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 2013. 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 2013 - 1 st January 2014. 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 01392 408937 or 07810 834996 between Christmas and New Year’s Eve. We are extending PRED4 until December 2014. The thiopurine induced pancreatitis arm of the study is now closed and we have added 2 new arms (below) which will open in January 2014. 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: 01392 403812 marian.parkinson@nhs.net Clare Heard Tel: 01392 403818 clare.heard@nhs.net Dr Tariq Ahmad (Chief Investigator) E-mail: tariq.ahmad1@nhs.net Claire Bewshea – IBD Research Project Manager E-mail: claire.bewshea@nhs.net Tel: 01392 406928 Mobile: 07828146468 Junior doctors: Dr Abhey Singh (TNF) abhey.singh@nhs.net ; Dr Graham Heap (TIP/TIM) grahamheap@nhs.net Dr Naomi Edney naomi.edney@nhs.net (PPI) Predicting Serious Drug Side Effects in Gastroenterology - PRED4 International IBD Genetics Consortium Projects www.ibdresearch.co.uk/pred4 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