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The Role of Vitamin D in Non-Scarring Alopecia.

Agnieszka Gerkowicz, Katarzyna Chyl-Surdacka, Dorota Krasowska, Grażyna Chodorowska
Review International journal of molecular sciences 2017 61 atıf
PubMed DOI CC-BY PDF
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Study Design

Çalışma Türü
Review
Müdahale
The Role of Vitamin D in Non-Scarring Alopecia. None
Karşılaştırıcı
Placebo
Etki Yönü
Positive
Yanlılık Riski
Unclear

Abstract

Non-scarring hair loss is a common problem that affects both male and female patients. Since any disturbances in the hair follicle cycle may lead to hair shedding, or alopecia, it is not surprising that the possible role of vitamin D in alopecia was investigated in many studies. Vitamin D has been shown to have many important functions. A growing body of evidence shows that vitamin D and its receptor are responsible for maintaining not only calcium homeostasis but also skin homeostasis. Moreover, vitamin D could also regulate cutaneous innate and adaptive immunity. This paper presents a review of current literature considering the role of vitamin D in alopecia areata, telogen effluvium, and female pattern hair loss. The majority of studies revealed decreased serum 25-hydroxyvitamin D levels in patients with different types of non-scarring alopecia, which could suggest its potential role in the pathogenesis of hair loss. According to the authors, vitamin D supplementation could be a therapeutic option for patients with alopecia areata, female pattern hair loss, or telogen effluvium. However, further studies on a larger group of patients are required.

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Tables

Table 1

AuthorsStudy Subjects (Number and Age)Severity of AlopeciaSerum Concentration of Vitamin D (25(OH)D)
Criteria for Vitamin D StatusMethod of Serum 25(OH)D MeasurementNotable Findings
Aksu Cerman et al., 2014 [12]AA—86 patientsV—44 patientsC—58 healthy controlsMean age of:AA—32.21 ± 9.60 yearsV—33.64 ± 11.51 years C—32.55 ± 9.78 yearsS1—71 patientsS2—15 patients D ≤ 20 ng/mL−1LC-MS/MSSignificantly higher prevalence of vitamin D deficiency in AA than in V and C (p = 0.003, p < 0.001 respectively).A significant negative correlation between AA severity and serum concentration of 25(OH)D (p < 0.001 r = −0.409).
D’Ovidio R et al., 2013 [13]AA—156 patients C—148 healthy controlsMean age of:AA—37.8 yearsC—34.5 yearsAA multilocularis—49 patientsOphiasis—69 patientsAT-AU—38 patientsMinimal hair loss in all groups: 25% of scalp areaD < 20 ng/mLCHL Presence of serum 25(OH)D levels < 20 ng/mL significantly higher in AA vs. C (p < 0.025).In AA higher compensatory levels of PTH (r = −0.24, p < 0.01);
Mahamid et al., 2014 [16]AA—23 patients C—20 healthy controlsMean age of:AA—24.2 ± 12.3 yearsC—27 ± 11.26 yearsPatchy AA—18Extensive AA—5S—30–50 ng/mLI < 30 ng/mLD < 20 ng/mLEIASerum 25(OH)D concentration significantly decreased in AA vs. C (p < 0.05);Serum 25(OH)D levels < 30ng/mL and CRP > 1 associated with AA occurrence (p = 0.02, p = 0.04, respectively).
Yilmaz et al., 2012 [33]AA—42 patients C—42 healthy controlsMean age of:AA—30.8 ± 8.2 yearsC—29.3 ± 7.4 yearsS1—30 patientsS2—6 patientsS3—3 patientsS4—2 patientsS5—1 patient25(OH)D—insufficient concentration < 50 nmol/L1,25(OH)2D—decreased concentrations ≤ 30 pg/mLELISA Significantly lower concentration of 25(OH)D and 1,25(OH)2D in AA vs. C (p < 0.001, p < 0.001 respectively).No correlation between the levels of 25(OH)D and 1,25(OH)2D and disease severity, duration, nail involvement.
Bakry et al., 2016 [34]AA—60 patients C—60 healthy controlsMean age of:AA—20.70 ± 10.85 yearsC—23.71 ± 7.45 yearsMild—24 patientsModerate—20 patientsSevere—16 patientsS > 75 nmol/LI—50–75 nmol/L D < 50 nmol/L ELISASignificantly lower levels of serum 25(OH)D in AA vs. C (p < 0.001).Significantly lower serum levels of 25(OH)D in severe AA vs. moderate and mild (p = 0.03, p = 0.002 respectively).
Ghafoor et al., 2017 [35]AA—30 patients C—30 healthy controlsMean age of:AA—23.77 ± 8.86 yearsC—24.03 ± 8.62 yearsS1—4 patientsS2—7 patientsS3—12 patientsS4—1 patientS5—6 patientsS—30 ng/dLI—20–29ng/dLD < 20 ng/dLEIA Significantly lower serum 25(OH)D levels in AA vs. C (p = 0.001).Lower serum 25(OH)D levels in patients with higher SALT Score.
Darwish et al., 2017 [36]AA—30 patients C—20 healthy controlsMean age of:AA—28.67 ± 10 yearsC—24.8 ± 6 yearsS1 (mild)—10 patientsS2 (moderate)—7 patientsS3–S5 (severe)—13 patientsNAELISA Significant decrease of serum 25(OH)D concentration in AA vs. C (p < 0.001).In AA significantly lower serum 25(OH)D level in males vs. females (p = 0.009).No correlation with SALT score.
Attawa et al., 2016 [37]AA—23 patientsC—23 healthy controlsMean age of:AA—26.44 ± 10.87 yearsC—29.39 ± 8.10 yearsS1—14 patientsS2—3 patientsS3–S5—6 patientsS > 30 ng/mLI—10–30 ng/mLD < 10 ng/mLELISASignificantly lower serum 25(OH)D levels in AA vs. C (p = 0.01).Significant difference between vitamin D status and AA severity (p = 0.02).
Erpolat et al., 2017 [38]AA—41 patients C—32 healthy controlsMean age of:AA cases—32.8 ± 7.5 yearsC—32.7 ± 7.5 yearsSingle patch—15 patientsMultiple patches—26 patientsS > 30 ng/mLI—20–30 ng/mLD < 20 ng/mLHPLC No significant difference in serum 25(OH) D levels between AA and control (p > 0.05).Vitamin D deficiency—93.8% patients with AA
Bhat et al., 2017 [39]AA—50 patients C—35 healthy controlsMean age of:AA cases—22.4 ± 8.6 yearsC—29.2 ± 7.6 yearsS1—38 patientsS2*—12 patientsD < 30ng/mLCHLSerum 25(OH)D levels significantly lower in AA vs. C (p < 0.001).A significant negative correlation between SALT score and serum vitamin D levels (p < 0.001; r = −0.730).
Unal et al., 2017 [40]AA—20 paediatric patients C—34 paediatric healthy controlsMean age of:AA M/F—12.4 ± 4.2/13.3 ± 4.4 years C—M/F 16.6 ± 0.8/16.5 ± 1.01 yearsS1—6 patientsS2—9 patientsS3—5 patientsD ≤ 20ng/mLNAVitamin D deficiency in both groups with no significant differences between the groups (p = 0.084).Significant inverse correlation between serum 25(OH)D levels and SALT score, disease duration and number of patches (p < 0.001, r = −0.831, p < 0.001, r = −0.997, p < 0.001 r = −0.989 respectively ).
Rasheed et al., 2012 [41]TE—42 patients FPHL—38 patients C—40 healthy controlsMean age of:TE and FPHL—29.8 ± 9.3 yearsC—30.8 ± 8.56 yearsTE:Mild—22 patientsModerate—6 patientsSevere—14 patientsFPHL:Mild—15 patientsModerate—13 patientsSevere—10 patientsS > 75 nmol/LI—25–75 nmol/LD < 25 nmol/LCompetitive enzyme immunoassaySignificantly lower serum 25(OH)D levels in TE and FPHL vs. C (p < 0.001).The highest serum 25(OH)D levels in mild vs. severe FPHL and TE (p = 0.035, p = 0.203 respectively).
Banihashemi et al., 2016 [42]FPHL—45 patients; C—45 healthy controlsMean age of: FPHL—29.11 ± 7.31 yearsC—28.82 ± 7.11 yearsLudwig I—28 patientsLudwig II—2 patientsLudwig III—2 patientsS > 30 ng/mLI—20–30 ng/mLD < 20 ng/mLELISALower serum 25(OH)D levels in FPHL vs. C (p = 0.04).No significant correlation between serum 25(OH)D levels and duration or severity of FPHL (p = 0.77, p = 0.92 respectively).
Moneib et al., 2014 [43]FPHL—60 patients C—60 healthy controlsMean age of: FPHL—26.4 ± 4.51 yearsC—25.85 ± 4.49 yearsLudwig I—34 patientsLudwig II—22 patientsLudwig III—4 patientsS > 30 ng/mLI—21–29 ng/mLD < 20 ng/mLIN > 150ng/mLRIA Significantly lower mean serum 25(OH)D level in FPHL vs. C (p = 0.0001).Significant difference between serum 25(OH)D levels and Ludwig’s three degrees (p = 0.006).The highest serum 25(OH)D levels in Ludwig III.
Nayak et al., 2016 [44]Diffuse hair loss—22 patients C—22 healthy controlsMean age of the study population—20.89 yearsNAI—25–75 nmol/LD < 20–25 nmol/LELISA Significantly lower serum 25(OH)D levels among cases vs. C (p = 0.007).
Karadag et al., 2011 [45]TE—63 patients C—50 healthy controlsMean age of: TE—29.0 ± 11.9 yearsC—28.4 ± 9.4 yearsAcute TE—29 patients Chronic TE—34 patientsNARIASignificantly higher serum 25(OH)D levels in TE patients vs. C (p < 0.01).Significantly increased risk for TE for patients with 25(OH)D levels in the highest quadrant vs. the lowest one (p < 0.0001).

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