Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, Seventh Edition


Disorders of Hair Follicles and Related Disorders


Image Human hair has little vestigial function:

Image Contributes to a psychological perception of beauty and attractiveness.

Image Tactile sensation.

Image Protects the scalp, face, and neck from UV solar radiation.

Image Reduces heat loss through the scalp.

Image Psychology of hair: Alteration of the “normal” quantity of hair is often associated with profound psychological impact. Loss of scalp hair is considered abnormal in many societies, associating balding with old age (pattern hair loss) or impaired health (chemotherapy).

Image Excess hair on the face (hirsutism, hypertrichosis) and extremities of women is often considered unattractive.

Biology of Hair Growth Cycles

Glossary of Terms

Hair Follicle Cycle

The hair follicle undergoes life-long cyclic transformations into three primary phases: anagen, catagen, and telogen (Fig. 31-1).


Figure 31-1. Hair growth cycle Diagrammatic representation of the changes that occur to the follicle and hair shaft during the hair growth cycle. (A) Anagen (growth stage); (B) Catagen (degenerative stage); (C) Telogen (resting stage). (Courtesy of Lynn M. Klein, MD.)

Anagen. Growth phase; lasts variable periods of time depending on body site and age; determines the ultimate length of hair at a site. Anagen hair matrix has rapidly proliferating epithelial cells and is exquisitely sensitive to drugs, growth factors, hormones, stress, and immunologic and physical injury. Destruction of epithelial stem cells results in permanent hair loss. Anagen hairs have pigmented malleable proximal ends (Fig. 31-2A). About 85-99% of hairs will be in this phase, with some individual variation.


Figure 31-2. Hair mount (A) Anagen: note the malleable proximal ends and (B) Telogen: club hairs. [From Goldsmith LA et al. (eds.). Fitzpatrick’s Dermatology in General Medicine, 8th edition. New York: McGraw-Hill, 2012.]

Telogen. Period of relative quiescence, prior to shedding. Telogen hairs are club hairs with depigmented rounded proximal ends (Fig. 31-2B). About 1-15% of hairs are in this phase at any given time.

Catagen. Apoptosis-driven phase between telogen and anagen phase. Duration: few weeks. Only about 1% of hairs are seen in this phase.

Exogen. Active process of hair shaft shedding.

Types of Hair

Lanugo Hair. Soft fine pigmented hair that covers much of fetus; usually shed before birth.

Vellus Hair. Fine, nonpigmented hair; growth not affected by hormones. Genetically determined to produce very small (but functionally fully active cycling) hair follicles located in the dermis.

Terminal Hair. Thick, pigmented hair found on scalp, beard, axillae, pubic area; growth is influenced by hormones. Eyebrow/eyelash hairs are terminal hairs. Produced by large hair follicles located in the subcutis.

Laboratory Examinations

Hair Pull. Scalp is gently pulled. Normally, three to five hairs are dislodged; shedding more hair suggests pathology.

Trichogram. Determines the number of anagen and telogen hairs and is made by epilating (plucking) 50 hairs or more from the scalp with a needle holder and counting the number of anagen and telogen hairs.

Scalp Biopsy. Offers insight into pathogenesis of alopecia.

Hair Loss: Alopecia ICD-9: 704.0 image ICD-10: L63-L66

Image Shedding of hair is termed effluvium or defluvium, and the resulting condition is called alopecia (Greek alópekia, “baldness").

Image Individuals are often aware of and very concerned about subtle thinning of the hair.

Image Alopecia classified into:

Image Noncicatricial alopecia: No clinical sign of tissue inflammation, scarring, or atrophy of skin.

Image Cicatricial alopecia: Evidence of tissue destruction such as inflammation, atrophy, and scarring may be apparent.

Nonscarring Alopecia (Table 31-1)



Pattern Hair Loss Image

Image Pattern hair loss is the most common type of progressive balding.

Image Occurs through the combined effect of:

Image Genetic predisposition

Image Action of androgen on scalp hair follicles

Image In males, pattern/extent of hair loss varies from bitemporal recession, to frontal and/or vertex thinning, to loss of all hair except that along the occipital and temporal margins ("Hippocratic wreath").

Image Synonyms: Males: Androgenetic alopecia (AGA), male-pattern baldness, common baldness. Females: Hereditary thinning, female-pattern baldness.

Etiology and Epidemiology

Etiology. Combined effects of androgen on genetically predisposed hair follicles. Genetics: (1) autosomal dominant and/or polygenic; (2) inherited from either or both parents.

Age of Onset

• Men: May begin any time after puberty, as early as the second decade; often fully expressed in 40s.

• Women: Later—in about 40% occurs in the sixth decade.

Sex. Men >> women.


Hamilton classified male-pattern hair loss into stages (Fig. 31-3 A):


Figure 31-3. Androgenetic alopecia: patterns in men and women (A) Hamilton classified the severity and pattern of hair loss in men into types I to V. (B) Ludwig classified hair loss in women into types I to III.

Type I: Loss of hair along frontal margin.

Type II: Increasing frontal hair loss as well as onset of loss of occipital (vertex or crown).

Types III, IV, and V: Increasing hair loss in both regions with eventual confluent and complete balding of top of scalp with sparing of sides.

Ludwig classified hair loss in women (Fig. 31-3B).


• Dihydrotestosterone causes growth of the prostate, growth of terminal hair, AGA, and acne.

• Testosterone causes growth of axillary hair and lower pubic hair, as well as sex drive, growth of the phallus and scrotum, and spermatogenesis.

• Testosterone is converted to (DHT) by 5α-reductase (5α-R). Two isozymes of 5α-R occur: type I and type II.

• Type I 5α-R is localized to sebaceous glands (face, scalp), chest/back skin/liver, adrenal gland, kidney.

• Type II 5α-R is localized to scalp hair follicle, beard, chest skin, liver, seminal vesicle, prostate, epididymis, and foreskin/scrotum.

• Finasteride inhibits conversion of testosterone to DHT by type II 5α-R.

Clinical Manifestation

Skin Symptoms. Most patients present with complaints of gradually thinning hair or baldness.

Skin Findings. Scalp skin is normal.

• In young women, look for signs of virilization (acne, excess facial or body hair, male-pattern escutcheon).

• With advanced pattern hair loss, scalp is smooth and shiny; orifices of follicles are barely perceptible with the unaided eye.

Hair (Fig. 31-4 to 31-7). Hair in areas of pattern hair loss becomes finer in texture (shorter in length, reduced diameter). In time, hair becomes vellus and eventually atrophies completely.


Figure 31-4. Pattern hair loss: male, Hamilton type III A 46-year-old male with bitemporal recession of hairline and frontal thinning of hair.


Figure 31-5. Pattern hair loss: male, Hamilton types IV to V A 37-year-old male with loss of hair in the frontotemporal and vertex areas in a male corresponding to Hamilton types IV and V.


Figure 31-6. Pattern hair loss: female, Ludwig type II A 66-year-old female with diffuse thinning of hair on the crown.


Figure 31-7. Pattern hair loss: female, Lugwig type III with basal cell carcinoma (BCC) A 67-year-old Greek female with advanced alopecia of the crown with BCC arising within it.


• Men usually exhibit patterned loss in the frontotemporal and vertex areas (Figs. 31-4 and 31-5). The end result may be only a rim of residual hair on the lateral and posterior scalp. In these regions, hair never falls out in pattern hair loss. Paradoxically, men with extensive pattern hair loss may have excess growth of secondary sexual hair, i.e., axillae, pubic area, chest, and beard.

• Women, including those who are endocrinologically normal, also lose scalp hair according to the male pattern, but hair loss is far less pronounced. Often hair loss is more diffuse in women, following the pattern described by Ludwig (Fig. 31-3B).

Systemic Findings. In young women with AGA, look for signs of virilization (clitoral hypertrophy, acne, facial hirsutism) and, if present, rule out endocrine dysfunction. However, most women with pattern hair loss are endocrinologically normal.

Differential Diagnosis

Diffuse Nonscarring Scalp Alopecia. Diffuse pattern of hair loss with alopecia areata, telogen defluvium, secondary syphilis, systemic lupus erythematosus (SLE), iron deficiency, hypothyroidism, hyperthyroidism, trichotillomania (pulling of one’s own hair, compulsive), seborrheic dermatitis.

Laboratory Examinations

Trichogram. In pattern hair loss, the earliest changes are an increase in the percentage of telogen hairs.

Dermatopathology. Abundance of telogenstage follicles is noted, associated with hair follicles of decreasing size and eventually nearly complete atrophy.

Hormone Studies. In women with hair loss and evidence of increased androgens (menstrual irregularities, infertility, hirsutism, severe cystic acne, virilization), determine the following:

• Testosterone: total and free.

• Dehydroepiandrosterone sulfate (DHEAS).

• Prolactin.

Other Studies. Treatable causes of thinning hair should be excluded with measurement of thyroid-stimulating hormone (TSH), T4, serum iron, serum ferritin, and/or total iron-binding capacity, complete blood count, antinuclear antibodies (ANA).


Clinical diagnosis is made on the history, pattern of alopecia, and family incidence of AGA. Skin biopsy may be necessary in some cases.


The progression of alopecia is usually very gradual, over years to decades.


Oral Finasteride. 1 mg po daily. Finasteride has no affinity for androgen receptors and therefore does not block other actions of testosterone (growth of the phallus and scrotum, spermatogenesis, libido). Most men who respond may begin to see benefit in slowing hair loss as early as 3 months. After 6 months, there is a regrowth of terminal hair on the vertex and anterior mid-scalp. If the drug is stopped, however, the hair that had grown will be lost within 12 months. Two percent of men taking finasteride report decrease in libido and erectile function; these effects were reversible when the drug was stopped and disappeared in two-thirds of those who continued taking finasteride.

Topical Minoxidil. Topically applied minoxidil, 2% and 5% solution, may be helpful in reducing the rate of hair loss or in partially restoring lost hair in both men and women.

Antiandrogens. In women with AGA who have elevated adrenal androgens, spironolactone, cyproterone acetate, flutamide, and cimetidine bind to androgen receptors and block the action of DHT. These must not be used in men.

Hairpiece. Wigs, toupees, prosthetics; hair weaves.

Surgical Treatment

Hair transplantation: Grafts of one or two follicles are taken from androgen-insensitive hair sites (peripheral occipital and parietal hairy areas) to bald androgen-sensitive scalp areas. Scalp reduction/rotation flaps.

Alopecia Areata Image

Image A localized loss of hair in round or oval areas with no apparent inflammation of the skin.

Image Nonscarring; hair follicle intact; hair can regrow.

Image Clinical findings: Hair loss ranging from solitary patch to complete loss of all terminal hair.

Image Prognosis: good for limited involvement. Poor for extensive hair loss.

Image Management: intralesional triamcinolone effective for limited number of lesions.


Etiology and Epidemiology

Etiology. Unknown. Association with other autoimmune diseases and immunophenotyping of lymphocytic infiltrate around hair bulbs suggests an anti-hair bulb autoimmune process; 10-20% of persons with alopecia areata (AA) have a familial history of AA.

Age of Onset. Young adults (<25 years); children are affected more frequently. Can occur at any age.

Prevalence. Relatively common; 1.7% of the US population experiences at least one episode of AA in a lifetime. Varies with geography and ethnicity.


• Chronic organ-specific autoimmune disease, mediated by autoreactive T cells affecting hair follicles and nails.

• Follicular damage occurs in anagen followed by rapid transformation to catagen and to telogen; then to dystrophic anagen status. While the disease is active, follicles are unable to progress beyond early anagen and do not develop normal hair.

• Follicular stem cell is spared; hair follicles are not destroyed (there is no scarring).

Clinical Manifestations

Duration of Hair Loss. Gradual over weeks to months. Patches of AA can be stable and often show spontaneous regrowth over a period of several months; new patches may appear while others resolve.

Associated Findings. Autoimmune thyroiditis. Down syndrome. Autoimmune polyendo-crinopathy-candidiasis-ectodermal dysplasia syndrome.


• Round patches of hair loss. Single or multiple. May coalesce. Alopecia often sharply defined with normal-appearing skin with follicular openings present (Figs. 31-8 through 31-10).

• “Exclamation mark” hairs. Diagnostic broken-off stubby hairs (distal ends are broader than proximal ends) (Fig. 31-8); seen at margins of hair loss areas.


Figure 31-8. Alopecia areata (AA) of scalp: solitary lesion An area of alopecia without scaling, erythema, atrophy, or scarring on the occipital scalp. The short, broken-off hair shafts (so-called exclamation point hair) appear as very short stubs emerging from the bald scalp.

• Scattered, discrete areas of alopecia (Fig. 31-9) or confluent with total loss of scalp hair (Fig. 31-10), or generalized loss of body hair (including vellus hair).


Figure 31-9. Alopecia areata of scalp: multiple, extensive lesions A 46-year-old male with multiple, confluent patches of alopecia areata.


Figure 31-10. Alopecia areata universalis (AAU) This patient has lost all scalp hair (alopecia totalis), eyebrows, eyelashes, beard, and all body hair (alopecia universalis) and has dystrophic ("hammered brass") nails.

• Diffuse AA of scalp (noncircumscribed) gives the appearance of thinned hair; can be difficult to differentiate from telogen effluvium (TE) or hair loss with thyroid disease.

• With regrowth of hair, new hairs are fine, often white or gray.

Sites of Predilection. Scalp most commonly. Any hair-bearing area. Beard, eyebrows, eyelashes, pubic hair.

• Alopecia arcata (AA): Solitary or multiple areas of hair loss (Figs. 31-8 and 31-9).

• AA totalis (AAT): Total loss of terminal scalp hair.

• AA universalis (AAU): Total loss of all terminal body and scalp hair (Fig. 31-10).

• Ophiasis: Bandlike pattern of hair loss over periphery of scalp.

Nails. Fine pitting ("hammered brass") of dorsal nail plate. Also: mottled lunula, trachyonychia (rough nails), onychomadesis (separation of nail from matrix) (see also Section 32).

Differential Diagnosis

Nonscarring Alopecia. White-patch tinea capitis, trichotillomania, early scarring alopecia, pattern hair loss, secondary syphilis (alopecia areolaris) ("moth-eaten” appearance in beard or scalp).

Laboratory Examinations

Serology. ANA (to rule out SLE); rapid plasma reagin (RPR) test (to rule out secondary syphilis).

KOH Preparation. Rule out tinea capitis.

Dermatopathology. Acute lesions show peribulbar, perivascular, and outer root sheath mononuclear cell infiltrate of T cells and macrophages; follicular dystrophy with abnormal pigmentation and matrix degeneration. May show increased number of catagen/telogen follicles.


• Spontaneous remission is common in patchy AA but is less so with AAT or AAU.

• Poor prognosis associated with onset in childhood, loss of body hair, nail involvement, atopy, family history of AA.

• If occurring after puberty, 80% regrow hair. With extensive involvement, <10% recover spontaneously.

• Recurrences of AA, however, are frequent.

• Systemic glucocorticoids or cyclosporine can induce remission of AA but do not alter the course.


• Treatment directed at inflammatory infiltrate. No curative treatment is currently available.

• In many cases, the most important factor in management of the patient is psychological support from the dermatologist, family, and support groups (The National Alopecia Areata Foundation, http://-www.naaforgl).

• Persons with extensive scalp involvement such as AAT may prefer to wear a wig or hairpiece.

• Makeup applied to eyebrows is helpful. Eyebrows can be tattooed.

Glucocorticoids. Topical. Superpotent agents not usually effective.

Intralesional Injection. Few and small lesions of AA can be treated with intralesional triamcinolone acetonide, 3-7 mg/mL, which can be very effective temporarily.

Systemic Glucocorticoids. May induce regrowth, but AA recurs on discontinuation; risks of longterm therapy therefore preclude their use.

Systemic Cyclosporine. Induces regrowth, but AA recurs when drug is discontinued.

Induction of Allergic Contact Dermatitis. Dinitrochlorobenzene, squaric acid dibutylester, or diphencyprone reported to be successful, but local discomfort due to allergic contact dermatitis and swelling of regional lymph nodes poses a problem.

Oral PUVA (Photochemotherapy). Variably effective, as high as 30%, and worth a trial in patients who are highly distressed about the problem. Entire body must be exposed.

Telogen Effluvium Image

Image Telogen effluvium is the transient increased shedding of normal club (telogen) hairs from resting scalp follicles.

Image Secondary to accelerated shift of anagen (growth phase) into catagen and telogen (resting phase).

Image Results in increased daily hair loss and, if severe, diffuse thinning of scalp hair.

Etiology and Epidemiology

Etiology. A reaction pattern to a variety of physical or mental stressors:

Endocrine: Hypo- or hyperthyroidism; postpartum; discontinuation or changing type of estrogen containing drugs.

Nutritional deficiency: Biotin, zinc, iron, essential fatty acid.

Rapid weight loss, caloric or protein deprivation, chronic iron deficiency, excessive vitamin A ingestion.

Physical stress: Febrile illnesses, catabolic illnesses (e.g., malignancy, chronic infection), major surgery, major trauma, acute or chronic psychological stress.

Psychological stress: Anxiety, depression, bipolar disorder.

Intoxication: Thallium, mercury, arsenic.

Drugs: See Table 31-2.




Inflammatory scalp disease: Seborrheic dermatitis, erythroderma.

Idiopathic: No obvious cause is apparent in a significant number of cases.

Age of Onset. Any age.

Sex. More common in women due to parturition, cessation of an oral contraceptive, and “crash” dieting.

Incidence. Second most common cause of alopecia after AGA.


• TE: many more hairs than normal are shed daily. The precipitating stimulus results in a premature shift of anagen follicles into the telogen phase. TE occurs in 3-4 months after the inciting event occurred. If the inciting cause is removed, shedding will resolve over the next few months. Hair density may take 6-12 months to return to baseline.

• Can become chronic with decreased hair density, always has potential for reversal, does not lead to total scalp hair loss, and rarely goes beyond 50% loss.

Clinical Manifestation

Skin Symptoms

• Patient presents with complaint of increased hair loss on the scalp that may be accompanied by varying degrees of hair thinning.

• Most individuals are anxious, fearing baldness.

Skin Lesions. No abnormalities of the scalp are detected.

Hair (Fig. 31-11). Diffuse shedding of the scalp hair. Gentle hair pull gathers several to many club or telogen hairs.


Figure 31-11. Telogen effluvium A clump of hair in the hand, associated with striking thinning of scalp hair. Using the fingers as shown, 30-40 hairs could be removed with each “hair pull.”

Distribution. Hair loss occurs diffusely throughout the scalp. Short regrowing new hairs are present close to the scalp; these hairs are finer than older hairs and have tapered ends.

Nails. The precipitating stimulus for TE may also affect the growth of nails, resulting in Beau lines (see Fig. 32-23), which appear as transverse lines or grooves on the fingernail and toenail plates.

Differential Diagnosis

Increased Shedding of Scalp Hair ± Nonscarring Alopecia. Pattern hair loss, diffuse-pattern alopecia areata, loose anagen syndrome, hyperthyroidism, hypothyroidism, SLE, secondary syphilis, drug-induced alopecia (Table 31-2).

Laboratory Examinations

Hair Pull. Compared with the normal hair pull, in which 80-90% of hair is in the anagen phase, TE is characterized by a reduced percentage of anagen hairs.

CBC. Rule out iron-deficiency anemia.

Chemistry. Serum iron, iron-binding capacity.

TSH. Rule out thyroid disease.

Serology. ANA, RPR.

Histopathology. Increase in the proportion of follicles in telogen.


Made on history, clinical findings, hair pull, and possible biopsy, excluding other causes.

Course and Prognosis

Complete regrowth of hair is the rule. In postpartum TE, if hair loss is severe and recurs after successive pregnancies, regrowth may never be complete. TE may continue for up to a year after the precipitating cause.


No intervention is needed or required. The patient should be reassured that the process is part of a normal cycle of hair growth.

Anagen Effluvium Image

Image Etiology: Radiation therapy to head; chemotherapy with alkylating agents; intoxications; protein malnutrition.

Image Onset is usually rapid and extensive (see Fig. 31-12).


Figure 31-12. Anagen effluvium: chemotherapy All scalp, facial, and bodily hair have fallen out. Close inspection reveals that scalp hair has begun to regrow.

Image Pathogenesis: Occurs after any insult to hair follicle that impairs its mitotic/metabolic activity.

Image More common and severe with combination chemotherapy than with the use of a single drug. Severity is generally dose dependent.

Image Manifestations: Scalp hair loss is diffuse, extensive; also: eyebrows/lashes, beard, etc. Nails show transverse banding or ridging.

Image Regrowth is usually rapid after discontinuation of chemotherapy.


Anagen cycle disrupted causing varying degrees of hair follicle dystrophy:

• Radiation therapy to head.

• Alkylating agents: see Table 31-2.

• Intoxications: mercury, boric acid, thallium.

• Severe protein malnutrition.


• Occurs after any insult to hair follicle that impairs its mitotic/metabolic activity.

• Anagen hairs break off within the follicle or at the level of the scalp, being shed without roots.

Clinical Manifestations

Skin. Appears normal.

Hair. Scalp hair loss is diffuse, extensive (Fig. 31-12). Hair breaks off at the level of the scalp. Eyebrows/lashes, beard, body hair may also be lost.

Nails. Show transverse banding or ridging.


• Hair regrows after discontinuation of chemotherapy.

• Regrowth after radiation depends on type, depth, dose fractionation; may result in irreversible hair follicle stem cell damage.


No effective preventive measures are available.

Cicatricial or Scarring Alopecia Image

Image Primary cicatricial (scarring) alopecia results from damage or destruction of the hair follicles stem cells by:

Image Inflammatory (usually noninfectious) processes.

Image Infection: e.g., “kerion” tinea capitis, necrotizing herpes zoster.

Image Other pathologic processes: surgical scar, primary or metastatic neoplasm.

Image Manifestations: Effacement of follicular orifices in a patchy or focal distribution, usually in scalp or beard.

Image The end result is effacement of follicular orifices and replacement of the follicular structure by fibrous tissue (Table 31-3).

Image Scarring is irreversible. Therapies are ineffective.



Chronic Cutaneous (Discoid) Lupus Erythematosus (CCLE): See Section 14.

• May occur without other manifestations or serologic evidence of lupus erythematosus.

• Manifestations:

• CCLE: erythematous plaques (Figs. 31-13 to 31-15). Keratotic follicular plugs ("carpet tacks"). Scattered. Variable in number. May become confluent. Postinflammatory hypopigmentation, and/or follicular plugging (see Fig. 31-14).


Figure 31-13. Scarring alopecia of scalp: chronic cutaneous lupus erythematosus (CCLE) A 41-year-old white male with multiple red discoid keratotic patches on the scalp for 1 year. A red scaling lesion with scarring alopecia is seen on the frontal scalp.


Figure 31-14. Diffuse and scarring alopecia of scalp: Systemic LE (SLE) and CCLE lesions A 36-year-old female with poorly controlled SLE for 3 years. Diffuse scalp alopecia is seen associated discrete discoid lesions with scarring alopecia.


Figure 31-15. This is the same patient as in Fig. 31-14. She has erythema of the ears and red areas of scarring alopecia on the scalp.

• SLE: diffuse scalp erythema with diffuse hair thinning (Fig. 31-14).

• Tumid LE: violaceous dermal inflammatory plaque with overlying hair loss.

• Dermatopathology: see “Lupus Erythermatosus” in Section 14.

Lichen Planopilaris (LPP). See “Lichen Planus” in Section 14.

• Follicular lichen planus (LP) is associated with cicatricial scalp alopecia, resulting in permanent hair loss (Fig. 31-16).


Figure 31-16. Scarring alopecia of scalp: pseudopelade of Brocq caused by lichen planus The scalp is smooth, shiny, devoid of hair and hair follicles in many areas; some of the remaining follicles are inflamed with perifollicular erythema and scale. Several hairs are seen emerging from a single site within the area of alopecia (arrows). The term pseudopelade implies that the lesions resemble alopecia areata.

• LPP may or may not be associated with lichen planus of skin or mucosa.

• Most commonly affects middle-aged women.

• Manifestations in scalp: Perifollicular erythema ± hyperkeratosis. Violaceous discoloration of scalp. Prolonged inflammation results in scarring alopecia. In some cases, follicular inflammation and scale are absent, with only areas of scarring alopecia, so-called footprints in the snow, or pseudopelade. Distribution: most common on parietal scalp; also affects other hair-bearing sites such as groin, axilla.

• Symptoms: scalp pain.

• Variants:

• Graham-Little syndrome: LP-like lesions + follicular “spines"/keratosis pilaris-like lesions in areas of alopecia on scalp, eyebrows, axillary, pubic areas.

• Frontal fibrosing alopecia: Frontotemporal hairline recession and eyebrow loss in postmenopausal women with perifollicular erythema (Fig. 31-17); histology shows LPP.


Figure 31-17. Scarring alopecia of scalp: lichen planopilaris (LPP) The frontal hairline has gradually receded; the area of alopecia lacks the pigmentation of forehead skin, which has had lifelong sun exposure. Both eyebrows have no hair; the eyebrow on the right is penciled in. The eyelashes appear normal. No other clinical findings of LP were detected. This clinical variant of LPP is called frontal fibrosing alopecia.

Pseudopelade of Brocq

• End stage of all noninflammatory scarring alopecias and a variety of initially inflammatory disorders.

• Manifestations:

• Early lesions: Discrete, smooth, skin- or pink-colored irregularly shaped areas of alopecia without follicular hyperkeratosis or perifollicular inflammation (Fig. 31-18).


Figure 31-18. Scarring alopecia of scalp: pseudopelade of Brocq Extensive scarring alopecia with residual islands of hair follicles and hair on the vertex. Note follicular tufting (several hair follicles emerging the scalp in groups) and the absence of erythema, scale, or crust.

• Pattern of alopecia: Early moth-eaten pattern with eventual coalescence into larger patches of hair loss ("footprints-in-the-snow").

• Dermatopathology: Similar to lichen planopilaris.

Central Centrifugal Scarring Alopecia

• Synonyms: follicular degeneration syndrome, hot comb alopecia, pseudopelade.

• Most commonly occurs in black women. Relation to chemical processing, heat, or chronic tension on the hair is uncertain, but they are best avoided.

• Slowly progressive alopecia begins in the crown/midvertex and advances centrifugally to surrounding areas.

• Dermatopathology: Earliest most distinctive change is premature desquamation of the inner root sheath with later changes through the outer root sheath (including migration of the hair shaft), a mononuclear infiltrate primarily at the isthmus, and, finally, loss of the follicular epithelium and replacement with fibrous tissue.

Alopecia Mucinosa (Follicular Mucinosis)

• Erythematous lesions (papules, plaques, or flat patches) of alopecia, occurring mainly on scalp and/or face.

• Dermatopathology: prominent follicular, epithelial/sebaceous gland mucin, perifollicular lymphohistiocytic infiltrate without concentric lamellar fibrosis.

• May be symptom of cutaneous T-cell lymphoma (See Section 20).

Folliculitis Decalvans

• Pustular folliculitis leading to hair loss. Surviving hairs clustered, emerging from a single follicular orifice (tufted folliculitis).

• Bogginess or induration of scalp/beard with pustules, erosions, crusts (Fig. 31-19), scale.


Figure 31-19. Scarring alopecia of scalp: folliculitis decalvans Erythema, inflammatory papules, crusts, and scarring of the scalp. Male pattern hair loss is also present.

• Staphylococcus aureus infection is common. Whether S. aureus infection is the primary process or secondary is uncertain.

• Dermatopathology: acute suppurative folliculitis, early.

• Scarring alopecia is irreversible. Systemic antibiotics, rifampin, systemic and/or topical and/or intralesional glucocorticoids, and systemic retinoid have been used. S. aureus infection should be documented and treated with appropriate antimicrobial agent.

Dissecting Folliculitis

• Synonyms: dissecting cellulitis, perifolliculitis abscedens et suffodiens.

• Race: most common in black men.

• Initial deep inflammatory nodules, primarily over the occiput, that progress to coalescing regions of boggy scalp (Fig. 31-20). Sinus tracts may form; purulent exudates can be expressed. S. aureussecondary infection is common.


Figure 31-20. Scarring alopecia of scalp: dissecting folliculitis A 46-year-old black female with longstanding abscess formation of the scalp has resulted in very severe hypertrophic scarring. There was associated cystic acne and hidradenitis suppurativa.

• Dermatopathology: early follicular plugging and suppurative follicular/perifollicular abscesses with mixed inflammatory infiltrate; later, foreign-body giant cells, granulation tissue, scarring with sinus tracts.

• Scarring alopecia is irreversible. S. aureus infection should be documented and treated with appropriate antimicrobial agent.

Follicultis Keloidalis Nuchae

• Synonym: acne keloidalis (nuchae).

• Occurs most commonly in black men.

• Usually occurs on the occipital scalp and nape of the neck, starting with a chronic papular or pustular eruption (Fig. 31-21). Keloidal scar formation may occur.


Figure 31-21. Scarring alopecia of scalp: folliculitis keloidalis A 31-year-old black male with papular scars of 3 years’ duration, and follicular pustules becoming confluent on the occipital scalp and neck.

• Distribution: nape of the neck, occipital scalp.

• Early mild involvement may respond to intralesional triamcinolone. If S. aureus is isolated on culture, treat with appropriate antimicrobial agent.

Pseudofolliculitis Barbae

• Synonym: “razor bumps.”

• Occurs commonly in black men who shave.

• Related to curved hair follicles. Cut hair retracts beneath skin surface, grows, and penetrates follicular wall (transfollicular type) or surrounding skin (extrafollicular type), causing a foreign-body reaction.

• Distribution: any shaved area, i.e., beard (Fig. 31-22), scalp, pubic.


Figure 31-22. Pseudofolliculitis barbae A 29-year-old black male with multiple follicular papular scars in the beard; the presence of follicular pustules usually indicates secondary Staphylococcus aureusfolliculitis. Folliculitis keloidalis is often seen on the occipital scalp and neck (see Fig. 31-21).

• Keloidal scarring in varying degrees occurs at involved sites.

• S. aureus secondary infection is common.

Acne Necrotica

• Pruritic or painful erythematous follicular-based papule with central necrosis, crusting, and healing with depressed scar.

• Lesions occur on anterior scalp, forehead, nose; at times, the trunk.

• Dermatopathology: lymphocytic necrotizing folliculitis.

• Poor response to treatment. Systemic antimicrobial agents and isotretinoin reported to be effective.

Erosive Pustular Dermatosis of Scalp

• A disease of the elderly, mainly women, although pediatric cases do occur.

• Manifestations: chronic, boggy, crusted plaque(s) on the scalp overlying exudative erosions and pustules, eventually leading to scarring alopecia.

• May follow trauma or treatment of actinic keratoses.

• Dermatopathology: lymphoplasmacytic infiltrate with or without foreign-body giant cells and pilosebaceous atrophy.

• Poor response to therapy. Treat documented S. aureus infection.

Laboratory Examination

Scalp Biopsy. 4-mm punch biopsy including subcutaneous tissue, prepared for horizontal section. A second 4-mm punch biopsy specimen for vertical sections and direct immunofluorescence, particularly if lupus is suspected.


Glucocorticoids. Topical high-potency and intralesional glucocorticoids (e.g., triamcinolone) are the mainstay of treatment, improving symptoms and hair growth.

Antibiotics. May be effective, especially if S. aureus infection is documented.

Excess Hair Growth ICD-9: 704.1 image ICD-10: L68

Image Excess hair growth occurs in two patterns.

Image Hirsutism: occurs in women at sites where hair is under androgen control.

Image Hypertrichosis: hair density or length beyond accepted limits of normal for age, race, sex (generalized, localized; lanugo, vellus, terminal hair).

Hirsutism Image

Image Excessive hair growth (women) in androgen-dependent hair patterns, secondary to increased androgenic activity.

Image Normally only postpubescent males have terminal hair in these sites.

Image Synonym: Unwanted hair.

Etiology and Epidemiology

Definition. Excessive hair growth (women) in androgen-dependent hair patterns, secondary to increased androgenic activity. However, varies with cultural and racial factors.

Etiology. See Table 31-4.



Risk Factors. Familial, ethnic, and racial influences. Hirsuteness: white > black > Asian.

Prevalence in the United States. Survey of college-aged women: 25% had easily noticeable facial hair; 33% had hair along linea alba below umbilicus; 17% had periareolar hair. Series of 100 patients: 15% idiopathic, 3% lateonset congenital adrenal hyperplasia (CAH) (varies within ethnic group).


• Androgens promote conversion of vellus to terminal hairs in androgen-sensitive hair follicles: beard area, face, chest, areolae, linea alba, lower back, buttocks, abdomen, external genitalia, inner thighs.

• Dihydrotestosterone, derived from conversion of testosterone by 5α-R at the hair follicle, is the hormonal stimulus for hair growth; 50-70% of circulating testosterone in normal women is derived from precursors, androstenedione, and DHEA; the rest is secreted directly, mostly by the ovaries. In hyperandrogenic women, a greater percentage of androgens may be secreted directly.

• In women, adrenal glands secrete androstenedione, DHEA, DHEA sulfate, and testosterone; ovaries secrete mainly androstenedione and testosterone.

Clinical Manifestation


• Family history

• Drug history

• Virilization symptoms: female pattern hair loss to male pattern balding, acne, deepened voice, increased muscle mass, clitoromegaly, increased libido, personality change. Relatively recent or rapid onset of symptoms and signs not associated with puberty.

• Other: Amenorrhea or changes in menstruation. New-onset hypertension.

Skin Findings. Note: acne, acanthosis nigricans, striae.

Hirsutism. (1) Note the amount of excess hair, (2) note all sites of hair, (3) evaluate progression and therapy.

• New growth of terminal hair (Fig. 31-23), especially on the face (Fig. 31-23A), chest (see Fig. 31-25B), abdomen, upper back, shoulders.



Figure 31-23. Hirsutism: face and chest. (A) Increased hair growth in androgen-dependent hair follicles of the sideburn area, associated with androgen excess. (B) Increased hair growth in androgen-dependent hair follicles of the presternal and periareolar regions.

Cushing Syndrome. Centripetal obesity, muscle wasting (especially peripheral muscle weakness), violaceous striae.

Pelvic Examination. If polycystic ovary syndrome is suspected.

Laboratory Evaluation of Hirsutism Serum Testosterone. If >200 ng/mL, exclude androgen-secreting tumor.

Serum-Free Testosterone and Dehydroepi-androsterone. More sensitive; most women with moderately elevated androgen levels have polycystic ovarian syndrome. If >800 μg/d, suggestive of adrenal tumor.

17-Hydroxyprogesterone. Raised level suggests CAH; confirm diagnosis by repeat measurement after ACTH stimulation.

Serum Prolactin. Hyperprolactinemia due to macro- or microprolactinoma or treatment with neuroleptic drugs; may have associated menstrual abnormalities, infertility, or galactorrhea.

Urinary 17-Ketosteroid. Helpful in evaluating the overall amount of androgen secretion. Results checked against age-appropriate normal levels; peak levels occur at 30 years (significant decline with age thereafter).

Oligomenorrhea/Amenorrhea. Prolactin, follicle-stimulating hormone, total testosterone.


Cosmetic Treatment. Bleaching: hydrogen peroxide. Temporary removal: Shaving, waxing, chemical (Nair). Eflornithine (Vaniqa) cream. LASER epilation. Electrolysis.

Weight Loss. May be helpful in obese patients; obesity increases free testosterone levels by reducing sex hormone-biding hormone and contributes to insulin resistance.

Endocrinology Consultation. For suspected lateonset CAH, Cushing syndrome, tumor.

Systemic Antiandrogen Therapy. Oral Antiandrogens. Spironolactone (100-200 mg daily). Cyproterone acetate. Finasteride.

Oral Contraceptives. Inhibit androgen synthesis by inhibiting output of gonadotropins; most effective if combined with antiandrogens.

Bromocriptine. For treatment of prolactinoma.

Hypertrichosis Image

Image Hypertrichosis is excessive hair growth (density, length) beyond accepted limits of normal for age, race, sex in areas that are not androgen sensitive (see Fig. 31-24).

Image May be generalized/universal or localized.

Image May consist of lanugo, vellus, or terminal hair.


Figure 31-24. Hypertrichosis of face Excessive hair growth in nonandrogen-sensitive areas of the face in a female treated with cyclosporine.


Congenital or hereditary; acquired (see “Acquired Hypertrichosis Lanuginosa,” below), drugs (minoxidil, phenytoin, cyclosporine, glucocorticoids, streptomycin, PUVA), porphyria, POEMS syndrome, hypothyroidism.

Clinical Manifestation

Localized Hypertrichosis. Trauma/scar/occupation-related sites of irritation. Drug-induced: topical minoxidil. Becker nevus.

Acquired Hypertrichosis Lanuginosa. Production of lanugo (wasp) hair in follicles previously producing vellus hair ("malignant down"). Hair may be >10 cm in length in nonscalp areas. Can involve entire body, except for palms and soles. In mild types, downy hair is limited to the face; hair on previously hairless areas such as the nose and eyelids is usually noticed first.

Universal Hypertrichosis (Fig. 31-24). Increase of lanugo, vellus, or terminal hair.


• Find and remove the inciting cause.

• Similar to “Cosmetic Treatment” of hirsutism (see above).

Infectious Folliculitis ICD-9: 704.8 image ICD-10: L73.8 Image

Image Infectious folliculitis begins in the upper portion of the hair follicle.

Image Etiologic agents: Bacteria, fungi, virus, mites.

Image Manifestations: Follicular papule, pustule, erosion, or crust at the follicular infundibulum.

Image Infection can extend deeper into the entire length of the follicle (sycosis).

Etiology and Epidemiology


Bacterial: S. aureus (Bockhart impetigo); Pseudomonas aeruginosa (hot-tub); gramnegative folliculitis.

Viral: Herpetic, molluscum contagiosum.

Fungal: Candida, Malassezia, dermatophytes.

Other: Syphilitic, Demodex.

Predisposing Factors

• Shaving hairy regions such as the beard area, axillae, or legs facilitates follicular infection. Extraction of hair such as plucking or waxing.

• Occlusion of hair-bearing areas facilitates growth of microbes.

• Topical glucocorticoid preparations.

• Systemic antibiotic promotes growth of gram-negative bacteria; diabetes mellitus; immunosuppression.

Clinical Manifestation

Symptoms. S. aureus and dermatophytic folliculitis can be chronic. Usually nontender or slightly tender; may be pruritic. Uncommonly, tender regional lymphadenitis.

Skin Lesions

• Papule or pustule confined to the ostium of the hair follicle, at times surrounded by an erythematous halo (Figs. 31-25 and 31-26). Rupture of pustule leads to superficial erosions or crusts.


Figure 31-25. Infectious folliculitis, superficial in axilla: MRSA A 25-year-old male with pruritic and tender axillary lesions for several weeks. Multiple follicular pustules and papules are seen in the vault of the shaved axilla. Shaving facilitates entry of S. aureus into the superficial hair follicle. The lesions resolved with minocycline.


Figure 31-26. Infectious folliculitis on forearm A 44-year-old male with HIV/AIDS and numerous pustules and papules with superimposed mild lichen simplex chronicus.

• Usually, only a small percentage of follicles in a region are infected.

• Superficial infection heals without scarring, but in darkly pigmented individuals, postinflammatory hypo- and hyperpigmentation can occur.

• Extension of infection can progress to abscess or furuncle formation.

Distribution. See Table 31-5.




S. aureus Folliculitis. Can be either superficial folliculitis (infundibular) (Fig. 31-25) or deep (sycosis) (extension beneath infundibulum) with abscess formation. In severe cases (lupoid sycosis), the pilosebaceous units may be destroyed and replaced by fibrous scar tissue (Fig. 31-27).


Figure 31-27. Infectious folliculitis A male patient with HIV/AIDS and persistent pruritic pustular and ruptured lesions on the cheek/beard for several months.

Gram-Negative Folliculitis. Occurs in individuals with acne vulgaris treated with oral antibiotics. “Acne” typically worsens, having been in good control. Characterized by small follicular pustules and/or larger abscesses on the cheeks.

Hot-Tub Folliculitis (Pseudomonas Aeruginosa). Occurs on the trunk following immersion in spa water (Fig. 31-28).


Figure 31-28. Infectious folliculitis ("hot tub"): P. aeruginosa A 31-year-old male with multiple painful follicular pustules 3 days after bathing in a hot tub. P. aeruginosa was isolated on culture from a lesion.

Dermatophytic Folliculitis. Infection begins in the perifollicular stratum corneum and spreads into follicular ostia and hair shafts (see Section 26) (Fig. 31-29).


Figure 31-29. Dermatophytic folliculitis: Trichophyton rubrum A 31-year-old male with HIV/AIDS had a pruritic rash on the buttocks for 1 year; topical glucocorticoids and antifungal agents had not been effective. Multiple follicular papules and scaling erythema are seen on the sacral area; tinea cruris and pedis were also present. KOH preparation showed septated hyphae. The lesions resolved with oral terbinafine.

Tinea Capitis (see Section 26).

In dermatophytic Majocchi granuloma, scattered papules, pustules, and nodules, usually associated with tinea cruris or tinea corporis.

Malassezia Folliculitis. More common in subtropical and tropical climates. Pruritic, monomorphic eruption characterized by follicular papules and pustules on the trunk, most often on the back (Fig. 31-30), upper arms, and less often on the neck and face; excoriated papules. Absence of comedones differentiates it from acne vulgaris (see Section 26). Synonym: Pityrosporum folliculitis.


Figure 31-30. Infectious folliculitis: Malassezia furfur A 41-year-old Hispanic male with multiple, discrete, follicular papulopustules on the chest.

Candida Albicans. Occurs in sites of occluded skin such as the back of a hospitalized febrile patient or under plastic dressing, especially if topical glucocorticoid preparations are used (see Section 26).

Herpetic Folliculitis. Occurs predominantly in the beard area (viral sycosis) in men. Characterized by follicular vesicles and later crusts (Fig. 31-31).


Figure 31-31. Infectious folliculitis: herpes simplex virus A 40-year-old healthy male with discrete and grouped pustules and erosions in the beard area for 3 weeks. Lesions resolved with oral acyclovir.

Molluscum Folliculitis. Presents as umbilicated skin-colored papules in a follicular and perifollicular distribution over the beard area.

Syphilitic (Luetic) Folliculitis: Secondary. Nonscarring alopecia of the scalp and beard (alopecia areolaris); “moth-eaten” appearance.

Demodicidosis. Clinical presentation: perifollicular scaling (pityriasis folliculorum) or rosacea-like erythematous follicular papules and pustules with a background of erythema on the face. Etiology: Demodex folliculorum.

Differential Diagnosis

Follicular Inflammatory Disorders. Acneiform disorders (acne vulgaris, rosacea, perioral dermatitis), HIV-associated eosinophilic folliculitis, chemical irritants (chloracne), acneiform adverse cutaneous drug reactions [epidermal growth factor receptor inhibitors (e.g., erlotinib), halogens, glucocorticoids, lithium], keloidal folliculitis, pseudofolliculitis barbae.

Regional Differential Diagnosis. Face: acne, rosacea, perioral dermatitis, keratosis pilaris, pseudofolliculitis barbae (ingrowing hairs). Scalp: folliculitis necrotica. Trunk: acne vulgaris, pustular miliaria, transient acantholytic disease (Grover disease). Axillae and groins: hidradenitis suppurativa.

Laboratory Findings

Direct Microscopy. Gram stain S. aureus: grampositive cocci. Also visualizes fungi.

KOH Preparation. Dermatophytes: hyphae, spores. M. furfur: multiple yeast forms; Candida: mycelial forms.

Culture Bacterial. S. aureus, P. aeruginosa; gramnegative folliculitis: Proteus, Klebsiella, Escherichia coli. In cases of chronic relapsing folliculitis, culture nares and perianal region for S. aureus carriage.

Fungal. Dermatophytes; C. albicans.

Viral. Herpes simplex virus.

Dermatopathology. Follicular and perifollicular infiltrate which may be lymphocytic (viral, fungal), neutrophilic (bacterial, fungal), granulomatous (viral, fungal) or mixed, with or without pilosebaceous involvement/destruction, Gram stain and fungal stains may be necessary to highlight microorganisms.


Clinical findings confirmed by laboratory findings.

Course and Prognosis

• S. aureus folliculitis can progress to deeper follicular and perifollicular infection with abscess (furuncle, carbuncle) or cellulitis.

• Infection of multiple contiguous follicles results in a carbuncle.

• Many types of infectious folliculitis tend to recur or become chronic unless the predisposing conditions are corrected.


Prophylaxis. Correct underlying predisposing condition. Washing with antibacterial soap or benzoyl peroxide preparation or isopropyl/ethanol gel.

Antimicrobial Therapy. Bacterial Folliculitis. Most will respond to natural penicillins but can consider dicloxacillin, amoxicillin, primary cephalosporins and clindamycin, usually for 7 to 10 days. Consider culture for resistant organisms. Minocycline, trimethoprim-sulfamethoxazole and quinolones may be necessary. There may be higher resistance to the erythromycin family.

Gram-Negative Folliculitis. Associated with systemic antibiotic therapy of acne vulgaris. Discontinue current antibiotics. Wash with benzoyl peroxide. In some cases, ampicillin (250 mg four times daily) or trimethoprim-sulfamethoxazole four times daily. Isotretinoin.

Fungal Folliculitis. Various topical antifungal agents. For dermatophytic folliculitis: terbinafine, 250 mg po for 14 days, or itraconazole, 100 mg twice daily for 14 days. For Candida folliculitis: fluconazole or itraconazole, 100 mg twice daily for 14 days.

Herpetic Folliculitis. See “Herpes Simplex Virus Infections” in Section 27.

Demodicidosis. Permethrin cream. Ivermectin, 200 μg/kg (usual range, 12-18 mg).

Pseudofolliculitis Barbae. Rule out secondary S. aureus infection. Discontinue shaving. Use beard clipper instead of safety razor. Destruction of hair follicle: electrolysis; laser hair removal.