{"id":58277,"date":"2023-08-10T09:11:31","date_gmt":"2023-08-10T08:11:31","guid":{"rendered":"https:\/\/www.touchendocrinology.com\/?p=58277"},"modified":"2023-11-20T15:31:24","modified_gmt":"2023-11-20T15:31:24","slug":"an-update-on-alopecia-and-its-association-with-thyroid-autoimmune-diseases","status":"publish","type":"post","link":"https:\/\/www.touchendocrinology.com\/thyroid\/journal-articles\/an-update-on-alopecia-and-its-association-with-thyroid-autoimmune-diseases\/","title":{"rendered":"An Update on Alopecia and its Association With Thyroid Autoimmune Diseases"},"content":{"rendered":"
Alopecia is a dermatological disorder characterized by hair loss from the scalp or body.1\u20133<\/sup><\/span>\u00a0It is one of the most common dermatological disorders worldwide and has several aetiologies, such as hereditary background, hormonal imbalance, infection or idiopathic causes.1,3,4<\/sup><\/span>\u00a0Alopecia can be classified into two main categories: scarring (or cicatricial) alopecia and non-scarring (non-cicatricial) alopecia (Figure 1<\/span><\/em>).1\u20133<\/sup><\/span><\/p>\n Scarring alopecia is a complex and heterogeneous group of hair disorders resulting in irreversible destruction of the hair follicle, which is then replaced by fibrous scar tissue, due to permanent follicular stem cell damage.1\u20133<\/sup><\/span>\u00a0Non-scarring alopecia is caused by an alteration in the capillary cycle, which causes temporary or partial damage to hair follicles, resulting in hair shedding followed by hair regrowth.1,3<\/sup><\/span><\/p>\n This comprehensive, focused review aims to serve as an up-to-date reference highlighting recent information on alopecia and its association with thyroid autoimmune diseases (TADs), focusing on case-control, retrospective, cross-sectional or cohort designs, and focused review articles published between 2011 and 2022.<\/p>\n Primary cicatricial alopecia, often termed scarring alopecia, describes a group of hair loss disorders in which the hair follicle is permanently destroyed and replaced by fibrous tissue.1\u20133,5\u20137<\/sup><\/span>\u00a0Most types of primary scarring alopecia, some of which overlap or occur simultaneously, are classified as inflammatory skin disorders.8<\/sup><\/span>\u00a0Primary scarring alopecia is less common than non-scarring alopecia, representing about 5\u20137% of cases.3,6<\/sup><\/span>\u00a0With scarring alopecia, the skin is bald, smooth and shiny inside the patches, and pores are absent due to a complete loss of follicular openings.6<\/sup><\/span><\/p>\n The hypotheses proposed to explain why scarring alopecia occurs include the loss of follicular immune privilege, alterations in the microbiota of the local pilosebaceous unit, abnormal lipid metabolism, the possible involvement of mast cells and an association with skin care products and sunscreens.8\u201311<\/sup><\/span>\u00a0The role of genetics in scarring alopecia also remains unclear.8,9<\/sup><\/span><\/p>\n Scarring alopecia is further subdivided into lymphocytic, neutrophilic and multiple causes (Figure 1<\/span><\/em>).1,3<\/sup><\/span><\/p>\n <\/p>\n <\/b>Discoid lupus erythematosus<\/span>\u00a0can occur in the absence of any systemic disease or in conjunction with systemic lupus erythematosus.9,12\u201314<\/sup><\/span>\u00a0It is known to progress with exposure to sunlight (ultraviolet light), so it mainly affects the scalp, face and ears, causing scarring alopecia and facial disfigurement.6,12\u201314<\/sup><\/span>\u00a0The clinical features of discoid lupus erythematosus include alopecia characterized by well-defined, coin-shaped persistent erythematous indurated plaques of varying size, followed by follicular hyperkeratosis, which is skin adherent.5,9,12\u201314<\/sup><\/span>\u00a0When the adhering scale is removed, follicle-sized keratotic spikes like carpet tacks can be observed (\u201ccarpet tack sign\u201d).5,9,12\u201314<\/sup><\/span>\u00a0The lesions slowly extend with active inflammation and hyperpigmentation at the periphery, resulting in depressed central atrophy, scarring, telangiectasia and hypopigmentation.\u00a0Discoid lupus erythematosus<\/span>\u00a0can lead to permanent scarring alopecia on the scalp.5,9,12\u201314<\/sup><\/span><\/p>\n Keratosis follicularis spinulosa decalvans is a rare genetic disorder that often starts in infancy or early childhood and predominantly affects males.9,15\u201318<\/sup><\/span>\u00a0It presents with progressive scarring alopecia of the scalp and eyebrows.9,15\u201318<\/sup><\/span><\/p>\n Lichen planopilaris<\/span><\/b>\u00a0is characterized by a lymphocytic invasion of hair follicles and is common in women between the ages of 40 and 60.19\u201321<\/sup><\/span>\u00a0Patients with lichen\u00a0planopilaris<\/span>\u00a0may experience itching, burning or tenderness of the scalp.19,20<\/sup><\/span><\/p>\n Frontal fibrosing alopecia<\/span><\/b>\u00a0is an irreversible chronic lymphocytic scarring alopecia; its cause is unknown.22,23<\/sup><\/span>\u00a0It is distinguished by progressive regression of the frontal and temporal hairlines, usually associated with loss of eyebrows and eyelashes.9,22\u201324<\/sup><\/span><\/p>\n Alopecia mucinosa<\/span>\u00a0refers to permanent hair loss that occurs when hair follicles are replaced by mucin.7,9,25 <\/sup><\/span>Clinically, it presents as erythematous-infiltrated plaques with follicular prominence, especially in the head and neck.25<\/sup><\/span><\/p>\n <\/b>Central centrifugal scarring alopecia<\/span>\u00a0(<\/span>CCSA<\/span>) typically manifests as irreversible hair loss on the crown of the scalp and progresses in a centrifugal pattern to the parietal scalp.5,9,26,27<\/sup><\/span>\u00a0The exact cause of CCSA is unknown and considered to be multifactorial. A gene variant was recently discovered in approximately 25% of patients with CCSA; however, the exact role of this variant in the occurrence of CCSA is unclear<\/span>.26\u201328<\/sup><\/span><\/p>\n Pseudopelade of Brocq<\/span>\u00a0is a rare, chronic and gradually progressive form of scarring alopecia that mainly affects middle-aged women.8,29<\/sup><\/span>\u00a0The vertex and parietal scalp are commonly involved, and it is distinguished by the clinical appearance of small skin-coloured alopecia patches that look similar to “footprints in the snow”, and mild-to-moderate atrophy with no evidence of folliculitis or significant inflammation.7\u20139,29<\/sup><\/span><\/p>\n Dissecting cellulitis of the scalp, or Hoffman\u2019s disease, is a rare form of neutrophilic alopecia of unknown aetiology that leads to irreversible hair loss.30\u201332<\/sup><\/span>\u00a0The clinical features of\u00a0dissecting cellulitis of the scalp<\/span>\u00a0are nodules, abscesses on the vertex and posterior scalp, draining sinuses and scarring alopecia.30\u201332<\/sup><\/span><\/p>\n <\/b>Folliculitis decalvans<\/span>\u00a0<\/span><\/span>is the most common type of neutrophilic alopecia.33\u201335<\/sup><\/span>\u00a0It is characterized by painful follicular pustules that expand centrifugally, erosions and scaly-crusty lesions localized in the scalp, which leave central scarring and hair loss.33\u201335<\/sup><\/span>\u00a0Folliculitis decalvans<\/span>\u00a0typically affects only the scalp; however, one report has mentioned the involvement of the limbs and trunk.34<\/sup><\/span><\/p>\n Acne keloidalis nuchae<\/span><\/b>\u00a0is a chronic inflammatory form of scarring folliculitis.36\u201340<\/sup><\/span>\u00a0The clinical features are the occurrence of keloid-like papules, pustules and plaques; it most commonly affects the occipital scalp and posterior neck.36,39<\/sup><\/span>\u00a0The exact aetiology of acne keloidalis nuchae is unclear. However, this condition may be caused by chronic mechanical irritation to the back of the neck and scalp, trauma, heat, humidity, infection, autoimmune disorder, medications, and excess of some hormones such as androgens.36\u201338<\/sup><\/span>\u00a0Treatment, which aims to improve the symptoms of the disease, is difficult and unsatisfactory; many treatments have been tried with varying degrees of success.38<\/sup><\/span><\/p>\n Acne necrotica<\/span>\u00a0is a bizarre and enigmatic rare follicular disorder that manifests as a necrotizing disorder of the hair follicle.7,9,40<\/sup><\/span>\u00a0It is characterized by the development of papules on the scalp with central necrosis in adult patients and causes pox-like scars.7,9<\/sup><\/span>\u00a0It represents a diagnostic challenge due to its distinct clinical pathological features.40<\/sup><\/span><\/p>\n <\/b>Erosive pustular dermatosis of the scalp<\/span><\/b>\u00a0is a rare chronic inflammatory skin disease that causes scarring alopecia and mainly affects older adults.41\u201343<\/sup><\/span>\u00a0The condition is commonly found on the scalp or legs but can occur anywhere on the skin.41<\/sup><\/span>\u00a0Clinical diagnosis may be difficult because it is similar to more common diseases, such as squamous cell carcinoma, infection, localized scarring pemphigoid (the Brunsting-Perry type), or folliculitis decalvans, and has non-specific clinical characteristics (crusts, atrophy, and pustules<\/span>).41\u201343<\/sup><\/span><\/p>\n Non-scarring alopecia, also called non-cicatricial alopecia, refers to recoverable hair loss.1,3,44<\/sup><\/span>\u00a0It is classified into androgenetic alopecia (AGA), telogen effluvium (TE), traction alopecia, trichotillomania and alopecia areata (AA) (Figure 1<\/span><\/em>).1,3,44<\/sup><\/span><\/p>\n <\/span>AGA, often called male pattern baldness, is an autosomal dominant disorder that gradually transforms terminal hairs into intermediate and vellus hairs.45\u201347<\/sup><\/span>\u00a0It is the most common progressive baldness in both men and women; however, clinical symptoms differ between genders. In men, AGA causes gradual thinning and vertex loss; in women, hair loss affects the frontal scalp and vertex, while the frontal hairline is spared, resulting in a more visible scalp.45,47 <\/sup><\/span>Testosterone metabolite and dihydrotestosterone are the most important mediators of AGA. They act on androgen receptors in the hair follicles, causing hair thinning in the anagen phase and extending the telogen phase of hair growth, leading to more immature hair and decreasing the new hair.45\u201347<\/sup><\/span>\u00a0Some studies linked AGA to systemic diseases such as metabolic syndrome, endocrine diseases, mental disorders and hypothyroidism.45,46<\/sup><\/span>\u00a0The treatment for AGA consists of oral finasteride, topical external use of minoxidil, low-intensity laser and hair transplantation; however, whether the treatments are successful remains controversial.45\u201347<\/sup><\/span><\/p>\n TE is a common non-scarring alopecia that mainly affects women.47\u201350<\/sup><\/span>\u00a0It consists of diffuse hair loss occurring 2\u20133 months after a triggering event and lasting about 6 months; this hair loss leads to an abnormal shift of scalp hair follicles from anagen to telogen, resulting in premature hair shedding.47\u201349<\/sup><\/span>\u00a0TE can be caused by low ferritin, vitamin B12 deficiency, thyroid dysfunctions, systemic diseases, drugs, medications, fever, stress, weight loss and giving birth.47\u201350<\/sup><\/span><\/p>\n Traction alopecia<\/span>\u00a0occurs in individuals who have hairstyles that exert a consistent pulling force on the hair roots.51,52<\/sup><\/span>\u00a0It is most common in\u00a0women of African descent<\/span>, who may braid their hair tightly and use chemical treatments to straighten it.51,52<\/sup><\/span> In the early stages, patients with traction alopecia usually present with patches of non-scarring hair loss and tensioned areas of the scalp; in its later stages, the disease can progress to irreversible scarring alopecia if left untreated.51<\/sup><\/span>\u00a0Patients may also report tenderness, itching and headaches.51<\/sup><\/span><\/p>\n Trichotillomania<\/span>\u00a0is a psychiatric condition classified as an obsessive\u2013compulsive disorder, in which a person pulls out hair from any part of their body regularly, resulting in hair loss.53\u201355<\/sup><\/span>\u00a0It can affect any part of the body; however, it most commonly affects the scalp, followed by the eyebrows and the pubic region.53\u201355<\/sup><\/span>\u00a0Clinically, it appears as patches of varying size and shape; however, the patches are not completely bald but are covered in an irregular pattern of broken hair.47<\/sup><\/span><\/p>\n AA is the most frequent cause of inflammation-induced, immune-mediated non-scarring hair loss disorder.56\u201358<\/sup><\/span>\u00a0It has an unpredictable course and a broad spectrum of manifestations (Figure 1<\/span><\/em>).<\/p>\n Although it is uncommon in children under 3 years, the vast majority of patients with AA are young. Up to 66% of patients are under 30, and only 20% of patients are older than 40.56\u201362<\/sup><\/span>\u00a0AA is characterized by a rapid onset, with patients experiencing hair loss in well-circumscribed patches, usually round or oval in shape, and entirely hairless and smooth.56,58,59,61<\/sup><\/span>\u00a0In 90% of clinical diagnoses, AA\u2019s most common clinical feature is a circumscribed area of bald skin on the scalp that is usually isolated from other patches.57,58,60<\/sup><\/span>\u00a0Since AA is a dynamic disorder (i.e. causing recurrent episodes of hair loss), patches may appear in other parts of the body, such as the elbows, arms and thighs.60<\/sup><\/span>\u00a0Furthermore, the disease may affect facial hair, including eyelashes, eyebrows and the beard area.60<\/sup><\/span>\u00a0One of the factors that may influence the onset of AA is stress.47,57,62\u201365<\/sup><\/span>\u00a0Some patients reported an emotional event or an identity crisis prior to the onset of AA.47,57,62\u201365<\/sup><\/span>\u00a0Other factors, such as infections, toxins, genetic factors and even food, could be triggers of the disease. AA is often associated with other diseases, such as systemic lupus erythematosus, autoimmune haemolytic anaemia, asthma, atopic dermatitis, vitiligo, allergic rhinitis, and thyroid diseases.47,57,62\u201365<\/sup><\/span><\/span><\/p>\nScarring alopecia<\/span><\/h1>\n
Lymphocytic primary scarring alopecia<\/span><\/h2>\n
Discoid lupus erythematosus<\/span><\/span><\/h3>\n
Keratosis follicularis spinulosa decalvans<\/h3>\n
Lichen planopilaris<\/h3>\n
Frontal fibrosing alopecia<\/h3>\n
Alopecia mucinosa<\/span><\/h3>\n
Central centrifugal scarring alopecia<\/h3>\n
Pseudopelade of Brocq<\/span><\/h3>\n
<\/b><\/span><\/b>Neutrophilic<\/b><\/span>\u00a0<\/b><\/span><\/span>primary scarring alopecia<\/b><\/span><\/h1>\n
Dissecting cellulitis of the scalp, or Hoffman\u2019s disease<\/h3>\n
Folliculitis decalvans<\/h3>\n
<\/span><\/b>Mixed<\/b><\/span>\u00a0<\/b><\/span><\/span><\/span>p<\/b><\/span>rimary scarring alopecia<\/b><\/span><\/h1>\n
Acne keloidalis nuchae<\/h3>\n
Acne necrotica<\/span><\/h3>\n
Erosive pustular dermatosis of the scalp<\/h3>\n
Non-scarring alopecia<\/span><\/h1>\n
Androgenetic alopecia<\/span><\/h2>\n
Telogen effluvium<\/span><\/h2>\n
Traction alopec<\/span><\/span>ia<\/h2>\n
Trichotillomania<\/span><\/h2>\n
Alopecia areata<\/span><\/h2>\n
Thyroid autoimmune diseases and alopecia<\/span><\/h1>\n