gastric atrophy.

AIM: To determine whether Helicobacter pylori (H pylori)infection caused hyperhomocysteinemia by altering serum vitamin B(12), serum folate and erythrocyte folate levels and whether eradication of this organism decreased serum homocysteine level. METHODS: The study involved 73 dyspeptic H pylori-positive patients, none of them had gastric mucosal atrophy based on rapid urease test and histology. Out of 73 patients, 41 (56.2%) showed a successful eradication of H pylori 4 wk after the end of treatment. In these 41 patients, fasting serum vitamin B(12), folate and homocysteine levels, and erythrocyte folate levels before and 4 wk after H pylori eradication therapy were compared. RESULTS: The group with a successful eradication of H pylori had significantly higher serum vitamin B(12) and erythrocyte folate levels in the post-treatment period compared to those in pre-treatment period (210+/-97 pg/mL vs 237+/-94 pg/mL, P<0.001 and 442+/-212 ng/mL vs 539+/-304 ng/mL, P = 0.024, respectively), but showed no significant change in serum folate levels (5.6+/-2.6 ng/mL vs 6.0+/-2.4 ng/mL, P = 0.341). Also, the serum homocysteine levels in this group were significantly lower after therapy (13.1+/-5.2 micromol/L vs 11.9+/-6.2 micromol /L, P = 0.002). Regression analysis showed that serum homocysteine level was positively correlated with age (P = 0.01) and negatively with serum folate level before therapy (P = 0.003). CONCLUSION: Eradication of H pylori decreases serum homocysteine even in patients who do not exhibit gastric mucosal atrophy. It appears that the level of homocysteine in serum is related to a complex interaction among serum vitamin B(12), serum folate and erythrocyte folate levels.

Autonomic neuropathy and gallbladder motility in patients with liver cirrhosis.

BACKGROUND/AIMS: Impaired gallbladder motility has been suggested as a contributor to increased incidence of gallstones in patients with liver cirrhosis. The purpose of this study was to determine gallbladder function and its relation with autonomic neuropathy in liver cirrhosis. MATERIALS AND METHODS: Gallbladder function was measured using ultrasonography in 48 patients with liver cirrhosis and in 31 controls. Autonomic neuropathy tests were applied in patients with liver cirrhosis. Patients with liver cirrhosis were analyzed in subgroups according to the severity of disease using the Child-Pugh classification. RESULTS: Fasting gallbladder volume was 16.2 mL (range: 2.1 mL-71.9 mL) in patients and 17.6 mL (range: 4.9 mL-76.6 mL) in controls. There were no differences in fasting gallbladder volume among the study groups (p>0.05). Gallbladder ejection fraction was significantly higher in patients compared with controls (84% vs. 65%) (p<0.001). No correlation was found between gallbladder ejection fraction and autonomic neuropathy (p>0.05). CONCLUSION: Our results indicate that liver cirrhosis does not impair gallbladder emptying, and that there is no association between gallbladder motility and autonomic neuropathy. Further investigations are required to explain increased gallbladder motility in liver cirrhosis.

The relationship of recurrent aphthous stomatitis and Helicobacter pylori, cytokine gene polymorphism and cobalamin.

BACKGROUND/AIMS: The aim of the present study was to investigate whether Helicobacter pylori causes or triggers recurrent aphthous stomatitis (RAS) through cytokine gene polymorphism and/or cobalamin deficiency. MATERIALS AND METHODS: Thirty-six patients with RAS and 130 patients without RAS were genotyped for IL-1ß (-511C/T) and IL-6 (-174G/C) and evaluated for H. pylori infection and serum cobalamin level. RESULTS: The patient groups according to RAS had similar rates of H. pylori gastritis and interleukin genotypes/alleles, and there was a non-significant difference between serum cobalamin levels (p>0.05). RAS patients with H. pylori gastritis showed a higher frequency (51.9%) of GC IL-6 genotype than RAS patients without H. pylori gastritis (11.1%) (p=0.036). Non-GG genotype and C allele were increased in patients without RAS and with H. pylori gastritis (p<0.05). Patients with H. pylori gastritis showed a lower value of serum cobalamin without statistical significance, although this difference was more prominent in RAS patients (p=0.07). CONCLUSION: The carriage of the C allele of IL-6 may lead a susceptibility to chronic gastric inflammation after contamination with H. pylori. If H. pylori infection is justified as a predisposing factor for RAS and its severity by further studies, we can speculate that subjects with genetic susceptibility to this infection may benefit from H. pylori eradication treatment with respect to RAS.

Helicobacter pylori has no effect on plasma ghrelin levels.

OBJECTIVE: Helicobacter pylori is the major etiologic agent for chronic active gastritis, and it also plays a crucial role in gastric and duodenal ulcer disease, as well as in gastric carcinoma. H. pylori infection has been shown to decrease plasma somatostatin (SST) and increase plasma gastrin concentrations. Ghrelin is a recently discovered peptide produced mostly in the stomach of rodents and humans and is secreted into the bloodstream. There is no data in the literature about the relationship between H. pylori and ghrelin. DESIGN: Thirty-nine age- and BMI-matched H. pylori infection positive and negative women, from whom biopsy specimens were taken during gastric endoscopy, were included in the study. METHODS: Total ghrelin was measured by enzyme immunoassay (EIA) in Medistek. All samples were measured in duplicate and averaged; results differing by more than 20% were re-assayed. Two biopsy specimens from antrum, corpus and fundus were obtained. RESULTS: Fifteen of the subjects were H. pylori negative and 24 were H. pylori positive. Age, BMI, lipid profile and insulin sensitivity indices of the groups were similar. Plasma ghrelin levels (375.92+/-7.10 vs 370.00+/-4.14 pmol/l; P>0.05) of H. pylori negative and positive groups did not differ significantly. CONCLUSION: H. pylori has no effect on plasma ghrelin concentration.