Update on vitamin D role in severe infections and sepsis

Abstract

Severe infections frequently require admission to the intensive care unit and cause life-threatening complications in critically ill patients. In this setting, severe infections are acknowledged as prerequisites for the development of sepsis, whose pathophysiology implies a dysregulated host response to pathogens, leading to disability and mortality worldwide.Vitamin D is a secosteroid hormone that plays a pivotal role to maintain immune system homeostasis, which is of paramount importance to resolve infection and modulate the burden of sepsis. Specifically, vitamin D deficiency has been widely reported in critically ill patients and represents a risk factor for the development of severe infections, sepsis and worse clinical outcomes. Several studies have demonstrated the feasibility, safety and effectiveness of vitamin D supplementation strategies to improve vitamin D body content, but conflictual results support its benefit in general populations of critically ill patients. In contrast, small randomised clinical trials reported that vitamin D supplementation may improve host-defence to pathogen invasion via the production of cathelicidin and specific cytokines. Nonetheless, no large scale investigations have been designed to specifically assess the impact of vitamin D supplementation on the outcome of critically ill septic patients admitted to the intensive care unit.

25-hydroxyvitamin D and parathyroid hormone in new onset sepsis: A prospective study in critically ill patients

“…Our findings are in accordance with previous data that demonstrate an increased prevalence of hypovitaminosis D in critically ill cases [ 11 , 19 , 20 , 28 ]. Evidence also suggests that decreased vitamin D is a risk factor for sepsis and a poor outcome [ 8 , 9 , 13 , 14 , 16 , 20 ]. A recent meta-analysis of 8 studies with 1736 cases showed that decreased 25(OH)D at admission was independently linked to an increased mortality in cases with sepsis [ 22 ].…”

“…In particular, vitamin D stimulates macrophages, induces regulatory T cells and Th2 response, inhibits B lymphocyte proliferation and differentiation, modulates dendritic cell maturation and tumor necrosis factor expression, suppresses pro-inflammatory cytokines and induces the synthesis of anti-inflammatory cytokines [ 11 , 12 ]. Additionally, vitamin D promotes barrier function and production of antibacterial peptides and reactive oxygen species [ 13 ]. Clinical studies suggest that hypovitaminosis D is a risk factor for bacterial and viral respiratory infections and sepsis [ [14] , [15] , [16] , [17] ].…”