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. 2023 Nov 16;10(2):123–128. doi: 10.1159/000534844

Androgenetic Alopecia in Children and Adolescents: From Trichoscopy to Therapy

Maria Rubi Losoya-Jaquez a, Arturo Lopez Yañez-Blanco a, Yonatan Armendariz-Barragan b, Nidia Gabriela Aguilar-Figueroa c, Lidia Rudnicka d, Luis Enrique Sanchez-Dueñas e
PMCID: PMC10987064  PMID: 38572189

Abstract

Introduction

Pediatric androgenetic alopecia is a product of hormonal and genetic factors. The diagnosis depends on recognizing the hair loss pattern in the context of a positive family history and a typical trichoscopy.

Methods

A multicenter retrospective study assessing medical data from January 2008 to January 2023 of two reference centers – one public and one private in west Mexico. Patients under 18 years old were included. The clinical features, trichoscopic findings, associated conditions, and treatment received were documented and analyzed.

Results

We found 145 patients, with a mean age of 16.08 ± 1.30 years, predominantly comprising males (72%). Trichoscopy was performed on 33 patients. The main trichoscopic findings were hair shaft thickness variability in 100% of the cases, vellus hair in 85%, and single-hair units in 79%. Vitamin D deficiency was found in 84% of the cases with laboratory determination, insulin resistance in 33%, and hyperandrogenemia in 12.5%. Topical minoxidil emerged as the main treatment modality in 24% of cases, demonstrating both efficacy and tolerability.

Conclusion

Pediatric androgenetic alopecia could be more prevalent than commonly perceived, potentially explained by the lower level of suspicion among medical practitioners. Distinctive trichoscopic findings offer valuable guidance for therapeutic strategies and ongoing management.

Keywords: Alopecia, Androgenetic alopecia, Pediatric trichology, Trichoscopy

Introduction

Androgenetic alopecia (AGA) is the most prevalent type of hair loss recorded after adolescence. It is characterized by the gradual replacement of terminal hair by vellus hair in the frontal and parietal scalp, with a decrease in the number of hair per hair unit follicle and a higher proportion of telogen hair [1].

The incidence and prevalence of this condition among adolescents remain unknown. In a large single-center retrospective analysis, González et al. [2] identified 57 adolescent patients with AGA. The mean age at presentation was 14.8 years, and the male-female ratio was skewed at 2:1.

Pediatric AGA (AGAped) is defined by the clinical and trichoscopic features of AGA manifesting before the age of 18. Both hormonal effect and genetic predisposition seem to play a role, with 83% of cases having a positive family history [35]. Its onset is associated with adrenarche and is commonly classified as pre- or postpubertal. By convention, this is based on the cut-off age of 12 years, when the initial physiological signs of dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione cannot be clearly determined [2]. Because high levels of androgens are not expected at this age, it may indicate an underlying condition such as metabolic syndrome, polycystic ovary syndrome, insulin resistance (IR), or endocrine disruptors triggering hyperandrogenism [4, 5]. Female patients with AGAped usually present diffuse thinning at the crown and preservation of the frontal hairline (“Christmas tree” pattern), while boys tend to present either a male adult pattern of AGA or diffuse thinning at the crown and varying degrees of biparietal thinning, which is considered a female pattern of alopecia [2, 6].

When assessing girls with AGAped and other androgenic manifestations like acne, hirsutism, and seborrhea, it is paramount to perform a thorough hormonal investigation that should include luteinizing hormone, follicle stimulating hormone, free testosterone, total testosterone, DHEA, DHEA-S, androstenedione, estradiol, 17-hydroxyprogesterone, prolactin, cortisol, and ACTH levels. For boys with female-pattern alopecia, precocious puberty must be ruled out [6].

The diagnosis of AGAped is established by recognizing the hair loss pattern in the context of a positive family history. Trichoscopic findings that further reinforce the diagnosis are: (1) follicular miniaturization; (2) variability in hair shaft thickness of more than 20%; (3) increased proportion of vellus hair; and (4) other features such as single-hair units, wavy hair, perifollicular pigmentation, yellow dots, and thin arborizing vessels [4, 5]. The two main differential diagnoses of AGAped are diffuse alopecia areata and telogen effluvium [2].

In regards to treatment, there is no standard therapy yet approved for the pediatric population, but topical and oral minoxidil have the safest profiles [6]. Different from other age groups, 5α-reductase inhibitors (topical or oral) and other antiandrogenics are contraindicated for childbearing-aged girls due to potential feminizing effects on male fetuses [4].

AGA is an under-recognized disease in children, so there is little epidemiological data available regarding its trichoscopy and response to treatment [4, 6]. By diving deeper into the clinical and trichoscopic manifestations of AGAped, we hope to shed light on its peculiarities and bridge the existing gap in physicians’ knowledge of this condition.

Methods

This was a cross-sectional, retrospective, and multicenter study of electronic data from January 2008 to January 2023 from two institutions: the Dermatology Department of the Dermatology Institute of Jalisco (“Dr. José Barba Rubio”), a public dermatologic center in Zapopan, Jalisco, Mexico, and the Hair Restoration Center in Dermika Laser Dermatologic Center, a private center specialized in hair and skin disorders located in Guadalajara, Mexico. We reviewed 15 years of data from electronic medical records ranging from 2008 to 2023. AGAped was defined as clinical and trichoscopic features of AGA manifesting before the age of 18 years. Demographic, clinical, and trichoscopic data were collected. Subjects with other disease-causing hair loss – alopecia areata, telogen effluvium, anagen effluvium, and trauma-related hair loss – were excluded.

Trichoscopy was performed with a handheld device (DL4N®, Dermlite Company; San Juan Capistrano, CA, USA) and digital trichoscopy (Fotofinder Medicam 1000®, Fotofinder Systems GmbH; Bad Birnbach, Germany) with a 10–20-fold magnification capacity. The images were analyzed for the following signs of AGAped: hair shaft thickness variability, vellus hair, single-hair units, wavy hair, perifollicular pigmentation, yellow dots, and focal atrichia.

Statistical Analysis

Data processing was executed using the statistical software IBM® SPSS Statistics v20 for the Windows platform (IBM Corp., Armonk, NY, USA). The normality distribution of variables was assessed using the Kolmogorov-Smirnov test. Descriptive statistics were employed to ascertain frequencies, means, and percentages as indicators of central tendency, while standard deviation was used to gauge data dispersion.

Results

We identified 145 patients with AGAped, 103 males and 42 females (71 and 21%, respectively). Age at diagnosis ranged from 13 to 17 years, with a mean of 16.08 years. Figure 1 presents the demographic data. We obtained trichoscopic images from 33 subjects. Table 1 shows the most common trichoscopic findings: increased hair shaft thickness variability (found in all 33 cases), vellus hair in 28 (85%), single-hair units in 26 (79%), wavy hair in 25 (76%), perifollicular pigmentation in 15 (45%), and yellow dots in three patients (9%). Focal atrichia was not observed.

Fig. 1.

Fig. 1.

Representative trichoscopic findings in AGAped. a Hair shaft thickness variability: normal hair alternating with thin hair (arrows). b Vellus hair (arrows). c Perifollicular discoloration (circle). d Single-hair units (arrows). e Yellow dots (circle). f Wavy hair (arrow).

Table 1.

Trichoscopic characteristics of the cases

n = 33 (22.8%) Positive, n (%) Negative, n (%)
Hair shaft thickness variability 33 (100) 0 (0)
Vellus hair 28 (85) 5 (15)
Single-hair units 26 (79) 7 (21)
Wavy hair 25 (76) 8 (24)
Perifollicular pigmentation 15 (45) 18 (55)
Yellow dots 3 (9) 30 (91)
Focal atrichia 0 (0) 33 (100)

One-fifth (n = 28) of the patients underwent further laboratory tests. Vitamin D deficiency was found in 11 out of the 13 tested for it (84%), three out of six had IR (33%), one out of seven had hyperandrogenemia (12.5%), two out of 14 had high cholesterol levels (14.3%), and two out of 13 were iron deficient (15.4%).

Treatment was appropriately given and documented for 46 patients (31.7% of our sample). Table 2 shows the frequency of each medication prescribed. Minoxidil 5% topical solution was prescribed for 23.4%, oral minoxidil for 2% (n = 3/145), finasteride for 1.3% (n = 2/145), dutasteride for 0.6% (n = 1/145), and spironolactone for 4.1% (n = 6/145). There were no significant side effects affecting patient compliance.

Table 2.

Laboratory, comorbid associations, and treatment

n = 28 (19.3%) Normal, n (%) Abnormal, n (%)
Hemoglobin 12 (100)
Iron 11 (84.6) 2 (15.4)
Lipid 12 (85.7) 2 (14.3)
Thyroid function 12 (100)
Ovarian function* 11 (100)
Testosterone 7 (87.5) 1 (12.5)
DHEA/DHEA-S 9 (90) 1 (10)
Insulin 6 (66.6) 3 (33.3)
Vitamin D 2 (15.4) 11 (84.6)
Vitamin B12 3 (100)
Zinc 3 (100)
Comorbidities, n = 34 (23%) n (%)**
 Acne 17 (50.0)
 Seborrheic dermatitis 8 (23.3)
 IR 6 (17.5)
 Obesity 2 (6.0)
 Atopic dermatitis 1 (3.0)
Treatment n (%)**
 Topical minoxidil 34 (23.4)
 Finasteride 3 (2.0)
 Dutasteride 2 (1.3)
 Spironolactone 2 (1.3)
 Total 46 (31.7)

DHEA, dehydroepiandrosterone; DHEA-S, dehydroepiandrosterone sulfate.

*Luteinizing hormone (LH), follicle stimulating hormone (FSH), progesterone, estrogens

**No adverse effects enough for withdrawal were documented.

Discussion

Our study found a mean age of 16.08 years at the time of diagnosis, slightly above the mean of 14.8 years reported by Gonzalez et al. [2]. The male-female ratio of 2.4:1 was similar to previous studies.

As described by Rossi et al. [7], certain dermatological diseases commonly seen in this group are acne, seborrheic dermatitis, atopic dermatitis, hirsutism, and endocrinological disorders such as polycystic ovarian syndrome and IR. One-fifth of our sample had an associated condition (n = 31). Acne was present 50.0% of the time, followed by seborrheic dermatitis (23.5%), IR (17.5%), obesity (6%), and atopic dermatitis (3%). Such findings highlight the importance of actively looking for associated conditions that may require multidisciplinary management.

According to Gomes et al. [6], a complete hormonal study should include luteinizing hormone, follicle stimulating hormone, free and total testosterone, DHEA, DHEA-S, androstenedione, estradiol, 17-hydroxyprogesterone, prolactin, cortisol, and adrenocorticotropic hormone. In our sample, the two metabolic abnormalities that stand out were vitamin D deficiency and elevated insulin levels. A diagnosis of AGAped should thus elicit an investigation of other disorders that may either be associated with or directly contribute to its clinical manifestations.

Among the 33 cases with available trichoscopy, the main abnormalities were increased hair shaft variability and vellus hair (present 100 and 85% of the time, respectively). These findings match the frequency reported by Özcan et al. [4] – 100 and 91%, respectively. However, we found a significantly higher proportion of single-hair units and wavy hair (79 and 76% vs. 35 and 26%, respectively, in their study). In our series, the frequency of perifollicular pigmentation (45%) and yellow dots (9%) also differed from Öskan et al. [8] (30%), perhaps due to subtle differences in our groups’s mean age, male predominance, or other genetic and racial factors. Further studies shall better explore certain trichoscopic peculiarities of AGAped. Interestingly, focal atrichia was not seen in our sample. A plausible explanation is that such finding often correlates with disease severity, and children tend to present a mild form compared to adults. Figure 2 correlates the clinical and trichoscopic findings that can help distinguish AGAped from more common causes of hair loss in children and adolescents, like telogen effluvium, alopecia areata, and trichotillomania.

Fig. 2.

Fig. 2.

Example of AGAped presenting symmetrical hair loss in androgen-dependent areas of the scalp (Christmas tree distribution).

Regarding the treatment, although there is no gold standard approved for this age group, 5% topical and low-dose oral minoxidil have been shown to be effective. In a recent study by John et al. [9] that involved 101 adolescents with AGA, oral or sublingual minoxidil given for an average of 20.1 months at a low dose (0.15–5 mg/day) was well tolerated. The most common adverse events were hypertrichosis, hypotension, nausea, and headache. There were no major adverse events, thus reinforcing its safe profile. In another large multicenter study comprehending 1,404 patients up to the age of 86, Vaño et al. [10] found a strong correlation between oral minoxidil and hypertrichosis when adjusted for age, weight, sex, and duration of treatment (OR 1.26 [95% confidence interval: 1.17–1.35], p < 0.001). The average dose was 1.4 mg.

In our study, only a third (31.7%) of the patients were medically treated. Topical minoxidil was used in most cases with no relevant side effects. Further studies, however, are required to confirm the efficacy and safety of different therapeutic modalities for AGA in pediatric patients.

Based on our research findings, we propose a classification system for AGAped into three clinical stages: early, intermediate, and late. We believe that such a classification can provide valuable guidance for treatment. Within this rationale, the early stage would comprehend variations in hair shaft thickness and changes in perifollicular pigmentation. The intermediate stage would involve the presence of single-hair units and wavy hair. Finally, the late (or advanced) stage would be hallmarked by yellow dots and the development of focal atrichia.

However, we acknowledge that in order to confirm this relationship, a larger sample size and a careful comparison with AGA affecting adults would be necessary. Limitations to our study include its retrospective format, the lack of relevant histopathological data as none of the patients underwent biopsy, and the heterogeneous composition of our sample.

Conclusion

In summary, our study has highlighted the distinctive clinical and trichoscopic characteristics of AGA in children and adolescents. To the best of our knowledge, this represents the most extensive case series of AGAped documented to date.

A comprehensive grasp of the epidemiological, clinical, and trichoscopic aspects of AGAped holds the potential to facilitate earlier diagnoses and more precise assessments. We believe this plays a pivotal role in determining the prognosis and guiding effective treatment strategies.

Despite the limitations posed by a relatively small sample size, our study elucidated the primary trichoscopic patterns of AGA within the pediatric population while also accentuating the persisting gaps in our understanding that await further exploration. Subsequent investigations may clarify the progression of the disease through its various stages, uncover additional clinical nuances, and identify optimal medications and dosages for managing these young patients. AGAped is not a novel ailment; rather, it constitutes a single link within the intricate chain of the hormonal androgen paradox.

Statement of Ethics

No photos or identifying data of patients were included in this work. Written informed consent was deemed unnecessary since verbal consent was obtained from the parents/guardians at the time of consultation. This is detailed and clarified in the approval report issued by the Ethics Committee that reviewed and authorized this publication. The study protocol was reviewed and approved by the Research Ethics Committee of “Centro de Estudios de Investigacion Basica y Clinica, S.C.,” Guadalajara, Jalisco, Mexico, approval number CEI-006-2023-02. In accordance with the Declaration of Helsinki (Fortaleza, Brazil; 2013) and Good Clinical Practices guidelines, the confidentiality of the participants was protected: at no time were they ever identified by name, and an assigned code ensured their anonymity. The authors did not receive economic support from the industry or any federal institution during the development of this study.

Conflict of Interest Statement

The authors have no conflicts of interest to declare.

Funding Sources

The authors did not receive economic support from the industry or any federal institution during the development of this study.

Author Contributions

Maria Rubi Losoya-Jaquez made substantial contributions in conceiving, designing, drafting, and approving the final version of this work. She assumed responsibility for all facets of the project, meticulously addressing queries concerning accuracy and integrity. Luis E. Sánchez-Dueñas significantly contributed to the study’s conception, design, data acquisition, analysis, and interpretation. His involvement extended to critically revising the content for intellectual significance and granting final approval for publication. He embraced full accountability for the work’s integrity and precision. Lidia Rudnicka made substantial contributions encompassing design, data analysis, and interpretation. Her thorough scrutiny of intellectual content enriched the study. Approving the version for publication, she undertook accountability for upholding the work’s accuracy and integrity. Arturo López Yañez-Blanco’s impact encompassed work design, data acquisition, analysis, and interpretation. He diligently drafted and critically revised the intellectual core. Approving the version for publication, he undertook complete accountability for ensuring the work’s accuracy and integrity. Yonatan Armendariz-Barragán’s contributions spanned work design, conceptualizing overarching research objectives, and applying statistical techniques for analysis. He demonstrated an unswerving commitment to addressing questions related to accuracy and integrity across all facets of the work. Nidia Guadalupe Aguilar-Figueroa excelled in crafting visual elements such as photos, diagrams, and graphics. Her meticulous attention to these details attested to her commitment to upholding accuracy and integrity in all aspects of the work.

Funding Statement

The authors did not receive economic support from the industry or any federal institution during the development of this study.

Data Availability Statement

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

References

  • 1. Kim BJ, Kim JY, Eun HC, Kwon OS, Kim MN, Ro BI. Androgenetic alopecia in adolescents: a report of 43 cases. J Dermatol. 2006;33(10):696–9. [DOI] [PubMed] [Google Scholar]
  • 2. Gonzalez ME, Cantatore-Francis J, Orlow SJ. Androgenetic alopecia in the paediatric population: a retrospective review of 57 patients. Br J Dermatol. 2010;163(2):378–85. [DOI] [PubMed] [Google Scholar]
  • 3. Tosti A, Iorizzo M, Piraccini BM. Androgenetic alopecia in children: report of 20 cases. Br J Dermatol. 2005;152(3):556–9. [DOI] [PubMed] [Google Scholar]
  • 4. Özcan D. Pediatric androgenetic alopecia: a retrospective review of clinical characteristics, hormonal assays and metabolic syndrome risk factors in 23 patients. An Bras Dermatol. 2022;97(2):166–72. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5. Griggs J, Burroway B, Tosti A. Pediatric androgenetic alopecia: a review. J Am Acad Dermatol. 2021;85(5):1267–73. [DOI] [PubMed] [Google Scholar]
  • 6. Gomes TF, Soares RO. Pediatric androgenetic alopecia: an updated review. J Dtsch Dermatol Ges. 2023;21(1):19–25. [DOI] [PubMed] [Google Scholar]
  • 7. Rossi A, D’Arino A, Pigliacelli F, Caro G, Muscianese M, Fortuna MC, et al. The diagnosis of androgenetic alopecia in children: considerations of pathophysiological plausibility. Australas J Dermatol. 2019;60(4):e279–83. [DOI] [PubMed] [Google Scholar]
  • 8. Hu R, Xu F, Han Y, Sheng Y, Qi S, Miao Y, et al. Trichoscopic findings of androgenetic alopecia and their association with disease severity. J Dermatol. 2015;42(6):602–7. [DOI] [PubMed] [Google Scholar]
  • 9. John JM, Sinclair R. Safety and tolerability of low-dose oral minoxidil in adolescents: a retrospective review. J Am Acad Dermatol. 2023;88(2):502–4. [DOI] [PubMed] [Google Scholar]
  • 10. Vañó-Galván S, Pirmez R, Hermosa-Gelbard A, Moreno-Arrones ÓM, Saceda-Corralo D, Rodrigues-Barata R, et al. Safety of low-dose oral minoxidil for hair loss: a multicenter study of 1,404 patients. J Am Acad Dermatol. 2021;84(6):1644–51. [DOI] [PubMed] [Google Scholar]

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 inquiries can be directed to the corresponding author.


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