Abstract Background: Vitamin D is a potent immunomodulator of innate immune responses, and
its deficiency was implicated in the activation of tuberculosis (TB). The effects of vitamin D are
exerted by the interaction with the vitamin D receptor (VDR) and may be influenced by polymorphisms
in the VDR gene.
Methods: We conducted a case–control study to identify 25(OH) D levels and FOK1 polymorphism
of the VDR gene in a group of newly diagnosed pulmonary TB patients and compared to the
findings in a group of healthy controls.
Results: Obtained results revealed that 25(OH) D levels were significantly lower in the patients
than in the controls (P < 0.0001), and the prevalence of vitamin D insufficiency was 72.5% in TB
patients. The frequencies of FokI genotypes determined from TB patients were 30% for FF , 50%
for Ff and 20% for ff, while in controls, the frequency of FF, Ff and ff were present in a percentage
of; 40%, 40% and 20%, respectively. There was no significant association between the genotype
groups, TB patient and normal control, for FokI polymorphism (P >0.05). Also, no association
between VDR genotype and 25(OH) D levels was found.
Conclusion: FokI polymorphisms in the VDR gene do not appear to be responsible for host susceptibility
to human tuberculosis in the Egyptian population. However, vitamin D deficiency may
be a cause of the susceptibility to tuberculosis.