Alopecia areata is a common nonscarring type of hair loss.
The disease is related to the following processes: auto-immune and has an incidence of about 0 / 100.000.
A characteristic feature is the presence of smooth, slightly erythematous or normal-colored apoplecic patches in hair . The presence of hair tapered near proximal end is pathognomic but this is not always seen. A positive result following a pull test shows active presence of the disease and thus more hair loss should be expected. Additionally, hair loss on other hair bearing areas equally favours the diagnosis. The most common presentation is the appearance of one or more round-oval denuded patches. No epidermal changes are associated with the hair loss.
Nail involvement is seen in 6.8 to 49.4% of patients and is most common in patients with severe forms of the condition. One of the most common findings is pitting.
Clinical features are the basis of alopecia areata diagnosis .
Trichoscopy can also help in differential diagnosis. During diagnosis, trichoscopy shows regularly distributed yellow dots known as hyperkeratotic plugs, small exclamation-mark hairs and black dots.
A biopsy is rarely needed. Histologic findings include peribulbar lymphocytic infiltrate. In some cases of inactive alopecia areata, inflammatory states may not be found. Other helpful findings include pigment incontinence in the hair bulb, follicular stelae as well as a shift in the anagen-to-telogen ratio towards higher telogen.
Since the condition is benign, treatment is not mandatory . This is also bearing in mind spontaneous remissions and recurrences. Treatments used are believed to stimulate hair growth but there is yet no clear evidence as to whether they affect the natural course of alopecia areata or not. Treatment modalities are often decided on based on the extent of hair loss as well as the age of the patient.
Topical treatments deployed include the use of corticosteroids, topical immunotherapy, anthralin and minoxidil. Systemic treatments include the use of psoralen plus, prednisone, cyclosporine, tacrolimus, interferon, dapsone and methotrexate.
In many cases which start as a small number of patches of hair loss, the hair grows back after a few months to a year . In cases where there is a greater number of patches, hair can either grow back or progress to more severe forms of the condition (Alopecia totalis or universalis).
The effect of this condition is mostly psychological, being loss of self-image as a result of hair loss. Loss of hair equally means more scalp sun burns following easy exposure to the sun. Loss of nasal hair increases severity of hay fever or other such similar allergic conditions. Since keratin forms both hair and nails, patients may witness aberrant nail formation.
Hair may grow back and fall out again later. This doesn’t indicate a recurrence of the condition. Rather it may be a natural cycle of growth and shedding. Onset of this condition before puberty predisposes the individual to chronic recurrences of the condition.
Alopecia areata is not contagious . It occurs more frequently in people who have family members affected by the condition which suggests a strong genetic predilection. Strong evidence of genetic association with increased risk for the condition was demonstrated by the identification of at least four susceptibility loci on chromosomes 6, 10, 16 and 18. It is also most likely to occur in people who have relatives with autoimmune conditions.
Alopecia areata is believed to be a systemic autoimmune disorder where the body attacks its own anagen hair follicles, suppressing or stopping hair growth .
On estimate, the global prevalence of alopecia areata is approximately 1 on 1000 people, with the lifetime risk put at approximately 2% . For many patients, the onset of the condition is before age 30. However, men and women are affected equally.
The pathophysiology for this condition is still open to debate. However, one hypothesis is commonly acccepted in different circles and this is the fact that alopecia areata is a T-cell mediated autoimmune condition with a higher possibility of occurrence in individuals that are genetically compromised for the condition . Over the course of history, there is a lot of evidence to support this hypothesis.
Although the process appears to be T-cell mediated, antibodies channeled to hair follicle have been seen more in patients with this condition when compared to the control subjects . With the aid of immunofluorescence, antibodies to anagen-phase hair follicles were seen in as much as 90% of patients with alopecia areata. This is in comparison to less than 37% of control subjects.
The autoantibody response is heterogenous and targets multiple structures of the anagen-phase hair follicle. The outer root sheath is the structure that is targeted most frequently and this is followed by the inner root sheath, the matrix and finally the hair shaft in that order. Whether these antibodies play a direct role in the pathophysiology is not yet known.
Since external etiologic factors are poorly documented and a genetic pathway has been established for the development of the disease, there is no clear way of preventing this disease.
Alopecia areata is a recurrent, nonscarring hair loss condition, affecting parts of the body with hair growing abilities . Clinically, alopecia areata can occur in a variety of patterns. It is of a benign nature but this doesn’t stop it from bringing about a great deal of emotional and psychosocial distress in people affected and those around them.
Alopecia areata is a condition that brings about hair loss on not just your scalp but the entire body. It can be as a result of heredity, certain medications consumed or other medical conditions. It is mostly seen in people in their 30s but can happen in people of all age groups.
The loss of hair takes different shapes and happens in any part of the body.
Treatment is not compulsory unless when the individual finds the condition to be worrying (more serious cases), in that case, medications or surgery can be used to bring back hair growth in the region affected.