Role of Inflammatory Markers on Left Ventricular Functions in Vitamin D Deficiency Rickets

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 serum 25(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 phosphtase (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, echocardiogrphic 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 correlation 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.