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Ear, Nose & Throat Journal 99(8)

Table 2. Classification, Nasal Signs, and Symptoms of Patients With
Allergic Rhinitis.
ARIA Classification

Number (%)

 Mild AR
 Moderate/severe AR

62 (51.6%)
58 (48.4%)

Clinical manifestations

Number (%)






115 (95.8%)
116 (96.6%)
108 (90%)
98 (81.6%)

Rhinorrhea
Sneezing
Nasal obstruction
Nasal itching

Abbreviations: AR, allergic rhinitis; ARIA, Allergic Rhinitis and its Impact on
Asthma.

Table 3. Relationship Between Total Nasal Symptom Score and
Vitamin D Levels.
Score

Number of Patients

25(OH)D Levels
(Mean [SD])

4-6
7-9
10-12

62
28
30

29.2 (14.7)
21.6 (11.8)
19.4 (12.5)

r

P

À.62

.002

Abbreviation: SD, standard deviation.

gender, socioeconomic status, and anthropometric data. No
significant differences were found on comparison of birth
month and season of birth between children with AR and
healthy controls.
Children with AR had significantly higher total serum
IgE and calcium levels than those of the healthy control
group (p < .0001 for each). The mean serum levels
25(OH)D and 1,25(OH)2D of were significantly lower in
AR group than in healthy children ( p < .001 and p < .0001
respectively, Table 1).
In the present study, only 23.3% of AR children had normal
serum 25-OHD concentration (>30 ng/mL) versus 52% of controls (p ¼ .002), 45.9% of the patient group had vitamin D
insufficiency (20-30 ng/mL) versus 40% in healthy controls
(p ¼ .4). Vitamin D deficiency (<20 ng/mL) was found
in 30.8% of AR group versus 8% of healthy children (p
< .0001, Table 1).
According to AR severity between both groups, we
found the mean 25-OHD3 levels in patients with moderate/severe AR were significantly lower than those with
mild AR (p < .001). Correlation analyses between vitamin
D levels and various parameters were done in our study.
We found a significant positive correlation between
25(OH)D and calcium (calcium levels (r ¼ .29, p ¼
.023). Besides, we found significant negative correlations
between mean 25(OH)D levels and TNSS (r ¼ À0.62, p ¼
.002, Table 3) and total IgE levels (r ¼ À0.27, p ¼ .013)
in AR group. No significant difference was found in comparison of birth month and season of birth between children with AR and healthy controls.

Discussion
Our study identified essential results in the growing area of
vitamin D levels and allergic children. This study investigated
vitamin D status in a large cohort of children with AR. We
observed that vitamin D deficiency is a frequent finding among
children with AR when compared to healthy controls. In line
with our report, Dogru and Suleyman10 studied 76 children
with AR and 65 healthy patients. They evaluated 25(OH)D3
levels in both groups, and the mean serum 25(OH)D3 levels of
AR children were significantly lower than healthy group (18.07
+ 6.1 ng/mL vs 24.03 + 9.43 ng/mL; p ¼ .001). However,
contrary to our finding, they failed to find any significant relationship between vitamin D deficiency and the severity of AR.
Another study (11) compared the levels of 1,25(OH)2D3 in 30
children with AR having recurrent tonsillitis and 30 controls.
The median levels of 1,25(OH)2D3 were significantly lower in
AR group when compared to healthy children (34.65 pg/mL vs
52.86 pg/mL; p ¼ .001). In the same report,11 the researchers
found significantly lower 1,25(OH)2D3 values (p < .05) in
children with severe nasal symptoms. Yenigun et al12 and Goksugur et al13 investigated 2 small groups of children with allergic rhinoconjunctivitis; they found significantly lower vitamin
D levels in patients with allergic rhino-conjunctivitis when
compared to controls. In recent years, the importance of vitamin D in the immune system and allergic diseases has received
much interest in research. There is a general agreement that the
shift from a Th1 to Th2 phenotype in CD4þ T cells is the
primary pathogenesis of AR, but the precise mechanism of
AR is still not clear. Current researches showed that Th17 and
T-regulatory cells are essential in the pathogenesis of AR.12,14
Vitamin D inhibits the proliferation of T-lymphocytes and
increases Th1 to Th2 switch by stimulation of the development
of Th2 cells. In addition, it enables the induction of Tregulatory cells and suppresses the development, transcription,
and bioactivity of Th17 cells.12,14 These data indicate that there
is a relationship between vitamin D and AR morbidity.15 Deficiency of vitamin D leads to contraction of the smooth muscles
and disturbance of prostaglandin regulation with impairment of
Th1-Th2 balance which increases airway inflammation.16
Some clinical and epidemiological studies have reported
significant associations between vitamin D intake during pregnancy and its serum level with the incidence of AR in different
ethnic groups. Two studies17,18 reported a positive relationship
between maternal vitamin D intake and AR. Erkkola et al17
reported an inverse relationship between maternal intake of
vitamin D during late pregnancy and the risk of asthma (confidence interval [CI]: 0.64-0.99) and AR (CI: 0.75-0.97) in
5-year-old children. Bunyavanich et al18 studied a cohort of
1248 mother-child pairs, and they found that the intake of each
100 IU of vitamin D/d during the first and second trimesters
was associated with 21% (odd ratio[OR]: 0.79 [95% CI: 0.670.92] and 20% (OR: 0.80 [95% CI: 0.68-0.93] reduced odds of
ever AR at school age. Bener et al19 reported that vitamin D
deficiency was significantly associated with AR children.
Another report by Jung et al20 used the data from the annual
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