Dr Ewan Pearson
Ewan Pearson qualified from Cambridge University Medical School in 1995. After a number of years of clinical training, he studied for a PhD in Andrew Hattersley’s lab in Exeter, where he carried out physiology and clinical phenotyping in patients with Maturity Onset Diabetes of the Young (MODY) and Neonatal diabetes. It was during this time that he established that patients with MODY due to HNF1A mutations are sulphonylurea sensitive; and that patients with 'insulin-dependent' neonatal diabetes due to potassium channel mutations can be treated with high dose sulphonylureas. Both findings have led to patients successfully transferring off insulin treatment.
Ewan moved to Dundee in 2005, where supported by a clinician scientist fellowship he pursued his research interest in genetic and phenotypic determinants of response to diabetes treatments. He was appointed to a clinical senior lecturer post at the University of Dundee in 2008. Ewan's current research areas are the pharmacogenetics of metformin, sulphonylureas and thiazolidinediones; clinical predictors of response to these agents; and pharmacovigilance.
Selected Publications
- Zhou K, Donnelly L, Burch L, Doney ASF, Leese G, Hattersley AT, McCarthy MI, Morris AD, Lang CC, Palmer CAN, Pearson ER. Loss of function CYP2C9 variants improve therapeutic response to sulfonylureas – A Go-DARTS study. Clin Pharmacol Ther. 2010 Jan;87(1):52-6. Epub 2009 Sep 30
- Zhou K, Donnelly LA, Kimber CH, Donnan PT, Doney AS, Leese G, Hattersley AT, McCarthy MI, Morris AD, Palmer CN, Pearson ER. Reduced-function SLC22A1 polymorphisms encoding organic cation transporter 1 and glycemic response to metformin: a GoDARTS study. Diabetes. 2009 Jun;58(6):1434-9.
- Donnelly LA, Morris AD, Pearson ER. Adherence in patients transferred from immediate release metformin to a sustained release formulation: a population-based study. Diabetes Obesity & Metabolism. 2009 Apr;11(4):338-42.
- Wagner VM, Kremke B, Schmidt D, Hiort O, Flanagan SE, Pearson ER. Transition from insulin to sulfonylurea in a child with heterozygous activating mutation in KCNJ11 encoding Kir6.2. requires high initial doses of sulfonylurea, rapid dose reduction and low maintenance dose in long term. European Journal of Paediatrics 2009 Mar;168(3):359- 61.
- Della Manna T, Battistim C, Radonsky V, Savoldelli RD, Damiani D, Kok F, Pearson ER, Ellard S, Hattersley AT, Reis AF. Glibenclamide unresponsiveness in a Brazilian child with permanent neonatal diabetes mellitus and DEND syndrome due to a C166Y mutation in KCNJ11 (Kir6.2) gene. Arq Bras Endocrinol Metabol. 2008 Nov;52(8):1350-5.
- deWet H, Proks P, Lafond M, Aittoniemi J, Sansom MSP, Flanagan SE, Pearson ER, Hattersley AT, Ashcroft FM. A mutation (Arg 826 Trp) in nucleotide-binding domain 1 of ABCC8 reduces ATPase activity and causes transient neonatal diabetes. EMBO reports. EMBO Reports. 2008 Jul;9(7):648-54.
- Evans JM, Ogston SA, Reimann F, Gribble FM, Morris AD, Pearson ER. No differences in mortality between users of pancreatic-specific and non-pancreatic-specific sulphonylureas: a cohort analysis. Diabetes Obes Metab. 2008 April 10(4):350-2.
- Pearson ER, Donnelly L, Doney ASF, Kimber C, Whitley A, McCarthy M, Hattersley AT, Morris AD, Palmer CNA. Variation in TCF7L2 influences therapeutic response to sulfonylureas: A GoDARTs study. Diabetes 2007 August 56(8):2178-82.
- Kimber CH, Doney AS, Pearson ER, McCarthy MI, Hattersley AT, Leese GP, Morris AD, Palmer CNA. TCF7L2 in the Go-DARTS study: evidence for a gene dose effect on both diabetes susceptibility and control of glucose levels. Diabetologia 2007 Jun;50(6):1186-91.
- Pearson ER, Flechtner I, Njolstad PR, Malecki MT, Flanagan SE, Larkin B, Ashcroft FM, Klimes I, Codner E, Iotova V, Slingerland AS, Shield J, Robert JJ, Holst JJ, Clark PM, Ellard S, Sovik O, Polak M, Hattersley AT; Neonatal Diabetes International Collaborative Group. Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations. New England Journal of Medicine 2006; 355(5):467-77.