Fontanellas, AntonioMartínez-Fresno, M.Garrido Astray, María ConcepciónPerucho, TeresaMorán-Jiménez, María JosefaGarcía-Bravo, MaríaMéndez, ManuelPoblete-Gutiérrez, PamelaFrank, JorgeHenriques-Gil, NunoEnríquez de Salamanca, Rafael2013-11-272013-11-272010Fontanellas, A., Martínez‐Fresno, M., Garrido‐Astray, M. C., Perucho, T., Morán‐Jiménez, M. J., García‐Bravo, M., ..., & Enríquez-Salamanca, R. (2010). Smoking but not homozygosity for CYP1A2 g‐163A allelic variant leads to earlier disease onset in patients with sporadic porphyria cutanea tarda. Experimental Dermatology, 19(8), e326-e328.http://hdl.handle.net/11268/735Porphyria cutanea tarda (PCT) results from decreased activity of hepatic uroporphyrinogen decarboxylase (UROD). Both sporadic and familial forms are characterised by typical cutaneous lesions triggered by genetic/environmental factors. Studies in rodents showed that cytochrome P4501A2 (CYP1A2) plays a central role in the synthesis of a competitive inhibitor of hepatic UROD, but there is little evidence in humans. The impact of smoking and CYP1A2 g-163C > A allelic variant upon first appearance of clinical signs was investigated in 102 patients (80 sporadic-PCT) and 150 healthy donors from Spain. We found an increase in the frequency of CYP1A2 g-163A allele in patients with PCT when compared with controls, although the more inducible A/A genotype had no effect on the onset age. In sporadic-PCT, smoking leads to earlier onset of clinically overt disease in moderate-to-heavy smokers (>or=10 cigarettes/day). In conclusion, this study provides evidence that smoking hastens the onset of cutaneous symptoms in sporadic-PCT patients.engjournal article10.1111/j.1600-0625.2009.01040.xrestricted accessEnfermedades de la piel