Alopecia Areata is a condition of hair loss that comes on suddenly at any age and may affect any hair bearing area.
It is unpredictable in its course, often starting as isolated patches of hair loss which may resolve spontaneously.
In a minority of cases it can progress to more extensive or complete hair loss.
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The cause of Alopecia Areata is unknown but it is likely to be due to a genetic predisposition as well as immune mechanisms.
Whether this immune reaction has an environmental or local trigger is the focus of much research.
Genetic predisposition:
It is likely that Alopecia Areata is a polygenic (meaning it comes from several genes) condition.
It is possible that certain genes account for the susceptibility to develop this condition whereas other genes might account for the severity of the condition in an individual.
The evidence for this genetic susceptibility comes from numerous family studies:
There is often a family history of Alopecia Areata (10-42%).
This is particularly true in individuals who have Alopecia Areata starting early in life.
There is a familial incidence of 37% in those individuals who had their first patch by the age of 30, whereas the familial incidence is only 7.1% if the first patch starts after the age of 30.
In the case of identical twins, if one twin develops the condition, there is a 55% chance of the other twin showing symptoms.
An association has been shown with the human leukocyte antigen genetic system (HLA) Class II.
There is an association between Alopecia Areata and the HLA Class II antigens -DR4, -DR5 and -DQ3.
Those individuals with HLA-DR5 have a higher rate of early onset Alopecia with more extensive hair loss.
Individuals with atopy and Down's syndrome (8.8%) have an increased incidence of Alopecia Areata.
This suggests that the genetic basis of Alopecia Areata involves several genes (polygenic).
Clearly this makes it more difficult to identify an underlying genetic defect.
Immune mechanisms:
If one looks at a hair follicle under the microscope from an affected patch of skin with Alopecia Areata, there are many immune cells gathered around the follicle.
Immune mechanisms clearly are important in the cause of Alopecia Areata.
These can be divided into organ-specific immune mechanisms and non-specific immunity.
Organ-specific Immune Mechanisms:
There are a number of reasons to support the concept that Alopecia Areata is an autoimmune condition:
Significant associations are seen with other conditions that are known as organ-specific autoimmune conditions.
Thyroid disease is more common in individuals with Alopecia Areata (8-11.8%) compared to the general population (2%).
Vitiligo is a condition of pigment loss of the skin and patients with Alopecia Areata have a four times increased incidence of this condition compared to the general population.
These, and other, associations support the possibility that Alopecia Areata is also an autoimmune condition.
To confirm this, scientists need to demonstrate a proven 'autoantibody' against, for instance, the hair follicles.
Several antibodies have been found against different components of the hair follicle, but further work is continuing as these antibodies are also found in a proportion of individuals who have no evidence of Alopecia Areata.
Non-specific Immunity:
Alopecia Areata can be temporarily reversed by using immune suppressing treatments such as oral steroids or cyclosporin (used in transplant recipients)
This supports an immune basis for this condition.
Environmental Triggers:
There are variable data suggesting the possibility of environmental factors being important in the aetiology or cause of Alopecia Areata.
Certain viruses have been implicated, most recently the cytomegalovirus (CMV).
The hypothesis is that the virus instigates an immune reaction against the hair follicle in a susceptible individual.
However, this association has not been confirmed by different laboratories.
The association of emotional stress preceding the onset of Alopecia Areata is also variable.
No one environmental factor appears to be responsible for provoking the onset of Alopecia Areata.
Local Triggers:
Certain local abnormalities have been described which might contribute to the onset or progression of Alopecia Areata:
Certain neuropeptides (calcitonin gene-related peptide, CGRP, and substance P) have been shown to be decreased in the scalp of patients with Alopecia Areata.
These neuropeptides are released from local nerve endings and can modify local inflammatory reactions (CGRP) and induce hair growth (Substance P).
Certain cytokines, which are immune-modulating proteins, have been shown to be abnormally expressed in the scalp of individuals with Alopecia Areata, and are known to affect hair follicle growth.
Whether this immune reaction has an environmental or local trigger is the focus of much research.
Genetic predisposition:
It is likely that Alopecia Areata is a polygenic (meaning it comes from several genes) condition.
It is possible that certain genes account for the susceptibility to develop this condition whereas other genes might account for the severity of the condition in an individual.
The evidence for this genetic susceptibility comes from numerous family studies:
There is often a family history of Alopecia Areata (10-42%).
This is particularly true in individuals who have Alopecia Areata starting early in life.
There is a familial incidence of 37% in those individuals who had their first patch by the age of 30, whereas the familial incidence is only 7.1% if the first patch starts after the age of 30.
In the case of identical twins, if one twin develops the condition, there is a 55% chance of the other twin showing symptoms.
An association has been shown with the human leukocyte antigen genetic system (HLA) Class II.
There is an association between Alopecia Areata and the HLA Class II antigens -DR4, -DR5 and -DQ3.
Those individuals with HLA-DR5 have a higher rate of early onset Alopecia with more extensive hair loss.
Individuals with atopy and Down's syndrome (8.8%) have an increased incidence of Alopecia Areata.
This suggests that the genetic basis of Alopecia Areata involves several genes (polygenic).
Clearly this makes it more difficult to identify an underlying genetic defect.
Immune mechanisms:
If one looks at a hair follicle under the microscope from an affected patch of skin with Alopecia Areata, there are many immune cells gathered around the follicle.
Immune mechanisms clearly are important in the cause of Alopecia Areata.
These can be divided into organ-specific immune mechanisms and non-specific immunity.
Organ-specific Immune Mechanisms:
There are a number of reasons to support the concept that Alopecia Areata is an autoimmune condition:
Significant associations are seen with other conditions that are known as organ-specific autoimmune conditions.
Thyroid disease is more common in individuals with Alopecia Areata (8-11.8%) compared to the general population (2%).
Vitiligo is a condition of pigment loss of the skin and patients with Alopecia Areata have a four times increased incidence of this condition compared to the general population.
These, and other, associations support the possibility that Alopecia Areata is also an autoimmune condition.
To confirm this, scientists need to demonstrate a proven 'autoantibody' against, for instance, the hair follicles.
Several antibodies have been found against different components of the hair follicle, but further work is continuing as these antibodies are also found in a proportion of individuals who have no evidence of Alopecia Areata.
Non-specific Immunity:
Alopecia Areata can be temporarily reversed by using immune suppressing treatments such as oral steroids or cyclosporin (used in transplant recipients)
This supports an immune basis for this condition.
Environmental Triggers:
There are variable data suggesting the possibility of environmental factors being important in the aetiology or cause of Alopecia Areata.
Certain viruses have been implicated, most recently the cytomegalovirus (CMV).
The hypothesis is that the virus instigates an immune reaction against the hair follicle in a susceptible individual.
However, this association has not been confirmed by different laboratories.
The association of emotional stress preceding the onset of Alopecia Areata is also variable.
No one environmental factor appears to be responsible for provoking the onset of Alopecia Areata.
Local Triggers:
Certain local abnormalities have been described which might contribute to the onset or progression of Alopecia Areata:
Certain neuropeptides (calcitonin gene-related peptide, CGRP, and substance P) have been shown to be decreased in the scalp of patients with Alopecia Areata.
These neuropeptides are released from local nerve endings and can modify local inflammatory reactions (CGRP) and induce hair growth (Substance P).
Certain cytokines, which are immune-modulating proteins, have been shown to be abnormally expressed in the scalp of individuals with Alopecia Areata, and are known to affect hair follicle growth.
Alopecia Areata affects men and women equally.
It can occur at any age but 60% of individuals lose their first patch of hair before the age of 20 years.
Hair loss is sudden and can occur in several different ways.
Nail changes can occasionally be seen.
Hair Loss:
Most individuals lose a circular patch of hair on any hair bearing area of the body but usually the scalp (img 1).
This patch is totally bald, smooth and not scarred and often shows the characteristic 'exclamation mark hairs'.
These are short broken off hairs, often seen at the edge of a patch and in the tapering shape of an exclamation mark. These are due to fragile hairs growing abnormally (indystrophic anagen).
The hair loss is usually asymptomatic although some people may feel some tingling, burning or itching before the hair is lost.
Hair loss may occur at other body sites than the scalp or may be more extensive on the scalp.
The majority (70%) of affected individuals regrow their hair within a few months.
Sometimes the hair grows back white at first but this usually repigments.
Others lose several patches of hair which can be recurrent.
Hair regrowth is less predictable and one in ten individuals progress to the chronic form
of Alopecia Areata with permanent and more extensive hair loss.
The hair loss may progress to involve the whole scalp (ALOPECIA TOTALIS) (img 2) or all the body hair (ALOPECIA UNIVERSALIS)
It is impossible to give an accurate prognosis in individuals with an isolated patch of Alopecia Areata.
Indicators of a poor prognosis are atopy, family history of Alopecia Areata, early onset of hair loss, extensive hair loss, pattern of hair loss around the ears (ophiasis) and nail dystrophy.
Nail Changes:
Changes can be seen in one, some or all the nails.
Most commonly, fine irregular pitting is seen (img 3).
Other changes are longitudinal striations resulting in a sandpaper like appearance (trachyonychia); superficial splitting of the free edge of the nail (onychorrhexis) and horizontal grooves (Beau's lines).
It can occur at any age but 60% of individuals lose their first patch of hair before the age of 20 years.
Hair loss is sudden and can occur in several different ways.
Nail changes can occasionally be seen.
Hair Loss:
Most individuals lose a circular patch of hair on any hair bearing area of the body but usually the scalp (img 1).
This patch is totally bald, smooth and not scarred and often shows the characteristic 'exclamation mark hairs'.
These are short broken off hairs, often seen at the edge of a patch and in the tapering shape of an exclamation mark. These are due to fragile hairs growing abnormally (indystrophic anagen).
The hair loss is usually asymptomatic although some people may feel some tingling, burning or itching before the hair is lost.
Hair loss may occur at other body sites than the scalp or may be more extensive on the scalp.
The majority (70%) of affected individuals regrow their hair within a few months.
Sometimes the hair grows back white at first but this usually repigments.
Others lose several patches of hair which can be recurrent.
Hair regrowth is less predictable and one in ten individuals progress to the chronic form
of Alopecia Areata with permanent and more extensive hair loss.
The hair loss may progress to involve the whole scalp (ALOPECIA TOTALIS) (img 2) or all the body hair (ALOPECIA UNIVERSALIS)
It is impossible to give an accurate prognosis in individuals with an isolated patch of Alopecia Areata.
Indicators of a poor prognosis are atopy, family history of Alopecia Areata, early onset of hair loss, extensive hair loss, pattern of hair loss around the ears (ophiasis) and nail dystrophy.
Nail Changes:
Changes can be seen in one, some or all the nails.
Most commonly, fine irregular pitting is seen (img 3).
Other changes are longitudinal striations resulting in a sandpaper like appearance (trachyonychia); superficial splitting of the free edge of the nail (onychorrhexis) and horizontal grooves (Beau's lines).
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 |
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The cause of Alopecia Areata is unknown but it is likely to be due to a genetic predisposition as well as immune mechanisms.
Whether this immune reaction has an environmental or local trigger is the focus of much research.
Genetic predisposition:
It is likely that Alopecia Areata is a polygenic (meaning it comes from several genes) condition.
It is possible that certain genes account for the susceptibility to develop this condition whereas other genes might account for the severity of the condition in an individual.
The evidence for this genetic susceptibility comes from numerous family studies:
There is often a family history of Alopecia Areata (10-42%). This is particularly true in individuals who have Alopecia Areata starting early in life.
There is a familial incidence of 37% in those individuals who had their first patch by the age of 30, whereas the familial incidence is only 7.1% if the first patch starts after the age of 30.
In the case of identical twins, if one twin develops the condition, there is a 55% chance of the other twin showing symptoms. An association has been shown with the human leukocyte antigen genetic system (HLA) Class II.
There is an association between Alopecia Areata and the HLA Class II antigens -DR4, -DR5 and -DQ3.
Those individuals with HLA-DR5 have a higher rate of early onset Alopecia with more extensive hair loss.
Individuals with atopy and Down's syndrome (8.8%) have an increased incidence of Alopecia Areata.
This suggests that the genetic basis of Alopecia Areata involves several genes (polygenic).
Clearly this makes it more difficult to identify an underlying genetic defect.
Immune mechanisms:
If one looks at a hair follicle under the microscope from an affected patch of skin with Alopecia Areata, there are many immune cells gathered around the follicle.
Immune mechanisms clearly are important in the cause of Alopecia Areata.
These can be divided into organ-specific immune mechanisms and non-specific immunity.
Organ-specific Immune Mechanisms:
There are a number of reasons to support the concept that Alopecia Areata is an autoimmune condition:
Significant associations are seen with other conditions that are known as organ-specific autoimmune conditions.
Thyroid disease is more common in individuals with Alopecia Areata (8-11.8%) compared to the general population (2%).
Vitiligo is a condition of pigment loss of the skin and patients with Alopecia Areata have a four times increased incidence of this condition compared to the general population.
These, and other, associations support the possibility that Alopecia Areata is also an autoimmune condition.
To confirm this, scientists need to demonstrate a proven 'autoantibody' against, for instance, the hair follicles.
Several antibodies have been found against different components of the hair follicle, but further work is continuing as these antibodies are also found in a proportion of individuals who have no evidence of Alopecia Areata.
Non-specific Immunity:
Alopecia Areata can be temporarily reversed by using immune suppressing treatments such as oral steroids or cyclosporin (used in transplant recipients)
This supports an immune basis for this condition.
Environmental Triggers:
There are variable data suggesting the possibility of environmental factors being important in the aetiology or cause of Alopecia Areata.
Certain viruses have been implicated, most recently the cytomegalovirus (CMV).
The hypothesis is that the virus instigates an immune reaction against the hair follicle in a susceptible individual.
However, this association has not been confirmed by different laboratories.
The association of emotional stress preceding the onset of Alopecia Areata is also variable.
No one environmental factor appears to be responsible for provoking the onset of Alopecia Areata.
Local Triggers:
Certain local abnormalities have been described which might contribute to the onset or progression of Alopecia Areata:
Certain neuropeptides (calcitonin gene-related peptide, CGRP, and substance P) have been shown to be decreased in the scalp of patients with Alopecia Areata.
These neuropeptides are released from local nerve endings and can modify local inflammatory reactions (CGRP) and induce hair growth (Substance P).
Certain cytokines, which are immune-modulating proteins, have been shown to be abnormally expressed in the scalp of individuals with Alopecia Areata, and are known to affect hair follicle growth.
Whether this immune reaction has an environmental or local trigger is the focus of much research.
Genetic predisposition:
It is likely that Alopecia Areata is a polygenic (meaning it comes from several genes) condition.
It is possible that certain genes account for the susceptibility to develop this condition whereas other genes might account for the severity of the condition in an individual.
The evidence for this genetic susceptibility comes from numerous family studies:
There is often a family history of Alopecia Areata (10-42%). This is particularly true in individuals who have Alopecia Areata starting early in life.
There is a familial incidence of 37% in those individuals who had their first patch by the age of 30, whereas the familial incidence is only 7.1% if the first patch starts after the age of 30.
In the case of identical twins, if one twin develops the condition, there is a 55% chance of the other twin showing symptoms. An association has been shown with the human leukocyte antigen genetic system (HLA) Class II.
There is an association between Alopecia Areata and the HLA Class II antigens -DR4, -DR5 and -DQ3.
Those individuals with HLA-DR5 have a higher rate of early onset Alopecia with more extensive hair loss.
Individuals with atopy and Down's syndrome (8.8%) have an increased incidence of Alopecia Areata.
This suggests that the genetic basis of Alopecia Areata involves several genes (polygenic).
Clearly this makes it more difficult to identify an underlying genetic defect.
Immune mechanisms:
If one looks at a hair follicle under the microscope from an affected patch of skin with Alopecia Areata, there are many immune cells gathered around the follicle.
Immune mechanisms clearly are important in the cause of Alopecia Areata.
These can be divided into organ-specific immune mechanisms and non-specific immunity.
Organ-specific Immune Mechanisms:
There are a number of reasons to support the concept that Alopecia Areata is an autoimmune condition:
Significant associations are seen with other conditions that are known as organ-specific autoimmune conditions.
Thyroid disease is more common in individuals with Alopecia Areata (8-11.8%) compared to the general population (2%).
Vitiligo is a condition of pigment loss of the skin and patients with Alopecia Areata have a four times increased incidence of this condition compared to the general population.
These, and other, associations support the possibility that Alopecia Areata is also an autoimmune condition.
To confirm this, scientists need to demonstrate a proven 'autoantibody' against, for instance, the hair follicles.
Several antibodies have been found against different components of the hair follicle, but further work is continuing as these antibodies are also found in a proportion of individuals who have no evidence of Alopecia Areata.
Non-specific Immunity:
Alopecia Areata can be temporarily reversed by using immune suppressing treatments such as oral steroids or cyclosporin (used in transplant recipients)
This supports an immune basis for this condition.
Environmental Triggers:
There are variable data suggesting the possibility of environmental factors being important in the aetiology or cause of Alopecia Areata.
Certain viruses have been implicated, most recently the cytomegalovirus (CMV).
The hypothesis is that the virus instigates an immune reaction against the hair follicle in a susceptible individual.
However, this association has not been confirmed by different laboratories.
The association of emotional stress preceding the onset of Alopecia Areata is also variable.
No one environmental factor appears to be responsible for provoking the onset of Alopecia Areata.
Local Triggers:
Certain local abnormalities have been described which might contribute to the onset or progression of Alopecia Areata:
Certain neuropeptides (calcitonin gene-related peptide, CGRP, and substance P) have been shown to be decreased in the scalp of patients with Alopecia Areata.
These neuropeptides are released from local nerve endings and can modify local inflammatory reactions (CGRP) and induce hair growth (Substance P).
Certain cytokines, which are immune-modulating proteins, have been shown to be abnormally expressed in the scalp of individuals with Alopecia Areata, and are known to affect hair follicle growth.
Information on Wigs and Hairpieces
If you have alopecia areata you are entitled to a prescription for a wig or a hairpiece. You will be able to get a very good wig from the National Health Service. This information sheet sets out the present arrangements for NHS Scotland.
Your hospital consultant will give you a prescription which you should take to the hospital’s Medical Appliance Officer. The hospital will have a contract with a number of hair studios and you will be given names and addresses of these but you have a right to choose any hair studio named on the contract. You must pay a prescription charge.
There are two types of wigs available and you may find what you are offered on prescription depends on the policy of your hospital Trust.
The two types of wig are acrylic and real hair wigs.
The prescription charges for each wig or item (from April 2005) are:
• acrylic wig £53. 90
• partial human hair wig £142.30
• full customised human hair wig £208. 10
Acrylic Wigs
The majority of people are prescribed an acrylic wig. There are four types of acrylic wig. It may help you to know how the staff at the hair studios will describe them. All of these wigs mentioned here are available on the NHS.
• In a wig with a “fully wefted base” fibre is sewn onto a strip of material. The wig or hairpiece is then made up using the wefted fibres.
• A wig described as having a ”monotop” will also be made from wefted fibres but its top will be constructed from fine monofilament material. This will make the top much lighter.
• A “hand tied” acrylic wig is made from fibre but the hair is hand knotted into a base. The base is made of fine net called a mesh. It is usually more comfortable to wear than the other types of acrylic wigs because it allows heat to escape and it reacts better in windy conditions.
You are entitled to two acrylic wigs on prescription per year. However, your entitlement is dependent on the advice of the consultant and he or she may prescribe more than two wigs per year if he or she feels that this is necessary.
Real Hair Wigs
There are many types of real hair wigs available on the NHS contract. They are made from taking a mould of the person’s scalp. Real hair wigs are usually more suitable for people who have no hair at all as they tend to slip if there is hair underneath. As these wigs are made to fit an individual they are called “customised”. It is also possible to get an “off the peg” real hair wig.
The consultant will decide how many real hair wigs that you should have during a period of time. Again it will be dependent on the policy of your hospital Trust.
• A “full hair wig” is made using real hair hand-knotted onto a net base. It can be quite heavy to wear. This type of wig must be dry cleaned and sent to the contractor for servicing if it made on a silk base.
• A wig made of real hair but with a base made of an acrylic monofilament material will be described by the fitter as a “full monofilament”. This type of wig held onto the scalp with tape. It is particularly suitable for those people with an active lifestyle because they can take part in most activities without worrying about it coming off. It can be handwashed at home but it will need to have hair added to it occasionally as it will moult.
Fitting and Maintenance
Whatever the type of wig you choose, it should fit your head snugly. It should be altered if it is not sitting comfortably on your scalp.
You should also be offered some sort of secure fastening if necessary, for instance, comb clips if you have some hair or some toupee tape on waxed silk if there is an area of your scalp that is quite bald.
Each supplier will explain how to look after your wig.
Accessories
There are also products available to help conceal bald patches such as hairpieces and a product called Couvre which are suitable for those people who do not need or want a full wig.
Wigs are except from Value Added Tax (VAT) when you buy privately and any extras are VAT free. If the extras are bought separately however ( for example, shampoo, conditioner or toupee tape) you must pay VAT.
Information updates on prescription charges
The Health Department of the Scottish Executive is responsible for issuing updates on prescription charges in Scotland.
The address is:
The Directorate of Service Policy and Planning
Health Planning and Quality Division
St Andrew’s House
Regent Road
Edinburgh EH1 3DG
Telephone: 0131 244 2434
If you have alopecia areata you are entitled to a prescription for a wig or a hairpiece. You will be able to get a very good wig from the National Health Service. This information sheet sets out the present arrangements for NHS Scotland.
Your hospital consultant will give you a prescription which you should take to the hospital’s Medical Appliance Officer. The hospital will have a contract with a number of hair studios and you will be given names and addresses of these but you have a right to choose any hair studio named on the contract. You must pay a prescription charge.
There are two types of wigs available and you may find what you are offered on prescription depends on the policy of your hospital Trust.
The two types of wig are acrylic and real hair wigs.
The prescription charges for each wig or item (from April 2005) are:
• acrylic wig £53. 90
• partial human hair wig £142.30
• full customised human hair wig £208. 10
Acrylic Wigs
The majority of people are prescribed an acrylic wig. There are four types of acrylic wig. It may help you to know how the staff at the hair studios will describe them. All of these wigs mentioned here are available on the NHS.
• In a wig with a “fully wefted base” fibre is sewn onto a strip of material. The wig or hairpiece is then made up using the wefted fibres.
• A wig described as having a ”monotop” will also be made from wefted fibres but its top will be constructed from fine monofilament material. This will make the top much lighter.
• A “hand tied” acrylic wig is made from fibre but the hair is hand knotted into a base. The base is made of fine net called a mesh. It is usually more comfortable to wear than the other types of acrylic wigs because it allows heat to escape and it reacts better in windy conditions.
You are entitled to two acrylic wigs on prescription per year. However, your entitlement is dependent on the advice of the consultant and he or she may prescribe more than two wigs per year if he or she feels that this is necessary.
Real Hair Wigs
There are many types of real hair wigs available on the NHS contract. They are made from taking a mould of the person’s scalp. Real hair wigs are usually more suitable for people who have no hair at all as they tend to slip if there is hair underneath. As these wigs are made to fit an individual they are called “customised”. It is also possible to get an “off the peg” real hair wig.
The consultant will decide how many real hair wigs that you should have during a period of time. Again it will be dependent on the policy of your hospital Trust.
• A “full hair wig” is made using real hair hand-knotted onto a net base. It can be quite heavy to wear. This type of wig must be dry cleaned and sent to the contractor for servicing if it made on a silk base.
• A wig made of real hair but with a base made of an acrylic monofilament material will be described by the fitter as a “full monofilament”. This type of wig held onto the scalp with tape. It is particularly suitable for those people with an active lifestyle because they can take part in most activities without worrying about it coming off. It can be handwashed at home but it will need to have hair added to it occasionally as it will moult.
Fitting and Maintenance
Whatever the type of wig you choose, it should fit your head snugly. It should be altered if it is not sitting comfortably on your scalp.
You should also be offered some sort of secure fastening if necessary, for instance, comb clips if you have some hair or some toupee tape on waxed silk if there is an area of your scalp that is quite bald.
Each supplier will explain how to look after your wig.
Accessories
There are also products available to help conceal bald patches such as hairpieces and a product called Couvre which are suitable for those people who do not need or want a full wig.
Wigs are except from Value Added Tax (VAT) when you buy privately and any extras are VAT free. If the extras are bought separately however ( for example, shampoo, conditioner or toupee tape) you must pay VAT.
Information updates on prescription charges
The Health Department of the Scottish Executive is responsible for issuing updates on prescription charges in Scotland.
The address is:
The Directorate of Service Policy and Planning
Health Planning and Quality Division
St Andrew’s House
Regent Road
Edinburgh EH1 3DG
Telephone: 0131 244 2434