DISCUSSION
Zona zoster is more common in women than men. Thoracic, lumbar,
trigeminal and cervical dermatomes are the most frequently affected
areas [3]. In our study, the most affected dermatomes were thoracic
and lumbar dermatomes, respectively.
With advanced age, the risk of developing shingles more severely
increases as a result of the decrease in the immune response specific to
varicella zoster virus in people with immunosuppressive disease or drug
use [1,3,9]. In humans, the main source of vitamin D is UVB-mediated
synthesis in the skin. Certain foods, such as fatty fish and dairy
products, contain vitamin D. Vitamin D activation involves two
hydroxylation steps, one in the liver and the other in the kidney. In
particular, final activation of vitamin D by 1-alpha hydroxylase also
occurs in extra kidney tissues, including epithelial and immune cells
[10].
The determination of the vitamin D receptor in peripheral blood
mononuclear cells has led to an emphasis on the regulatory role of
vitamin D in the immune system [6,11]. 25 (OH) –Vitamin D enters
the monocyte and, after being converted to 1,25-(OH)2-D in the mitochondria, binds to the vitamin D
receptor (VDR) and ultimately acts as a transcription factor for human
cathelicidin, an antimicrobial peptide. Defensins can also inhibit viral
replication and cause direct degradation of the viral membrane [12].
After pathogen exposure, monocytes and macrophages increase the number
of vitamin D receptors to increase cathelicidin production [13,14].
Cathelicidin effectively inhibits herpes simplex virus type 1 and
retrovirus replication in LL-37 peptide form. In addition, severe
1,25-(OH) 2-D deficiency has been associated with
clinically advanced human immunodeficiency virus (HIV) infection, and
vitamin D supplementation significantly inhibits hepatitis C virus (HCV)
proliferation [7]. B cells infected with Epstein-Barr virus (EBV)
exhibit significantly lower levels of VDR expression compared to
uninfected cells [7]. Activation of B and T lymphocytes has been
shown to result in VDR expression. In addition, 1,25-(OH)2-D stimulates T lymphocyte maturation, increases the
regulatory T lymphocyte ratio, and plays a role in limiting inflammation
triggered by microbial invasion [6,13]. HIV infection weakens VDR
activity. The decrease in VDR expression or activity levels leads to the
impairment of innate immunity, thus allowing intracellular pathogens
such as viruses to remain. However, vitamin D itself exhibits antiviral
effects in vitro [7]. In a study of the effects of vitamin D-related
antimicrobial peptides on herpes viruses, cathelicidine was shown to
reduce HSV-1 viral titers isolated from patients with
keratoconjunctivitis [13]. It has been shown that vitamin D
deficiency correlates with increased mental stress. Stress can affect
the activation of CD8 + T lymphocytes through the induction of
neuroendocrine factors that regulate the transition between viral
latency and reactivation in neurons. In this way, vitamin D deficiency
causes the weakening of immunity and predisposes to the development of
zona [7]. In a study of patients undergoing dialysis for chronic
kidney failure, it was found that the risk of zona reactivation was
significantly lower in patients who received vitamin D supplements
[6]. Chao et al. suggested that vitamin D may also play a role in
controlling VZV replication during zona zoster management, as the
control of most episodes of viral infection depends on cell-mediated
immunity and related cytokines [7]. Vitamin D can inhibit
neuroinflammation through down-regulation of pro-inflammatory cytokines
and up-regulation of anti-inflammatory cytokines. Chen et al. showed in
their study that hypovitaminosis D was significantly higher in
postherpetic neuralgia patients compared to controls [15]. In a
study by Han et al. with 30 zoster patients, the incidence of herpes
zoster decreased as 25 hydroxyvitamin D3 increased [16]. In our
study, 25-(OH)-D vitamin levels were found to be lower in patients with
zona zoster than in the control group.
A cohort study concluded that while low vitamin D levels were associated
with a higher risk of progression to AIDS in HIV-infected patients,
vitamin D supplementation did not affect mortality, CD4 cell count, and
viral load [13]. Chao et al found that both serum total and
bioavailable vitamin D levels were positively associated with zoster
antibody levels [7].
In a study conducted in Canada, low 25-OH-vitamin D levels were
associated with an increased risk of viral upper respiratory tract
infections in children [17]. In another study by Sabetta et al,
including healthy adults, it was found that those with 25-OH-D vitamin
over 38 ng / ml had a lower risk of acute viral respiratory tract
infection [18]. In a meta-analysis by Bergman et al., vitamin D
supplementation was found to have a protective effect against
respiratory tract infections [10].
The fact that our study was retrospective and the clinical course and
complications of disease could not be evaluated are among the
limitations of our study. This study revealed that 25-OH vitamin D
levels were significantly lower in zona zoster patients compared to the
control group. 25-OH vitamin D deficiency may increase the risk of VZV
reactivation, and vitamin D supplementation in patients with vitamin D
deficiency in zona zoster may help mild and reduce the disease and
complications such as postherpetic neuralgia. Controlled prospective
studies are needed on this subject.