Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT06391437 |
| Other study ID # |
RC17-4-2023 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
May 1, 2023 |
| Est. completion date |
March 31, 2024 |
Study information
| Verified date |
April 2024 |
| Source |
Benha University |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
Aim of the work is to assess the prevalence of vitamin A deficiency in critically ill
children with sepsis and the association between vitamin A deficiency and clinical outcomes
Description:
Vitamin A plays an essential role in a large number of physiological functions that encompass
vision, growth, reproduction, hematopoiesis, and immunity.
Despite major advances in the knowledge of vitamin A biology, its deficiency is still a
serious public health problem that affects an estimated 127 million preschool children. In
children, vitamin A deficiency results in increased risks of mortality and morbidity from
infections, blindness and anemia. Many of these effects can be linked to the immunological
functions of vitamin A.
Vitamin A modulates immunity through its active metabolite retinoic acid (RA), which acts on
retinoid receptors in various cell types. Studies utilizing various animal models of vitamin
A or retinoid receptor deficiency have revealed an integral role for RA in immunity and
tolerance.
Retinoic acid (RA) has been reported to promote anti-inflammatory regulatory T cell (Treg)
differentiation and inhibit interleukin (IL)-6-induced proinflammatory T helper 17 (Th17)
cells, which could balance pro- and anti-inflammatory immunity.
Vitamin A deficiency (VAD ) is associated with adverse health outcomes due to an increased
risk of infection in children. VAD could impact immunity at multiple levels, including
disturbing the integrity of the gastrointestinal mucosal barrier, decreasing monocyte and
natural killer (NK) cell numbers, and impairing the function of macrophages, dendritic cells,
and neutrophils.
Sepsis, a life-threatening organ dysfunction caused by a dysregulated host response to
infection, contributes to millions of deaths worldwide each year, with a mortality rate of
more than 25%. Remarkably, sepsis is a common cause of death in children. The mortality of
severe sepsis was reported to be as high as 34.6% in children.
As a public health problem, sepsis has posed a significant burden on extensive health care
resources for many years. It is reported as a complicated immune disorder characterized by
both a hyperinflammatory immune response in the early stage and immunosuppression in the
later stage.
Most deaths from sepsis occur due to opportunistic pathogen superinfections or latent viral
reactivation resulting from immunosuppression.
VA is an immunomodulatory, and its deficiency may cause an imbalance between pro- and
anti-inflammatory factors and impaired immune function, which are found in sepsis. There is a
biological rationale that VAD may be a contributing factor related to poor clinical outcomes
in patients with sepsis. Importantly, VAD is highly prevalent in children, especially in
preschool children. However, there is limited data regarding the correlation between VAD and
sepsis, so we hypothesize that VAD may play an important role in the pathogenesis and
progression of sepsis in children.
