Transcript Management of Alopecia

ALOPECIA
EZEIKE OBINNA
OUTLINE
 Introduction
 Types
 Epidemiology
 Pathophysiology
 Presentation
 Diagnosis
 Differential Diagnosis
 Management
 Prognosis
 Conclusion
Introduction
3 stages in hair growth
ANAGEN
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growth phase ( scalp 3 - 7yrs, brow 4yrs)
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80-90% of scalp hair in this phase
CATAGEN
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resting phase lasts 3-4wks
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Hair protein synthesis stops
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Follicle retreats towards the surface
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10-20% of hairs in this phase
TELOGEN
- shedding stage
- no growth
- lasts months
- at the end hair sheds, and new follicles start to grow
- 25-100 hairs shed per day
Introduction Contd
 Alopecia affects both men and women
 Normally lose 25-100 hairs per day
 Hair grows one cm a month
 About 100,000 hairs on the scalp
Epidemiology
Prevalence
 Ibadan (Ogunbiyi et al 2004) – 3.4%
 Kaduna (Yahya et al 2007) – 3.3%
 Enugu (Nnoruka et al 2005) - 1.3%
 Lagos (Ekpudu et al 2008) – 4.6%
Forms of Alopecia
 Scarring : associated fibrosis, inflammation, and
loss of hair follicles.
 Non-scarring : hair shafts are gone, but the hair
follicles are preserved; reversible
 May also be focal or diffused.
Causes of non-scarring Alopecia
 A. PRIMARY CUTANEOUS DISORDERS
 1. Telogen effluvium
 2. Anagen effluvium
 3. Androgenetic alopecia
 4. Alopecia areata
 5. Tinea capitis
 6. Traumatic alopecia
 B. Drugs
Non-scarring contd
 C. Systemic diseases
 1. Systemic lupus erythematosus
 2. Secondary syphilis
 3. Hypothyroidism
 4. Hyperthyroidism
 5. Hypopituitarism
 6. Deficiencies of protein, iron, biotin, and zinc
SCARRING (CICATRICAL) ALOPECIA
 About 7-8% of alopecia.
 May be primary or secondary
 Primary: the hair follicle is the target of the
destructive inflammatory process.
 Secondary: destruction of the hair follicle is
incidental to a non-follicle-directed process. May be
systemic (scleroderma, discoid lupus erythematosus)
or external injury, such as burns, radiation, traction
etc.
Scarring hair loss:
Primary cicatricial alopecia
 Primary cicatricial alopecias, further classified by type of inflammatory
cells that destroy the hair follicle during the active stage of the disease.
 Lymphocytic
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Chronic cutaneous LE
Lichen planopilaris
Classic pseudopelade
Central centrifugal cicatricial alopecia
Alopecia mucinosa
Keratosis follicularis spinulosa decalvans
 Neutrophilic
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Folliculitis decalvans
Dissecting folliculitis (perifolliculitis abscedens et suffodiens)
 Mixed
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Folliculitis keloidalis
Folliculitis necrotica
Erosive pustular dermatosis
 Non-specific
SCARRING ALOPECIA
 Are not contagious
 Majority of patients have no family history of a
similar condition.
 However, Central centrifugal cicatricial alopecia
primarily affects women of African ancestry, and
may occur in several women in the same family.
 May be symptomless or have symptoms such as
itching, pain, tenderness, or burning
DLE ( Scarring Alopecia)
Scarring Alopecia
DIAGNOSIS
 Hair pull test (rarely done nowadays, painful)
 Microscopic exam/ trichogram
 Of the hair bulb of the hairs pulled
 To differentiate b/w normal and dystrophic telogen
 To determine anagen/telogen ratio
 An excess of loose anagen hairs can be indicative of
active disease.
 Scalp biopsy is essential for the diagnosis: shows
type of inflammation present, location and amount
of inflammation, and other changes in the scalp.
TREATMENT
 Treatment, different for each subtype.
 Lymphocytic group: anti-inflammatory
medications.
 Oral medications may include hydroxychloroquine,
doxycycline, mycophenolate mofetil, cyclosporine, or
corticosteroids.
 Topical medications may include corticosteroids,
tacrolimus, pimecrolimus.
 Triamcinolone may be injected into inflamed,
symptomatic areas of the scalp.
TREATMENT CONT’D
 Neutrophilic group: . Oral antibiotics are mainstay. Topical
antibiotics may be used to supplement the oral antibiotics. In
dissecting cellulitis, pathogenic microbes are not usually present.
Isotretinoin may be helpful.
 Mixed group: antimicrobials, isotretinoin, and anti-inflammatory
medications.
 Treatment continued until symptoms stop.
 Hair regrowth uncommon, but possible if tx commenced early.
Topical minoxidil might help.
 Hair restoration surgery or scalp reduction may be considered if dx
is inactive for 1-2 yrs.
 Hair pieces, wigs, toupees, hats recommended.
Dissecting cellulitis
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Chronic folliculitis affecting predominantly young black males.
Presents with papules and pustules over the occipital region of the scalp
with hair loss. If severe, the back of the scalp becomes a boggy swelling
(discharging pus) with areas of scarring alopecia.
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Can be complicated by keloid scar formation (‘acne keloidalis nuchae’).
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Treatment is difficult but prolonged courses of low-dose antibiotics are
worth trying in early disease.
Prolonged courses of isotretinoin can help a few individuals and deep
surgical excision can be used in recalcitrant cases.
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Combined rifampicin and clindamycin (both 300 mg × 2) can be used in
resistant cases.
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(acne keloidalis nuchae).
Non-scarring alopecia
 refers to hair loss without permanent
destruction of the hair follicle.
Non-scarring alopecia
 Androgenetic alopecia,
 Anagen effluvium
 Telogen effluvium,
 Alopecia areata,
 folliculitis (mild),
 inherited disorders of the hair shaft
 traumatic alopecia
TELOGEN EFFLUVIUM
 Cause of diffuse hair loss. The disease results in
reversible diffuse loss of mature, terminal hairs,
usually following a significant stressful event.
 Reversible.
 Treatment involves controlling precipitating
condition.
Causes of telogen effluvium
 Endocrine
Hypo/hyperthyroidism
 Post-partum
 Peri/post-menopausal
 Nutritional
 Biotin deficiency
 Iron deficiency
 Kwashiokor/marasmus
 Zinc deficiency
 Essential FA deficiency
 Stress
 Anaemia
 Surgery
 Systemic illness
 Psychological stress
 Pregnancy/ abortion
 Severe weight loss
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Drugs
 ACEI
 β-blockers
 Anticoagulants
 Cytotoxics
 Interferon
 Lithium
 OC pills
 Retinoids
 Valproic acid
 Vit A excess
 Benze-imidazoles
Anagen effluvium
 Anagen effluvium involves loss of growing
(anagen) hair
Anagen effluvium
 alkylating, eg busulphan, melphalan, chlorambucil
 antimitotic, eg vinblastin, vincristine, paclitaxel
 Immunotherapeutic medications (eg, cyclosporine).
 Radiation therapy.
TRAUMATIC ALOPECIA
 mechanical traction,
 chemical trauma, and
 trichotillomania (nervous, self-induced hair pulling).
 Styling techniques that call for chronic tension on the hair,
 repeated use of lye-containing chemicals for hair
straightening
 hot oils for styling may cause a reversible loss of hair
Trichotillomania
tight curlers:
Traction alopecia secondary to braiding:
Hot-comb alopecia:
Tinea capitis
 Varies from scaling with minimal hair loss to discrete
patches with "black dots" (broken hairs) to boggy
plaque with pustules (kerion).
 Invasion of hairs by dermatophytes, most commonly
Trichophyton tonsurans.
 Oral griseofulvin or terbinafine plus 2.5% selenium
sulfide or ketoconazole shampoo; examine family
members
ANDROGENIC ALOPECIA
 Genetically determined disorder xterized by the gradual
conversion of the pigmented terminal hairs into
indeterminate, and finally into nonpigmented vellus, hairs. It
is a common condition that affects men and women.
 As condition progresses, the anagen phase shortens with the
telogen phase remaining constant. As a result, more hairs are
in the telogen phase, and the patient may notice an increase in
hair shedding.
 Androgenetic alopecia may mimic diffuse alopecia areata.
 Association was found between balding at the vertex and
Prostate cancer. (Amoretti et al)
Androgenetic Alopecia
 most common cause of alopecia
 three distinct forms recognized-MPAA, FPAA,
diffuse AA
 Caucasians most commonly affected
 More in males than females
 In women, more common post menopausal
 mode of inheritance unclear
 presence of androgens (esp. DHT) essential
 mechanism of action on follicles unclear
PRESENTATION
 MALES
 Men note a gradual recession of the frontal hairline early in the
process with gradual thinning in the temporal areas, producing a
reshaping of the anterior part of the hairline
 For the most part, the evolution of baldness progresses according to
the Norwood/Hamilton classification of frontal and vertex thinning.
 FEMALES
 Hair generally is lost diffusely over the crown; this produces a
gradual thinning of the hair rather than an area of marked baldness.
 The frontal hairline is often preserved in women
 Bitemporal recession does occur in women but usually to a lesser
degree than in men.
 May be associated with Polycystic ovary syndrome, adrenal dx etc.
PATHOPHYSIOLOGY
 Patients with androgenetic alopecia have a reduction
in the terminal-to-vellus hair ratio, normally about
4:1
 Studies have identified 2 major genetic risk loci for
androgenetic alopecia. These are the X-chromosomal
AR/EDA2R locus and the PAX1/FOXA2 locus on
chromosome 20.
 More recent studies have identified a third gene:
HDAC9
CONT’D
 Locus with strongest evidence for linkage to androgenetic
alopecia was the 3q26 site on the X chromosome. In
addition, an association between androgenetic alopecia
and chromosome 20pll and the androgen-receptor gene
has been reported.
 Androgen is necessary for progression of androgenetic
alopecia, as it is not found in males castrated prior to
puberty.
 Postulated to be a dominantly inherited disorder with
variable penetrance and expression. However, it may be
of polygenic inheritance.
 This suggests that systemic or external factors may play a
role in androgenetic alopecia.
DIAGNOSIS
 History and the physical examination, most important aspects of
diagnosis.
 Dehydroepiandrosterone (DHEA)-sulfate and testosterone analysis:
In women, if virilization is evident
 Dermoscopy: brown peripilar casts and miniaturized hairs (Schmidt
et al)
 Biopsy and histology
 A biopsy is rarely necessary to make the diagnosis of androgenetic
alopecia.
 Although the condition is considered a noninflammatory form of
hair loss, a superficial, perifollicular, inflammatory infiltrate is
noted at times. A mildly increased telogen-to-anagen ratio is often
observed.
Differentials
 Alopecia Areata
 Anagen Effluvium
 Telogen Effluvium
Management
 The following drugs have been approved by the FDA for the
treatment of androgenetic alopecia:
 Minoxidil: Androgen-independent hair-growth stimulator:
Minoxidil appears to lengthen the duration of the anagen phase,
and it may increase the blood supply to the follicle. Regrowth is
more pronounced at the vertex than in the frontal areas and is not
noted for at least 4 months.
 Side effects: Central chorioretinopathy (reversible),
 Finasteride: 5-Alpha reductase type 2 inhibitor. It is not an
antiandrogen. Inhibits conversion of testosterone to
dihydrotestosterone.
 The drug can be used only in men because it can produce
ambiguous genitalia in a developing male fetus. Used indefinitely.
Mgt Cont’d
 Other drugs: (androgen receptor antagonists)
spironolactone, cyproterone acetate; oral
contraceptives.
 Dutasteride: inhibits type I and type II 5-a reductase
isoenzymes and is felt to be 3 times as potent as
finasteride in inhibiting the type II enzyme and 100
times as potent in inhibiting the type I enzyme. Still
under trials.
 Topical Latanoprost.
 HairMax LaserComb. (Low-level laser light therapy)
Surgical Management
 punch-graft hair transplantation
 minigrafts and micrografts
 scalp reduction
 extensive scalp reduction
 tissue expansion
 transposition flaps
Male pattern
Female pattern
Female pattern baldness
Traction Alopecia
Alopecia Areata
INTRODUCTION
 Alopecia areata is a recurrent nonscarring type of hair loss that can affect
any hair-bearing area and can manifest in many different patterns .
Although, benign it can cause emotional and psychosocial distress.
 No known risk factors exist for alopecia areata, except a positive family
history. Autoimmune condition.
 The exact role of stressful events remains unclear, but they most likely
trigger a condition already present in susceptible individuals, rather than
acting as the true primary cause.
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Associated with other autoimmune diseases viz:
Thyroid disease
Diabetes mellitus
Inflammatory bowel disease
Systemic lupus erythematosus
Rheumatoid arthritis
Psoriasis and psoriatic arthritis
Vitiligo
INTRO cont’d
 Other comorbid conditions found included the following:
 Atopy (allergic rhinitis, asthma, and/or eczema) - 38.2%
 Contact dermatitis and other eczema - 35.9%
 Mental health problems (depression or anxiety) - 25.5%
 Hyperlipidemia - 24.5%
 Hypertension - 21.9%
 Gastroesophageal reflux disease - 17.3%
 Down syndrome
 Stressful life events in the 6 months before onset, febrile
illnesses, drugs, pregnancy, trauma may be precipitating
factor.
Signs and symptoms
 Alopecia areata most often is asymptomatic, but some patients
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(14%) experience a burning sensation or pruritus in the affected
area. The condition usually is localized when it first appears, as
follows:
Single patch - 80%
Two patches - 2.5%
Multiple patches - 7.7%
No correlation exists between the number of patches at onset and
subsequent severity.
Frequency of involvement at particular sites is as follows:
Scalp - 66.8-95%
Beard - 28% of males
Eyebrows - 3.8%
Extremities - 1.3%
CLASSIFICATION (areata)
 Reticular - Hair loss is more extensive and the
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patches coalesce
Ophiasis - Hair loss is localized to the sides and
lower back of the scalp
Sisaipho (ophiasis spelled backwards) - Hair loss
spares the sides and back of the head
Alopecia totalis - 100% hair loss on the scalp
Alopecia universalis - Complete loss of hair on all
hair-bearing areas
PATCHY ALOPECIA AREATA
OPHIASIS
SISIAPHO
DIFFUSE ALOPECIA AREATA
Presentation
 The presence of smooth, slightly erythematous (peach
color) or normal-colored alopecic patches is xteristic.
Presence of exclamation point hairs (ie, hairs tapered
near proximal end) is pathognomonic but not always
found.
 A positive result from the pull test at the periphery of a
patch usually indicates active disease, and further hair
loss can be expected.
 Additionally, hair loss on other hair-bearing areas also
favors the diagnosis. The most common presentation is
the appearance of one or many round-to-oval denuded
patches.
Nail changes
Seen in 6.8-49.4% of patients. Common with
severe forms of alopecia areata:
 Pitting (most common)
 Opacification
 Dystrophic changes,
 Others include: Trachyonychia, Beau lines,
Onychorrhexis, Onychomadesis, Koilonychias,
leukonychia etc.
PATHOPHYSIOLOGY
 Exact pathophysiology of alopecia areata remains
unknown. Most widely accepted hypothesis is of a
T-cell–mediated autoimmune condition that occurs
in genetically predisposed individuals.
 Using immunofluorescence, antibodies to anagenphase hair follicles were found in as many as 90% of
patients with alopecia areata compared with less
than 37% of control subjects.
 Histologically, lesional biopsy findings of alopecia
areata show a perifollicular lymphocytic infiltrate
around anagen-phase hair follicles. The infiltrate
consists mostly of T-helper cells and, to a lesser
extent, T-suppressor cells.
PATHOPHYSIOLOGY CONT’D
 Genetics: Two studies demonstrated that HLA DQ3
(DQB1*03) was found in more than 80% of patients with
alopecia areata, which suggests that it can be a marker
for general susceptibility to alopecia areata. The studies
also found that HLA DQ7 (DQB1*0301) and HLA DR4
(DRB1*0401) were present significantly more in patients
with alopecia totalis and alopecia universalis.
 Interleukin 1 receptor antagonist gene, may correlate
with disease severity.
 High association of Down syndrome with alopecia areata
suggests involvement of a gene located on chromosome
21.
EPIDEMIOLOGY
 Prevalence in the general population is 0.1-0.2%.
 All races are affected equally by alopecia areata
 Peak incidence appears to occur from age 15-29
years.
 Some studies show slight female preponderance.
DIAGNOSIS
 Diagnosis usually clinical. A scalp biopsy seldom is needed.
 HISTOLOGY: Horizontal sections usually are preferred to
vertical sections because they allow examination of multiple
hair follicles at different levels.
 Most characteristic feature is a peribulbar lymphocytic
infiltrate, which appears similar to a swarm of bees. The
infiltrate often is sparse and usually involves only a few of the
affected hairs in a biopsy specimen.
 A significant decrease in terminal hairs is associated with an
increase in vellus hairs, with a ratio of 1.1:1 (normal is 7:1).
Other helpful findings include pigment incontinence in the
hair bulb and follicular stellae.
 A shift in Anagen: Telogen ratio (usually about 9:1) in favour
of telogen.
DIAGNOSIS CONTD
 Dermoscopy
 Presence of yellow dots (95% of pxs). Following
histopathological correlation, these yellow dots
represent degenerated follicular keratinocytes and
sebum contained within the ostium of hair follicles.
 Although occasionally seen in advanced malepattern hair loss, yellow dots are not seen in cases of
female-pattern hair loss, scaring alopecia, or telogen
effluvium
DIFFERENTIALS
 Androgenetic Alopecia
 Pseudopelade, Brocq
 Telogen Effluvium
 Tinea Capitis
 Trichotillomania
TREATMENT
 Treatment is not mandatory as condition is benign, and
spontaneous remissions are common. Treatment can be
topical or systemic.
 Patients with alopecia totalis or alopecia universalis
usually have a poorer prognosis, and more treatment
failure .
 CORTICOSTEROIDS
 Intralesional corticosteroid therapy is usually
recommended with less than 50% involvement viz:
 Triamcinolone acetonide (Kenalog) is used most
commonly; concentrations vary from 2.5-10 mg/ml;
every 4-6 weeks. Side effects: transient atrophy, pain
during injection.
TREATMENT CONT’D
 TOPICAL CORTICOSTEROIDS may be useful,
esp in children
 Fluocinolone acetonide cream 0.2% twice daily or
betamethasone dipropionate cream 0.05%
 For refractory alopecia totalis or alopecia universalis,
2.5 g of clobetasol propionate under occlusion with a
plastic film 6 days/wk for 6 months helped a
minority of patients
 Tx must be continued for a minimum of 3 months
before regrowth can be expected, and maintenance
therapy often is necessary
TREATMENT CONTD
 Systemic corticosteroids not recommended. May be used for rapidly
progressive alopecia areata.
 Immunotherapy (> 50% scalp involvement)
 Topical immunotherapy is the induction and periodic elicitation of
an allergic contact dermatitis by topical application of potent
contact allergens
 Commonly used agents include squaric acid dibutylester (SADBE)
and diphencyprone (DPCP). Adverse effect: cervical
lymphadenopathy, pigment changes.
 Anthralin 0.2-1% (Synthetic derivative of a tree bark extract)
 Minoxidil appears to be effective in the treatment of extensive
disease (50-99% hair loss) but is of little benefit in alopecia totalis
or alopecia universalis.
 Initial regrowth can be seen within 12 weeks. Continued application
needed to achieve cosmetically acceptable regrowth.
TREATMENT CONTD
 Psoralen plus UV-A
 Both systemic and topical PUVA therapies have been used
 Most patients relapse within few months (4-8 months) after treatment is
stopped
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Other agents
Topical cyclosporine has shown limited efficacy
Topical tacrolimus
Methotrexate, with or without systemic corticosteroids, has shown mixed
results
Biologics did not show efficacy.
Phototherapy.
Cosmetic treatment
Dermatography has been used to camouflage the eyebrows of patients with
alopecia areata.
Hairpieces are useful for patients with extensive disease
Surgical intervention has no role in the treatment of alopecia areata.
Prognosis
 Natural history of alopecia areata is unpredictable.
 Most patients have only a few focal areas of alopecia, and
spontaneous regrowth usually occurs within 1 year.
 Less than 10% of patients experience extensive alopecia
and less than 1% have alopecia universalis.
 Patients with extensive long-standing conditions are less
likely to experience significant long-lasting regrowth.
 Adverse prognostic factors include nail abnormalities,
atopy, onset at a young age, and severe forms of alopecia
areata.
Patient Education
 Patient education is a key factor in alopecia areata.
Inform patients of the chronic relapsing nature of
alopecia areata. Reassure patients that the condition
is benign and does not threaten their general health.
 Inform patients that expectations regarding therapy
should be realistic.
ALOPECIA AREATA (BEARD)
ALOPECIA AREATA (FOREARM)
Localized Alopecia areata
Localized Alopecia areata
alopecia totalis
alopecia totalis
CONCLUSION
 Alopecia affects both males and females.
 Alopecia can be scarring (7-8%) or non-scarring
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(92%)
Scarring alopecia may be primary or secondary.
Primary scarring may be Lymphocytic, Neutrophilic
or mixed.
Mainstay of tx of lymphocytic is anti-inflammatory.
Mainstay of tx of neutrophilic is antibiotics.
Surgery not usually indicated.
Conclusion Contd
 Non-scarring more common.
 Androgenic alopecia commonest form. Results from
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excess androgens (female) or increased sensitivity to
antigens (males).
Minoxidil, finasteride, androgen receptor
antagonists beneficial
Surgery beneficial
Alopecia areata basically auto-immune.
Immunosupressants/ Immunomodulatory tx
mainstay.
Surgery of little benefit.