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. 2021 Sep 14;7(6):454–459. doi: 10.1159/000518042

A Retrospective Study on Alopecia Areata in Children: Clinical Characteristics and Treatment Choices

Christina Stefanaki a,*, George Kontochristopoulos a, Eleni Hatzidimitraki b, Aravella Stergiopoulou b,**, Alexandra Katsarou a, Vasiliki Vosynioti a, Eleni Remountaki a, Dimitrios Rigopoulos b
PMCID: PMC8613625  PMID: 34901176

Abstract

Background

Although children are affected frequently with alopecia areata (AA), data are limited on clinical characteristics and treatment choices.

Materials and Methods

We retrospectively reviewed the records of the pediatric dermatology department over a 12-year period to identify children with AA. Clinical data were collected.

Results

Three hundred and sixty-four children with AA were identified, aged 1–12 years, 214 males and 150 females. The mean age of onset was 6.6 years (±3.3). The disease presented with patches on the scalp in the majority (90.7%), whereas only 6 children had alopecia totalis or universalis. The most commonly prescribed treatment was topical steroids (69.1%), followed by the combination of topical steroids and minoxidil 2% (14.3%). Oral steroids were prescribed in only 16 children. Follow-up at 3 months was available for only 70 children and the majority (84.3%) had some hair regrowth. Hair regrowth was unrelated to the number of plaques (p = 0.257), disease location (p = 0.302), and atopy (p = 0.999). Hair regrowth only correlated with the type of treatment (p = 0.003) with potent topical and intralesional steroids giving the best results.

Conclusion

AA usually presents with a mild form in children, and potent topical steroids are the mainstay of treatment.

Keywords: Alopecia areata, Topical steroids, Minoxidil, Males, Ophiasis

Introduction

Alopecia areata (AA) is a common dermatologic disorder resulting from an autoimmune attack of the hair follicle, leading to nonscarring alopecia. Although it can affect any age, it is the third most common dermatosis in children and approximately in 40% of the patients, the disease presents before age 20 and 20% of all AA cases occur in infancy [1, 2, 3]. A lower prevalence in adults than children has been reported [4].

Clinical and epidemiologic characteristics of the disease have been well described in adults but data in children are limited [1, 5, 6, 7, 8]. Therefore, we conducted this study to explore the clinical and epidemiologic characteristics of AA in children and their response to treatment.

Material and Methods

We reviewed data between years 2005 and 2017 (12 years) on children diagnosed with AA in the Pediatric Dermatology Unit of Andreas Sygros University Skin Hospital, Athens, Greece. Diagnosis was made clinically, and information about age, gender, family history in a first-degree relative, past medical history of autoimmune diseases (thyroid disease, lupus, celiac disease, and vitiligo) or atopic dermatitis, coexistence of Down syndrome, and triggering factors (stress, viral illness, and vaccines) was collected. Disease characteristics including the number of patches (1–2, 3–5, >6), the type of disease (AA totalis, universalis, and ophiasis), nail involvement, and involvement of eyebrows or eyelashes were also recorded. Type of treatment, response to treatment at 3 months, and relapse after 1–2 years were also extracted for analysis. Relapse was defined as the recurrence of the disease manifesting with at least 1 patch of hair loss.

Statistical Analysis

Statistical analyses were performed using Stata, version 13 (StataCorp. 2013. Stata Statistical Software: release 13. StataCorp LP, College Station, TX, USA). Differences in means of continuous variables were assessed with Student's t test and one-way ANOVA tests. Differences in proportions of categorical variables were assessed through the χ2 test or Fisher's exact test as appropriate. A 2-tailed value of p < 0.05 was considered significant.

Results

A total of 364 children with AA were examined during the study period. Age at onset of the disease ranged from 1 to 12 years, and in almost half of the children the disease presented between 1 and 5 years (40.5%) and in the other half between 6 and 10 years (44.7%). The mean age of onset was 6.6 years (±3.3). There were 214 (58.8%) males and 150 (41.2%) females and males tended to develop the disease at an earlier age (p = 0.044) and particularly between the ages 1–5 (p = 0.0949) (Table 1).

Table 1.

Age of onset and gender distribution in children with AA

Gender
Total (n = 360) p value
female (n = 148) male (n = 212)
Age of onset (mean, ± SD) 7.0 (3.1) 6.4 (3.0) 6.6 (3.1) 0.044*
Age
 0–5 51 (34.5) 95 (44.8) 146 (40.5) 0.094**
 6–10 70 (47.3) 91 (42.9) 161 (44.7)
 >10 27 (18.2) 26 (12.3) 53 (14.7)

Four missing. AA, alopecia areata.

*

t test.

**

χ2 test.

Clinical and demographic characteristics of children with AA and treatment choices are described in Table 2. The majority of children (73.8%, 76/103) did not have a positive family history in a first-degree relative and did not have any comorbidities (81.8%, 108/132). The most common comorbidity was thyroid disease, whereas children with atopic dermatitis represented 24.6%. Triggering factors were sought in 101 children, and stress was the only one that seemed to occur more frequently (38, 41.3%).

Table 2.

Demographic, clinical characteristics, main therapeutic modalities, and long-term outcomes of 364 children with AA

Variable Frequency, n (%)
Children 364
Gender
 Female 150 (41.2)
 Male 214 (58.8)
Age of onset (mean, SD) 6.6 (3.1)
Unknown 4
Comorbidities
 No 110 (83.4)
 Thyroid disease 11 (8.3)
 Growth retardation 4 (3.0)
 Rheumatic disease 3 (2.3)
 Anemia 2 (1.5)
 Vitiligo 1 (0.8)
 Down syndrome 1 (0.8)
 Unknown 232
Disease location
 Scalp 304 (91.3)
 Eyebrows or eyelashes 8 (2.4)
 Eyebrows and eyelashes 4 (1.2)
 Scalp and eyebrows 5 (1.5)
 Scalp and eyelashes 5 (1.5)
 Scalp, eyelashes, and eyebrows 1 (0.3)
 Totalis 6 (1.8)
 Unknown 31
Plaques
 1–2 123 (66.1)
 3–5 38 (20.4)
 >6 12 (6.5)
 Diffuse 4 (2.2)
 Totalis 7 (3.8)
 Ophiasis 2 (1.1)
 Unknown 178
Nails
 Yes 12 (12.9)
 No 81 (87.1)
 Unknown 271
Family history
 Yes 27 (26.2)
 No 76 (73.8)
 Unknown 261
Atopy
 Yes 32 (24.6)
 No 98 (75.4)
 Unknown 234
Triggering factors
 No 39 (42.4)
 Stress 38 (41.3)
 Viral and other infections 9 (9.8)
 Other (surgery, head lice, etc.) 6 (6.5)
 Unknown 263
Treatment
 No 6 (1.8)
 Topical steroids 232 (69.1)
 Minoxidil 2% 2 (0.6)
 Topical steroids and minoxidil 2% 48 (14.3)
 Anthralin 1% 3 (0.9)
 Topical steroids and anthralin 1% 10 (3.0)
 Topical steroids and minoxidil 2% and anthralin 1% 8 (2.4)
 Systemic steroids 16 (4.8)
 Intralesional triamcinolone acetonide 2 (0.6)
 Topical steroids and calcineurin inhibitors 7 (2.1)
 Calcineurin inhibitors 2 (0.6)
 Unknown 28
Hair regrowth
 Yes 59 (84.3)
 No 11 (15.7)
Percent of hair regrowth
 20% 4 (6.8)
 30% 5 (8.5)
 40% 1 (1.7)
 50% 4 (6.8)
 60% 1 (1.7)
 100% 44 (74.6)
 Unknown 294
Relapse
 Yes 21 (67.7)
 No 10 (32.3)
 Unknown 333

AA, alopecia areata.

The disease presented with patches on the scalp in the majority (90.7%), whereas only 4 children presented with the diffuse form of AA and only 6 with alopecia totalis or universalis. Eyebrows or eyelashes were affected in 23 children and nails in 12 (12/93). Most of the children (66.1%) had 1–2 patches of alopecia, and ophiasis involving the margins of the scalp was a rare occurrence. The most commonly prescribed treatment was topical steroids (69.1%), followed by the combination of topical steroids and minoxidil 2% (14.3%). Oral steroids in the form of gradually tapered prednisolone over 6 weeks were prescribed in only 16 children.

Follow-up at 3 months was available for only 70 children and the majority (84.3%) had some hair regrowth, whereas 74.6% had full hair regrowth. No difference in disease severity was found between children attending for follow-up and those who did not (p = 0.205). Hair regrowth was unrelated to the number of patches (p = 0.257), the location of the disease (p = 0.302), and personal history of atopy (p = 0.999) (Table 3). Hair regrowth correlated with the type of treatment (p = 0.003) with potent topical and intralesional steroids giving the best results. Interestingly, the combination of topical steroids with minoxidil 2% or anthralin 1% did not offer any advantage over topical steroids alone. Systemic steroids did not result in hair regrowth in half of the children treated with this modality. Unfortunately, no follow-up was available for children treated with anthralin alone or with calcineurin inhibitors.

Table 3.

Correlation of response to treatment with various factors

Variable Hair regrowth, n (%)
p value
total yes no
Plaques, n
 1–2 50 (74.6) 42 (75.0) 8 (72.7)
 3–5 11 (16.4) 10 (17.9) 1 (9.1)
 >6 2 (3.0) 2 (3.6) 0 (0.0) 0.257
 Totalis 3 (4.5) 1 (1.8) 2 (18.2)
 Ophiasis 1 (1.5) 1 (1.8) 0 (0.0)
Disease location
 Scalp 63 (90.0) 54 (91.5) 9 (81.8) 0.302 0.302
 Eyebrows or eyelashes ± scalp 7 (10.0) 5 (8.5) 2 (18.2)
Treatment
 Topical steroids 49 (70.0) 46 (78.0) 3 (27.3)
 Topical steroids and anthralin 1% and/or minoxidil 2% 14 (20.0) 8 (13.6) 6 (54.6) 0.003
 Systemic steroids 5 (7.1) 3 (5.1) 2 (18.2)
 Intralesional steroids 2 (3.4) 2 (3.4) 0 (0.0)
Atopy
 Yes 5 (20.8) 4 (20.0) 1 (25.0) 0.999
 No 19 (79.2) 16 (80.0) 3 (75.0)

The p value derived from Fisher's exact test.

Follow-up after 1–2 years was available in only a small number of children (31) and 67% of them relapsed. No difference in disease severity was found between children attending for long-term follow-up and those who did not (p = 0.806). Relapse was unrelated to the number of patches (p = 0.999), the location of the disease (p = 0.999), and the type of treatment (p = 0.484) (Table 4). Unfortunately, we were not able to identify any predisposing factors for a relapsing disease.

Table 4.

Correlation of relapse to various factors

Variable Relapse, n (%)
p value
total yes no
Plaques, n
 1–2 15 (71.4) 7 (63.6) 8 (80.0)
 3–5 5 (23.8) 3 (27.3) 2 (20.0) 0.999
 Ophiasis 1 (4.8) 1 (9.1) 0 (0.0)
Disease location
 Scalp 29 (93.6) 20 (95.2) 9 (90.0) 0.999
 Eyebrows or eyelashes ± scalp 2 (6.5) 1 (4.8) 1 (10.0)
Treatment
 Topical steroids 19 (63.3) 11 (55.0) 8 (80.0)
 Topical steroids and anthralin 1% and/or minoxidil 2% 6 (20.0) 4 (20.0) 2 (20.0) 0.484
 Systemic steroids 4 (13.3) 4 (20.0) 0 (0.0)
 Intralesional steroids 1 (3.3) 1 (5.0) 0 (0.0)

The p value derived from Fisher's exact test.

Interestingly, only 1 girl presenting with severe patchy AA (multiple patches) at the age of 5 years progressed to alopecia totalis in a 2-year follow-up. However, 16 children progressed from mild AA, presenting with <3 patches, to a more severe disease with multiple patches. All 16 children were males and the disease presented at an earlier age <6 years. Two boys had a protracted course with severe disease from the onset. One can speculate that males with a very early disease onset have a tendency for a more severe course.

Discussion

A predominance of AA in females has been reported in the literature in contrast to our results. We found a family history in 26%, whereas this percentage ranges in the literature from 8.4% to 51.6% [1, 5, 6, 7, 8].

AA has been associated with other autoimmune diseases but the majority of patients are healthy individuals [9, 10]. Comparable to our results, the strongest association reported in the literature is thyroid disease [11, 12], followed by vitiligo [1, 3, 11] but other autoimmune and metabolic disorders have also been associated [11]. A high percentage of patients (28.6–34.4%) present with a history of atopic dermatitis [1, 3, 11, 13], and atopic dermatitis has been associated with the most severe disease [3]. In our study, 24.6% of our children reported a history of atopic dermatitis.

AA typically presents with localized patches of non­scarring alopecia on the scalp but in more severe cases it may spread to involve the entire scalp (AA totalis) or the whole body (AA universalis) [10]. Other less common forms are AA ophiasis with patches of alopecia at the occipital area and the periphery of the scalp and ophiasis inversa, typically involving the central vertex [10]. Another variant of AA more recently described is the diffuse form with diffuse and extensive hair shedding [10].

The typical localized form of AA was the most prevalent in our cohort, and most of the children (66%) presented with 1–2 patches of alopecia, whereas the severe forms (totalis and universalis) affected only a small number of children (4.9%). The diffuse form was observed in only 4 children. Severe cases have been found to represent a small percentage (0.025–7%) of children with AA [13, 14] and the majority usually present with a mild disease [3, 5, 6, 7, 8]. Only specialized hair clinics report greater percentages of severe forms (20–60%) [1, 3]. Although there is no cure for AA, current treatments include topical, intralesional, or oral corticosteroids; minoxidil; light-based therapies; topical immunotherapy; systemic therapies, including methotrexate and antitumor necrosis factor inhibitors such as etanercept and Janus kinase inhibitors [9, 15].

Usually, topical corticosteroids are the first-line treatment for pediatric patients with AA because of the minimal side effects and ease of application, with class I and II typically used. In our study, the vast majority of the children (69%) used only potent topical steroids (clobetasol propionate) and in 20%, topical steroids were combined either with minoxidil and/or anthraline. Only topical potent steroids showed the highest efficacy, and hair regrowth was achieved in 46/49 children, with combinations offering no advantage. However, the efficacy of topical steroids may be questioned, given the high percentage (50%) of spontaneous regrowth observed in children with AA [10], particularly with mild disease. The efficacy of topical corticosteroids remains controversial; however, few studies have shown promising results, including a randomized controlled trial demonstrating 50% hair regrowth in 78% of treated children [9, 16, 17].

Data about the effectiveness of minoxidil are limited; however, it is commonly used in pediatric AA. In our study, it was used in combination with steroids. Minoxidil carries certain risks if used over large surface areas in children, even at lowest concentration of 2%, such as cardiovascular side effects and generalized hypertrichosis [9, 18]. There is a better quality of evidence about the effectiveness of minoxidil 5% compared to 1 or 3% in children and adults; however, it remains controversial [19].

Unfortunately, follow-up was not available in children treated only with short contact anthralin 1% and the result from the combination with steroids was not very satisfactory. In a small comparative study, it has been found less effective than topical steroids [20]. In general, response rates ranging between 63 and 85% have been reported but in severe cases a limited response (20–30%) has been noted [21, 22]. Stinging, irritation, and brown staining of the scalp, clothing, and bathtubs are the major drawbacks from its use [9].

Despite the fact that intralesional steroids can give excellent results [23], we chose this form of treatment in only 2 children because of the pain of the procedure that cannot be easily tolerated by children. Both had full hair regrowth.

Apart from systemic steroids for a short period of time (6 weeks), no other systemic agents were tried in our study and those were reserved for severe cases. However, 2/5 of the children treated with systemic steroids did not have a cosmetically acceptable hair regrowth in a 3-month follow-up. Both had alopecia totalis. Patients with AA have been found to respond better to systemic steroids than patients with alopecia totalis, and a 60% response rate has been reported [9, 24, 25, 26] but most fail to maintain a sustainable result. Intravenous pulse corticosteroid therapy is another option; however, 80% of patients after an initial improvement relapse [27, 28]. Apart from the high relapse rate, systemic steroids may cause various adverse effects in children including weight gain and growth retardation among others [9].

Although experts consider topical immunotherapy as a first-line option in children with AA [15, 29, 30], we did not offer this modality. According to the results of a recent systemic review, topical immunotherapy is commonly used in children with AA; however, it is characterized by lower efficacy than topical glucocorticosteroids [15].

No particular treatment seemed to prevent recurrence of the disease and we could not identify any prognostic factors for a relapsing course, like atopy, involvement of eyebrows or eyelashes, or extent of the disease. Only speculations can be made regarding the association of a more severe course with male sex and an earlier disease onset. According to the literature, atopy, a family history of AA, and extensive hair loss have all been associated with poor prognosis [29, 30, 31, 32, 33].

A major limitation of our study is the small number of children available on short- and long-term follow-up; therefore, no definite conclusions can be drawn. This can be easily explained by the retrospective design of our study. More studies are needed in children to shed light on difficult ones to treat disease like AA.

Statement of Ethics

The study was approved by the Andreas Sygros University Skin Hospital's Institutional Review Board. Date: March 12, 2018.

Conflict of Interest Statement

The authors have no conflicts of interest to declare.

Funding Sources

We did not use any funding sources for this work.

Author Contributions

Christina Stefanaki has collected all data and written the study; George Kontochristopoulos contributed on writing the study; Eleni Hatzidimitraki, Alexandra Katsarou, Vasiliki Vosynioti, and Eleni Remountaki contributed on the collection of the data; Aravella Stergiopoulou was responsible for the statistics; and Dimitris Rigopoulos reviewed the manuscript.

Data Availability Statement

All data generated or analyzed during this study are included in this article. Further enquiries can be directed to the corresponding author.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

All data generated or analyzed during this study are included in this article. Further enquiries can be directed to the corresponding author.


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