Rheumatology and Internal Medicine

The Behçet's disease is a chronic inflammatory disease, recurrent, multisystem of unknown etiology. All events are self-limited except the ocular condition. It characterized by periods of exacerbation remission and unpredictable frequency and duration. Is based the diagnosis is based on the association of especially bipolar aphthosis, skin manifestations, uveitis and affectation of great vessels. In the absence of these signs is more difficult to confirm the diagnosis. The lesions of the gastrointestinal tract and central nervous system is less frequent, even so may threaten the patient's life. The susceptibility of Behçet´s disease is strongly associated with the presence of HILA -B51 allele. The neurological manifestations are signs of malignancy.

The majority of individuals with traditional cardiovascular risk factors contributing in heart failure (HF) risk exhibited increased serum levels  of  uric  acid.  The  role  of  SUA  in  HF  manifestation  appears  to  be  controversial.  First  controversy  affects  the  fact  that  SUA  plays  an  important role in inducing oxidative stress, inflammation, neuro humoral activation, and endothelial dysfunction. Being natural antioxidant uric acid contributes in prevention of cell damage and thereby may restore vascular function leading to reversion of endothelial dysfunction. Interestingly,  there  is  a  large  body  of  evidence  regarding  that  uric  acid  is  able  to  regulate  an  activity  of  endogenous  repair  system  through  epigenetic  mechanisms  and  activation  of  intracellular  signaling,  such  as  STAT3  and  Akt.  Indeed,  uric  acid  mediates  a  survival  of  endothelial  precursors, mediate their mobbing and differentiation, as well as coordinate a turn-over effect of metabolic memory phenomenon into repair capability  of  cell  precursors.  Probably,  these  controversies  could  have  taken  into  consideration  when  clinical  results  of  several  studies  are  discussed. Although elevated SUA levels were found a strong predictor of adverse clinical outcomes in HF patients, there is assumption that final result of elevated uric acid may depend on cooperation between metabolic and epigenetic factors contributing in HF evolution. The short communication is depicted the importance of new clinical data to confirm the emerging reparative ability of SUA in HF and its role as promising target for treatment in cardiac failure.