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Thiopurines Crohn disease

Thiopurine methyltransferase (TPMT) catalyzes the S-methylation of thiopurine dmgs, such as 6-mercaptopurine (6-MP), 6-thioguanine and azathioprine, to inactive metabolites [29-32]. Thiopurines form part of the routine treatment for patients with acute lymphoblastic leukemia, rheumatoid arthritis, and autoimmune diseases such as SLE and Crohn s disease, and are used as an immunosuppressant following organ transplantation. [Pg.494]

Fig. 13.2 Thiopurine methyl transferase (TPMT) methylator genotypes in Crohn s disease during azathioprine/6-mercaptopurine (AZA/6-MP) treatment influences the time in months to development of severe myelosuppression. However, only 27% of patients with Crohn s disease and myelo-suppression during AZA therapy had mutant alleles of the TPMT gene associated with enzyme deficiency. Myelosuppression is more often caused by other factors. Continued monitoring of blood cell counts remains mandatory in patients treated with AZA. (Reproduced from ref 35.)... Fig. 13.2 Thiopurine methyl transferase (TPMT) methylator genotypes in Crohn s disease during azathioprine/6-mercaptopurine (AZA/6-MP) treatment influences the time in months to development of severe myelosuppression. However, only 27% of patients with Crohn s disease and myelo-suppression during AZA therapy had mutant alleles of the TPMT gene associated with enzyme deficiency. Myelosuppression is more often caused by other factors. Continued monitoring of blood cell counts remains mandatory in patients treated with AZA. (Reproduced from ref 35.)...
Colombel IF, Ferrari N, Debuy sere H et al. Genotypic analysis of thiopurine 5-methyltransferase in patients with Crohn s disease and severe myelosuppression during azathioprine therapy. Gastroenterology 2000 118 1025-1030. [Pg.198]

Kaskas BA, Louis E, Hindorf U et al. Safe treatment of thiopurine S -methyltransferase deficient Crohn s disease patients with azathioprine. Gut 2003 52 140-142. [Pg.200]

Azathioprine and 6-MP are important agents in the induction and maintenance of remission of ulcerative colitis and Crohn s disease. Although the optimal dose is uncertain, most patients with normal thiopurine-S-methyltransferase (TPMT) activity (see below) are treated with 6-MP, 1-1.5 mg/kg/d, or azathioprine, 2-2.5 mg/kg/d. After 3-6 months of treatment, 50-60% of patients with active disease achieve remission. These agents help maintain remission in up to 80% of patients. Among patients who depend on long-term glucocorticoid therapy to control active disease, purine analogs allow dose reduction or elimination of steroids in the majority. [Pg.1328]

Mazor Y, Koifman E, Elkin H (2013) Risk factors for serious adverse drug reactions to thiopurines in patients with Crohn s Disease. Curr Drug Saf 8 181-185... [Pg.704]

Pancreas In a retrospective, multicenter study in 241 patients with inflammatory bowel disease and 108 patients with vasculitis the cumulative incidence of thiopurine-induced acute pancreatitis in Crohn s disease equalled that in ulcerative colitis and vascuhtis (2.6%, 3.7%, and 1.9% respectively) [165 ]. [Pg.634]

Of 135patients with Crohn s disease (n — 88) or ulcerative colitis (n = 47), 65 stopped taking it because of adverse events after 25 (8-92) days the other 70 patients tolerated mercaptopurine and were followed up for 736 (362-1080) days [109 ]. Mercaptopurine was tolerated in 12 of 17 patients with hepatotoxicity and in 13 of 19 with arthral-gia/myalgia during azathioprine treatment. Previous abdominal surgery was more common in those who had adverse reactions to mercaptopurine (39/65 vs. 27/70), and thiopurine methyltransferase activity was higher in those who were tolerant of mercaptopurine. [Pg.825]

Pancreas During 82 episodes of acute pancreatitis, most cases were attributed to drug exposure azathioprine/mercapto-purine (n = 46) and mesalazine (n = 6) [121 ]. In those with acute pancreatitis due to thiopurines, female sex (OR = 3.4 95% Cl = 1.3, 9.3) and Crohn s disease (OR = 5.8 95% Cl = 1.6,21) were susceptibility factors. [Pg.826]

Liver In a retrospective study in 30 patients with Crohn s disease who had failed treatment with thiopurines with or without methotrexate, thioguanine 40 mg/ day was used instead [156 ]. Seven stopped taking it because of adverse reactions seven developed abnormal liver function tests during treatment, mostly transient and mild, and one developed portal hypertension, which resolved after withdrawal. Of 11 liver biopsies, none showed nodular regenerative hyperplasia. [Pg.830]

Costantino G, Furfaro F, Belvedere A, Alibrandi A, Fries W. Thiopurine treatment in inflaimnatory bowel disease response predictors, safety, and withdrawal infoUow-up. J Crohns Colitis June 2012 6(5) 588-96. PubMed PMID 22398045. Epub 2012/03/09. eng. [Pg.601]

Smith MA, Blaker P, Marinaki AM, Anderson SH, Irving PM, Sanderson JD. Optimising outcome on thiopurines in inflammatory bowel disease by co-prescription of allopurinol. J Crohns Colitis October 2012 6(9) 905-12. PubMed PMID 22386736. Epub 2012/03/06. eng. [Pg.601]


See other pages where Thiopurines Crohn disease is mentioned: [Pg.657]    [Pg.254]    [Pg.144]    [Pg.384]    [Pg.64]    [Pg.658]    [Pg.830]    [Pg.1119]   
See also in sourсe #XX -- [ Pg.598 ]




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