Table 1.
| Study | Year | Study type (Sample origin) | Demographics (AA cases)† | Sample Size Total (Detail) | Measures and outcomes |
|---|---|---|---|---|---|
| Vitamin D receptor studies | |||||
| Fawzi et al. [42] | 2016 | Case-control (Hospital- based) | Sex: 12M/8F Age: 26.10 ± 9.431 Country: Egypt |
40 (20 AA cases and 20 age- and sex- matched controls from neurosurgery department) | Serum and tissue VDR levels lower in AA cases (serum 9.990 ± 1.6973 ng/mL; tissue 199.710 ± 33.3802 ng/mL) vs controls (serum 13.605 ± 1.6612 ng/mL; tissue 333.910 ± 46.6220) (P = 0.000; P = 0.000) |
| Serum level studies | |||||
| Bakry et al. [43] | 2016 | Case-control (Not described) | Sex: 36M/24F Age: 20.70 ± 10.85 Country: Egypt | 120 (60 AA cases and 60 age-, gender-, and body mass index-matched healthy controls | Serum 25(OH)D lower in AA cases (44.04 ± 15.61 nmol/L) vs controls (66.07 ± 17.40 nmol/L) (P < 0.001) Prevalence of vitamin D deficiency* in AA (83.3%) vs controls (23.3%) (P < 0.001) Inverse association between mean serum vitamin D and disease severity (mild: 58.59 nmol/L; moderate 42.18 nmol/L; severe: 35.39 nmol/L) |
| Thompson et al. [47] | 2016 | Prospective cohort | Sex: 55,929F Age: 63.4 ± 6.4 Country: USA |
55,929 (133 AA cases) | No difference in hazard ratio (HR) for incident AA between highest vs lowest quartiles of surrogate vitamin D score: multivariate HR 1.08 (95 % CI 0.68–1.73); No difference in HR for AA comparing highest versus lowest quartiles of dietary, supplemental, and total vitamin D intake |
| Çerman et al. [32] | 2014 | Case-control (Hospital- based) | Sex: 56M/30F Age: 32.21 ± 9.60 Country: Turkey |
188 (86 AA cases, 44 vitiligo cases, and 58 age- and sex-matched controls from volunteer hospital staff) | Serum 25(OH)D lower in AA cases (11.84 ± 6.18 ng/mL) vs vitiligo (16.15 ± 7.93 ng/mL) and vs healthy controls (23.57 ± 9.03 ng/mL) (P = 0.001 and P < 0.001); Prevalence of vitamin D deficiency*; in AA (91%) vs vitiligo (71%) vs controls (33%) (P = 0.003 and P < 0.001); Inverse association between 25(OH)D level and severity of alopecia (P < 0.001, r = −0.409) |
| Mahamid et al. [33] | 2014 | Case-control (Hospital- based) | Sex: 14M/9F Age: 24.2 ± 12.3 Country: Israel |
43 (23 AA cases and 20 control cases, recruited from clinics and who had no history of AA) | Serum 25(OH)D lower in AA cases vs controls (11.32 ± 10.18 vs 21.55 ± 13.62 ng/mL, P < 0.05); Prevalence of vitamin D deficiency* in AA (69.5%) vs controls (25%) (P < 0.05); Multivariate analysis for vitamin D < 30ng/mL: odds ratio (OR) 2.3 (95% CI, 2.2–3.1, P = 0.02); CRP levels in AA group were elevated (P < 0.05) |
| d’Ovidio et al. [34] | 2013 | Case-control (Registry- based) | Sex: 45M/111F Age: 37.8 Country: Italy |
304 (156 AA cases enrolled in the National Mediterranean Alopecia Areata Association and 148 controls (no further control detail) | Prevalence of vitamin D deficiency*; in AA (42.4%) vs controls (29.5%) (P < 0.025) Inverse association between Vitamin D and PTH levels (r = −0.24, P < 0.01) |
| Yilmaz et al. [35] | 2012 | Case-control (Hospital- based) | Sex: 14M/28F Age: 30.8 ± 8.2 Country: Turkey |
84 (42 AA cases and 42 healthy controls) | Serum 25(OH)D concentration lower in AA cases (33.4 ± 17.7 nmol/L) vs controls (51.2 ± 21.1 nmol/L) (P < 0.001)* |
| Genetic polymorphism studies | |||||
| Akar et al. [37] | 2007 | Case-control (Not described) | Sex: 30M/2F Age: 24.1 ± 7.5 Country: Turkey |
59 (32 AA cases and 27 healthy controls) | Genes studied: BsmI, ApaI, TaqI
No difference in prevalence of polymorphisms in AA vs. controls |
| Akar et al. [36] | 2004 | Case-control (Not described) | Data not available | 52 (25 AA cases and 27 healthy controls) | Genes studied: FokI
No difference in prevalence of polymorphisms in AA vs. controls |
| Vitamin D treatment studies | |||||
| Narang et al. [44] | 2017 | Clinical trial (no placebo) | Sex : 12M/10F Age : 30.4 ± 10.8 Country: India |
22 | Regimen: 0.005% calcipotriol lotion applied 2x/day for 12 weeks (or until complete regrowth) Results: 59.1% of patients had hair re-growth with onset at 4.21 ± 2.13 weeks; response stratified by percent change in SALT score: 9 patients with 0% change, 4 patients with <25% change, 3 patients with 26–50% change, 6 patients with >50% change |
| Çerman et al. [38] | 2015 | Clinical trial (no placebo) | Sex: 26M/22F Age: 33 ± 11.14 Country: Turkey |
48 | Regimen: 0.005% calcipotriol cream applied 2x/day for 12 weeks Results: Lower mean SALT score at 12 weeks (P = 0.001) Hair regrowth ≥50% in 75% of patients; regrowth ≥75% in 62.5%; complete regrowth in 27.1% |
| Kim et al. [39] | 2012 | Case-report | Sex: M Age: 7 Country: Korea |
1 | Regimen: calcipotriol solution 50 μg/mL applied daily for 3 months Results: Complete hair regrowth at 3 months; no relapse 9 months |
| Orecchia et al. [40] | 2009 | Clinical trial | Data not available | 28 | Results: Failure of calcipotriol to potentiate squaric acid dibutylester effectiveness |
| Berth-Jones et al. [41] | 2009 | Clinical trial | Data not available | 20 | Results: No response to calcipotriol in patients with alopecia totalis and alopecia universalis |
AA alopecia areata, CI confidence interval, CRP c reactive protein, HR hazard ratio, OR odds ratio, PTH parathyroid hormone, SALT severity of alopecia tool
*
Vitamin D deficiency defined as ≤20 ng/mL or ≤50nmol/L
†
BMI and Age given as mean ± standard deviation