Alopecia areata (AA) is a common chronic autoimmune disease of the hair follicle characterized by patchy, non-scarring hair loss, with a global lifetime risk estimated at 1–2% of the general population (1,2). Although its exact pathogenesis is not fully elucidated, it is believed to involve a breakdown of immune privilege of the hair follicle, leading to T-cell–mediated inflammation and premature follicle regression (3). Genetic predisposition, environmental triggers, and associated autoimmune conditions contribute to disease onset and chronicity (4,5).

Among systemic associations, autoimmune thyroid disease (AITD) is one of the most frequently reported in AA patients. Both conditions share common genetic and immunological pathways, including aberrant T-helper cell activity and increased prevalence of autoantibodies such as anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg) (6,7). Previous studies have shown that thyroid dysfunction, particularly hypothyroidism, is more prevalent in AA patients compared to the general population (8,9). Furthermore, clinical severity and chronicity of AA may correlate with higher risk of thyroid autoimmunity.

Therefore, the present study was undertaken to evaluate the prevalence of autoimmune thyroid dysfunction in patients with chronic alopecia areata and to explore its association with clinical disease characteristics.

Study Design and Population

A total of 120 patients with clinically diagnosed chronic alopecia areata (defined as disease duration ≥12 months) were enrolled. Diagnosis was established based on history, clinical examination, and dermoscopic findings.

Inclusion and Exclusion Criteria

Patients aged 18–60 years with chronic alopecia areata affecting the scalp were included. Exclusion criteria were: (i) patients on systemic corticosteroids or immunosuppressive drugs within the past three months, (ii) presence of other autoimmune diseases such as vitiligo, rheumatoid arthritis, or systemic lupus erythematosus, (iii) known thyroid disease under treatment, and (iv) pregnancy or lactation.

Data Collection

Detailed demographic and clinical information, including age, sex, duration of disease, pattern and extent of alopecia, and family history of autoimmune disorders, was recorded using a structured proforma. The severity of alopecia was classified using the Severity of Alopecia Tool (SALT) score.

Laboratory Investigations

Venous blood samples were obtained after overnight fasting. The following parameters were measured:

• Thyroid-stimulating hormone (TSH) and free thyroxine (fT4) using chemiluminescence immunoassay.
• Anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies using enzyme-linked immunosorbent assay (ELISA).

Reference values followed the institutional laboratory standards. Subclinical hypothyroidism was defined as elevated TSH with normal fT4, overt hypothyroidism as elevated TSH with reduced fT4, and hyperthyroidism as suppressed TSH with elevated fT4.

Imaging

Patients with abnormal thyroid function or positive antibody tests underwent thyroid ultrasonography to assess gland morphology and exclude nodular disease.

Statistical Analysis

Data were entered into Microsoft Excel and analyzed using SPSS version 25.0 (IBM Corp., Armonk, NY, USA). Categorical variables were expressed as frequencies and percentages, whereas continuous variables were presented as mean ± standard deviation. Chi-square test and Fisher’s exact test were applied for categorical comparisons. Logistic regression was performed to determine predictors of thyroid dysfunction. A p-value <0.05 was considered statistically significant.

Baseline Characteristics

A total of 120 patients with chronic alopecia areata were included in the study. The mean age was 34.2 ± 10.5 years (range: 18–58 years). Females constituted 68 patients (56.7%), and males 52 patients (43.3%), giving a male-to-female ratio of 1:1.3. The mean duration of disease was 3.8 ± 1.9 years. A positive family history of autoimmune disease was noted in 18 patients (15%) (Table 1).

Table 1. Baseline demographic and clinical characteristics of study participants (n = 120).

Thyroid Function Status

Thyroid dysfunction was detected in 28 patients (23.3%). Subclinical hypothyroidism was the most frequent abnormality (15 patients; 12.5%), followed by overt hypothyroidism (8 patients; 6.7%) and hyperthyroidism (5 patients; 4.1%). The remaining 92 patients (76.7%) had normal thyroid function (Table 2).

Table 2. Distribution of thyroid function abnormalities among patients with alopecia areata.

Thyroid Autoantibodies

Anti-TPO antibodies were positive in 20 patients (16.7%), while anti-Tg antibodies were positive in 12 patients (10%). Co-positivity of both antibodies was observed in 7 patients (5.8%) (Table 3).

Table 3. Distribution of thyroid autoantibodies among study population.

Association with Clinical Features

Thyroid dysfunction was more frequent in patients with extensive alopecia areata (12 of 32; 37.5%) compared to those with limited disease (16 of 88; 18.2%), showing a statistically significant difference (p = 0.02). Patients with disease duration >2 years also had a higher prevalence of thyroid dysfunction (20 of 66; 30.3%) than those with ≤2 years (8 of 54; 14.8%; p = 0.01) (Table 4).

Table 4. Association of thyroid dysfunction with clinical variables in alopecia areata.

*Statistically significant (p < 0.05).

The present study highlights a significant association between chronic alopecia areata (AA) and autoimmune thyroid dysfunction. In our cohort, thyroid abnormalities were identified in approximately one-fourth of patients, with subclinical hypothyroidism being the most prevalent. These findings are consistent with earlier reports that described hypothyroidism, particularly of autoimmune origin, as the most frequent thyroid abnormality in AA patients (1,2).

The prevalence of thyroid dysfunction observed in our study (23.3%) lies within the wide range reported in literature, varying from 8% to 30% depending on geographic location, study design, and patient selection (3,4). A systematic review by Lee et al. demonstrated an overall increased risk of thyroid disease in AA, particularly in women and those with severe or chronic forms (5). Similarly, Kasumagic-Halilovic et al. reported a higher frequency of thyroid autoantibodies in AA patients compared to controls (6).

Our findings showed that anti-TPO positivity was more frequent than anti-Tg positivity, which aligns with other studies indicating that anti-TPO is a more sensitive marker for detecting autoimmune thyroiditis in AA patients (7,8). The presence of these autoantibodies suggests a shared autoimmune mechanism, with dysregulation of T-helper lymphocytes and loss of immune privilege in both thyroid and hair follicle structures (9,10).

Notably, thyroid dysfunction was more frequent in patients with extensive scalp involvement and longer disease duration, highlighting that chronic and severe AA may predispose to systemic autoimmune comorbidities. Kakourou et al. observed a similar trend in children and adolescents, where thyroid autoimmunity was more common in severe AA (11). This underscores the importance of screening high-risk patients for early detection and management.

The association of family history of autoimmunity with thyroid dysfunction further strengthens the genetic predisposition hypothesis. Genome-wide studies have identified susceptibility loci shared between AA and autoimmune thyroiditis, supporting a polygenic model of autoimmunity (12,13).

From a clinical perspective, identifying thyroid abnormalities in AA patients is essential, as untreated thyroid disease can exacerbate fatigue, hair loss, and metabolic imbalance, potentially worsening quality of life. Early diagnosis through thyroid function testing and antibody screening allows timely intervention, which may not only improve systemic health but could also influence the course of alopecia areata (14,15).

Limitations

This study has certain limitations. Being cross-sectional, causal relationships could not be established. The sample size was modest and limited to a single center, which may restrict generalizability. Furthermore, long-term follow-up was not performed to assess the effect of thyroid disease management on AA progression.

Our results emphasize that thyroid dysfunction, particularly subclinical hypothyroidism with anti-thyroid antibody positivity, is common in patients with chronic alopecia areata. Screening for thyroid disease, especially in extensive or long-standing cases, should be integrated into routine clinical evaluation to ensure comprehensive care.

1. Park SM, Oh YJ, Lew BL, Sim WY. The association among thyroid dysfunction, thyroid autoimmunity, and clinical features of alopecia areata: a retrospective study. J Am Acad Dermatol. 2019 Aug;81(2):602-5. doi: 10.1016/j.jaad.2018.04.051. PMID: 29753058.
2. Lee S, Lee YB, Kim BJ, Lee WS. Screening of thyroid function and autoantibodies in patients with alopecia areata: a systematic review and meta-analysis. J Am Acad Dermatol. 2019 May;80(5):1410-3.e4. doi: 10.1016/j.jaad.2018.10.066. PMID: 30447313.
3. Patel D, Li P, Bauer AJ, Castelo-Soccio L. Screening guidelines for thyroid function in children with alopecia areata. JAMA Dermatol. 2017 Dec 1;153(12):1307-10. doi: 10.1001/jamadermatol.2017.3694. PMID: 28973128.
4. Wang S, Ratnaparkhi R, Piliang M, Bergfeld WF. Role of family history in patchy alopecia areata. Dermatol Online J. 2018 Oct 15;24(10):13030/qt0n19r7ps. PMID: 30677822.
5. Baars MP, Greebe RJ, Pop VJ. High prevalence of thyroid peroxidase antibodies in patients with alopecia areata. J Eur Acad Dermatol Venereol. 2013 Jan;27(1):e137-9. doi: 10.1111/j.1468-3083.2011.04420.x. PMID: 22226373.
6. Seyrafi H, Akhiani M, Abbasi H, Mirpour S, Gholamrezanezhad A. Evaluation of the profile of alopecia areata and the prevalence of thyroid function test abnormalities and serum autoantibodies in Iranian patients. BMC Dermatol. 2005 Oct 31;5:11. doi: 10.1186/1471-5945-5-11. PMID: 16259629.
7. Kakourou T, Karachristou K, Chrousos G. A case series of alopecia areata in children: impact of personal and family history of stress and autoimmunity. J Eur Acad Dermatol Venereol. 2007 Mar;21(3):356-9. doi: 10.1111/j.1468-3083.2006.01931.x. PMID: 17309458.
8. Seo HM, Kim TL, Kim JS. The risk of alopecia areata and other related autoimmune diseases in patients with sleep disorders: a Korean population-based retrospective cohort study. Sleep. 2018 Sep 1;41(9):zsy111. doi: 10.1093/sleep/zsy111. PMID: 29955877.
9. Sharma VK, Dawn G, Kumar B. Profile of alopecia areata in Northern India. Int J Dermatol. 1996 Jan;35(1):22-7. doi: 10.1111/j.1365-4362.1996.tb01610.x. PMID: 8838924.
10. Han TY, Lee JH, Noh TK, Choi MW, Yun JS, Lee KH, Bae JM. Alopecia areata and overt thyroid diseases: a nationwide population-based study. J Dermatol. 2018 Dec;45(12):1411-7. doi: 10.1111/1346-8138.14648. PMID: 30222206.
11. Noso S, Park C, Babaya N, Hiromine Y, Harada T, Ito H, Taketomo Y, Kanto K, Oiso N, Kawada A, Suzuki T, Kawabata Y, Ikegami H. Organ specificity in autoimmune diseases: thyroid and islet autoimmunity in alopecia areata. J Clin Endocrinol Metab. 2015 May;100(5):1976-83. doi: 10.1210/jc.2014-3985. PMID: 25734250.
12. Sorrell J, Petukhova L, Reingold R, Christiano A, Garzon M. Shedding light on alopecia areata in pediatrics: a retrospective analysis of comorbidities in children in the National Alopecia Areata Registry. Pediatr Dermatol. 2017 Sep;34(5):e271-2. doi: 10.1111/pde.13238. PMID: 28884897.
13. Du Vivier A, Munro DD. Alopecia areata, autoimmunity, and Down's syndrome. Br Med J. 1975 Jan 25;1(5951):191-2. doi: 10.1136/bmj.1.5951.191. PMID: 122906.
14. Saylam Kurtipek G, Cihan FG, Erayman Demirbaş Ş, Ataseven A. The frequency of autoimmune thyroid disease in alopecia areata and vitiligo patients. Biomed Res Int. 2015;2015:435947. doi: 10.1155/2015/435947. PMID: 26355833.
15. Kasumagić-Halilović E. Thyroid autoimmunity in patients with alopecia areata. Acta Dermatovenerol Croat. 2008;16(3):123-5. PMID: 18812059.