Search

Abstract Background Although lateral internal sphincterotomy is the gold-standard treatment for chronic anal fissure, intrasphincteric injection of botulinum toxin seems to be a reliable new option. The aim of this non-randomized study is to compare the effect of lateral internal sphincterotomy and botulinum toxin injection treatments on the outcome and reduction of anal sphincter pressures in patients with chronic anal fissure. Methods Patients with chronic anal fissure were treated with either botulinum toxin injection or lateral internal sphincterotomy by their own choice. Maximal resting pressure and maximal squeeze pressure measurements were performed before and 2 weeks after treatments by anal manometry. Patients were followed for fissure relapse during 14 months. Results Twenty-one consecutive outpatients with posterior chronic anal fissure were enrolled. Eleven patients underwent surgery and ten patients received botulinum toxin injection treatment. Before the treatment, anal pressures were found to be similar in both groups. After the treatment, the maximal resting pressures were reduced from 104 ± 22 mmHg to 86 ± 15 mmHg in the surgery group (p < 0.05) and from 101 ± 23 mmHg to 83 ± 24 mmHg in the botulinum toxin group (p < 0.05). The mean maximal squeeze pressures were reduced from 70 ± 27 mmHg to 61 ± 32 mmHg (p > 0.05) in the surgery group, and from 117 ± 62 mmHg to 76 ± 34 (p < 0.01) in the botulinum toxin group. The fissures were healed in 70 percent of patients in the botulinum group and 82 percent in the surgery group (p > 0.05). There were no relapses during the 14 months of follow up. Conclusion Lateral internal sphincterotomy and botulinum toxin injection treatments both seem to be equally effective in the treatment of chronic anal fissure.

Background/aims: Inflammatory bowel diseases (IBD) impairs patients' quality of life (QoL). Inflammatory bowel disease questionnaire (IBDQ) is created to measure the health-related QoL specific for IBD. We planned to investigate the validation and reliability of the Turkish translation of IBDQ., Materials and Methods: Patients filled self-report questionnaires (Turkish Inflammatory bowel disease questionnaire (TrIBDQ) and Short Form-36 (SF-36)) themselves under a physician's supervision, and they were free to ask questions about the questionnaires. The participants then filled the same questionnaire after at least two weeks. Construct validity, discriminant ability, reliability, and susceptibility to change were analyzed separately for the IBD patients. Intra-class correlation coefficient (ICC) was used to assess test-retest reliability. Cronbach's alpha values were used to assess internal consistency., Results: A hundred patients enrolled in the study, 53 with Crohn's disease (CD), 47 with ulcerative colitis (UC). We found a moderate to high positive correlation between the TrIBDQ domains and the SF-36 dimensions. In UC and CD, TrIBDQ was able to differentiate active disease and remission. We found Cronbach's alpha for TrIBDQ domains ranged from 0.76-0.94 in CD and from 0.79-0.92 in UC. The total Cronbach's alpha for TrIBDQ was 0.96 in CD and 0.95 in UC. Sensitivity-to-change analyses of the bowel, systemic, and emotional scores showed statistically significant differences between their baseline and follow-up values., Conclusion: TrIBDQ is a valid and reliable tool for assessing the quality of life in Turkish speaking IBD patients. Thus it can be used in clinical research and practice.

Background/aims: Anorectal diseases, including fecal incontinence, are prevalent and have an enormous impact on the quality of life. Therefore, investigating their etiological factors may help to reduce the incidence and/or the severity of the underlying diseases., Materials and Methods: Referral complaints (constipation, strained defecation, and incontinence) and medical and anorectal manometry records of 883 (562 female/321 male, ages 45.17±1.00 and 48.41±0.63 years, respectively) patients were evaluated retrospectively. Maximal resting pressure (MRP) and maximal squeeze pressure (MSP) measured by stationary pull-through technique, volume of rectoanal inhibitory reflex, and sensory threshold to rectal balloon distention (ST) were obtained by water perfusion system. Data were compared according to referral complaints, age, gender, parity, and underlying diseases., Results: Incontinence was the most frequent referral complaint in 61.2% of females and 67.6% of males. MRP and MSP were significantly lower in incontinent females than in the other groups. In incontinent males, MSP was lower than the strained defecation group, and ST was higher than the constipation group. Age was negatively correlated with MRP for both of the genders and in all groups. Obstetric trauma (85%) and number of parity (3.40±2.59) were significantly higher in incontinent females. Moreover, the most prevalent underlying disease was diabetes in incontinent females (13.7%) and neurological diseases, including traumas, in incontinent males (41.5%)., Conclusion: Increasing awareness of labor safety, controlling diabetes mellitus, and preventing obstetric traumas may reduce the prevalence of fecal incontinence.

Background/aims: To determine the incidence rate and distribution of anemia types over time from an Inflammatory Bowel Disease (IBD) patient cohort spanning 18 years., Materials and Methods: Between January 1995 and November 2013, the University Hospital digital databases as well as hard copies of patients' files were reviewed retrospectively. IBD patients with at least one complete blood count (CBC) report were included in this study., Results: We obtained 941 IBD patients' records; 375 (39.9%) patients were diagnosed with Crohn's disease (CD), and 566 (60.1%) patients had ulcerative colitis (UC). Anemia was detected in 548 (58.2%) patients. Female patients were more frequently anemic than male patients (68.4% vs. 49.7%, p=0.001). The frequency of anemia was slightly higher in patients with CD (62.1%) than in patients with UC (55.7%) (p=0.04). The incidence rate of anemia for the entire IBD patient cohort was calculated as 103.45 per 1,000 patient-years. The correlation between the age of the IBD disease and the presence of anemia exhibited a high correlation coefficient of Pearson's r=0.702., Conclusion: This is the first study to report the incidence rate of anemia (103.45 per 1,000 patient-years) in a long-term cohort of IBD patients.

To study the prevalence major rheumatic diseases in western Turkey. This survey was conducted in Havsa which have a total population of 18,771. Physicians and interns visited every household, interviewed face to face a questionnaire about the symptoms of rheumatic disorders. The individuals replied positively to any question were examined at the nearest health center. Those have no objective findings related to any rheumatic diseases were excluded. People could not be clinically diagnosed were asked to come to the hospital for further evaluation. A total 17,835 of 18,771 residents participated. We estimated the prevalence of Behçet's Disease (BD) as 0.019%; ankylosing spondylitis: 0.120%; rheumatoid arthritis: 0.321%; knee osteoarthritis (OA): 5.351%; hand OA: 1.110%; hand and knee OA: 1.958%; total OA: 8.420%; primary Raynaud's: 1.192%; psoriasis: 0.424 %; psoriatic arthritis: 0.050%; rheumatic fever: 0.318%; rheumatic heart disease: 0.200%; inflammatory bowel disease: 0.023%; lupus: 0.059%; gout: 0.018%; systemic sclerosis: 0.022%; juvenile rheumatoid arthritis: 0.032%; temporal arteritis: 0.020%, and familial Mediterranean fever (FMF) as 0.006%. Figures were adjusted for age-sex of the general Turkish population. The prevalence's of BD and FMF are considerably lower in Havsa as compared to other regions in Turkey.

Background: Increasing evidence suggests that innate immune system may have a key role in the pathogenesis of the inflammatory bowel disease (IBD). Bactericidal/permeability increasing protein (BPI) has an important role in the recognition and neutralization of gram-negative bacteria by host innate immune system. The polymorphism on BPI gene called Lys216Glu is on the suspected list of IBD pathogenesis., Methods: We studied the Lys216Glu polymorphism on BPI gene, in a Turkish IBD patient population. A total of 238 IBD patients; 116 Crohn's disease (CD) and 122 ulcerative colitis (UC), besides 197 healthy controls were included in this study., Results: The Glu/Glu genotype and allele frequencies were found to be statistically higher compared to healthy control group not only in CD patients [P: 0.03, OR: 1.87 (CI 95% 1.02-3.42) and P: 0.00001 (OR: 2.07 CI 95% 1.47-2.91) respectively] but also in UC patients [P: 0.0002, OR: 2.71 (CI 95% 1.53-4.80) and P: 0.00002 (OR: 2.71 CI 95% 1.53-4.80) respectively]., Conclusions: BPI polymorphism (Lys216Glu) is associated both to CD and UC. Our findings differ from the two Western European studies; one without any association and the other indicating an association only with CD. Our study is the first one reporting a novel association between BPI gene mutation (Lys216Glu) and UC., (Copyright © 2010 European Crohn's and Colitis Organisation. All rights reserved.)

P53 tumor suppressor protein is one of the pivotal regulators for genome integrity, cell cycle and apoptosis. The most commonly and extensively studied single nucleotide polymorphism (SNP) of p53 is Arg>Pro substitution on codon 72 (R72P). Although we know that the SNP has unique functional effects on the protein, its clinical significance is not clearly identified yet. Aim of the study was to access the relationship between R72P genotype distribution and clinical variables in patients with ulcerative colitis (UC) and colorectal cancer (CRC). Genomic DNA samples were extracted from 95 UC, 50 CRC, and 219 healthy controls. R72P genotype analysis was carried out with polymerase chain reaction following by restriction enzyme digestion. We observed that Pro allele carriage is a strong risk factor for CRC (OR = 3.03; 95%CI = 1.91-2.40; p = 0.003), but only modest association with UC (OR = 1.61; 95%CI = 0.98-2.65; p = 0.059) (Pro/Pro and Pro/Arg genotypes vs. Arg/Arg genotype). We did not find any correlation between genotype distribution of the polymorphism and clinical parameters of CRC, but in UC, Pro/Pro genotype was significantly related to an inflammatory bowel disease family history (OR = 8.0; 95%CI = 1.68-38.08, p = 0.015), and Arg/Pro genotype was significantly associated with the history of disease-related colectomy (OR = 17.77; 95%CI = 0.98-323.34, p = 0.012) and steroid use (OR = 10.14; 95%CI = 2.63-39.12, p = 0.0002). Our data suggest that R72P variant seems to be associated with high risk for development of CRC but carries low risk for development of UC. R72P genotypes might be a useful predictive marker for surgical and medical treatment of UC.

Background/aims: Somatostatin receptors have been shown on hepatic stellate cells, and somatostatin infusion has been shown to inhibit hepatic stellate cells activation. We aimed to test the effects of a long-acting somatostatin analogue, lanreotide, on bile duct ligation-induced liver fibrosis in rats., Methods: Thirty-seven Wistar rats were divided into 5 groups as follows: Group 1, bile duct ligation+lanreotide; Group 2, bile duct ligation; Group 3, sham+lanreotide; Group 4, sham; and Group 5, control group. Lanreotide-autogel (20 mg/kg/month) or saline in intraperitoneal doses was administered. Serum biochemical parameters, liver collagen level, and oxidative stress and histological parameters were determined after 28 days., Results: The tissue collagen level, biochemical parameters (AST, ALT, bilirubins, alkaline phosphatase, γ-glutamyl transpeptidase) and oxidative stress parameters (malondialdehyde, luminal, lucigenin) in the bile duct ligation groups were higher than in the sham-operated and control groups (p<0.001 for all). Lanreotide improved malondialdehyde and glutathione levels in the bile duct ligation+lanreotide group. In histopathological examination, bile duct ligation groups showed stage-3 liver fibrosis, while all the controls were normal. Lanreotide did not improve the liver fibrosis histologically or biochemically., Conclusions: A monthly active somatostatin analogue, lanreotide, improved malondialdehyde and glutathione; however, it was not able to improve bile duct ligation-induced liver fibrosis in rats. Although lanreotide is a long-acting medication, it did not show anti-fibrotic effects in the model.

Orlistat, an inhibitor of digestive lipases, is widely used for the treatment of obesity. Previous reports on the effect of orally ingested orlistat together with a meal on gastric emptying and secretion of gut peptides that modulate postprandial responses are controversial. We investigated the effect of ingested orlistat on gastric emptying and plasma responses of gut peptides in response to a solid mixed meal with a moderate energy load. In healthy subjects, gastric emptying was determined using scintigraphy and studies were performed without and with 120 mg of orlistat in pellet form in random order. Orlistat shortened t lag and t half and decreased the area under the gastric emptying curve. Orlistat significantly attenuated the secretion of glucose-dependent insulinotropic polypeptide (GIP) but did not alter the plasma responses of cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), pancreatic polypeptide (PP), and insulin. There was no peptide YY (PYY) response. Area under the curve of gastric emptying was positively correlated with integrated secretion of GIP (r=0.786) in orlistat and was negatively correlated with integrated plasma response of GLP-1 (r=-0.75) in control experiments, implying that inhibition of fat absorption modifies determinants of gastric emptying of a meal. Orlistat administered similar to its use in obesity treatment accelerates gastric emptying of a solid mixed meal with a moderate energy load and profoundly attenuates release of GIP without appreciably altering plasma responses of CCK, GLP-1, and PP. Since GIP is being implemented in the development of obesity, its role in weight control attained by orlistat awaits further investigation.

We could not reproduce the model described by Lieber et al for nonalcoholic steatohepatitis model in rats. In our trial the high fat liquid diet group of rats gained nearly 100 g or less weight compared to the mean weight gain stated in the original article. However, the fasting glucose level was statistically higher in this group as compared to the chow diet group. Some pathological abnormalities in the duodenum and jejunum samples were observed in the high fat liquid diet group. We do not know the exact reason for these changes. Overall, our study results arose some suspicions about the reproducibility of the model. Furthermore, to the best of our knowledge, no study using the proposed model has been published so far.

We present a case of Budd-Chiari syndrome (BCS) having two risk factors, Behcet's disease (BD) and oral contraceptive (OC) usage. A 33-year-old woman with BD was admitted to the Emergency Unit with nausea, vomiting, abdominal pain, abdominal distention, and confusion started 12 days ago before admission. Since the patient was in a shock state, she was taken to the Intensive Care Unit (ICU) with the suspicion of abdomen-originated sepsis. Abdominal ultrasound showed massive hepatosplenomegaly and moderate ascites. Abdominal MRI revealed an inferior vena cava (IVC) obstruction starting above the renal veins and diffuse thrombosis of the right and medial hepatic veins. An extensive thrombosis of the IVC and the hepatic veins (BCS) which led to shock was diagnosed. In addition to BD, the unnotified OC usage for a year by the patient without her doctor's knowledge was recognized as possible precipitating factor of BCS. Pulse methylprenisolone was started for three consecutive days to treat active BD-induced vasculitis. IVC digital subtraction angiography (DSA) showed occlusion of the IVC below the hepatic veins with extensive collateral circulation originating at the occlusion level suggesting that obliteration had a subacute or chronic course. Since intralesional thrombolytic therapy failed, the patient was transferred to a liver transplantation center. While waiting for an appropriate donor, the patient died due to hepatic failure. Since BCS is mortal and deemed multi-factorial, every patient with a thrombotic risk factor such as BD should be questioned for other possible causes of thrombosis.

The value and/or limitations of computed tomography (CT) in assessment of hepatosteatosis are not well studied in nonalcoholic fatty liver disease (NAFLD). We prospectively evaluated the accuracy of CT in assessing the amount of hepatosteatosis in NAFLD patients and the impact of demographic and histopathologic variables on CT images. Forty patients with biopsy-proven NAFLD were eligible. Of these, 10 exhibited hepatic iron overload. Liver and spleen attenuation measurements were obtained and spleen-minus-liver attenuation difference (DeltaS-LA) was calculated. A good correlation between DeltaS-LA and pathological hepatosteatosis was observed (r = 0.837, P < 0.0001). Liver iron overload did not affect this correlation, although the mean DeltaS-LA was significantly lower in patients with iron overload. No correlation was detected between DeltaS-LA and hepatic inflammation, fibrosis, or body mass index. We conclude that DeltaS-LA derived from CT may be a useful tool for predicting the amount of hepatosteatosis in NAFLD patients as it is not affected by various individual factors.

Goals: A retrospective study of pretransplantation risk factors predisposing to liver injury following bone marrow transplantation (BMT)., Background: Liver complications are a major cause of morbidity and mortality following BMT. Determination of the pretransplantation factors that are likely to lead to liver injury may allow earlier diagnosis after BMT and may possibly improve prognosis., Study: Medical records of BMT patients were reviewed, and results of serial liver function tests and HBV/HCV serology during the pre- and posttransplantation 1-year period were noted. Presence of liver injury was defined as alanine aminotransferase levels twice the upper limit of normal. Forty-four allogeneic and 17 autologous BMTs, performed between 1990 and 2000, were analyzed in the study., Results and Conclusion: One-year survival was 77% (34 of 44 patients) for allogeneic BMT and 52% (9 of 17 patients) for autologous BMT. Seventy-two percent (32 of 44) of allogeneic transplant recipients and 47% (8 of 17) of autologous transplant recipients had liver injury during the first year of BMT. The most frequent causes of liver injury were graft-versus-host disease and drug hepatotoxicity for allogeneic BMT and drug hepatotoxicity for autologous BMT. Fulminant hepatic failure occurred in one allogeneic transplant recipient who was a pretransplantation HBV carrier and led to death. Multivariate regression analysis showed that pretransplantation HBV/HCV positivity and pretransplantation elevated liver enzyme levels of any cause were predictive risk factors for post-BMT liver injury, and close follow-up, early diagnosis, and treatment are highly recommended for BMT patients with these risk factors.

Objective: Acute and chronic use of non-steroidal anti-inflammatory drugs can increase gastrointestinal permeability. Celecoxib, which selectively inhibits the enzyme cyclooxygenase-2, is a novel anti-inflammatory drug with minimal gastrointestinal toxic effects while retaining anti-inflammatory efficacy. Our aim was to assess the potential effects of celecoxib on gastric permeability in comparison with placebo and ibuprofen., Design: We conducted a prospective, double-blind, cross-over study., Setting: This study is carried out at Marmara University Hospital., Participants: Twenty-five healthy subjects entered the study but 19 subjects completed the treatment., Intervention: Subjects were randomized to celecoxib 100 mg twice daily, ibuprofen 600 mg twice daily or placebo for 7 days in pre-defined sequences. Treatments were separated by a 7 day washout period., Main Outcome Measure: Gastric permeability was assessed by measuring urinary excretion of sucrose spectrophotometrically., Results: Ibuprofen 600 mg twice daily produced greater increases in gastric permeability compared with placebo or celecoxib (geometric mean of urinary sucrose recovery was 59.15, 32.65 and 33.11 mg/h for ibuprofen, placebo and celecoxib, respectively) (P < 0.001). Celecoxib was generally better tolerated than ibuprofen., Conclusions: When compared with ibuprofen, celecoxib 100 mg twice daily has no significant effect on gastric mucosa in healthy subjects.

We investigated the effect of acarbose, an alpha-glucosidase and pancreatic alpha-amylase inhibitor, on gastric emptying of solid meals of varying nutrient composition and plasma responses of gut hormones. Gastric emptying was determined with scintigraphy in healthy subjects, and all studies were performed with and without 100 mg of acarbose, in random order, at least 1 wk apart. Acarbose did not alter the emptying of a carbohydrate-free meal, but it delayed emptying of a mixed meal and a carbohydrate-free meal given 2 h after sucrose ingestion. In meal groups with carbohydrates, acarbose attenuated responses of plasma insulin and glucose-dependent insulinotropic polypeptide (GIP) while augmenting responses of CCK, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). With mixed meal + acarbose, area under the curve (AUC) of gastric emptying was positively correlated with integrated plasma response of GLP-1 (r = 0.68, P < 0.02). With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. The results demonstrate that acarbose delays gastric emptying of solid meals and augments release of CCK, GLP-1, and PYY mainly by retarding/inhibiting carbohydrate absorption. Augmented GLP-1 release by acarbose appears to play a major role in the inhibition of gastric emptying of a mixed meal, whereas CCK and PYY may have contributory roles.

The role of gender and the menstrual cycle in small bowel motility has not been clearly elucidated. Jejunal motility was recorded with a nasojejunal catheter incorporating five solid-state pressure transducers in ambulatory menstruating women and men of comparable age over 24 h. All women were studied twice, in the early follicular (early-F) and midluteal (mid-L) phases of the menstrual cycle, verified by determining serum levels of gonadal steroids and gonadotropins. The propagation velocity of phase III was slow and the contraction amplitude was high in both menstrual cycle phases compared with men, and these parameters were correlated with serum estrogen levels in the mid-L phase. In the early-F phase, migrating motor complex (MMC) cycle duration during sleep was long compared with other groups and positively correlated with estrogen concentrations, whereas in the mid-L phase MMC cycle duration during sleep was negatively correlated with serum progesterone levels. In all groups, the frequency of phase III contractions was low and the intercontractile interval measured from pressure peak to peak was long during sleep compared with the awake state. Postprandial motility did not display gender difference in any parameter examined. The results demonstrate that the majority of patterns of motility are similar in menstruating women and men, whereas certain aspects of the MMC, most conspicuously propagation velocity and phase III contraction amplitude, differ. We have also documented circadian variation of phase III contraction frequency in both women and men.

Objective: The aim of the present study was to investigate whether corticosteroid therapy alters gastroduodenal mucosal permeability and whether permeability alteration is associated with macroscopic mucosal damage., Methods: Eight patients taking oral corticosteroid therapy (total prednisone-equivalent dose, 1.5+/-0.1 g; duration, approximately 30 days), nine patients with multiple sclerosis taking high-dose intravenous methyl-prednisolone therapy (total dose, 11.7+/-0.5 g; duration, approximately 9 days), and 20 age- and gender-matched controls were studied. Gastroduodenal permeability was determined using sucrose as a site-specific permeability probe. Five-hour urine was collected after ingesting 100 g of sucrose and its urinary excretion rate was measured using high-pressure liquid chromatography. Gastroduodenal endoscopy was performed before steroid therapy to exclude subjects with evidence of macroscopic mucosal lesions. The sucrose test and endoscopy were repeated after completion of corticosteroid therapy., Results: The urinary sucrose excretion rates were similar in the control group and in patient groups before corticosteroid therapy. The median excretion rate of sucrose increased four (one to 28)- and eight (two to 35)-fold, respectively, as compared with pretreatment values in patients taking oral steroid and high-dose intravenous methyl-prednisolone therapy (p < 0.01). Considering all patients together, subjects who received a mean prednisone-equivalent dose of 8.4+/-1.5 g exhibited mucosal lesions, whereas patients who received 3.3+/-1.8 g did not (p = 0.06). The post-therapy increments in sucrose excretion rates were associated with neither the presence of macroscopic lesions nor with the total steroid dose received., Conclusions: Corticosteroid therapy augments gastroduodenal permeability and high doses are associated with macroscopic mucosal lesions. Steroid-induced permeability increase does not appear to be associated with the presence of macroscopic mucosal lesions.

Objective: Enteric-coated tablets are designed to resist gastric fluids and to disrupt and dissolve in the alkaline medium of the small intestine. Main objective of the present study was to investigate whether the increase in gastric pH due to omeprazole treatment alters the release rate of a drug from enteric-coated formulation. To this end, we have compared the single dose pharmacokinetics of a single-unit enteric-coated salicylate to that of uncoated acetylsalicylic acid tablets in the presence and absence of omeprazole treatment., Methods: Study was carried out according to 4 x 4 Latin square design. Eight healthy subjects received either uncoated acetylsalicylic acid tablets or single-unit enteric-coated sodium salicylate tablets alone or following 4 days of treatment with single-dose 20 mg omeprazole, and blood samples were collected for 24 hours. Serum salicylate levels were determined by the modified spectrophotometric method of Brodie et al. [1994]., Results: Salicylate was absorbed rapidly from uncoated tablets but absorption of salicylate from enteric-coated tablets was delayed, as expected. According to our results, omeprazole treatment did not influence the bioavailability from uncoated acetylsalicylic acid tablets but the absorption rate of salicylate from enteric-coated tablets was increased significantly., Conclusion: Findings of the present study demonstrate that omeprazole treatment significantly increases the rate of absorption of single-unit enteric-coated medication. Enhanced rate of absorption is most probably due to an early disruption of enteric coating and the intragastric release of the drug secondary to an omeprazole-mediated increase in gastric pH. The results of the present study also corroborate previous findings which have demonstrated highly variable absorption of enteric-coated single units.

Recently described distinct associations of HLA class II genes with ulcerative colitis (UC) suggest a genetic heterogeneity for disease susceptibility. In this study, HLA-DRB alleles of UC patients (n = 59) from Turkey were investigated and compared with healthy controls (n = 244). Using molecular genotyping by polymerase chain reaction (PCR) and sequence-specific oligonucleotide hybridization, we have shown a positive association of UC patients with the HLA-DRB1*1502 allele (10/59 vs. 16/244; P = 0.02; OR: 2.9) and a negative association with the DRB1*13 allele (7/59 vs. 64/244; P = 0.03; OR: 0.38) compared to controls. HLA-DRB1*0701 was significantly increased in perinuclear antineutrophil cytoplasmic antibody (pANCA)-positive UC patients compared to pANCA-negative patients (8/32 vs. 0/27; P = 0.005), whereas DRB1*1502 was observed more frequently in pANCA-negative patients (8/27 vs. 2/32; P = 0.03). These results extended the reported positive association of DRB1*1502 with UC to another population and supported the genetic susceptibility associated with HLA genes for disease development.

Exogenous administration of glucagon-like peptide-1-(7-36) amide (GLP-1), an insulinotropic hormone, inhibits gastric emptying and acid secretion in humans. The role of GLP-1 as a regulator of gastric function is elusive. In gastric fistula rats, vagal afferent denervation and peripheral administration of the GLP-1 receptor antagonist exendin-(9-39) amide enhanced emptying of a glucose meal, whereas intracerebroventricular exendin was ineffective. The rate of saline emptying was attenuated by peripheral as well as by central administration of GLP-1, and pretreatment with exendin by the respective routes reversed the inhibition by GLP-1. Vagal afferent denervation abolished the central and peripheral action of GLP-1 on gastric emptying. Neither peripheral cholinergic nor adrenergic blockade altered the delay of methyl cellulose meal emptying by intracisternal GLP-1 injection. Acid secretion in conscious pylorus-ligated rats was inhibited by intracisternal GLP-1 administration, whereas systemic GLP-1 was ineffective. These results support the notion that GLP-1 receptors participate in the central and peripheral regulation of gastric function. Furthermore, vagal afferent nerves mediate the inhibitory action of GLP-1 on gastric motor function. GLP-1 may be a candidate brain-gut peptide that acts as a physiological modulator of gastric function.