Impact of Vitamin D Deficiency on Systemic Inflammatory Markers and Left Ventricular Functions in Rachitic Infants

Background: Circulating 25 hydroxyvitamin D (25 (OH)D), an accurate measure of
vitamin D status, is markedly reduced in rachitic infants. Aside from the known
relationship between vitamin D and bone, vitamin D has also been implicated in
cardiovascular homeostasis, immune function and inflammation. Furthermore, a
mass of evidence is accumulating that vitamin D deficiency could lead to
cardiovascular complications and imbalance of cytokines profile. Our objective was
to study the relationship between vitamin D status (as determined by serum25(OH) D
concentrations) and inflammatory markers and left ventricular function in rachitic
infants, also to evaluate the effect of vitamin D supplementation on the above
parameters. Subjects and methods: This study included two groups; vitamin D
deficiency rickets (VDDR) group (25 infants) and an age matched control group (15
infants). After subsiding of the acute illness, the rachitic infants received vitamin D
supplementation for 6 months. Blood samples were collected in the morning before
the start of treatment and analyzed for serum 25(OH)D, intact parathyroid hormone
(iPTH), Alkaline phosphatase (ALP), calcium (Ca), Phosphorus (Ph) and
inflammatory markers [interleukin-6 (IL-6), and C-reactive protein (CRP)].
Electrocardiogram (ECG) and echocardiography measuring left ventricular functions
were done. The biochemical variables, ECG and echocardiography were assessed at
baseline and after 6 months of vitamin D supplementation. Results: VDDR group had
significant lower 25(OH)D, Ca, Ph and significant higher iPTH, ALP, IL-6 and CRP
compared to the age matched control group at baseline. Echocardiographic finding
revealed significant increase in LVEDD and LVESD and significant decrease in EF%
and FS% in VDDR group compared to the age matched control group at the study
entry. Also, ECG finding showed abnormality in some patients at baseline. The
biochemical, echocardiographic and ECG variables improved significantly after 6
months of vitamin D supplementation and reached to those levels found in the age
matched control group. Finally, we found negative correlations between 25(OH)D
level and IL-6, CRP, LVEDD and LVESD. Also, positive correlations were found
between 25 (OH)D and EF% and FS%. These correlations were observed at baseline
and after 6 months of vitamin D treatment. Conclusion: VDDR is associated with
increased inflammatory markers and impairment of left ventricular functions in
rachitic infants. Vitamin D supplementation ameliorated these effects. Also, results
gleaned from this investigation support the possible contributing role of the elevated
inflammatory markers in the pathophysiology of left ventricular impairment in
vitamin D deficiency rachitic infants. More studies are needed to fully characterize
the relationship between Vitamin D induced inflammation and cardiac function in
rachitic infants.