In the name of God

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In the name of God
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Alopecia areata

• Dr Giti Sadeghian
• Dermatologist

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• Introduction
• Alopecia aerata is a chronic inflammatory
  disorder affecting hair follicles and sometimes
  the nails that produces non scarring hair loss.

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• Patient typically
• Develop discrete Arera of complete
• Hair loss

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• Epidemiology
• The estimated prevalence of alopecia areata is
  approximately
• 1 in 1000 people, with a lifetime risk of
  approximately 2 percent.
• Men women
• Alopecia areata can started at any age although
  in most patients the onset is before age 30.

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• Patho physiology
• the hair follicle pathology of AA is probably
  mediated by auto
• reactive T lymphocytes.
• Hair follicle auto antibodies are frequently
  present in sera from AA patients but their
  pathogenic role is uncertain.
• Other autoimmune diseases, such as
  vitilligo,thyroiditis,and pernicious anemia, may
  be associated with AA.

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• Approximately 20 of patient have a family
  history of AA, indicating a genetic
  predisposition to the disease. this is thought
  to be polygenic in nature and association with a
  variety of genes, predominantly immune response
  genes, have been reported.

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• A variety of factors, such as infections, drugs,
  and vaccinations, have been implicated in
  triggering episodes of AA.
• Some patients report severe stress, especially
  emotional stress as a precipitating event,
  although many patients have no such history.

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• Clinical features
• Patients with AA have smooth, circular, discrete
  area of complete hair loss that develop over a
  period of a few weeks, followed by regrowth over
  several months. These patches may enlarge and
  coalesce into bizarre patterns.
• Short hairs broken off a few millimeters from the
  scalp are found at the edges of expanding patches
  .

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• Area overgrowth often are characterized initially
  by fine , white vellus hairs.
• Alopecia most commonly occurs on the scalp, but
  may be found on any hair bearing area .

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• There also can be nail involvement with fine
  pitting or roughening of the nail plates.

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• Eye abnormalities, including the rare early
  development of cataract, may occur in patients
  with AA

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• Spontaneous regrowth occurs in the majority of
  patients.
• Around 80 of those with limited patchy hair loss
  will recover within a year, although almost all
  will experience more than one episode of the
  disease.
• However, alopecia areata may persist for several
  years and sometimes hair growth never recovers.

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• In a minority of patients there is progression to
  total loss of scalp hair (alopecia totalis) or
  loss of the entire scalp and body hair (alopecia
  universalis).

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• Ikeda,s categories
• Type 1 the common type
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• Age 20-40
• Total course les than 3 years
• Alopecia totalis develops in only 6

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• Type2atopic type
• 10
• The onset is in childhood
• Disease course is 10 years
• Alopecia totalis develops in 75

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• Type 3prehypertention type
• 4
• Young adults
• Disease course is rapid
• Alopecia totalis develops in 39

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• Type 4 combined type
• 5
• Patients are over 40 years
• Course is prolong
• Alopecia totalis develops in 10

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• Prognosis

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The following factors are associated with a poor
prognosis and /or high likelihood of relapse

• Onset in childhood
• Severe disease, specially alopecia totalis or
  alopecia universalis.
• Duration of more than one year.
• Involvement of peripheral scalp (ophiasis)
• Nail disease
• Atopy

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• Diagnosis

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• The diagnosis of AA is suspected in patients
  with the following
• Smooth, discrete area of hair loss affected skin
  may be slightly reddened but show no other
  changes.
• Exclamation point hair at the margins of patches
  these are short broken hairs which can be
  extracted with minimal traction and where the
  proximal end of the hair is narrower than the
  distal end.
• Exclamation point hair can be difficult to see
  their absence does not exclude AA.

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• Biopsy specimens are usually not necessary to
  confirm the diagnosis, but may be needed in cases
  where the diagnosis is uncertain.
• If obtained ,it is best to perform two 4mm punch
  biopsies into the subcutaneous fat and have one
  specimen processed with routine vertical
  sectioning and the other with horizontal
  sectioning.

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• If only a single specimen is obtained, horizontal
  sections will give a better representation of the
  histology.
• Biopsy taken early in the course of the disease
  show the majority of follicles in telogen or
  late catagen.
• Some anagen hair bulbs are situated at a higher
  level in the dermis than normal.

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• A peribulbar lymphocytic infiltration is seen
  around foliclles, this being more dens in early
  lesions.
• The infiltrater consiss procominantly of Tcells
  with increases of langerhans cells.
• The infiltrate disappears during regrowth.

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• Because of the association between AA and other
  autoimmune disorders, it is responsible to screen
  for thyroid disorder or pernicious anemia in the
  patients with a suggestive history or physical
  examination.

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• Differential diagnosis

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• Tinea capitis-
• tinea capitis may be associated with pruritus
  and produces scaling and inflammation in area of
  hair loss
• AA produces smooth area of hair loss, without any
  scaling .
• Adenophaty may be present in tinea capits.
• Tinea capitis should always be considered in
  children presenting with patchy hair loss.

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• Nervous hair pulling (trichotillomania)
• Trichotillomania pruduces unusual pattern of
  broken hair of varying length which lead to a
  characteristic Wire brush, feel, as compared
  with the smooth hair loss of AA.
• However, AA and trichotillomania can co-exist on
  the same scalp.
• A biopsy in the area of alopecia will help
  differentiate the two conditions.

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Trichotillomania
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Trichotillomania
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Cicatricial Aopecia

• Cicatricial alopecia may be the result of diverse
  pathologies, including lichen plano-pilaris,
  discoid lupus eryhematosu
• and folliculitis decavans.
• All are characterized by permanent, distraction
  of hair follicles. Hair loss is usually patchy
  and there is loss of follicular orifices.
• Additional features are variable and depending on
  the primary pathology may include erythema
  scaling follicular plugging and pustulation.

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Cicatricial Aopecia
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Androgenic Alopecia

• Onset of hair loss is gradual in androgenic
  alopecia and in a typical distribution patern.
• There are no exclamation point hairs.
• AA occasionally presents as diffuse hair loss,
  which may resemble androgenetic alopecia but the
  progression is most wide spreadand more rapid.
• A biopsy may be necessary in doubtful cases.

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Secondary syphilis

• Area of hair loss appear moth- eaten in patients
  with secondary syphilis rather than the smooth
  and discrete area seen with AA. Serologic
  testing may be necessary for differentiation.

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Counseling

• Counseling of patients on the nature of AA its
  prognosis and the treatment options is essential.
• For the majority of patients AA is a cosmetic
  issue although it can occasionally cause physical
  disabilities ,where there is eyelash involvement
  or marked nail dystrophy.

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• Nevertheless the cosmetic importance of hair loss
  is such that AA can cause sever emotional problem
  particularly in children
• and young women, thought by no means restricted
  to these groups.
• In view of limited efficacy of current forms of
  treatment the clinician has an important role in
  helping patients adapt to their lack of hair .

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• This is not an easy task and input from other
  health professionals, such as a clinical
  psychologist ,may be needed .
• Many patients though not all are helped by
  involvement in patient support groups. With
  children it is often the parents whose reaction
  must be addressed for the child adjust to the
  hair loss.

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Treament
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Treament

• Treatment is not mandatory because the condition
  is benign, and spontaneous remissions and
  recurrences are common.
• Treatments used are believed to stimulate hair
  growth, but no evidence indicates they can
  influence the ultimate natural course of alopecia
  areata.
• Treatment modalities usually are considered first
  according to the extent of hair loss and the
  patient's age.

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Treament
Not all patients require treatment. Up to 80
percent of patients with alopecia areata that is
limited and of less than one year's duration may
expect spontaneous regrowth of hair. Because
alopecia areata is believed to be an autoimmune
condition, different immunomodulators have been
used to treat this condition. Additional
treatment options for alopecia areata include
minoxidil and other treatment modalities.
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Topical treatmentsCorticosteroids

• Intralesional corticosteroids We suggest
  intralesional corticosteroids as the preferred
  therapy for adults with isolated patches of hair
  loss who desire treatment

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• Triamcinolone acetonide (Kenalog) is used most
  commonly concentrations vary from 2.5-10 mg/mL.
  The lowest concentration is used on the face. A
  concentration of 5 mg/mL is usually sufficient on
  the scalp.
• Less than 0.1 mL is injected per site, and
  injections are spread out to cover the affected
  areas (approximately 1 cm between injection
  sites see image below).

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• New growth is usually visible within four weeks.
  The treatment may be repeated as necessary every
  four to six weeks.
• Local skin atrophy is a consistent side
  effect(10) but usually resolves within a few
  months. Other side effects of therapy include
  telangiectasia, hypopigmentation, and systemic
  absorption.

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Topical steroids

• Topical steroids have not been extensively
  evaluated, although they are frequently used to
  treat alopecia areata, especially in children.
• 0.2 fluocinolone acetonide cream
• betamethasone dipropionate 0.05 percent (cream,
  lotion, ointment)
• Twice daily applications

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• Therapy should be evaluated after three months of
  use topical corticosteroids may also be combined
  with other topical agents or injected
  glucocorticoids

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Anthralin

• Anthralin is an irritant agent.
• Both short-contact and overnight treatments have
  been used.
• Anthralin concentrations varied from 0.2-1.
• Adverse effects include pruritus, erythema,
  scaling folliculitis, local pyoderma, and
  regional lymphadenopathy
• Withholding treatment for a few days results in
  rapid disappearance of adverse effects

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• Treatment then can be reinstituted, but anthralin
  should be left on for shorter periods. Staining
  of clothes and skin can be a concern.
• The mechanism of action of anthralin is unknown.
  Most likely, it creates inflammation by
  generating free radicals, which have
  antiproliferative and immunosuppressive actions.

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• Use for three months before reevaluating for
  treatment effectiveness given that treatment with
  anthralin is uncomfortable and of limited
  efficacy, we generally do not recommend it, and
  are particularly hesitant to use it in children.

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Minoxidil

• Minoxidil appears to be effective in the
  treatment of alopecia areata in patients with
  extensive disease (50-99 hair loss). Response
  rates in that group vary from 8-45.
• Minoxidil was of little benefit in patients with
  alopecia totalis or alopecia universalis.

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Minoxidil

• Minoxidil Over the counter minoxidil is
  sometimes used twice daily alone or in
  combination with betamethasone dipropionate or
  anthralin in children and adults.
• The 5 solution appears to be more effective
• Minoxidil should be tried for three months before
  evaluating effectiveness.

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• Minoxidil usually is well tolerated. Adverse
  effects include distant hypertrichosis (5) and
  irritation (7).
• The exact mechanism of action of minoxidil
  remains unclear

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• mitogenic effect on epidermal cells, both in
  vitro and in vivo.
• Anagen-phase hair bulbs plucked showed a
  significant increase in proliferation index as
  measured by DNA flow cytometry.
• prolong the survival time of keratinocytes in
  vitro
• Finally, minoxidil may oppose intracellular
  calcium entry.

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• Calcium influx normally enhances epidermal growth
  factors to inhibit hair growth. Minoxidil is
  converted to minoxidil sulfate, which is a
  potassium channel agonist and enhances potassium
  ion permeability, thus opposing the entry of
  calcium into cells
• Local vasodilatation does not appear to play a
  primary role in hair growth associated with
  minoxidil

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Immunotherapy

• Topical immunotherapy is defined as the induction
  and periodic elicitation of an allergic contact
  dermatitis by topical application of potent
  contact allergens.

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• The mechanism of action of topical immunotherapy
  is unknown. Antigenic competition has been
  hypothesized. That is, the introduction of a
  second antigen can initiate a new infiltrate
  containing T-suppressor cells and suppressor
  macrophages that may modify the preexisting
  infiltrate and allow regrowth.

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• Commonly used agents for immunotherapy include
  squaric acid dibutylester (SADBE) and
  diphencyprone (DPCP).
• The median time to achieve significant regrowth
  was 12.2 months.
• The relapse rate after reaching significant
  regrowth was 62.6.

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• Treatment is provided weekly.
• The patient first is sensitized directly on the
  scalp with a 2 concentration on a small area (2
  cm).
• The following week, a low concentration (0.0001)
  is applied.
• The concentration is increased slowly every week
  as needed until a mild tolerable allergic contact
  dermatitis is elicited. Many concentrations are
  available that achieve this goal.

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Phototherapy

• Phototherapy and photochemotherapy are potential
  treatments for alopecia areata. Narrowband UVB is
  thought to act as an irritant, but there is
  little documented evidence of efficacy .
• Psoralen plus UVA therapy (PUVA) can be
  administered with the psoralen delivered
  topically as a gel or paint, or orally.
• Several uncontrolled series have suggested
  efficacy rates of PUVA of 60 to 65 percent,
  though with a high relapse rate . Other series
  have found efficacy rates no higher than might be
  expected without therapy .

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• Treatment is usually for four to six months,
  which can result in high cumulative doses.
  However, a trial of photochemotherapy may be
  reasonable in patients with extensive alopecia
  areata (more than 75 percent of scalp involved),
  alopecia totalis, or alopecia universalis when
  topical immunotherapy is contraindicated or
  unacceptable to the patient.

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PUVA

• PUVA is a relatively safe treatment modality
  adverse effects include burning and, possibly, an
  increased risk of skin cancer.

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Oral corticosteroids

• Systemic steroids most likely are effective via
  their immunosuppressive effects.
• An initial benefit may occur by using systemic
  prednisone in some patients, but the relapse rate
  is high, and it does not appear to alter the
  course of the condition.
• Systemic prednisone is not an agent of choice for
  alopecia areata because of the adverse effects
  associated with both short- and long-term
  treatment.

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Cyclosporine

• Cyclosporine has been used both topically and
  systemically in the treatment of alopecia areata.
• Topical cyclosporine has not proven to be
  effective in severe alopecia .
• The mechanism of action of cyclosporine remains
  unclear. It may act through its immunosuppressive
  effect

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• In conclusion, topical cyclosporine has shown
  limited efficacy. Although systemic CsA appears
  to be effective in alopecia areata, the adverse
  effect profile, the recurrence rate after
  treatment discontinuation, and thus, the
  inability to produce long-term remissions, make
  CsA unattractive for the treatment of alopecia
  areata.

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Tacrolimus

• Regrowth was shown on the application site of
  topical tacrolimus in 2 studies using the DEBR
  model. Oral tacrolimus was ineffective. No
  benefit was shown in the use of topical
  tacrolimus for alopecia areata in a small 2005
  study by Price et al that included 11
  patients.25

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Interferon

• A study of 11 patients with alopecia areata
  ranging from patchy alopecia areata to alopecia
  universalis showed no benefit using intralesional
  interferon alfa-2 (1.5 million IU, 3 times per wk
  for 3 wk).

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• Dapsone, Methotrexate, latanoprost,nitrogen
  mustard, massage and relaxation, isoprinosine,
  acupuncture, and aromatherapy
• efficacy of these treatments needs to be
  demonstrated in larger, placebo-controlled trials
  before they can be recommended

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Biological agents

• including adalimumab, alefacept, etanercept and
  infliximab) in the treatment of alopecia areata
  did not show efficacy, and some patients
  developed alopecia areata while under treatment
  with biologic agents for other conditions.

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Nonpharmacologic methods

• A systematic MEDLINE search could not find any
  study with sufficient validity to provide
  scientific evidence of benefit with complementary
  and alternative medicine therapies for alopecia
  areata

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• A study on hypnosis for refractory alopecia
  areata did not show efficacy of regrowth, but it
  did show that hypnosis can improve depression,
  anxiety, and quality of life in affected patients

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• COSMETIC APPROACHES Female patients with
  extensive alopecia areata will usually require a
  wig or hairpiece. Wigs are generally less
  successful in men where hair styles, such as
  shaving the scalp, are often a more acceptable
  approach. Temporary tattooing can be helpful for
  loss of eyebrows.

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• INFORMATION FOR PATIENTS
• Explain in detail that although any of the
  treatments discussed can induce resumption of
  normal hair growth, none will "cure" the disease
  or prevent recurrence after healing.
• In the United States, patients can be encouraged
  to contact the National Alopecia Areata
  Foundation, a national support group that
  publishes a newsletter and provides names of
  local support groups.

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• SUMMARY AND RECOMMENDATIONS
• Patients with alopecia areata typically have
  smooth, circular, discrete areas of complete hair
  loss that develop over a period of a few weeks,
  followed by regrowth over several months. .
• The diagnosis of alopecia areata is typically
  made on clinical grounds. Patients have smooth
  discrete areas of hair loss, and exclamation
  point hairs may be seen at the margins of
  patches. .
• The cosmetic effects of alopecia areata can cause
  severe emotional distress counseling in such
  patients is essential. .

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• Not all patients with alopecia areata require
  treatment up to 80 percent of patients with
  limited alopecia areata of less than one year's
  duration will experience spontaneous regrowth of
  hair.
• There is relatively little evidence on treatment
  from well-designed clinical trials. For patients
  who desire treatment, we suggest the following

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• We suggest that localized scalp alopecia areata
  be treated with intralesional injections of
  corticosteroids .
• Clinicians should consider referral to a
  dermatologist if facial steroid injections are
  required. .
• In children or adults with limited disease and
  who have concerns about exposure to intralesional
  steroids, we suggest treatment with topical
  corticosteroids .

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• If intradermal or topical corticosteroid therapy
  produces an inadequate response, we suggest a
  trial of topical 5 percent minoxidil either alone
  or in combination with continued corticosteroid
  therapy .
• We suggest that patients with extensive alopecia
  areata, including alopecia totalis, as well as
  patients with more limited disease who do not
  respond to the above therapies be treated with
  topical immunotherapy .

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• Patients should generally be referred to a
  dermatologist for such therapy and any additional
  management.
• Photochemotherapy is another option for
  patients with extensive disease when topical
  immunotherapy is contraindicated or unacceptable.
  Long-term photochemotherapy should be avoided.

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• Patients who do not desire treatment may benefit
  from cosmetic interventions. Wigs (particularly
  in women) and shaving the scalp (in men) may
  produce an acceptable cosmetic result. Temporary
  tattooing can be helpful for loss of eyebrows.

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The End