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Journal of Clinical Medicine
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31 January 2023

Study of the Thyroid Profile of Patients with Alopecia

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1
Department of Dermatovenerology, “Carol Davila University” of Medicine and Pharmacy & “Elias” University Emergency Hospital, 011461 Bucharest, Romania
2
Department of Endocrinology, “Carol Davila” University of Medicine and Pharmacy & “C.I. Parhon” National Institute of Endocrinology, 011461 Bucharest, Romania
3
Department of Cellular and Molecular Biology, and Histology, Faculty of Medicine, “Carol Davila” University of Medicine and Pharmacy & National Institute for Mother and Child Health Alessandrescu-Rusescu, 011461 Bucharest, Romania
4
Department of Obstetrics and Gynaecology, “Carol Davila” University of Medicine and Pharmacy & University Emergency Hospital, 011461 Bucharest, Romania
J. Clin. Med.2023, 12(3), 1115;https://doi.org/10.3390/jcm12031115
This article belongs to the Special Issue Alopecia: Etiopathogenesis, Symptoms & Management
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Abstract

Thyroid hormones are required for the physiological growth and maintenance of hair follicles. We aim to study the thyroid profile of patients with alopecia. This is a narrative review. PubMed literature was searched from 2013 to 2022. We followed different types of alopecia: alopecia areata (AA), androgenic alopecia in males and females, telogen effluvium (TE), frontal fibrosing alopecia (FFA), lichen planopilaris, and alopecia neoplastica (AN). AA shares a common autoimmune background with autoimmune thyroid diseases, either sporadic or belonging to autoimmune polyglandular syndromes. Some data suggested that AA is more severe if thyroid anomalies are confirmed, including subclinical dysfunction or positive antithyroid antibodies with normal hormone values. However, routine thyroid screening for patients with AA, if the patients are asymptomatic from a thyroid point of view and they have negative personal and family history of autoimmunity, remains controversial. TE, apart from the autoimmune type, associates thyroid anomalies of a hormonal assay (between 5.7% and 17%). FFA, mostly a postmenopausal entity (however, not exclusive), associates a higher prevalence of thyroid conditions (up to 50%) than the general population. However, these might have an age-dependent pattern, thus the association may be incidental since there are a limited number of studies. Overall, alopecia remains a very challenging condition for patients and physicians; a multidisciplinary team is required to improve the outcome and quality of life. The common autoimmune background is suggestive of some types of alopecia and thyroid disorders, yet, the underlying mechanisms are still a matter of debate. AA, TE, FFA, LPP, and, potentially, female pattern hair loss have been found to be connected with thyroid entities, thus a state of awareness from a dual perspective, of trichology and endocrinology, is helpful.

1. Introduction

Human hair plays a major role in social communication and different behaviours, and its loss (alopecia) is typically associated with a decreased sense of personal wellbeing, low self-esteem, and social disengagement. Despite recent progress, alopecia remains a challenging condition due to its complexity, multidisciplinary implications, and difficulties in management in many situations. It is characterized by diffuse or patches of hair loss, total hair loss of the scalp (alopecia totalis), and/or of the entire body (alopecia universalis). The pathogenesis is incompletely described, however, a connection to immune and cytokines status, as well as to the endocrine field, including the thyroid domain, should be taken into consideration [1,2,3,4,5].

1.1. Thyroid Hormones (THs) and Hair Follicles

THs are required for the physiological growth and maintenance of hair follicles, suggesting that hair loss could be a sign of a thyroid disorder [1]. When it comes to the thyroid panel in relationship to alopecia, there are several levels of approach. On one hand, the role of THs at the level of the skin may be stratified in terms of endocrine, paracrine, and autocrine roles. On the other hand, associated pathologies to the thyroid diseases themselves might play a role in the development of alopecia as does gonadal status, including androgens levels, insulin resistance, metabolic complications, vitamin D deficiency, etc., as well as the connection with thyroid autoimmunity [1,2,3,4,5,6,7,8,9,10]. TH actions at a peripheral level in terms of receptors (TR) are related to skin and hair follicles, acting as endogenous modulators of dermal proliferation and local inflammation. KO mice for TRα1 and TRβ present a decreased level of keratinocyte proliferation (at the interfollicular epidermis) by involving a down-regulation of cyclin D1 and an upregulation of cyclin-dependent kinase inhibitors p19 and p27, respectively [3]. Lack of TRs might influence the bulge stem cells responsible for hair cycling (at the level of hair follicles). Further on, the dysfunction of these mentioned cells underlines abnormal Smad signaling and beta-catenin pathways [4]. These findings suggest that the dermal actions of THs are part of the local environment concerning hair follicles [3,4].

1.2. Alopecia: From General Considerations to Thyroid Connections

In terms of epidemiological impact, androgenic alopecia, the most prevalent cause of hair loss in the general population, is followed by alopecia areata (AA) and telogen effluvium (TE), affecting approximately half of all men and women. It is typically described as a most probable genetically determined condition that results in permanent hair loss in both men and women. The SOX gene has been proposed as a master regulator of hair shaft cuticle development [4]. However, alopecia may be incidental to a certain thyroid entity, considering its high prevalence in some populations.
With respect to the autoimmunity background, the prevalence of thyroid illness in alopecia patients ranges from 8% to 28% depending on the studied population, the types of alopecia, the types of thyroid diseases, etc. [1]. Kasumagić-Halilović described a significant link between alopecia and thyroid autoimmunity, with a higher prevalence of antithyroid antiantibodies (25.7%) in alopecia patients when compared to healthy people (3.3%) [2]. AA, a particular immune-mediated chronic disorder with periodic relapses, causes nonscarring hair loss; about 2% of the general population develops the disease with cosmetic disadvantages, impairing quality of life. Hair follicles are retained in AA, with the possibility of regeneration. Although scalp hair follicles are the primary targets, extra-scalp involvement, which manifests as facial hair loss (eyebrows, eyelashes, beard) or body hair loss, is found in AA, being linked to other systemic disorders such as atopic, autoimmune, and rheumatoid diseases [6].
Alopecia in subjects with chronic autoimmune Hashimoto’s thyroiditis is either first referred to a dermatologist or the patient is already under endocrine surveillance. CD8+ positive lymphocyte infiltration, as found in chronic thyroiditis, is dependent on an interferon-mediated response, and this aspect is identified in other types of alopecia like frontal fibrosing alopecia (FFA). This represents a scarring lymphocytic alopecia which is accompanied by the absence of eyebrows, being reported in some cases of severe hypothyroidism, and generally, it remains of a less clearly understood cause [7,8,9,10,11]. Early-onset type I interferonopathy is caused by monogenic STING gain-of-function mutations, with symptoms ranging from catastrophic vasculopathy to moderate chilblain lupus. The underlying molecular processes of the varied phenotype-genotype connections are still unknown. Alopecia, photosensitivity, and thyroid dysfunctions are among the characteristics of STING-associated vasculopathy with onset in infancy (SAVI), also involving livedo reticularis, skin vasculitis, nasal septum perforation, face erythema, and bacterial infections [12]. An extremely rare type is alopecia neoplastica (AN), an uncommon form of cutaneous metastasis originating from visceral tumours, including thyroid cancer [13].

1.3. Aim

We aim to analyse thyroid profiles in individuals with different types of alopecia.

2. Methods

This is a narrative review. A PubMed literature search was conducted using the terms: “alopecia” and “thyroid” (or “thyroiditis”), from 2013 to 2022. We followed different types of alopecia: alopecia areata (AA), androgenic alopecia in males and females, telogen effluvium (TE), alopecia neoplastica (AN), frontal fibrosing alopecia (FFA), and lichen planopilaris (LPP), and included only clinically relevant studies (full-length papers and excluded case reports) that provided enough information on the dermatological issues in relation to thyroid diseases.

4. Discussion

4.1. From Alopecia to Thyroid Anomalies

A large number of data connect alopecia with the field of thyroid conditions, in terms of abnormal function and/or positive antibodies. It is undeniable that severe changes in TH serum levels have an effect on human skin and appendages, both TRα and TRß being extensively expressed in the dermis, including in the hair follicles. While congenital hypothyroidism is associated with hair loss in infants, high telogen hair counts on the scalp might be a sign of hypothyroidism in adults [32,33,34]. Some data showed that AA seems more severe if thyroid anomalies are confirmed in one patient, including subclinical dysfunction or serologic positive profile for antithyroid antibodies with normal hormone values. However, routine thyroid screening in AA remains controversial if the patients are asymptomatic from an endocrine point of view (for instance, concerning the patients with alopecia who do not actually present typical signs, symptoms, and even complications of untreated hypothyroidism as somnolence, bradycardia, cardiac insufficiency, dyspnea, even coma of unknown cause, persistently dry skin, and slow intestinal transit) and they have a negative personal and family autoimmunity [51,52,53].
Of note, the majority of thyroid involvement that has been studied in relation to alopecia involves anomalies of function (hypothyroidism or hyperthyroidism) and/or positive antithyroid antibodies, mainly TPO-Ab and Tg-Ab, which are consistent for Hashimoto’s thyroiditis and TR-Ab that offers the confirmation of Basedow-Graves’s disease. However, both autoimmune conditions are included in the spectrum of thyroiditis. A patient in either category of autoimmune thyroid condition might suffer from hyperfunction or hypofunction at a certain point in time, and also might present euthyroidism, either spontaneous or medically induced (for instance, by being treated with levothyroxine replacement in cases of hypothyroidism or with antithyroid drugs for Graves’ disease). Thus the clinical relevance of many studies (especially those cross-sectional) is limited concerning the association between the thyroid profile and alopecia [2,6] (Figure 4).
Figure 4. The relationship between thyroid hormonal profile and thyroid autoimmunity: Hashimoto’s thyroiditis and Graves’s disease belong to the spectrum of autoimmune thyroid diseases; most patients with Hashimoto’s thyroiditis have hypo or euthyroidism, but flare-up thyrotoxicosis might be present; Graves’s disease associates hyperthyroidism, however, normal thyroid function may be spontaneously or iatrogenic achieved while iatrogenic intervention (thyroidectomy, radioiodine therapy and anti-thyroid drugs) or copresence of blocking antithyroid antibodies causes hypothyroidism. Abbreviations: TPO-Ab = anti-thyroperoxidase antibodies; TG-Ab = antithyroglobulin antibodies; TR-Ab = TSH-receptor antibody.
Deregulation of the immune system results in an immunological attack on the thyroid gland, which causes ATD [54]. Underlying the immune process in AA, peribulbar lymphocytes around the bulb region of anagen hair follicles are a tell-tale sign of active AA [55,56]. Natural killer group 2D (NKG2D) ligand in this area draws killer CD8 T cells to this infiltration [57]. Innate and acquired immunity are involved in AA [58,59]. The undulant pattern of autoimmunity is also reflected in the clinical pattern of AA. Multiple episodes of spontaneous regrowth are reported in a subject with AA. Within one year, the hair may return in 50–80% of patchy AA. Remission may be sustained, or the lesions are irreversible [60], which is why the AA impact of correcting thyroid dysfunction is still an open issue, and further interventional trials are needed. Autoimmunity is also involved in autoimmune TE, but generally, TE (which sometimes is clinically mistaken as AA) may associate with an abnormal hormonal profile regardless of the subtype [34,61,62,63,64,65,66].

4.2. Cicatricial Alopecia and Thyroid Status

Another chapter includes the thyroid profile in individuals with cicatriceal alopecias (FFA and LPP) [67,68,69,70]. FFA brings the menopausal panel as the main endocrine aspect, despite not being exclusively after menopause [71,72,73,74]. We still need evidence with regard to thyroid disease, including the mutual influence of thyroid anomalies and FFA [75,76,77,78,79,80]. The loss of the hair follicle’s immunological privilege would be the first step in the emergence of scarring alopecias [81,82,83,84]. Interferon may be the cause of this bulge immunological privilege collapse [85,86,87]. An important role in FFA is played by a Th1-biased cytotoxic T cell autoimmune response directed towards the hair follicles [88]. In the bulge region of LPP, downregulation of the hair follicle epithelial progenitor cell marker keratin 15 is found [89,90]. In FFA, and LPP, the lower melanocyte count found in the upper follicle indicates that the melanocytes of the hair follicle may be an antigenic target in FFA [91,92,93]. It has been suggested that the early causes of inflammation in LPP are the downregulation and abnormal action of the peroxisome proliferator-activated receptor (PPAR); PPAR being essential for sebocyte differentiation and maturation as well as lipid homeostasis [90,94,95]. Targeted ablation of PPAR in mice from follicular stem cells causes a scarring alopecia-like appearance [94,95,96,97,98].
Additionally, since the menopausal population is mainly affected by FFA, the role of androgen/oestrogens status has been incriminated [96,97]. The panel of postmenopausal dermatological and endocrine comorbidities might suggest a common pathogenic mechanism. For instance, subjects with FFA associate a higher risk of systemic lupus erythematosus, while FFA and vitiligo are reported to be associated with the same individuals with ATD [97,98,99].
Additionally, neutrophil-associated subtypes of primary cicatricial alopecia have been studied with regard to thyroid status. We identified one study from 2004 to 2013 that estimated an overall incidence of 6.1 (95% CI 5.62–6.6) per 100,000 person years and an overall prevalence of 20.93 (95% CI 17.97–23.86) per 100,000 person years, and logistic regression analysis confirmed a statistically significant association with thyroid diseases OR = 1.64 (p < 0.001) [100].

4.3. Polyglandular Autoimmune Syndrome

A very challenging condition from a multidisciplinary perspective, as it is not only dermatological or endocrine, is represented by autoimmune polyglandular syndrome type 1 (APS-1), a rare autosomal recessive condition (a prevalence of 2.6 cases/million) with childhood onset (AIRE gene) that, in addition to the classical triad (chronic candidiasis, adrenal insufficiency, and autoimmune hypoparathyroidism) may present with alopecia, vitiligo, and ATD [101]. AA, either patchy (most frequent), totalis, or universalis, is reported in APS-2, and APS-3, as well [102,103,104]. For instance, the rarest variant-AA universalis was recently identified as the onset of APS-3, before an ATD and type 1 diabetes mellitus diagnosis [103]. AA and vitiligo are regarded as “sister diseases” [104], one is due to an immune attack at the level of the hair follicle, the other, at the level of melanocytes. Also, psoriasis and lichen planus should be listed among dermatological illnesses with an immunologic component in other organs, including the thyroid [105,106]. A study of 158 patients with APS-1 showed a prevalence of 24% for alopecia, 17% for vitiligo, and 27.8% for ATD, respectively [107]. In addition to ATD, other AA comorbidities include asthma, atopic dermatitis, and allergic rhinitis. A recent study on 61,899 individuals with AA from 2012 to 2019 confirmed these associations. Of note, the prevalence of AA increased from 0.16% in 2012 to 0.27% in 2019, as an effect of modern society and autoimmunity issues [108].

4.4. Endocrine Perspective of Alopecia

Changing the perspective, a patient with alopecia may be first admitted to endocrinology, depending on the copresence of hormonal issues. Alopecia opens up several chapters. As mentioned, AA and ATD are reported together due to a common autoimmune background. Other thyroid conditions including abnormal hormones assays seem associated with TE, FFA, and LPP, as well as a few findings concerning thyroid cancer-associated AN with a low level of statistical evidence (Table 1) [13,16,17,18,19,21,25,29,30,33,34,39,40,41,42,43,44,45,46,47,48,49,50].
Table 1. introduces the most clinically relevant study from a dermatologic perspective of alopecia and thyroid findings. The articles are displayed starting with 2013 (please see references [13,16,17,18,19,21,25,29,30,33,34,39,40,41,42,43,44,45,46,47,48,49,50]).
The assessments of thyroid hormones and antithyroid antibodies are mandatory in cases with particular aspects of AA (for instance, severe forms of AA, paediatric populations, patients with suspected or confirmed thyroid dysfunction, individuals with personal or familial medical history of autoimmune endocrine conditions like hypophysitis, chronic adrenal insufficiency, premature ovarian failure, type 1 diabetes mellitus, autoimmune hypoparathyroidism, polyglandular autoimmune syndromes, etc. or nonendocrine autoimmune comorbidities such as celiac disease, chronic autoimmune hepatitis, etc.), autoimmune TE, and LPP [109,110,111]. Hyperandrogenemia-related alopecia (associated or not with other clinical and biochemical elements of virilisation) is caused by androgen excess in females, of either an ovarian or adrenal cause like polycystic ovary syndrome (affecting 10% of women of reproductive age), ovarian tumours with virilisation potential, Cushing syndrome, congenital adrenal hyperplasia, etc. [112,113,114,115,116]. Anomalies of growth hormone signalling pathways, as seen in Laron syndrome, are associated with alopecia and also, rarely, hypopituitarism and hyperprolactinemia [84,117]. Among many other roles, vitamin D is a key player in trichology and skin metabolism through its local receptor; hypovitaminosis D might manifest with alopecia [118,119]. Loss of function in the vitamin D receptor (hereditary vitamin D-resistant type of rickets) associates hair loss with the paediatric onset and poor response to calcitriol treatment [120,121]. Some data showed a certain efficacy with regard to intralesional injections of vitamin D3 in AA [122]. When it comes to endocrine issues of a dermatologic approach concerning alopecia, especially AA, the topic and general administration of glucocorticoids is advised (selected cases) and traditional side effects of this medication should be taken into consideration [123,124].
Finally, an individual with alopecia may be admitted to a dermatologic and/or endocrine unit; and some aspects like personal medical history, family history in genetic conditions (like APS), and general phenotype (like myxoedema) are essential clues in order to decide the case management. Further studies are necessary to point out if a subgroup of patients with thyroid entities are prone to develop alopecia and, on the opposite, which is the protocol of thyroid panel assessment in subjects with alopecia without obvious signs of a thyroid disorder and, moreover, which is the extend of influencing alopecia amid hormonal dysfunction correction.

5. Conclusions

Overall, alopecia represents a very challenging condition for patients and physicians. A multidisciplinary team is required to improve the outcome and the quality of life. The common autoimmune background is suggestive of some types of alopecia and ATD. Yet, the underlying mechanisms are still a matter of debate. Non-AN types of alopecia (AA, FPHL, TE, FFA, or LPP) are studied in relationship with thyroid entities and some pointed out a higher prevalence than the general population, thus a state of awareness from a dual perspective, of trichology and endocrinology, is helpful. According to the data we have so far, a careful selection of patients with alopecia in order to address the thyroid evaluation depends on a multifactorial equation that includes dermatologic features (type of alopecia, other skin conditions with potential endocrine connections like vitiligo, etc.), the presence of hormonal anomalies, and of autoimmune background. Further, we need specific protocols of a dual perspective (dermatologic and hormonal) to help with the individual decisions of investigations and surveillance.

Author Contributions

Conceptualization, A.P., M.C. and F.S.; methodology, M.C., M.C.D. and D.C.; software, D.C. and C.-E.N.; validation, A.P., M.C., M.C.D. and F.S.; formal analysis, M.C. and D.C.; investigation, D.C., C.-E.N., F.S., A.P. and M.C.; resources, A.P.; data curation, A.P., C.-E.N., F.S. and M.C., writing—original draft preparation, M.C., A.P. and F.S., writing—review and editing, M.C., A.P., D.C., C.-E.N. and M.C.D.; visualization, A.P., C.-E.N., M.C.D. and M.C.; supervision, A.P. and F.S.; project administration, A.P., M.C. and F.S. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Data Availability Statement

Not applicable.

Conflicts of Interest

The authors declare no conflict of interest.

Abbreviations

AAalopecia areata
Abantibodies
ANalopecia neoplastica
ATDautoimmune thyroid disease
APS-1autoimmune poly-endocrine syndrome type 1
CIConfidence Interval
FFAfrontal fibrosing alopecia
FPHLfemale pattern hair loss
HLAHuman Leukocyte Antigen
LPPlichen planopilaris
IFNinterferon
IQRinterval inter-quartile
OROdds Ratio
NKGNatural Killer Group
NOSNo other specified
MPAmale pattern alopecia
PPARperoxisome proliferator-activated receptor
SAVISTING-associated vasculopathy with onset in infancy
TEtelogen effluvium
THthyroid hormones
TG-Abanti-thyroglobulin antibodies
TR-AbTSH-receptor antibody
TPO-Abantithyroperoxidase antibodies
TRthyroid hormones receptor
T3Triiodothyronine
T4thyroxine
TSHThyroid Stimulating Hormone

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