A STUDY OF THE ROLE OF URINARY POTASSIUM IN ULCERATIVE COLITIS PATIENTS, ITS CORRELATION WITH DISEASE ACTIVITY | ||||
| ALEXMED ePosters | ||||
| Article 17, Volume 2, Issue 2, October 2020, Page 51-51 | ||||
| Document Type: Preliminary preprint short reports of original research | ||||
| DOI: 10.21608/alexpo.2020.47222.1057 | ||||
 View on SCiNiTO | ||||
| Author | ||||
Dina Mohamed naguib GadAllah 
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| Internal medicine, faculty of medicine ,alexandria main university hospital, alexandria, egypt | ||||
| Abstract | ||||
| Inflammatory bowel disease (IBD) has been a global healthcare problem with increasing incidence. It includes two major forms, Crohn’s disease (CD) and ulcerative colitis (UC), which are distinct chronic bowel-relapsing inflammatory disorders. Worldwide, UC is more common than CD. The etiopathogenesis of UC is incompletely understood, but immune-mediated mechanisms are responsible for dysregulated immune responses against intraluminal antigens in genetically predisposed individuals. The diagnosis is based on the history, clinical, laboratory markers, radiological, endoscopic and histological features. Apart from the genetic factors that affect the pathogenesis of UC, environment plays a major role in regulating the balance between the immune tolerance and inflammation in the gut. One such factor is salt, high sodium intake and excretion (a reflection of sodium intake) has been associated with increased inflammation, higher cardiovascular morbidities, cancer and renal inflammation in chronic kidney disease (CKD) patients. High NaCl inhibits IL-10 secretion and suppressive function of Foxp3+ regulatory T cells thereby promoting the proinflammatory response. In addition, high salt exacerbates the immune response by activating the pro-inflammatory M1 macrophages. while alternatively reducing the activation of anti-inflammatory M2 macrophage. On the opposite side, potassium enhanced the generation of FoxP3+ Treg cells in the presence of TGFβ1 and reinforced the Foxp3 expression in Th17 cells by activating Smad2/3 and inhibiting Smad 7 expression. In a human report, potassium supplementation reduced IL-17A which was markedly enhanced by a high salt diet by inhibiting p38/MAPK-SGK1 pathway. | ||||
| Keywords | ||||
| urinary potassium; ulcerative colitis; FoxP3+ Tregcells | ||||
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