Antioxidative potential of a combined therapy of anti TNFα and Zn acetate in experimental colitis.

AIM: To evaluate whether combination therapy with anti-tumour necrosis factor α (TNFα) antibody and Zn acetate is beneficial in dextran sodium sulphate (DSS) colitis. METHODS: Colitis was induced in CD1-Swiss mice with 5% DSS for 7 d. The experimental mice were then randomised into the following subgroups: standard diet + DSS treated (induced colitis group); standard diet + DSS + subcutaneous 25 μg anti-TNFα treated group; Zn acetate treated group + DSS + subcutaneous 25 μg anti-TNFα; standard diet + DSS + subcutaneous 6.25 μg anti-TNFα treated group and Zn acetate treated group + DSS + subcutaneous 6.25 μg anti-TNFα. Each group of mice was matched with a similar group of sham control animals. Macroscopic and histological features were scored blindly. Homogenates of the colonic mucosa were assessed for myeloperoxidase activity as a biochemical marker of inflammation and DNA adducts (8OH-dG) as a measure of oxidative damage. RESULTS: DSS produced submucosal erosions, ulcers, inflammatory cell infiltration and cryptic abscesses which were reduced in both groups of mice receiving either anti-TNFα alone or combined with zinc. The effect was more pronounced in the latter group (vs Zn diet, P < 0.02). Myeloperoxidase activity (vs controls, P < 0.02) and DNA adducts, greatly elevated in the DSS fed colitis group (vs controls, P < 0.05), were significantly reduced in the treated groups, with a more remarkable effect in the group receiving combined therapy (vs standard diet, P < 0.04). CONCLUSION: DSS induces colonic inflammation which is modulated by the administration of anti-TNFα. Combining anti-TNFα with Zn acetate offers marginal benefit in colitis severity

Risk factors for non-adherence to medication in inflammatory bowel disease patients

Background: Inflammatory bowel diseases are chronic conditions requiring medication throughout life to treat the disease and control the risk of relapse and colorectal cancer. Adherence to prescribed drugs is therefore crucial to their management. Aim: To identify determinants and potential risk factors of non-adherence in inflammatory bowel disease patients. Methods: An anonymous 24-item questionnaire (available online as Supplementary material) was administered to 485 out-patients attending a tertiary referral centre. Results: Sixty-one per cent of the patients reportedly adhered to their treatment. No differences emerged between inflammatory bowel disease and socio-demographic characteristics other than age, non-adherence being significantly associated with cases under 40 years (43% vs. 34%, P = 0.041). The most common reasons for non-adherence vs. adherence were forgetfulness (61% vs. 44%, P = 0.000), disease remission (25% vs. 10%, P = 0.000), recent diagnosis (24% vs. 15%, P = 0.000) and full-time employment (55% vs. 26%, P = 0.000). Oral therapy was associated with a significantly better adherence than rectal therapy (60% vs. 32%, P = 0.001). Communication affects patient adherence: a significant interaction was found for adherence and patients <40 years who had a good relationship with their doctors. Conclusions: Risk factors for non-adherence are younger age, busy working life, recent diagnosis and disease remission. Good communication with the doctor might improve adherence