The effect of the systemic inflammatory response on plasma vitamin 25 (OH) D concentrations adjusted for albumin

Plasma 25-hydroxyvitamin D (25(OH) D) deficiencies are associated with several diseases. The magnitude of systemic inflammatory response, as evidenced by C-reactive protein (CRP), is a major factor associated with lower 25(OH)D. Other aspects of the systemic inflammatory response may be important in determining plasma 25 (OH)D concentrations.

To examine the relationship between plasma 25(OH)D, CRP and albumin concentrations in two patient cohorts.

5327 patients referred for nutritional assessment and 117 patients with critical illness were examined. Plasma 25 (OH) D concentrations were measured using standard methods. Intra and between assay imprecision was <10%.

In the large cohort, plasma 25 (OH) D was significantly associated with CRP (r(s)  =  -0.113, p<0.001) and albumin (rs = 0.192, p<0.001). 3711 patients had CRP concentrations ≤ 10 mg/L; with decreasing albumin concentrations ≥ 35, 25-34 and <25 g/l, median concentrations of 25 (OH) D were significantly lower from 35 to 28 to 14 nmol/l (p<0.001). This decrease was significant when albumin concentrations were reduced between 25-34 g/L (p<0.001) and when albumin <25 g/L (p<0.001). 1271 patients had CRP concentrations between 11-80 mg/L; with decreasing albumin concentrations ≥ 35, 25-34 and <25 g/l, median concentrations of 25 (OH) D were significantly lower from 31 to 24 to 19 nmol/l (p<0.001). This decrease was significant when albumin concentration were 25-34 g/L (p<0.001) and when albumin <25 g/L (p<0.001). 345 patients had CRP concentrations >80 mg/L; with decreasing albumin concentrations ≥ 35, 25-34 and <25 g/l, median concentrations of 25 (OH) D were not significantly altered varying from 19 to 23 to 23 nmol/l. Similar relationships were also obtained in the cohort of patients with critical illness.

Plasma concentrations of 25(OH) D were independently associated with both CRP and albumin and consistent with the systemic inflammatory response as a major confounding factor in determining vitamin D status.