NON-CICATRICIAL AlOPECIA

BY: MOHAMMED ALSAIDAN

APPROACH

Approach

History• Duration• Pattern• Thinning vs. shedding (hair root? Breaking?)• FH• Hair care products • Systemic disease, e.g. thyroid • Heavy mestruation, menstrual irregularity• Child birth, surgery, stress• New medication ? When was started?• Diet : caloric intake

Approach

Examination • Distribution • Hair line ?• Signs of Androgenism • Inflammation ? Scale ?• Scarring ?• TESTS TO ASSES HAIR

How to assess the quantity of hair lost ?

Assessment

• Daily hair counts• Hair pull test • Hair wash• 60 second hair count• Hair pluck trichogram• Global photography• Dermoscopy • Contrasting felt examination

Hair pull test

• Scalp: 100 000 hair follicle• Telogen normally=10% (10 000)• Average of daily lost hair =10 000/100day= 100• Some studies are estimating normality as (10-250) ?

• 20-60 hairs are grasped between the thumb, index and middle fingers from the base of the hairs near the scalp and firmly, but not forcefully, pulled away from the scalp.

• >10% hairs are pulled away implies active hair shedding.

• The patient must not shampoo for at least 24h.

Hair wash

• Washing hair in closed sink after 5 days of no wash then count hair

• Hairs counted and divided into ≤3cm and ≥5 cm in length.

• The 'modified hair wash test' demonstrates that in FAGA 58.9% of hair is vellus, whereas in chronic telogen effluvium (CTE), there are only 3.5%

60 second hair count

• Before shompooing, comb hair for 60 second over a pillow or white sheet

• Start combing from back top of the scalp moving to front and count hair

• Repeat it before 3 consequetive shampooing, e.g. every 2nd or 3rd day using the same comb or brush

• Repeat it monthly

Hair pluck trichogram

• 50 hair pulled with a hemostat covered with rubber, along the angel of insertion, on the fifth day after the last shampoo

• The hair is cut about 1 cm from the root, placed on a wet-mount microscope slide & viewed at 10X

• DACA (4-dimethylaminocinnamaldehye) reacts with an internal root sheath amino acid allowing differentiation of anagen from telogen hairs. (+ve in anagen)

Trichogram - 50-80 hairs are grasped with a hemostat covered with rubber and are plucked, twisting and lifting the hair shafts rapidly in the direction of emergence from the scalp

Preparing the trichogram slide - the plucked hairs are arranged side by side on a glass slide and taped

Anagen hair - showing the darkly pigmented triangular or delta-shaped bulbs with an angle to the hair shaft ('hockey-stick' appearance) and presence of inner root sheath

early telogen hair showing the hypopigmented, club-shaped bulb with absence of inner root sheath

A Telogen fibers showing a club shape .B Anagen fibers with attached root sheaths, demonstrating pigmented, distorted bulbs appearing

like the end of broom sticks .C Ruffled cuticle of loose anagen hair

Global Photography

• a stereotactic positioning device (with a camera and flash) on which the patient's chin and forehead are fixed

• To ensure that the view, magnification and lighting are the same at consecutive study visits.

• ask patients to keep the same hair style and color

• Four standard views (vertex, midline, frontal and temporal) are advocated

CONTRASTING FELT EXAMINATION

• After making a parting in the hair, the index card is held along the scalp

• miniature hairs can be seen in patients with androgenetic alopecia.

• In a regrowing telogen effluvium, a classic short frontal fringe is seen

Approach

Labs:• TSH, ferritin +/- (vit.D , Zinc, ESR)• Hormonal essay if needed ( free testosterone + DHEAS)• ANA • Skin Biopsy if needed

Male/Female Pattern Hair Loss (AGA)

• The most common cause of hair loss , age related, men >women

• Almost all caucasian men show recession of hair line after puberty

• by age 70, 80% of Caucasian men, 40% of women show evidence of AGA

• Association with CAD, DM, HTN ??

Etiology

• Testosterone: • presence of terminal pubic and axillary hair fibers• increased muscle mass• growth of the phallus and scrotum• voice change, sex drive

• DHT :• temporal scalp hair recession• development of terminal hairs in the beard region, external ears,

nostrils, and limbs• acne• growth of the prostate gland

Etiology

• Polygenic

• Miniaturization is the hallmark of AGA

• Vellus hairs may be present in large amounts prior to permanent shedding

• 5α-reductase activity and DHT levels are increased compared to non-balding scalp skin , once low -> reversal of AGA

• Absence of type II 5α-reductase prevents development of male androgenetic alopecia

Clinical features

• Symmetrical and prgressive

• Pattern : Hamilton, Norwood, ludweg

• Men: Recession of frontal hair line + balding of vertex

• Female: involving crown and frontal scalp, maintaining hair line

• Signs of androgenisim ?

Ludwig grade I : minimal widening of the part widthLudwig grade II : with moderate thinningLudwig grade III :with significant thinning and widening of the part width

Ludwig scale

Ludwig 1-1The central parting of a woman with no hair loss.

Ludwig 1-2 1-3 1-4The width of the parting gets progressively wider indicating thinner hair along the center of scalp.

Ludwig 2-1 2-2Diffuse thinning of the hair over the top of the scalp.

Ludwig 3A woman with extensive diffuse hair loss on top of the scalp, but

some hair does survive .

Ludwig scale

Ludwig AdvancedA woman with extensive hair loss and little to no surviving hair in the alopecia affected area. Very few women ever reach this stage and if they do it is usually because they have a condition that causes significant, abnormally excessive androgen hormone production.

Ludwig FrontalA woman with a pattern of hair loss that is described as "frontally accentuated". That means there is more hair loss at the front and center of the hair parting instead of just in the top middle of the scalp

Differential diagnosis

• FPHL vs TE ?

• FPHL + TE ?

• FPHL + AA

• Hyperandrogenism ?

Telogen effluvium

• TE is the most common form of hair loss seen in association with systemic disease

• begins approximately 3 months after an event, Thinning of the hair involving the entire scalp

• chronic TE (> 6 months) affects women between the ages of 30 and 60 years without any precipitating cause and is a diagnosis of exclusion

• Telgen >15% presumptive, >20% diagnostic (kligman ?)

Medical treatment of androgenetic alopecia in men–finasteride (n = 219) versus placebo (n = 15) five-year clinical trial. The figure shows the mean difference in hair

count after 5 years (p<0.001) .

Treatment:

• (hairDX test): CAG repeat score• A smaller CAG test score is associated with• higher risk for significant hair loss • increased response to Finasteride • increased risk of developing BPH

Trichotellomania

• Usually present in early childhood to adolescence.

• The most frequent site of hair pulling is the scalp

• grouped under the ‘impulse-control disorders not elsewhere classified causing clinically significant distress or impairment'’

Trichotellomania

• patchy or full alopecia of the scalp, centrifugal or wave like pattern, hairs in the occiput tend to be spared

• bizarre shapes, irregular borders, and contain hairs of varying lengths and hair shaft fractures

• ‘hair growth window’ by repeatedly (weekly) shaving a small area of involved scalp to demonstrate normal, dense regrowth, will support the diagnosis

Trichotellomania

• The differential diagnosis includes tinea capitis and alopecia areata

• Histopathology: Trichomalacia and pigment casts

• No specific treatment

• Hypnosis, behavioral modification therapy.

• The recommended first-line medication is clomipramine or (SSRI)

• N-actyl-cysteine ?

Temporal Triangular Alopecia

• Could be congenital or acquired during the first decade of life then persist for life.

• rarely, occur outside the temporal area

• Lesions appear hairless, but very fine vellus hairs can be seen with magnification.

Temporal Triangular Alopecia

• The lancet-shaped lesions are a few centimeters in width, may be unilateral or bilateral, and are oriented so that that the tip of the ‘lancet’ points superiorly and posteriorly.

• Hair transplant can help

Lipedematous Alopecia (Lipedematous Scalp)

• thick boggy scalp and hair

• primarily in women with darkly pigmented skin.

• doubling of scalp thickness as a result of edema and subsequent expansion of the subcutaneous fat layer.

• in scalp biopsy specimens, follicular structures appear normal but ectatic lymphatic vessels are sometimes found

Postoperative (Pressure-Induced) Alopecia• in patients who have undergone lengthy surgical procedures,

usually the upper occiput.

• Less commonly, 2ry to blunt trauma to the scalp.

• Early on, erythema and induration are found in the central portion of the affected area.

• Few weeks later typically presents as a solitary, oval patch

• Usually, complete hair regrowth occurs, although ( cicatricial) hair loss have been reported.

Alopeia areata

BY: MOHAMMED ALSAIDAN

Alopecia areata

• Alopecia areata affects all age groups and different ethnicities, with equal sex distribution

• occur in 0.1% to 0.2 % of the general population

Clinical features

• Classic AA lesions are well demarcated, round or oval, completely bald, smooth-surfaced patches

• Patches can be mildly reddened or peachy in color

• A characteristic finding that is frequently seen in (or at the border of) the patches is ‘‘exclamation mark hairs.’’

• hair pull test may be positive at the periphery of lesions

• Initial sparing of white hairs in patients with graying hair

Pattern

• ophiasis type, band-like hair loss in parieto-temporo-occipital area

• Ophiasis inversus (sisapho), very rare band-like hair loss in the fronto-parieto-temporal area

• Reticular patches of hair loss

• diffuse thinning over part or all of the scalp.

• Acute diffuse and total alopecia: rapid progression and extensive involvement, along with a favorable prognosis

DDx

• Trichotillomania and tinea capitis are the most important differential diagnoses in children

• Lupus , secondary syphilis and congenital atrichia

• diffuse AA can be easily misdiagnosed as telogen effluvium

Prognosis

• the most important prognostic factor is the extent of AA involvement or an ophiasis pattern

• Other factors: long duration , atopy, a positive family history, other autoimmune diseases, nail involvement, and young age of first onset

• Up to 50% of patients will recover within 1 year even without treatment

• Approximately 5% of cases will progress to AT/AU.

• In AT/AU, the chance of full recovery is less than 10%

Associations

• AA can be associated with nail changes in as many as 66% of patients

• Autoimmune diseases, particularly thyroiditis, are the most significant association (8% and 28%)

• Other associations include vitiligo, atopy, down syndrome, psychiatric and asymptomatic ophthalmologic changes 41%

• IDDM ?

Labs

• Routine testing is not indicated in AA

• Potassium hydroxide, fungal culture, lupus serology, syphilitic screening, and a scalp biopsy may be necessary

Pathology

• A peribulbar lymphocytic infiltrate ‘‘swarm of bees’’ characterizes the acute phase of AA

• In subacute cases, large numbers of catagen and telogen hairs will be present

• Hair follicle miniaturization with minimal or no inflammation is seen in chronic cases

Treatment:

INTRALESIONAL CORTICOSTEROIDS

• Intralesional corticosteroids are the treatment of choice for adults

• triamcinolone acetonide 5mg/mL to the scalp and 2.5mg/mL to the face every 4 to 6 weeks

• Treatment should be stopped if there is no improvement after 6 months

Treatment:

TOPICAL CORTICOSTEROIDS

• Topical midpotent corticosteroids are the treatment of choice in children

• The authors combine topical corticosteroids with minoxidil 5%

• Minoxidil 5% is mainly used as adjuvant treatment to conventional therapy

Treatment:

Anthralin

• Anthralin 0.5% to 1% short contact therapy is used as alternative treatment

• Mild irritation should develop in order for it to work

• Anthralin should not be combined with corticosteroids

• Treatment may be stopped if there is no improvement after 3 months

Treatment:

TOPICAL IMMUNOTHERAPY

• Diphenylcyclopropenone (DPCP) is the treatment of choice for adults with more than 50% scalp involvement

• Treatment should be stopped if there is no improvement after 6 months

• Squaric acid dibutylester is an alternative in patients who do not develop allergic reaction to DPCP (DNCP: MUTAGENIC)

• The success rate is 50% to 60%, with a relapse rate up to 62% at a median period of 2 and a half years

Initially, 2% DPCP in acetone is applied to a 4 -4-cm circular area of the scalp

Two weeks later, a 0.001% DPCP solution is applied to the same half of the scalp

The concentration of DPCP is increased gradually each week until a mild dermatitis reaction is

obtained .

The goal is to achieve a low-grade erythema and mild pruritus

DPCP should be left on the scalp for 48 hours, with sun avoidanceLag for evident clinical improvement 3-12 month

Treatment:

Capsaicin

• Capsaicin was previously shown to induce vellus hair regrowth in AA• More recently, a study showed that topical capsaicin and clobetasol

0.05% are comparable

Bexarotene

• In a single recently published study, bexarotene 1% gel resulted in a 26% hair regrowth rate

• Dermal irritation is a common side effect

Topical calcineurin inhibitors • failed to show hair regrowth in AA

Treatment:

Systemic corticosteroids

• Daily, weekly, and monthly pulse corticosteroids have been used with varying success

• The use of systemic corticosteroids is limited by their side effect profile and a higher rate of relapse

Treatment:

Cyclosporine

• Cyclosporine has been used alone or in conjunction

• with corticosteroids with a success rate up to 76.6%

• Cyclosporine use is limited by its side effects and high relapse rate

Treatment:

Sulfasalazine

• Sulfasalazine up to 1.5 g twice daily is successful in about quarter of the patients

• The relapse rate is 45.5%

• One in three patients may have side effects

Treatment:

Methotrexate• Methotrexate in conjunction with low-dose

prednisone showed success in 64% of patients with AT/AU in one study

Biologics• Several reports of multiple biologics, including

etanercept, efalizumab, adalimumab, and infliximab failed to show improvement in AA

Treatment:

Photochemotherapy

• Systemic and topical psoralen plus ultraviolet A light phototherapy have been used with limited success

• Long-term safety, side effects, and a high relapse rate have curtailed the use of psoralen plus ultraviolet A light phototherapy

Treatment:

Other phototherapies

• Excimer laser may be helpful in limited patchy AA

• Infrared irradiation as monotherapy or adjunctive to conventional therapy showed some success

Treatment:

Psychological support

Thank you