on pathogenesis, the course of the disease, and the best presumed/proven therapy is
determined. Although according to the law of large numbers the majority of
patients profit, practice shows that a minority of patients are partially or completely
refractory to treatment. Through deductive reasoning and individualization, per-
sonalized medicine tries to explain the differences between patients suffering from
the same disease and determines the best possible treatment for the individual
patient. Although the daily treatment approach has always been individualized
(type of drug, dose, duration of therapy), the difference is that individualization
thus far has been mainly based on the trial and error method, relying on the
physician’s experience and‘gut feeling,’while in personalized medicine it is
based on objective parameters. Through personalized medicine, we try to determine
the right dosage of the right drug for the right patient at the right time, basing the
decision on all available data—the phenotype of the disease, the genotype of the
patient, and the exposure to environmental factors.^2
Limitations of personalized medicine are linked to all the problems modern
society faces, namely unequal access to high-tech methods (genetic testing) due to
geographical and/or economical disparity, ethical and legal problems related to the
ownership of genetic data, health insurance policies for individuals with increased
risk of genetic disorders, and the possible misuse of such data. Cost benefit analyses
will play a major role in defining clinical usefulness and the level of implementation
of personalized medicine in everyday practice.^3
2 Personalized Medicine in Gastroenterology
The complexity of the gastrointestinal (GI) tract and its residing intestinal micro-
flora is best observed through the fact that the number of intestinal bacteria (10^13 –
1014 ) overwhelms the number of the host’s (human) cells present in the entire
organism and that the total bacterial genome has 100-fold more genes than the
entire human genome.^4 In such a complex system, pathogenesis and manifestation
of inflammatory bowel diseases (Crohn’s disease and ulcerative colitis) are a direct
result of the interaction of the human genome, the bacterial genome (microbioma),
as well as exposure to environmental factors.^5 Research is currently undertaking the
task of discovering genetic (predisposing) and serological (existing) markers of the
disease (Table 1 ).^6 Personalized medicine seems to be a must since the difference in
the expression of effector molecules, inflammatory markers, and microbioma
structure results in such a variety of disease phenotypes.^7
(^2) Hamburg and Collins ( 2010 ).
(^3) Issa ( 2007 ).
(^4) Gill et al. ( 2006 ).
(^5) Patel and Babyatsky ( 2008 ).
(^6) Barrett et al. ( 2008 ), Somma et al. ( 2013 ), Tesˇija Kuna ( 2013 ), and Mendoza and Abreu ( 2009 ).
(^7) Patel and Babyatsky ( 2008 ).
258 D. Sˇtimac and N. Franjic ́