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Dr. Christopher Tzermias

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ALOPECIAS

Alopecia is the most common disorder of hair growth with significant effects on both the appearance and the mood of people, depending on its stage, the time of onset, the duration and the permanence of the problem.

The term “alopecia” describes the absence or thinning of hair on the scalp or other parts of the body and it is caused by the weakened functioning of hair follicles.

Alopecia occurs when the hair follicles stop producing the normal number of hairs (i.e. one to four hairs per follicle) or when the hairs produced are thinner or of worst quality. Hair follicles bristles produce abnormally thick and abnormal quality. Hair follicles are shrinking and minimalisation occurs, while gradually hair production is reduced, or only vellus hair is produced, or no hair at all.

There are two types of alopecias:

  1. Non-cicatricial (non-scarring) alopecia
  2. Cicatricial alopecia

Non-cicatricial Alopecias

a) Normal alopecias

Immediately after birth, the hair of the head are usually replaced, something that is not even noticeable most of the times. When this process is evident, alopecia occurs, starting from the frontal part of our head. In some babies normal alopecia becomes evident at the occipital area, probably due to the contact with the pillow.

During adolescence, a greater number of boys and a smaller number of girls see hair loss at the frontal hairline, resulting in differentiations in terms of the curvature of the hairline at the frontal-parietal region with a shape that resembles a triangle.

In humans, normal hair loss is stable process. In some individuals it may appear in a similar way as a seasonal increase of hair growth rates.

b) Alopecia areata

This is an autoimmune disorder of the hair follicle. It is characterised by the heterogeneous hair thinning, which develops on normal scalp, with hair that look like an exclamation mark around the boundaries of the areas with alopecia.

In most cases alopecia is confined in one or more areas of the scalp. However, in more severe cases total hair loss may occur on the scalp only (“alopecia totalis”) or on the whole body (“alopecia universalis”).

c) Androgenetic alopecia

Androgenetic alopecia, commonly known as baldness, is caused by the increased sensitivity of the receptors which are normally present in hair follicles, the androgens that circulate in the body, independently of the number of circulating androgens.

In 5% of men the onset of this disorder is before the age of 20 years old, showing a symmetric thinning of the hair at the frontotemporal region along the frontal hairline. As the individual gets older hair loss rate increases and, depending on the severity, androgenetic alopecia can be measured using the Hamilton-Norwood.

In women alopecia usually starts at a later point and its progress is slower. Hairs become thinner and hair loss usually starts from the parting of the hair although it may affect other areas of the scalp, too. In women classification of hair loss is conducted according to the Ludwig scale.

d) Other forms of non-cicatricial alopecia due to the effects of other harmful factors

During mitosis, the maternal cells of the hair are really vulnerable in various harmful factors, which affect cells’ mechanisms, leading to partial or full inhibition of hair loss. Depending on the severity of the disorder, alopecias can be distinguished in (a) telogen, in which the proportion of follicles in the telogen phase increases as compared to hair follicles in the anagen phase, (b) dystrophic, in which the proportion of dystrophic hair follicles is increased, and (c) mixed, in which both the proportion of telogen and dystrophic hair follicles is affected.

Classification of diffuse alopecias depending on the phototrichogram’s imaging

i) TELOGEN EFFLUVIUM

Its main characteristic is the great amount of hairs that are lost due to the early or sudden completion of the anagen phase and the onset of the telogen phase. This results in hair loss within two to three months. In this type of alopecia, hair loss is reversible, as it is caused by certain harmful factors, which may be more or less severe. High-fever, severe diseases or disorders, surgical procedures, psychological stress, medications or iron insufficiency are some of these adverse factors.

Another important thing to note is that sometimes telogen alopecia may occur after the end of pregnancy or when contraceptive medication administrations stops. The sudden interruption of the pre-existing extended period of the anagen phase and the onset of the telogen phase is the cause of telogen alopecia in many occasions.

ii) ANAGEN EFFLUVIUM

In this type of alopecia, hair follicles’ functioning is inhibited at the anagen phase due to the effects of potent harmful agents. The result of this is the production of thinner and fragile hairs, which are usually lost within one to four weeks. This particular type of hair loss may be reversible or irreversible, depending on the damage and on whether necrosis of the hair follicle has occurred. In cases of patients undergoing chemotherapy total hair loss may occur within a few days.

iii) MIXED ALOPECIA

In this type of alopecia, harmful factors affect in different ways hair follicles, which leads to early termination of the anagen phase in some individuals, while in others leads to disruption of hair growing at the anagen phase.

Classification of diffuse alopecias depending on the time of onset

There are 3 different types of events signifying the onset of diffuse alopecia:

  1. Acute alopecia, in which hair loss starts suddenly
  2. Subacute alopecia, in which hair loss occurs in several months
  3. Chronic alopecia, in which the hair thinning cycle tends to be repeated, a process that usually lasts more than 6 months.

The interruption of the normal lifecycle of the hair is usually the result of a systematic disorder of the organism, metabolic stress (chemotherapy, pregnancy, adolescence, surgical procedure, intense stress, severe chronic diseases), or it may be the result of psychological distress or trauma.

Hair thinning may start becoming visible up to 3 months after an intense event has occurred. Due to this delay in the onset of hair loss as compared to the triggering event, the individual may notice hair loss when s/he has already been treated from the disease or psychological distressed that was the triggering factor at first, which is why it is difficult sometimes to specify the exact cause of alopecia.

Classification of alopecias depending on the harmful agent/factor

i) Diffuse alopecia due to endocrine alterations

In hypothyroidism, diffuse alopecia is observed on the scalp, while at a later stage it may also appear on the body. Moreover, thinning of hair may also be evident in the eyebrows and the armpits.

Diffuse alopecia may also occur in cases of hyperthyroidism, which is severe in rare cases and it is reversible.

In cases of hypoparathyroidism the hairs of the scalp become thinner; they may be dry and coarse, while the appearance of hair loss may be irregular at certain areas of the scalp.

In individuals with uncontrolled diabetes mellitus diffuse alopecia may occur.

As already discussed, during pregnancy or when contraceptive pill administration stops, the sudden interruption of the pre-existing extended period of the anagen phase and the onset of the telogen phase may be the cause of telogen alopecia.

ii) Diffuse alopecia due to medications and chemical compounds

In case of accidental intake of insecticides, or if an individual intakes insecticides to commit suicide, the onset of alopecia is usually after ten days, appearing as a diffuse apoptosis of hairs. Depending on the dose of the substance that was taken, alopecia may be dystrophic and it may last for 3-4 months.

In some individuals, antithyroid drugs may cause diffuse alopecia when administered for extended periods.

Anticoagulants may also cause diffuse alopecia, a condition that is reversible.

Chemotherapeutic drugs can cause diffuse alopecia when the follicles that are in the anagen phase enter early into the catagen-telogen phase, or in cases of shrinkage of the inhibitors of the hair matrix or full breakage of hair.

Antipsychotic drugs disrupt the process of keratinisation, something that makes hair coarser and thinner.

In the case of hypervitaminosis of Vitamin A, hairs become thinner, the scalp becomes dryer and more sensitive, while sometimes hypermelachrosis may also occur..

Boric acid can also cause diffuse alopecia following prolonged use.

iii) Diffuse alopecia due to nutritional and metabolic disorders

Diffuse alopecia may be caused by protein insufficiency, iron deficiency, poor iron storage, deficiency in zinc, magnesium, vitamin D and B12, folic acid and fatty acids, as well as due to certain hereditary disorders of amino acids’ metabolism.

e) Traumatic Alopecias

i) Trichotillomania

This type of traumatic alopecia, in which a person pulls his /her hair out due to a nervous tick, may lead to the development of a region with partial alopecia. The shape of these areas is usually unnatural and hair thinning is not full but sporadic, while the eyelashes and the eyebrows may be affected, too.

ii) Traction alopecias

Prolonged and continuous tension on the hair due to the use of rollers, the hairstyle and other cosmetic procedures in general can cause inflammation of the hair follicle and scarring, leading to permanent hair loss. Peripheral alopecia is more common.

Cicatricial alopecias

This condition is more common among women and it usually presents with perifollicular erythema and keratotic plugs at the margins of expanding alopecia. It may be due to various causes, including the following:

  • Developmental disorder and hereditary conditions: skin aplasia, epidermal nevi, porokeratosis of Mibelli, ichthyosis, Darier disease, etc.
  • Defects due to natural causes: mechanical traumas, burns, x-ray dermatitis.
  • Microbial infections: tinea/ringworm infections, bacterial infections (lupus vulgaris, leprosy, syphilis tritogonos, furuncle, psefdanthrax, folliculitis, acne necrotising), leishmaniasis, viral infections (herpes zoster, chickenpox, smallpox).
  • Neoplasias: basal cell carcinoma, cicatricial (scarring) basal cell carcinoma, metastatic carcinomas.
  • Various other dermatoses/skin diseases of unknown aetiology: lichen planus, lupus erythematosus, scleroderma, lipoid necrobiosis, sarcoidosis, benign mucous membrane pemphigoid, follicular mucinosis, etc..

Lichen planopilaris

Lichen planopilaris, also known as follicular lichen planus, is a clinical syndrome that consists of lichen planus and it is associated with cicatricial alopecia of the scalp. The condition is more common among women, and presents with perifollicular erythema and keratotic plugs at the margins of the expanding alopecia. The follicular involvement is limited to the infundibulum (pituitary stalk) and the isthmus, both of which demonstrate lichenoid inflammation. The main complications of follicular lichen planus are atrophy and scarring, with permanent hair loss.

Three forms of lichen planopilaris are recognised:

  1. Classic lichen planopilaris
  2. Graham-Little syndrome, which is characterised by the following:
  • multifocal scalp cicatricial alopecia
  • non-scarring alopecia of the axilla and/or groin
  • keratotic follicular papules
  1. Frontal fibrosing alopecia that affects mainly postmenopausal women and appears as cicatricial alopecia of the frontoparietal hairline and is associated with non-scarring alopecia of the eyebrows

Management strategy

Therapeutic management for lichen planopilaris is difficult and challenging. However, if the associated inflammation can be controlled in its early stages, follicular units may be preserved and hair regrowth may be possible.

A good therapeutic response would include a reduction in associated symptoms along with stabilization of the disease and some regrowth of hair in the active perimeter of the alopecic patch. For the most part, therapeutic reports are anecdotal. Oral antihistamines may be used to control pruritus, and high-potency topical corticosteroids are used to control the inflammation in early lesions. Intra-lesional injections of 3–5mg/mL of triamcinolone acetonide are effective in well-developed lesions.

It has been shown that retinoids have some effect in the treatment of lichen planus and therefore provide a possible alternative to corticosteroid treatment. Additional treatment modalities include the antimalarials, in particular hydroxychloroquine. Other agents that have been reported to be of use are ciclosporin and mycophenolate mofetil.

Biologic agents are included among the other agents that have been reported as being useful in the treatment of lichen planopilaris, such as the tumour necrosis factor (TNF)-blocking agents for this condition.

 

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