Table of Contents
What is Alopecia Areata?
Alopecia areata is a recurring type of hair loss that can affect any area of hair.
Clinically, alopecia areata can occur in many different forms. Although medically this is considered as a benign condition, alopecia areata can cause tremendous emotional and psychosocial distress in the affected patients and their families.
Alopecia areata is hair loss in one or more round spots on the scalp, which can grow bigger, confluent and lead to complete hair loss.
Alopecia areata can occur at any age – from birth to the later decades of life.
There are also congenital cases. The peak incidence of the condition is seen at the age 15-29 years.
Nearly 44% of people with alopecia areata have the onset of the condition before the age of 20. First symptoms of alopecia areata are observed in less than 30% after 40 years of age of all patients affected.
According to The National Center of Advancing Translational Sciences „…the prevalence of alopecia areata … is estimated to be 0.1% to 0.2% of all people. This would mean that approximately 318,000 to 636,000 people in the United States are affected with alopecia areata.” 
The exact pathophysiology of alopecia areata remains unknown. The most common hypothesis is that alopecia areata is a T-cell autoimmune disease that is most likely to occur in genetically predisposed individuals.
In many cases, the disease or recurrences occur after psychological trauma – shock, severe mental traumas (exams, psychological stress, etc.) as well as some endocrine disorders (such as thyroid crisis, diabetes, etc.)
Such conditions are often combined with alopecia areata. Circular alopecia is sometimes combined with vitiligo, diabetes, thyroid disorder, anemia, hypogammaglobulinemia, various autoimmune diseases such as pernicious anemia, chronic hepatitis, dermatitis, and psychiatric disorders.
There is evidence supporting the hypothesis that alopecia areata is an autoimmune condition. The process appears to be an organ-restricted and T-cell mediated. It has been found that there is an increased frequency of patients antibodies directed to the structures of the hair follicle.
The response of the antibodies is diverse and focuses on different structures to the hair follicles in the anagen phase .
The outer root sheath is the most common target structure, followed by the inner root sheath, matrix and hair shaft. Whether these antibodies have a direct role in the pathogenesis or whether they are secondary phenomenon is left unknown yet.
Clinical forms on an alopecia areata include:
• Diffuse alopecia areata–
A diffuse hair loss  all over the scalp
Diffuse alopecia – the disease characterized by hair loss over the entire surface of the scalp in both men and women. This is a disease resulting from a violation of the hair due to adverse effects on the body.
Among the main causes of diffuse alopecia can be identified genetic predisposition expressed by a high level or dihydrotestosterone receptor hypersensitivity of this hormone in the hair follicle. Decreased function of the hair follicles and the gradual loss of hair may be due to an excess of dihydrotestosterone in the body.
In addition, diffuse alopecia may be due to the presence of chronic infection in the body or emotional tension and stress, as well as the impact of various chemicals. Most often, diffuse alopecia is caused by disorders of the endocrine system (thyroid, adrenal, ovaries).
Episodes of localized alopecia areata (<50% affected) are usually self-limiting. Spontaneous regrowth occurs in most patients within a few months with or without treatment.
Extensive forms of alopecia areata (> 50% effect) are less common. Alopecia totalis or alopecia universalis occur in 7% of patients. Alopecia areata consisting of more than 40% hair loss, was observed in 11%.
In 30% of patients with alopecia totalis has experienced total hair loss within 6 months after the onset of illness.
Differential diagnosis is made with androgenetic alopecia, syphilis, trichotillomania, tinea capitis, telogen effluvium, psevdopelada Brock.
The diagnosis can usually be made on clinical grounds.
Biopsy of the scalp is rarely necessary but can be helpful when the clinical diagnosis is less certain. Histological diagnosis of alopecia areata may be done when there are some particular characteristics.
The most characteristic feature is peribulbar lymphocytic infiltrate, which is described in the appearance similar to a bee swarming. Sometimes undetected inflammation can occur, which can lead to diagnostic difficulties.
Other useful findings include pigment incontinence in the hair bulb. Degenerative changes in the matrix of the hair can be rarely found.
Treatment is not required since the condition is benign and spontaneous remissions and recurrences are very common.
There is data related to the natural progression of the condition. For example, in patients with less than 40% damage to the scalp, studies showed no benefit from the treatment (1% minoxidil and topical immunotherapy) versus placebo.
Patients with extensive alopecia areata (> 40% hair loss), there is little evidence of natural evolution. The frequency of spontaneous remission appears to be less than in patients with less than 40% damage to the scalp.
The recurrence rate is higher in patients with severe forms of alopecia areata. Patients with alopecia totalis and alopecia universalis usually have a poor prognosis.
Since alopecia areata is considered an autoimmune disease, various immunomodulators have been used to treat this condition.
Further options for the treatment of alopecia areata include minoxidil, corticosteroids, anthralin, psoralen + UV-A, prednisone, interferon, dapsone, methotrexate, biological agents, hair transplants.
Alopecia areata monocularis
Describes hair loss in only one place, it can appear anywhere on the head
Partial scalp alopecia
It means a partial loss of normal hair growth on the scalp affecting only certain limited area(s) of it.
Partial scalp alopecia may be due to a syndrome-Spanlang Tapeyner (Spanlang-Tapeiner), Syndrome X-linked mental retardation as a result of a point mutation is expressed by partial scalp alopecia, mental retardation, spastic paraplegia, the immaturity of premaxillary bones, strabismus, underdeveloped ears, bones of the feet and genitals, cryptorchidism and others.
Alopecia areata multilocularis
The condition refers to a plurality of areas of hair loss.
The areas affected can range from the size of a dime to as big as an adult’s palm and can even merge forming a large bald area. The development of this type of alopecia can vary from a month to a year depending on the severity of this autoimmune disorder.
Alopecia Ophiasis refers to hair loss in the form of wave
Аlopecia areata barbae
Alopecia areata barbae is confined to the beard
Тotal alopecia (alopecia totalis)
This means a complete hair loss
Alopecia (kapitis) totalis is an autoimmune disease that leads to loss of all the hair on the scalp, including hair on the face, eyebrows and eyelashes. Sometimes it is an intermediate state between alopecia areata and alopecia universalis.
Two types of alopecia (kapitis) totalis are observed:
-a sudden loss of hair of the head
-the slower process starting as alopecia areata and leads to complete loss of hair on the scalp
Although the disease can affect individuals of all ages, it is more commonly seen in children and adults under 40 years of age.
Nail dystrophy is a general term that describes malformed fingernails and toenails; in this condition, the nails are often ridged, pitted, or abnormally curved.
The condition is autoimmune, i.e. the immune system attacks its own hair follicles. In most cases, the chance of recovery is minor, though there are cases of complete recovery.
Treatment of alopecia (kapitis) totalis focuses on immunomodulation. Oral and topical corticosteroids are usually applied. They are used for mild cases of hair loss (below 60% of hair loss).
Minoxidil solutions are also applied topically (Minoxidil stimulates hair growth and to slow balding) as well as oral Ciclosporin (Cyclosporine inhibits the activation of helper T cells that may be pathogenic in alopecia areata. ). 
- Universal Alopecia (alopecia universalis) – complete loss of hair on the head and whole body
Alopecia universalis is a condition characterized by a complete lack of hair on the body. The Affected individuals are born without eyebrows and eyelashes and do not develop axillary and pubic hair.
Anatomically, there are hair follicles detected but they are devoid of hair.
Alopecia universalis is inherited in an autosomal recessive pattern and is caused by a gene mutation. Alopecia universalis is said to be the most severe form of alopecia areata.
It is possible to develop such condition at any age.
Individuals with alopecia universalis are healthy but have a tendency to develop thyroid disease or vitiligo. Usually, the affected individuals are born with light hair, which quickly disappears.
Besides the genetic predisposition, there are no other predisposing factors discovered yet.
Alopecia universalis can be combined with changes in the fingernails and toenails.
The condition can also be acute, transient or permanent. Hair growth is possible even in subjects with complete absence of hair for many years.
There is no definitive treatment for alopecia universalis. The best treatment is the local immunotherapy.
The goal of treatment is to stimulate hair follicles by placing chemical irritants on the skin.
The natural course of alopecia areata is unpredictable. Most patients have several areas, affected by alopecia and their spontaneous regrowth usually occurs within one year.
Studies indicate that there are less than 10% of all patients experiencing extensive alopecia and less than 1% have alopecia universalis.
Patients with extensive long-term conditions are less likely to develop significant long-term regrowth. Adverse prognostic factors include nail abnormalities, atopy , the occurrence of the condition at a younger age and severe forms of alopecia areata.
- Androgenetic alopecia
Androgenetic alopecia is an extremely common disease that affects both men and women. The incidence of androgenic alopecia usually considered to be greater in men than in women.
Androgenic alopecia is represented by thinning and hair loss symmetrically on the scalp. Most often the condition affects genetically predisposed individuals, which can be induced by the effects of androgenic hormones.
Androgenetic alopecia is an extremely common disease that affects about 50% of men and perhaps many women older than 40 years.
The incidence of androgenic alopecia increases significantly in postmenopausal women and according to various studies, it can affect 75% of women aged over 65 years.
Androgenic alopecia is considered a cosmetic disorder. It affects the patient psychologically, androgenic alopecia causing hair loss allows ultraviolet light to reach the scalp and thus increases the amount of actinic damage.
Men with androgenetic alopecia may have an increased incidence of myocardial infarction. Increased incidence of benign prostatic hypertrophy is also associated with androgenic alopecia.
Androgenic alopecia is a genetically conditioned disorder.
The beginning of the androgenic alopecia is gradual.
In men, the condition begins after the age of 20.
Men are manifested by a gradual thinning of the hair in the temporal areas, creating in reshaping the front of the hairline.
In the majority of cases the evolution of alopecia progresses through frontal and vertex thinning hair, and over time the two sections merge.
The process is progressing slowly without subjective complaints. At the beginning of the hairs are replaced by thin, dystrophic and depigmenting hairs that also fall out.
The scalp becomes smooth, shiny and over time atrophic. Typically the hair located in the occipital area is not affected.
Women with androgenic alopecia usually presented with diffuse thinning hairs in the frontal area and the crown of the scalp, which begins much later.
The condition leads to a gradual thinning of the hair rather than forming an area of evident baldness.
This alopecia often preceded by seborrhea (here are the best treatment products) and pityriasis simplex and usually causes severe itching.
Differential diagnosis is made with alopecia areata, telogenic effluvium, and anagen effluvium.
The most important aspects in the diagnosis of the condition are the anamnesis and the physical examination.Trichogram
Trichogram  is often necessary in order to prove that the number of telogen hairs (during a remission period) is increased. A biopsy is rarely needed for the diagnosis of the disease. A biopsy is needed to verify the reduction of hair follicles in size.
Later, some of these follicles completely disappear.
Although androgenic alopecia is considered a non-inflammatory form of hair loss, sometimes perifollicular, inflammatory infiltrate is observed.
A biopsy is rarely needed for the diagnosis of the disease. A biopsy is needed to verify the reduction of hair follicles in size. Later, some of these follicles completely disappear.
Although androgenic alopecia is considered a non-inflammatory form of hair loss, sometimes perifollicular, inflammatory infiltrate is observed.
Only two medications have been shown to be effective in the treatment of androgenetic alopecia: minoxidil and finasteride. Minoxidil  is applied topically and is available as a 2% or 5% solution.
Finasteride  can be orally administered. The surgical treatment is practically a transplantation of hair follicles from the occipital region of the head in the affected areas.
The effect of oral cyclosporine in the treatment of severe alopecia areata.
What is atopy? Sidestepping semantics.
Premature androgenic alopecia and insulin resistance. Male equivalent of polycystic ovary syndrome?
Androgenetic alopecia, metabolic syndrome, and insulin resistance: Is there any association? A case–control study
Minoxidil Response Testing in Males With Androgenetic Alopecia
Dutasteride Versus Placebo and Finasteride in Men With Androgenetic Alopecia
The unit area trichogram in the assessment of androgen-dependent alopecia.
Expression of HLA-DR by anagen hair follicles in alopecia areata.
Clinical and histological challenge in the differential diagnosis of diffuse alopecia: female androgenetic alopecia, telogen effluvium and alopecia areata – Part II*