Alopecia

Alopecia classified into: Alopecia areata

▪ Non-cicatricial Alopecia : No clinical sign of tissue inflammation, scarring, or atrophy of skin . • A localized loss of hair in round or oval areas with no apparent inflammation of the skin. Most
▪ Cicatricial alopecia : Evidence of tissue destruction such as inflammation, atrophy, and scarring is apparent. common on scalp.
• Nonscarring; hair follicle intact; hair can regrow.
Classification of acquired alopecia • Clinical findings: Hair loss ranging from solitary patch to complete loss of all terminal hair.
Can occur globally or focally : ( Causes of hair loss ) • Prognosis: good for limited involvement. Poor for extensive hair loss.
• Management: intralesional triamcinolone effective for limited number of lesions.
Diffuse (global) hair loss
Non-scarring PATHOGENESIS DIFFERENTIAL DIAGNOSIS
1- Failure of follicle production • Chronic organ
organ-specific
specific autoimmune disease, Nonscarring Alopecia :
2- Hair shaft abnormality mediated by autoreactive T cells affecting hair • White-patch tinea capitis,
3- Abnormality of cycling (shedding) follicles and nails. • Trichotillomania,
• Telogen effluvium • Early scarring alopecia,
• Associated autoimmune disorders:
• Anagen effluvium • Pattern hair loss,
• Loose anagen syndrome Autoimmune thyroid disease in adults.
• Secondary
econdary syphilis (alopecia areolaris)
• Alopecia areata • Follicular damage occurs in anagen followed by (“moth-eaten”
eaten” appearance )
rapid transformation to catagen and to
Focal (patchy, localized) hair loss telogen
telogen; then to dystrophic anagen status.
status
LABORATORY EXAMINATIONS
Non-scarring Scarring (cicatricial) alopecia • Serology :
While the disease is active, follicles unable to
1- ANA (to rule out SLE);
3- Production decline : 1- Lymphocytic : progress beyond early anagen and do not
2- rapid plasma reagin (RPR) test (to rule
• Triangular alopecia • Chronical cutaneous (discoid) lupus erythematosus develop normal hair.
out secondary syphilis).
• Pattern hair loss (androgenetic alopecia) • Lichen planopilaris (LPP) CLINICAL MANIFESTATIONS • KOH Preparation: Rule out tinea capitis.
• Classic pseudopelade of Brocq
Age: Any age , but peak between 20 – 50 years • Dermatopathology :
4- Hair breakage : • Central centrifugal cicatricial alopecia
Acute lesions show :
•
Trichotillomania • Alopecia mucinosa Sex : affect both sexes.
•
- peribulbar, perivascular, and outer root
•
Traction alopecia Kertosis folliclaris spinulosa decalvans Duration of Hair Loss sheath mononuclear cell infiltrate of T cells
•
Infection (tinea capitis) Gradual over weeks to months. and macrophages;
•
Primary or acquired hair shaft abnormality 2- Neutrophilic :
• Folliculitis decalvans Skin Symptoms - follicular dystrophy
hy with abnormal
5- Unruly hair. • Dissecting folliculitis (cellulitis) Disfiguring bald patch. pigmentation and matrix degeneration.
MANAGEMENT
3- Mixed : Associated Findings No curative treatment is currently available.
6- Abnormality of cycling :
• • Autoimmune thyroiditis.
• Alopecia areata Folliculitis keloidalis Treatment for AA is unsatisfactory.
• Folliculitis necrotica • Down syndrome.
• Secondary
econdary syphilis (alopecia areolaris) Treatment directed at inflammatory infiltrate
(“moth-eaten”
eaten” appearance in beard or scalp). • Erosive pustular dermatosis • Autoimmune polyendocrinopathy
polyendocrinopathy-
and growth inhibitor factors produced by
candidiasis
candidiasis–ectodermal
ectodermal dysplasia syndrome.
inflammation.
4- Non-specific :
• Trauma.
Skin Findings
1- General measures :
• Chemical or physical burn. - Usually none.
• Psychological support ( very important ).
• Surgical wound - Possibly minimal erythema in area of hair loss.
• Persons with extensive scalp involvement
• Neoplasm (Basal cell carcinoma ,Squamous
, cell carcinoma) such as AAT may prefer
efer to wear a wig or
Hair
Scarring (cicatricial) alopecia Round patches of hair loss. hairpiece.
• Primary cicatricial alopecia (PCA) results from damage or destruction of the hair follicles stem cells by: • Single or multiple. May coalesce. • Makeup applied to eyebrows is helpful.
- Inflammatory (usually noninfectious) processes • It's often sharply defined. Eyebrows can be tattooed.
- Infection: e.g., “kerion” tinea capitis, necrotizing herpes zoster • Normal
Normal-appearing skin with follicular 2- Glucocorticoids
- Other pathologic processes: surgical scar, primary or metastatic neoplasm. openings present . • Glucocorticoids Topical :
• Manifestations: Effacement of follicular orifices in a patchy or focal distribution, usually in scalp or beard. • “Exclamation mark” hairs (Fig. 32-8) : Superpotent agents not usually effective.
• The end result is effacement of follicular orifices & replacement of the follicular structure by fibrous tissue. Diagnostic broken
broken- off stubby hairs • Intralesional Injection :
• Scarring is irreversible. Therapies are ineffective. (distal ends are broader than proximal ends) Few and small lesions of AA can be treated
TELOGEN EFFLUVIUM ANAGEN EFFLUVIUM seen at margins of hair loss areas. with intralesional triamcinolone acetonide,
• Telogen effluvium (TE) is the transient increased • Etiology: See below • Scattered, discr
discrete areas of alopecia (Fig. 32-9)
32
3–77 mg/mL, which can be very effecJve
shedding of normal club (telogen) hairs from resting
• Onset is usually rapid & extensive. or temporarily.
scalp follicles.
•
Confluent with total loss of scalp hair (Fig. 32--10), • Systemic Glucocorticoids :
• Secondary to accelerated shift of anagen (growth Pathogenesis: Occurs after any insult to hair
phase) into catagen and telogen (resting phase) follicle that impairs its mitotic/metabolic or May induce regrowth, but AA recurs on
• Results in increased daily hair loss and, if severe, activity. Rapid growth arrest or damage to generalized loss of body hair (including vellus hair). discontinuation; risks of long-term
term therapy
diffuse thinning of scalp hair. anagen hairs that skip catagen and telogen Diffuse AA of scalp (noncircumscribed) gives the therefore preclude their use.
phases and are shed. appearance of thinned hair; can be difficult to
Etiology: differentiate from pattern hair loss of telogen
3- Systemic Cyclosporine
A reaction pattern to a variety of physical or mental • More common and severe with combination Induces regrowth, but AA recurs when drug is
effluvium, hair loss with thyroid disease.
stressors : chemotherapy than with the use of a single discontinued.
drug. Severity is generally dose dependent. • With regrowth of hair, new hairs are fine,
often white or gray. 4- Induction of Allergic Contact Dermatitis -
• Endocrine : • Manifestations: By Dinitrochlorobenzene ( DNCP ) , but local
1- Hypo- or hyperthyroidism ; Scalp hair : loss is diffuse, extensive; also: Sites of Predilection discomfort due to allergic contact dermatitis
2- postpartum ; eyebrows/lashes, beard, etc. - Scalp ( most commonly ) and swelling of regional lymph nodes poses a
3- discontinuation or changing type of estrogen Nails: show transverse banding or ridging. - Any hair
hair-bearing area : Beard, eyebrows, problem.
containing drugs • Regrowth is usually rapid after discontinuation eyelashes, pubic hair.
of Chemotherapy 5- Oral PUVA (Photochemotherapy)
Photochemotherapy) :
• Nutritional: • Alopecia areata (AA):
1- Deficiency: biotin, zinc, iron, essential fatty acid
Entire body must be exposed,
Solitary or multiple areas of hair loss.
in that the therapy is believed to be a form of
2- Rapid weight loss, Etiology: • AA totalis (AAT):
3- caloric or protein deprivation, systemic immune suppression.
Anagen cycle disrupted causing varying degrees Total loss of terminal scalp hair.
4- excessive vitamin A ingestion • AA universalis (AAU):
of hair follicle dystrophy : • Patchy alopecia :
• Physical stress : Total loss of all terminal body & scalp hair. o Intralesional corticosteroids :
• Radiation therapy to head . • Ophiasis:
1- Febrile illnesses, Up to 2 mL injected/session and repeated at
2- catabolic illnesses (e.g., malignancy, chronic • Alkylating agents: Bandlike pattern of hair loss over periphery intervals.
infection), busulfan, carboplatin, carmustine, BCNU, of scalp . o Potent topical steroid (1-2×/day).
2×/day).
3- major surgery, chlorambucil, cisplatin, dacarbazine, o Topical anthralin (0.1%-2.0%
2.0% once daily) :
4- major trauma, Nails Wash off after 10-20 20 min, steadily increase
estramustine, fotemustine,
fotemustine ifosamide,
5- acute or chronic psychological stress • Fine pitting (“hammered brass”) of dorsal contact duration, switch to higher dose if no
lomustine, mechlorethamine, nitrogen nail plate. significant irritation.
• Psychological stress : mustard, melphalan, oxaliplatin, procarbazine,
• mottled lunula, o Minoxidil loJon (5%) twice daily.
1- Anxiety, streptozocin, temozolomide, thiotepa.
• trachyonychia (rough nails), • Extensive or rapidly progressive alopecia.
2- depression, • onychomadesis (separation of nail from matrix). o Contact immunotherapy.
3- bipolar disorder • Intoxications:
o Systemic corticosteroids.
mercury, boric acid, thallium, colchicine. FIGURE 32-8
• Intoxication : Thallium, mercury, arsenic Solitary lesion
Benefits are uncertain and must be weighed
against risk of systemic corticosteroid therapy.
• Drugs : • Severe protein malnutrition. o Wig or hairpiece.
1- Antimitotic agents (dose dependent): cancer • Alopecia totalis/universalis
The short, broken-off hair
shafts (so-called
called exclamation
chemotherapy, benzimidazoles. o Contact immunotherapy.
point hair) appear as very
2- Antihypertensives: captopril short stubs emerging from the o Topical/systemic steroids.
3- Anticoagulants bald scalp.
o Wig or hairpiece.
4- CNS drugs: lithium, valproic acid
FIGURE 32-9
5- Cholesterol-lowering
lowering drugs multiple, extensive lesions
6- Colchicine COURSE
7- Cytostatic drugs Multiple, confluent, involved
sites on the scalp with
• Spontaneous remission is common in patchy AA
8- Interferon “exclamation point hairs.” but is less so with AAT or AAU.
9- Penicillamine • Poor prognosis associated with onset in
10- Retinoids: vitamin A excess, retinoids childhood, loss of body hair, nail involvement,
(isotretinoin, acitretin, indinavir) atopy, family history of AA.
11- Selective serotonin reuptake inhibitors • If occurring aMer puberty, 80% regrow hair. With
12- Inflammatory scalp disease: Seborrheic FIGURE 32-10 extensive AA, AAT, AAU, <10% recover
dermatitis, erythroderma AA totalis spontaneously.
• Idiopathic : • Recurrences of AA, however,, are frequent.
freq
No obvious cause is apparentt in a sign
significant number • Systemic glucocorticoids or cyclospor
yclosporine can induce
of cases. remission of AA but do not alter the course.