Clinical evidence of VVS and vitamin B12/folate deficiency
There is some clinical evidence of the association between vitamin B12
deficiency and VVS in pediatric patients;22, 23nonetheless, there is scarce and weak evidence in adults and the
elderly.24 In a case-control study, pediatric patients
with VVS (N=125) were more likely to have vitamin B12 deficiency (47.2%
versus 18.0%; P<0.001) and lower serum vitamin B12 (352.8
versus 411.3 pg/mL; P<0.001) compared to healthy controls
(N=50); however, there was no difference in serum levels of
folate.22 Another study revealed that pediatric
patients with VVS and a positive HUTT (N=80) are more likely to have
vitamin B12 deficiency (80.0% versus 52.5%; P=0.001) and lower serum
vitamin B12 (282 versus 358 pg/mL; P=0.01) compared to HUTT negative
patients (N=80).23
Despite this evidence in pediatric patients <18 years of age,
there are only some descriptive studies in other age
groups.24, 32, 33 These studies showed that the
prevalence of vitamin B12 deficiency might be as high as 70% in
adult24 or 23% in eldely33 patients
with VVS and a positive HUTT; nevertheless, no comparison was made with
a control group. Notably, supplementation with intramuscular vitamin B12
in patients with deficiency reduced HUTT-induced syncope by 50-60% in a
six-month follow-up.24 Although these findings may
imply the association of vitamin B12 and VVS in adults, the lack of a
proper control group limits their generalizability. Furthermore, our
results do not support this association, at least in a general
population of patients with VVS who were referred to our syncope unit.
This is in contrast with the current evidence in pediatric patients.
This discrepancy may be attributed to the physiologic differences in
dietary needs and growth between adults and adolescents, as most of the
pediatric patients included in the abovementioned studies were older
than ten years.22, 23