ezeike obinna alopecia. outline introduction types epidemiology pathophysiology presentation...

EZEIKE OBINNA

ALOPECIA

OUTLINE

IntroductionTypesEpidemiologyPathophysiologyPresentationDiagnosisDifferential DiagnosisManagementPrognosisConclusion

Introduction3 stages in hair growth

ANAGEN growth phase ( scalp 3 - 7yrs, brow 4yrs) 80-90% of scalp hair in this phase

CATAGEN resting phase lasts 3-4wks Hair protein synthesis stops Follicle retreats towards the surface 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 womenNormally lose 25-100 hairs per dayHair grows one cm a monthAbout 100,000 hairs on the scalp

Epidemiology

PrevalenceIbadan (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 effluvium2. 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 Chronic cutaneous LE Lichen planopilaris Classic pseudopelade Central centrifugal cicatricial alopecia Alopecia mucinosa Keratosis follicularis spinulosa decalvans

Neutrophilic Folliculitis decalvans Dissecting folliculitis (perifolliculitis abscedens et suffodiens)

Mixed Folliculitis keloidalis Folliculitis necrotica Erosive pustular dermatosis

Non-specific

SCARRING ALOPECIA

Are not contagiousMajority 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

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.

Can be complicated by keloid scar formation (‘acne keloidalis

nuchae’).

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.

Combined rifampicin and clindamycin (both 300 mg × 2) can be used in resistant cases.

(acne keloidalis nuchae).

Non-scarring alopecia

refers to hair loss without permanent destruction of the hair follicle.

Non-scarring alopecia

Androgenetic alopecia, Anagen effluviumTelogen 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

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, alkylating, eg busulphan, melphalan, chlorambucil chlorambucil

antimitotic, eg vinblastin, vincristine, antimitotic, eg vinblastin, vincristine, paclitaxelpaclitaxel

Immunotherapeutic medications (eg, Immunotherapeutic medications (eg, cyclosporine).cyclosporine).

Radiation therapy.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

straighteninghot oils for styling may cause a reversible loss of

hair

Trichotillomania

Traction alopecia due to the use Traction alopecia due to the use of tight curlersof tight curlers:

Traction alopecia secondary to braidingTraction alopecia secondary to braiding::

Hot-comb alopecia: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 alopeciathree distinct forms recognized-MPAA,

FPAA, diffuse AACaucasians most commonly affectedMore in males than femalesIn women, more common post menopausalmode of inheritance unclearpresence of androgens (esp. DHT) essentialmechanism 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 AreataAnagen EffluviumTelogen 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 transplantationminigrafts and micrograftsscalp reductionextensive scalp reductiontissue expansiontransposition 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.

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 syndromeStressful 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 (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 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 scalpAlopecia 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 anagen-phase 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

DermoscopyPresence 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 male-pattern hair loss, yellow dots are not seen in cases of female-pattern hair loss, scaring alopecia, or telogen effluvium

DIFFERENTIALS

Androgenetic AlopeciaPseudopelade, BrocqTelogen EffluviumTinea CapitisTrichotillomania

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 .

CORTICOSTEROIDSIntralesional 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

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

(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 excess androgens (female) or increased sensitivity to antigens (males).

Minoxidil, finasteride, androgen receptor antagonists beneficial

Surgery beneficialAlopecia areata basically auto-immune.Immunosupressants/ Immunomodulatory tx

mainstay.Surgery of little benefit.Counselling essential