Citations 2
Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for Thiopurine Dosing Based on TPMT and NUDT15 Genotypes: 2025 Update
Maillard, M., Schwab, Matthias, Whirl-Carrillo, Michelle, Moyer, AM , Suarez‐Kurtz, Guilherme , Pui, CH, Stein, C Michael, Klein, Teri E. , Spahn, Claire , Kwon, Sooyeon, Boer, Nanne K de, Ahmad, Tariq, Antillon-Klussmann, Federico Guillermo, Caudle, Kelly E. , Yeoh, Allen E J, Schmiegelow, K., Yang, Jun J, Schwab, Matthias , Maillard, Maud , Maillard, Maud , Schwab, Matthias , Whirl-Carrillo, Michelle , Caudle, Kelly E , Kato, Motohiro , Klein, Teri E , Whirl‐Carrillo, Michelle , Stein, C. Michael, Hartono, Juanda Leo , Ahmad, Tariq , Antillon‐Klussmann, Federico Guillermo, Kato, Motohiro , Yeoh, Allen Eng Juh
Clinical Pharmacology & Therapeutics | January 31, 2026 | Volume: 119 | Issue: 4 | Pages: 916-927
Thiopurine methyltransferase (TPMT) and Nudix hydrolase 15 (NUDT15) are key enzymes that catabolize thiopurines. Decreased or no‐function alleles in TPMT and NUDT15 are associated with reduced or no enzyme activity and predictive of pronounced adverse effects, including severe myelosuppression, that may occur among individuals treated with standard doses of thiopurines. Genetic variants in these genes are present in all world populations; however, their frequency varies by ancestry. In this updated guideline, we provide recommendations for adjusting starting doses of mercaptopurine, thioguanine, and azathioprine based on TPMT and NUDT15 genotypes, including for individuals with variants in both genes (updates on www.clinpgx.org ).
The Global Evolution of Inflammatory Bowel Disease across Four Epidemiologic Stages
Hracs, Lindsay , Gorospe, Julia, Buie, Michael , Quan, Joshua , Goddard, Quinn , Caplan, Léa , Markovinović, Ante , Abbey, Yvonne , Abdullah, Murdani , Balderramo, Domingo , Bernstein, Çharles N. , Burisch, Johan , Chong, Vui Heng , Dotan, Iris , Ouali, Sara El , Forss, Anders, Dao, Hang Viet , Baños, Fabián Juliao , Kaibullayeva, Jamilya , Kobayashi, Taku , Miao, Yinglei , Ng, Ka Kei , Olén, Ola , Simadibrata, Marcellus , Sun, Yang , Turner, Dan , Vergara, Beatriz, Wei, Shu Chen, Yang, Suk‐Kyun , Kobayashi, Taku , Kaplan, Gilaad G. , Windsor, Joseph W. , Cummings, Michael K. , Coward, Stephanie B. , Williamson, Tyler S. , Abreu, María T. , Ahuja, Vineet , Ali, Raja Affendi Raja , Altuwaijri, Mansour A. , Banerjee, Rupa , Benchimol, Eric I. , Bernstein, Charles Noah , Brunet, Eduard , Dutta, Usha , Forbes, Angela J. , Forss, Anders, Gearry, Richard B. , Hartono, Juanda Leo , Hilmi, Ida Normiha , Hodges, Phoebe , Jones, Gareth‐Rhys , Kelly, Paul , Kotze, Paulo Gustavo , Lakatos, Péter L. , Lees, Charlie W. , Limsrivilai, Julajak , Lo, Bobby Zhao Sheng , Loftus, Edward V. , Ludvigsson, Jonas F. , Mak, Joyce Wing Yan , Okabayashi, Shinji , Panaccione, Remo , Paudel, Mukesh Sharma , Quaresma, Abel Botelho , Rubin, David T. , Suzuki, Hidekazu , Toro, Martín , Wei, Shu Chen, Yamamoto-Furusho, Jesus , Ng, Siew C.
No container title available | January 23, 2024 | Volume: No volume available | Issue: No issue available | Pages: No page available
Abstract During the 20th century, inflammatory bowel disease (IBD) was considered a disease of early-industrialized regions in North America, Europe, and Oceania. At the turn of the 21st century, incidence of IBD increased in newly-industrialized and emerging regions in Africa, Asia, and Latin America, while prevalence in early-industrialized regions started to grow steadily. Changes in incidence and prevalence denote evolution of IBD across four epidemiologic stages: Stage 1 (Emergence), characterized by low incidence and prevalence; stage 2 (Acceleration in Incidence), characterized by rapidly rising incidence and low prevalence; and stage 3 (Compounding Prevalence), characterized by decelerating, plateauing, or declining incidence and steadily rising prevalence. A fourth stage (Prevalence Equilibrium) has been proposed where the slope of prevalence plateaus due to shifting demographics of an aging IBD population, but it has not yet been evidenced. To date, these stages have been theoretical without specific incidence/prevalence indicators defining transition points. Using real-world data from 490 population-based studies comprising 80 global regions and spanning over a century (1920–2023), we show spatiotemporal transitions across stages 1–3 and model transition towards stage 4. Understanding the evolution of IBD across epidemiologic stages allows healthcare systems to better prepare for the future worldwide burden of IBD.