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.