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Additional resources for INFLAMMATORY BOWEL DISEASE
25h; ). These results imply that the lowest enzymatic activity, resulting from the fast degradation of a protein, is connected with the alleles TPMT*3A and TPMT*2. This hypothe‐ sis is supported by the phenotype-undetectable metabolic activity of enzymes in patients with the variant alleles TPMT*3A and TPMT*2 in their genotype. 2. 19) is one of the ubiquitous cytosol enzymes. It catalyzes the reaction of inosine triphosphates hydrolysis to inosine monophos‐ phate. Even though the activity in various types of cells is different and the role of the en‐ zyme in the cell is not clearly understood; it is supposed that it prevents the accumulation of false nucleotides, which could be incorporated in the DNA and RNA molecules instead of standard nucleotides, and therefore damage these macromolecules.
In monozygous twins with CD, 7 out of 9 cases showed a corre‐ spondence to the disease location, and in 6 out of 9 cases the disease was diagnosed within 2 years. However, the disease behaviour did not reveal any correspondence . Available data imply that the mutation in the gene CARD15/NOD2 can be connected with the affected ileum, or preferential occurrence of inflammation in the ileocaecal area  and with the sten‐ otic form of the disease [59,60]. There has also been a discussion regarding the impact of mu‐ tation in this gene on the onset age of Crohn’s disease .
An important outcome of these population studies is that clinically significant variant alleles or their polymorphisms are present in all populations; therefore, the same diagnostic meth‐ ods based on the determination of genotype can be used. . From the phenotype per‐ spective, the overall protein stability of TPMT is the most important. In vitro and in vivo studies confirm that the quantity of expression of variant alleles is comparable with the ex‐ pression of the variant allele TPMT*1.