Beliefs About Medicines and Adherence to Treatment in Turkish Patients with Inflammatory Bowel Disease.

BACKGROUND: Although studies are investigating the perception and beliefs about treatment and adherence to treatment in different societies related to inflammatory bowel disease, there are no studies on this subject in Turkish people with different sociocultural structures. In our study, we aimed to evaluate the beliefs about treatment and its effect on adherence to treatment in the Turkish population with inflammatory bowel disease. METHODS: In the study, the "Medication Adherence Report Scale" and "Beliefs about Medicines Scale" scales were used to evaluate the treatment compliance and perception and beliefs about treatment. Characteristics that could affect treatment compliance were evaluated by statistical analysis. RESULTS: A total of 253 patients, 167 with ulcerative colitis and 86 with Crohn's disease, were included in the study. The non-adherence rate to the treatment was found as 41.9% in ulcerative colitis and 24.4% in Crohn's disease (P = .006). Intentional (29.3% in ulcerative colitis and 16.3% in Crohn's disease [P = .031] and unintentional non-adherence to treatment (28.1% in ulcerative colitis, 16.3% in Crohn's disease [P = .037] were significantly higher in ulcerative colitis than in Crohn's disease. Female gender (odds ratio = 2.59, P = .005), low education level (odds ratio = 4.8, P = .015), distal involvement in ulcerative colitis (P = .014), and thoughts about the disease would last too soon in Crohn's disease (odds ratio = 4.17, P = .049) were risk factors for non-adherence to treatment. CONCLUSION: The negative perception of treatment in inflammatory bowel disease affects adherence to the treatment. Considering some social factors that affect adherence to the treatment and taking measures to enhance the adherence to treatment will increase the success of treatment.

Investigation of IL23R, JAK2, and STAT3 gene polymorphisms and gene-gene interactions in Crohn's disease and ulcerative colitis in a Turkish population.

BACKGROUND/AIMS: Inflammatory bowel diseases are chronic, relapsing, inflammatory conditions. They have a genetic backround resulting in patient susceptibility. The aim of our study is to investigate the involvement of IL23R, JAK2, and STAT3 polymorphisms in inflammatory bowel diseases in a Turkish population. MATERIALS AND METHODS: Polymorphisms in IL23R (rs11209026), JAK2 (rs10758669), and STAT3 (rs3816769, rs2293152, rs744166, rs957970, rs8074524) were genotyped in 69 Crohn's disease patients, 157 ulcerative colitis patients, and 89 healthy controls. RESULTS: The presence of (C) in rs10758669, (T) and (TT) in rs957970, and (TT) in rs744166 were found to increase the susceptibility to Crohn's disease (p=0.049, p=0.016, p=0.010, p=0.035, respectively), while rs2293152 (GC), rs744166 (CT), and rs957970 (CT) provide protection against Crohn's disease (p=0.007, p=0.043, p=0.043, respectively). While rs2293152 (GC) was protective, rs2293152 (CC) increased the susceptibility to ulcerative colitis (p=0.009, p=0.001). All the polymorphisms were associated with age-at-diagnosis, except rs11209026. Furthermore, rs2293152 was associated with an extension in ulcerative colitis, while rs10758669, rs3816769, rs744166, rs2293152, and rs957970 were associated with the subphenotype in Crohn's disease. The presence of rs10758669 (AC) was protective against perianal Crohn's disease (p=0.016). Additionally, rs10758669 and rs2293152 in Crohn's disease and rs8074524, rs3816769, and rs10758669 in ulcerative colitis were associated with the requirement of immunsuppression. Finally, rs8074524 and rs10758669 in Crohn's disease and rs11209026 in ulcerative colitis were associated with disease-related operation. CONCLUSION: This is the first study of the single marker association of IL23R, JAK2, and STAT3 polymorphisms with ulcerative colitis and Crohn's disease in a Turkish population. It was demonstrated that these polymorphisms may be effective in the etiology of inflammatory bowel disease in this Turkish population.

Tyrosine kinase-2 gene polymorphisms are associated with ulcerative colitis and Crohn's disease in Turkish Population.

BACKGROUND AND OBJECTIVE: Inflammatory bowel disease is a group of chronic inflammatory conditions affecting gastrointestinal tract. Lots of genes have been identified resulting in susceptibility to inflammatory bowel disease. Any polymorphism leading to functional modifications in tyrosine kinase-2 may precipitate excessive immune response in the intestinal mucosa. The aim of our study is to investigate the involvement of tyrosine kinase-2 polymorphisms in the patients with inflammatory bowel disease in Turkish population. METHODS: Four single nucleotide polymorphisms in tyrosine kinase-2 (rs280523, rs2304256, rs280519 and rs280496) were genotyped in 60 Crohn's disease, 151 ulcerative colitis patients and 89 unrelated healthy controls. These polymorphisms were detected by real-time polymerase chain reaction. RESULTS: The presence of genotype (CC) in rs2304256 and (AA) in rs280519 were found to increase the susceptibility to ulcerative colitis (P=0.024, 0.025, respectively). rs2304256 (CA) and rs280519 (AG) have provided protection against ulcerative colitis (P=0.021, 0.012, respectively). rs280519 (AG) was protective against Crohn's disease (P=0.045). rs2304256 (CC) increased the susceptibility to inflammatory Crohn's disease (P=0.014). The presence of rs2304256 (A) increased the susceptibility to perianal Crohn's disease (P=0.03). Both rs280519 and rs2304256 polymorphisms were associated with the requirement of corticosteroid and immunosuppressive therapy in ulcerative colitis. CONCLUSION: This study is the first demonstration of the single marker association of tyrosine kinase-2 polymorphisms with ulcerative colitis and Crohn's disease in Turkish population. They may be effective in the etiology of inflammatory bowel disease in our population. Disparity between our study and others may be related to ethnic differences.

The role of serum cytokines in the pathogenesis of hepatic osteodystrophy in male cirrhotic patients.

Objective. In this study, we aimed to investigate the possible role of serum cytokines in the development of hepatic osteodystrophy. Matherial and Methods. 44 consecutive male cirrhotic patients (17 alcoholic, 20 hepatitis B, 7 hepatitis C), 15 age- and sex-matched chronic alcoholics without liver disease, and 17 age- and sex-matched healthy controls were included in the study during one year period. Bone mineral density was measured by dual X-ray absorptiometry in the lumbar vertebrate and femoral neck. Serum interleukin levels were measured by ELISA method. Results. Although osteopenia frequency between our cirrhotic patients was 20%, there was no difference in T-scores among the controls and other groups. Serum interleukin-1, interleukin-8, and tumor necrosis factor-alpha levels were not different between all groups. Serum interleukin-2 and interleukin-6 levels were higher in the cirrhotics than controls (P < 0.001). However, there were no significant difference between osteopenic and nonosteopenic cirrhotics. Conclusion. According to the results of the study in this small population of 44 male cirrhotic patients, frequency of hepatic osteopenia is small and serum interleukins 1, 2, 6, 8, and tumor necrosis factor-alpha may not play a role in the pathogenesis of hepatic osteodystrophy. Further studies in which large number of patients involved are necessary in this field.

The relationship between virulence factors of Helicobacter pylori and severity of gastritis in infected patients.

The outcome of Helicobacter pylori infection has been related to specific virulence-associated bacterial genotypes. The best known genotypic virulence factors of H. pylori are cytotoxin-associated gene A (cagA) and vacuolating cytotoxin gene A (vacA). The objective of this study was to assess the relationship between H. pylori cagA and vacA status and histopathological findings. Esophagogastrodoedonoscopy was performed in 80 dyspeptic patients. Antrum and corpus biopsies were obtained for isolation of H. pylori and for histopathological assessment. The polymerase chain reaction was used to detect cagA and vacA genes of H. pylori using specific primers. Biopsy samples were stained with hematoxylin and eosin, and histopathological findings were graded using the "updated Sydney system". H. pylori from 57 of the 80 patients was incubated. Of the 57 patients, 44 were cagA positive. In the corpus biopsy specimens there was a significant relationship between the density of H. pylori colonization (P = 0.02) and chronic inflammation (P = 0.02) and cagA-positive genotypes. In the antrum specimens there was a significant relationship between cagA positivity and neutrophil activity (P = 0.003) and glandular atrophy (P = 0.002), but not with H. pylori density, chronic inflammation, and intestinal metaplasia. The odds ratio of cagA-positive vs. cagA-negative strains for the presence of glandular atrophy, irrespective of grading and of gastric localization, was 4.62 (95% CI, 1.18-18.08, P = 0.041). No significant relationships were observed between vacA s1 and s2 genotypes and histopathological parameters. Corpus neutrophil infiltration was found to be more severe in the m1 group than in the m2 group (P = 0.004). Other histopathological features showed no difference between m1 and m2 genotypes. In conclusion H. pylori strains showing cagA positivity are associated with more severe gastritis in some histological features but virulence factors of H. pylori do not appear to determine the overall pattern of gastritis.