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Chapter 21. Alopecia
Acne
Keloidalis
Cellulitis
Scarring
(Cicatricial)
Dissecting
CCCA
Lupus
Discoid
429
Alopecia
(MPHL)
Hair Loss
Male Pattern
Female
Pattern Hair
Loss (FPHL)
Anagen
Effluvium
Non-Scarring
(Non-cicatricial)
Diffuse Pattern (Androgenetic) Lymphocytic Neutrophillic Mixed
Telogen
Effluvium
Focal
Traction Tr ichotillomania
Areata
Alopecia
F . Hair loss algorithm
430
C. Barranco and K. Krishnamurthy
telogen effluvium and anagen effluvium. Patterned alopecia, also known as androgenetic, includes female pattern hair loss and male pattern hair loss.

Decision-Making/Differential Diagnosis

The first step to assessing hair loss is to determine whether a scarring or non-scarring process is occurring. Generally speaking, scarring alopecia includes forms of alopecia where the hair follicles are permanently lost. Some alopecias, includ­ing alopecia areata, androgenetic alopecia, and traction alo­pecia, may demonstrate a non-scarring process early in the disease course and permanent hair loss in later stages.

Non-scarring Alopecias

Androgenetic Alopecia
(Synonyms: Male Pattern and Female Pattern Hair Loss [MPHL and FPHL], Common Balding, Hereditary Balding or Thinning)
Androgenetic alopecia represents the most common sub-
type of the non-scarring alopecias and in fact is the most common cause of hair loss overall. It is due to a genetically determined sensitivity to androgens of the scalp hair follicles [1]. It can begin any time after puberty, when androgens begin to be synthesized [3, 4].
Features:
• Gradual thinning without noticeable shedding.
• Strong genetic disposition, with a high concordance among monozygotic twins.
• Male pattern hair loss: symmetric and progressive, typi­cally affecting the frontoparietal area with frontal reces­sion as well as vertex thinning (Fig.21.2).
Chapter 21. Alopecia
F . Classic pattern of androgenetic alopecia in a male involving the bitemporal and crown of the scalp [5]
431
• Female pattern hair loss: diffuse central thinning of the crown with preservation of the frontal hairline. A “Christmas tree” pattern results with widening of the cen­tral part width (Fig.21.3).
• Treatment options include antiandrogenic medications (Table21.1).
Focal Hair Loss
Alopecia Areata. This is usually a hair-specific autoimmune
phenomenon in which T-cells interact with follicular antigens. It is characterized by abrupt onset usually before the second decade [2]. Alopecia areata can be associated with other
C. Barranco and K. Krishnamurthy
432
F . Classic “Christmas tree” pattern seen in androgenetic alopecia in a female [5]
T . Non-scarring alopecia treatment Androgenetic alopecia
• Minoxidil 5% topical solution (1mL BID)
• Finasteride 1mg/day × at least 3months (with oral contraceptives)
• Spironolactone 100–200mg/day
• Surgical hair transplant
Chapter 21. Alopecia
T . (continued)
Alopecia areata • Intralesional steroid 2.5–5mg/mL (0.5–1- cm
intervals)
• Topical clobetasol propionate 0.05%
ointment, desoximetasone 0.25% cream, or betamethasone valerate foam BID
• Diphencyprone (DCP) and squaric acid dibutyl ester (SADBE): 0.001% for 2weeks and gradually increase weekly over time (0.01%, 0.1%, 0.2%, 0.5%, 1%, and 2%)
• Topical minoxidil
• Topical anthralin
• Systemic corticosteroids (for totalis or universalis): 40mg triamcinolone IM monthly or daily oral prednisone tapered over 6–8weeks
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Trichotillomania
Telogen effluvium
Scarring alopecia treatment
Discoid lupus Erythematosus
Central centrifugal Cicatricial alopecia
Dissecting cellulitis
Acne keloidalis
• Behavioral modification therapy, hypnosis, insight-oriented therapy
• Clomipramine 25mg daily, gradually increase to 100mg/day (divided with meals) over 2weeks
• Treat underlying thyroid or iron deficiency
• Reassurance
• Oral hydroxychloroquine.
• Topical, oral, or intralesional corticosteroids.
• Combination of doxycycline or minocycline + topical clobetasol or fluocinonide.
• Oral isotretinoin (0.5–1.5mg/kg daily until 4months after achieving a clinical remission).
• Doxycycline+potent topical corticosteroids.
434
cd
C. Barranco and K. Krishnamurthy
ab
ef
F . Clinical variants of alopecia areata (AA). (a) Classic round patch of hair loss seen in alopecia areata. (b) Multiple round patches of hair loss. (c) Reticulate pattern of AA. (d) Ophiasis pat­tern: band- like loss of hair across the temporal and occipital scalp. (e) Sisaipho pattern. (f) Alopecia universalis [7]
autoimmune diseases, including Hashimoto’s thyroiditis, vit­iligo, inflammatory bowel disease, and type I diabetes [6] (Fig.21.4).
Features:
• Typically presents as discrete bare patches of hair loss, in a patchy or multifocal distribution.
• Other presentations include:
• Alopecia totalis: loss of all scalp hair.
• Alopecia universalis: loss of all scalp and body hair.
• Ophiasis pattern: band-like pattern of hair loss that occurs along the periphery of the temporal and occipital scalp.
• Alopecia involving the beard area.
• Multiple treatment options are available, including but not limited to corticosteroids, topical immunotherapy (SADBE, Table21.1), excimer laser therapy.
Traction Alopecia. Occurs due to physical stress on the
hair follicle secondary to tight hairstyles, including ponytails, braids, and hair weaves:
• Hair thinning mainly noted along the marginal hairline— frontally, temporally, and occipitally [2]
• Mostly affects African Americans.
Chapter 21. Alopecia
Trichotillomania. Can have various presentations, but
there will be rough, irregular patches of hair loss with broken or twisted hairs on closer examination. It is a result of inten­tional pulling of hair from the scalp [1]:
• Onset in childhood and more commonly seen in females (4:1 ratio) [8].
• Grouped with DSM IV OCD disorders.
• Patients may pull hairs out from other hair-bearing areas such as the eyebrows, eyelashes, face, extremities, and pubic area.
• Treatment options include behavioral modification and clomipramine [1, 9] (Table21.1).
435

Diffuse Hair Loss

1. Telogen Efuvium. Patients experience excessive hair shedding over the entire scalp:
• Often preceded by a physical or emotional stressor
approximately 3 months prior to the start of the hair loss.
• Acute telogen effluvium, <3-months duration; chronic
telogen effluvium, >6-months duration.
• Causes include severe infections, postsurgical, postpar-
tum, hypothyroidism, anemia, malnutrition, and drugs (especially beta-blockers) [10].
• In many instances, a discernible precipitating cause can-
not be found. Chronic telogen effluvium may be a pre­cursor to patterned hair loss.
2. Anagen Efuvium. Abrupt and striking loss of hair (90% of hairs are in anagen phase):
• It typically is caused by chemotherapy.
• Occurs within days to weeks of initiation and is entirely
reversible.
• Hair regrowth typically occurs after a delay of
3–6months.
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C. Barranco and K. Krishnamurthy

Scarring Alopecia

Generally refers to all forms of alopecia in which there is permanent loss of hair follicles. Clinically, one will observe a smooth scalp with absence of follicular ostia and replacement with scar tissue. Patients may experience symptoms, including pain, itching, erythema, and burning sensations. This occurs as a result of continued inflammation that targets the follicle. Histopathologic correlation is often needed. As such, the classification scheme is typically divided into the type of inflammatory infiltrate involved: lymphocytic, neutrophilic, or mixed [2] (Fig.21.1).
Lymphocytic
Central Centrifugal Cicatricial Alopecia (CCCA) (Fig.21.5)
• A chronic, progressive disease with eventual spontaneous burnout.
• Alopecia centered on the crown or vertex and expands peripherally in a symmetric fashion.
• It is found almost exclusively in African Americans.
• Early and mild disease can be effectively treated. Long­acting oral tetracycline and topical corticosteroid can usu­ally halt progression (Table21.1).
Discoid lupus erythematosus. A form of cutaneous lupus
erythematosus that occurs most commonly on the face, ears, and scalp (Fig.21.6):
• Discoid lesions usually demonstrate erythema, epidermal atrophy, and dilated, plugged follicular ostia.
• Central hypopigmentation with peripheral hyperpigmen­tation is evident in dark-skinned individuals.
• Patients typically do not have systemic disease.
• Diagnosis requires biopsy.
Chapter 21. Alopecia
437
F . Central centrifugal cicatricial alopecia. Characteris­tic central scarring alopecia that will eventually expand centrifu­gally [11]
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C. Barranco and K. Krishnamurthy
F . (a) Figure A demonstrates a fibrotic plaque with peripheral hyperpigmentation and central hypopigmentation, which are classic findings in the scarring alopecia of discoid lupus. (b) Enhanced view of a scarring alopecic plaque of discoid lupus show­ing loss of hair follicles centrally, follicular keratotic plugging, and central hypopigmentation with peripheral hyperpigmentation [12]
Mixed Neutrophilic andLymphocytic
Acne Keloidalis
• Presents with small, firm papules and pustules on the occipital scalp and posterior neck.
• Usually affects young African American men and occa­sionally women and rarely will be seen in Caucasians.
• Often seen in conjunction with CCCA, but the cause remains uncertain.
Neutrophilic
Dissecting cellulitis. Involves multiple, firm scalp nodules
most often on the mid-posterior vertex and upper occiput:
• A part of the “follicular occlusion triad.”
• It most often affects young adult black men.
• Over time, the nodules become boggy, fluctuant, and inter­connected and will discharge purulent material.
1
Group of disorders in which the hair follicle becomes blocked with keratin, including hidradenitis suppurativa, acne conglobata, and dissect­ing cellulitis.
1