Published online Nov 9, 2021. doi: 10.5409/wjcp.v10.i6.192
Peer-review started: November 11, 2020
First decision: April 6, 2021
Revised: April 18, 2021
Accepted: July 6, 2021
Article in press: July 6, 2021
Published online: November 9, 2021
Processing time: 361 Days and 20.2 Hours
Alopecia areata (AA) is an inflammatory disease with autoimmune, environmental, and inherited components directed at the hair follicle, either limited to patchy hair loss over the scalp (Focalis, AF), total loss of scalp hair (Totalis, AT), or total loss of both scalp and body hair (Universalis, AU). Despite multiple treatment modalities, no therapy exists. Vitamin D deficiency in patients with AA/AT/AF influences disease severity and duration, inversely correlating with inflammation histologically.
Three girls presented with AT (P1), AU (P2), and AF (P3) at the ages of 1, 5, and 5 years, respectively. For P1-P2, all available treatments implemented for 2 years had failed. We started an initial 6-mo repletion with oral cholecalciferol 2000/4000 IU/d, with no apparent effect. Then we attempted immunomodulation using oral calcitriol and its analog paricalcitol. On calcitriol, 0.5 mcg/d P1 regrew hair within 6 mo. After 4 years, a relapse with loss of eyebrow hair was resolved after doubling the calcitriol dose to 0.5 mcg × 2/d; the results have been maintained for 6 years to date. On calcitriol, 0.25 mcg × 3/d P2 led to the development of asymptomatic hypercalcemia-hypercalciuria, which was immediately resolved by switching to paricalcitol 2 mcg × 3/d; mild tolerable hypercalciuria was main
Vitamin D may have immunomodulating therapeutic impact on AT/AU/AF, which needs to be explored with further pilot clinical trials.
Core Tip: Alopecia areata (AA) is an inflammatory disease with autoimmune, environmental, and inherited components directed at the hair follicle, either limited to patchy hair loss over the scalp (Focalis, AF), total loss of scalp hair (Totalis, AT), or total loss of both scalp and body hair (Universalis, AU). Despite multiple treatment modalities, there is no current therapy. Three girls aged 3, 7, and 5 years with AT, AU, and AF were treated with oral calcitriol, paricalcitol, and cholecalciferol, showing hair regrowth at 6, 6, and 3 mo, respectively but only as fur for P2 with AU. Vitamin D may have an immunomodulating therapeutic impact on AT/AU/AF, which needs to be explored with further pilot clinical trials testing the effectiveness and establishing the optimal form and dosage of vitamin D.
