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Tips which we have found helpful to identify PPI and TNF patients Talk to your Neurologists, Rheumatologists and Dermatologists (and Neurophysiology) Contact.

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Presentation on theme: "Tips which we have found helpful to identify PPI and TNF patients Talk to your Neurologists, Rheumatologists and Dermatologists (and Neurophysiology) Contact."— Presentation transcript:

1 Tips which we have found helpful to identify PPI and TNF patients Talk to your Neurologists, Rheumatologists and Dermatologists (and Neurophysiology) Contact imaging for MRI scans and cross check with codes for UC (K51) and CD (K50); Arthropathies (M00-M25) and Spondyloarthropathies (M45-M49); G35-G37 (Demyelinating diseases of the CNS); or other conditions for which the Anti-TNFα is being used. Codes for identifying patients with PPI induced renal failure: M13.1 (Percutaneous needle biopsy of lesion of kidney) + N10 and N12 (Acute tubulo-interstitial nephritis) OR Y53 (Side effects from Gastrointestinal drugs) If you have clinic letters available in an electronic format, ask your IT department do a search for patients seen by the Renal team with PPI / omeprazole etc. in the “Diagnosis” or “Medical History” sections. We have found that raising the profile of the Anti-TNF/ PPI study to our neurology and renal colleagues has also been very successful. E.g. MDT meetings or at lunch time presentations. We can also provide you with laminated inclusion criteria to place in clinic rooms. Thank you all very much indeed for your fantastic support over We have recruited a total of 936 patients to PRED4, which is a great achievement. We have until the end of 2013 to reach our initial target of 1100 patients. The Pharmacogenetics Office will be closed 24 th December st January You may still send samples over this period as lab staff will be working over this period. If you have any urgent queries you may call our Research nurse Suzie Marriott on or between Christmas and New Year’s Eve. We are extending PRED4 until December The thiopurine induced pancreatitis arm of the study is now closed and we have added 2 new arms (below) which will open in January The NEXT Steps…… We thought it would be an idea to share with you what happens to the blood samples and case report forms when they are received in Exeter. The blood samples are delivered to our molecular genetics laboratory where the DNA is extracted and then stored until the genetic wide association studies (GWAS) are performed. The case report forms are all ‘adjudicated’ by an expert panel of consultants. The panel look at each case/patient to evaluate how likely it is that the drug caused the adverse event. The patients are graded as definite or probable or possible or unlikely cases of drug induced serious adverse events. DNA from definite and probable cases are then sent for genotyping and analyses. Marian Parkinson Tel: Clare Heard Tel: Dr Tariq Ahmad (Chief Investigator) Claire Bewshea – IBD Research Project Manager Tel: Mobile: Junior doctors: Dr Abhey Singh (TNF) ; Dr Graham Heap (TIP/TIM) Dr Naomi Edney (PPI) Predicting Serious Drug Side Effects in Gastroenterology - PRED4 International IBD Genetics Consortium Projects Sulphasalazine Induced Neutropaenia History of inflammatory bowel disease or Rheumatoid arthritis History of Sulphasalazine exposure in the previous 30 days Normal total white cell count and neutrophil count at baseline Fall in neutrophil count to ≤0.5 x10 9 /L Medical opinion implicating Sulphasalazine leads to dose reduction or drug withdrawal (even if temporary) Thiopurine induced Liver Injury History of inflammatory bowel disease Normal ALT and bilirubin at baseline No pre-existing liver disease Elevation of ALT and/or bilirubin to ≥ 5 times upper limit of normal (defined by local lab) History of thiopurine exposure in the previous 30 days prior to this abnormal blood test Medical opinion implicating thiopurine in development of hepatotoxicity

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