Vitamin D and inflammation

Abstract

Abbreviations: CRP, C-reactive protein; CXCL9, CXC chemokine ligand 9; E-selectin, ESR, erythrocyte sedimentation rate, F1C2, prothrombin fragment 1C2; IFG, impaired fasting glucose; IL, interleukin; MCP-1, monocyte chemoattractant protein-1; NGAL, neutrophil gelatinase-associated lipocalin; NGT, normal glucose tolerance; ns, not stated; PAI-1, plasminogen activator inhibitor-1; sICAM-1, soluble intracellular adhesion molecule-1; sTNF-R2, soluble tumor necrosis factor a receptor type 2; TAT, thrombin antithrombin complex; TGF-b, transforming growth factor-b; TNF-a, tumor necrosis factor-a Seventeen found significantly reduced inflammatory markers, 19 did not, one was mixed and one showed adverse results. With few exceptions, studies in normal subjects, obesity, type 2 diabetics, and stable cardiovascular disease did not find significant beneficial effects. However, we found that 6 out of 7 RCTS of vitamin D 3 in highly inflammatory conditions (acute infantile congestive heart failure, multiple sclerosis, inflammatory bowel disease, cystic fibrosis, SLE, active TB and evolving myocardial infarction) found significant reductions. We found baseline and final 25(OH)D predicted RCTs with significant reduction in inflammatory markers. Vitamin D tends to modestly lower markers of inflammation in highly inflammatory conditions, when baseline 25(OH)D levels were low and when achieved 25(OH)D levels were higher. Future inquiries should: recruit subjects with low baseline 25(OH)D levels, subjects with elevated markers of inflammation, subjects with inflammatory conditions, achieve adequate final 25(OH)D levels, and use physiological doses of vitamin D. We attempted to identify all extant randomized controlled trials (RCTs) of vitamin D that used inflammatory markers as primary or secondary endpoints.

Assessment of vitamin D status – a changing landscape

“…However, at present it is controversial whether 25-OHD reduces inflammation or whether inflammation reduces 25-OHD concentrations. It is possible that both mechanisms are active and not mutually exclusive: vitamin D may decrease inflammation, while oxidative stress from inflammation may interfere with the metabolism of vitamin D and thus lower 25-OHD [56]. Randomized controlled trials of vitamin D have given inconsistent results.…”

Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact

“…Cerebral ischemic damage is due to the activation of several inflammatory events, including the infiltration of circulating immune cells and activation of microglia, astrocytes, and endothelial cells [160]. In stroke individuals, the mechanism involved in vessel disease mediated by vitamin D deficit might consist of a release of atherogenic pro-inflammatory cytokines, that foster atherosclerotic vascular changes, and might induce plaque instability [161][162]. Vitamin D plays an additional role for the regulation of inflammation process, through prostaglandin inhibition, reduction of mitogen-activated protein kinase (MAPK) and reducing the expression of the nuclear factor kappa B (NF-κB) pathways [163][164][165].…”

Vaikų, Sergančių Cistine Fibroze, Vitamino D Koncentracija Kraujyje

“…Vertinant priešuždegiminį vitamino D poveikį, vienos nuomonės nėra. Atlikti tyrimai rodo atvirkštinę priklausomybę tarp 25(OH)D ir uždegi-mo mediatorių, tačiau vis dar neaišku, ar 25(OH)D mažina uždegimą, ar dėl esamo uždegimo sumažėja 25(OH)D [5].…”