Vitamin D Status in Scarring and Non-Scarring Alopecia

Vitamin D is produced in the skin and is an important factor in the regulation of hair follicle cycling, which implicates it in hair loss.¹ Serum vitamin D levels are collected routinely during evaluation of hair loss, allowing institute clinicians to address this controversial issue.

Patients diagnosed with alopecia areata (AA), androgenic alopecia (AGA), central centrifugal scarring alopecia (CCCA), lichen planopilaris (LPP), and telogen effluvium (TE) over a 1-year period and not taking vitamin D supplements were identified (N = 358). Vitamin D deficiency was defined as vitamin D levels < 30 ng/ml, and were further categorized into mild (21–29 ng/ml), moderate (12–20 ng/ml), or severe (< 12 ng/ml) deficiency.²

Most patients had TE, followed by AA, and AGA. Median age was 49.5 years (range 4.2–85) with LPP patients tending to be older and AA patients younger (P < 0.001). Males comprised 9.8% (N = 35) of patients, and were most likely to have AA (P < 0.001). Vitamin D deficiency was present in 64.8% of patients, with 32.96% having mild, 17.60% moderate and 14.25% severe deficiency.

Comparison of Demographic Characteristics and Vitamin D Levels Among Different Types of Alopecia (N = 358)

2009 – 2010

Using logistic regression, patients with LPP were 8.3 times more likely to present with severe vitamin D deficiency than those with AA (P < 0.001), while TE patients were 3.7 times more likely to have severe vitamin D deficiency than those with AA (P ≤ 0.024), after adjusting for sex, age, and race. African Americans had 6.3-fold increased odds (P ≤ 0.001) and Asians 6.1-fold increased odds (P = 0.04) of severe vitamin D deficiency compared with Caucasians.

Logistic Regression for Dichotomized Vitamin D (N = 358ᵃ)

2009 – 2010

Vitamin D inhibits the adaptive immune system and improves the innate immune response, with some studies suggesting an increase in autoreactive T-cells as a result of altered maturation and function of dendritic cells, which maintain self-tolerance.³⁻⁴ Limitations include collection at a tertiary care center, and lack of a control group.

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  2. Ross AC. Vitamin D. The 2011 report on dietary reference intakes for calcium and vitamin D. Public Health Nutr. 2001 May;14(5):938-939.
  3. Prietl B, Treiber G, Pieber TR, Amrein K. Vitamin D and immune function. Nutrients. 2013 Jul;5(7):2502-2521.
  4. Antico A, Tampoia M, Tozzoli R , Bizzaro N. Can supplementation with vitamin D reduce the risk or modify the course of autoimmune diseases? A systematic review of the literature. Autoimmun Rev. 2012 July;12:127-136.