An Australian Audit Of Vaccination Status In Children And Adolescents With Inflammatory Bowel Disease

This includes invasive pneumococcal disease and influenza. The primary aim of this study was to describe compliance with current Australian guidelines for vaccination of children and adolescents diagnosed with IBD. A secondary aim was to review the serological screening for VPD. Methods A random sample of patients (0-18 years at diagnosis), were selected from the Victoria Australia state based Pediatric Inflammatory Bowel Disease Register. A multi-faceted retrospective review of immunization status was undertaken, with hospital records audited, a telephone interview survey conducted with consenting parents and the vaccination history was checked against the primary care physician and Australian Childhood Immunization Register (ACIR) records. The routine primary childhood vaccinations and administration of the recommended additional influenza and pneumococcal vaccines was clarified. Results This 2007 audit reviewed the immunization status of 101individuals on the Victorian Pediatric IBD database. Median age at diagnosis was 12.1 years, 50% were on active immunosuppressive therapy. 90% (38/42) [95% confidence intervals (CI) 77%; 97%] with complete immunization information were up-to-date with routine primary immunizations. Only 5% (5/101) [95% CI 2%; 11%] received a recommended pneumococcal vaccine booster and 10% (10/101) [95% CI 5%; 17%] had evidence of having ever received a seasonal influenza vaccine. Those living in rural Victoria (p = 0.005) and younger at the age of diagnosis (p = 0.002) were more likely to have ever received an influenza vaccine Serological testing, reviewing historical protection from VPD, identified 18% (17/94) with evidence of at least one serology sample. Conclusion This study highlights poor compliance in IBD patients for additional recommended vaccines. A multi-faceted approach is required to maximize protection from VPD in this vulnerable special risk population. Keywords:

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Australian Gastroenterology Week (AGW) 2007 & Developments in Ulcerative Colitis

Morning shower or two. Cookies must be enabled. Enabling Cookies in Internet Explorer 7, 8, 9 + Open the Internet Browser Click Tools (or “gear” icon at top right hand corner) > Internet Options > Privacy > Advanced Check Override automatic cookie handling For First-party Cookies and Third-party Cookies click Accept Click OK and OK Click Tools > Options > Privacy Select Privacy > Content settings Check ‘Allow local data to be set (recommended)’ Click ‘Done’ Under ‘History’ select Firefox will: ‘Use custom settings for history’ Check ‘Accept cookies from sites’ and then check ‘Accept third-party cookies’ Click OK Enabling Cookies in Google Chrome Open the Google Chrome browser Chrome > Preferences Click ‘Show advanced settings’ at the bottom. Under Privacy select ‘Content settings’ Under ‘Cookies’ select ‘Allow local data to be set (recommended)’ Click ‘OK’ Under ‘Block cookies’ check ‘Never’ Enabling Cookies in Mobile Safari (iPhone, iPad) Go to the Home screen by pressing the Home button or by unlocking your phone/iPad Select the Settings icon. Select Safari from the settings menu. Select ‘accept cookies’ from the safari menu. Select ‘from visited’ from the accept cookies menu. Press the home button to return the the iPhone home screen. Select the Safari icon to return to Safari. Before the cookie settings change will take effect, Safari must restart. To restart Safari press and hold the Home button (for around five seconds) until the iPhone/iPad display goes blank and the home screen appears. Select the Safari icon to return to Safari.

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Gluten free definition worries specialist

These peaks were significantly sensitive for 5-ASA. What we need to do now is to apply these results in a clinical context. Genes Implicated in IBD – IL23R is an IBD Susceptibility Gene (confirmation in an Australian cohort) and GLI1 gene a Risk Factor for Ulcerative Colitis With advances in research and from results of clinical studies, additional insight into the causes and genetics behind ulcerative colitis has been obtained. For example, variations in particular receptors such as the IL 23 receptor has recently been shown to be associated with both Crohn’s and ulcerative colitis. Another gene called the GLI1 gene plays a significant role in the formation and maintenance of a healthy lining for our gut. Defects in the GLI1 gene have been implicated in patients with ulcerative colitis. Patterns of Medication use in Inflammatory Bowel Disease PatientsThere is a wide range of therapies for ulcerative colitis – depending on the location of disease, different combinations of treatments are employed. In disease limited to the rectum, the mainstay of therapy includes topical aminosalicyclate (5-ASA) suppositories (small masses of medication that are designed to melt when inserted into a body cavity). Topical therapy refers to local application of treatment directly onto the surface of a body part. In more extensive cases where disease affects larger parts of the bowels, combination therapy involving 5-ASA agents (both oral and topical), steroids and other immunosuppressive agents is recommended. In a recent study conducted by Barclay et al, an increased use of medications which act to alter the immune response (immunomodulators) was demonstrated. Out of 1421 patients with inflammatory bowel disease, the use of immunomodulators including azathioprine, 6 mercaptopurine and methotrexate was investigated. Oral 5-ASA treatments were used in 77% of ulcerative colitis patients. Use of these medications correlated with increasing disease extent. In conclusion, IM use was high in these patients, compared with previous studies.

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