MEDICINE

The Diagnosis and Treatment of Hair

and Scalp Diseases
Hans Wolff, Tobias W. Fischer, Ulrike Blume-Peytavi

air is of both physiological and psychological

SUMMARY
Background: Hair loss is caused by a variety of hair growth
H importance. It protects against the sun’s ultra-
violet rays and serves a biological signaling function.
disorders, each with its own pathogenetic mechanism. In the Western world at least, long and full women’s
Methods: This review is based on pertinent articles hair is considered beautiful and a sign of youth, while
retrieved by a selective search in PubMed, on the current thick pigmented men’s hair signifies youth and vitality
German and European guidelines, and on the authors’ (1). It is thus hardly surprising that people with
clinical and scientific experience. excessive hair loss often seek medical help.
Results: Excessive daily hair loss (effluvium) may be
physiological, as in the postpartum state, or pathological, Learning objectives
due for example to thyroid disturbances, drug effects, iron Reading this article should enable readers to
deficiency, or syphilis. Androgenetic alopecia generally ● understand the normal physiology and patho-
manifests itself in women as diffuse thinning of the hair physiology of hair growth,
over the top of the scalp, and in men as receding temporal ● know the most common and cosmetically most
hairlines and loss of hair in the region of the whorl on the disturbing types of increased hair loss and alope-
back of the head. Alopecia areata is patchy hair loss cia, and
arising over a short time and involving the scalp, ● carry out the indicated treatments in collaboration
eyebrows, beard, or entire body. The hair loss of alopecia with a dermatologist.
areata is reversible in principle but hard to treat.
Folliculitis decalvans is a form of alopecia with scarring, Anatomy and physiology of hair growth
characterized by inflamed papules, pustules, and crusts at Healthy men and women generally have 80 000 to
the edges of the lesions. Lichen planopilaris generally 120 000 vital terminal hairs on the scalp. Hair is
presents with small patches of baldness, peripilar composed of keratin and is produced in the hair
erythema, and round areas of skin scaling. Kossard’s follicles. All hair follicles go through repeated cycles of
frontal fibrosing alopecia is characterized by a receding growth and rest (2).
hairline and loss of eyebrows. During the growth (anagen) phase, which is 2–6
Conclusion: Hair loss is a symptom, not a diagnosis. The years long, a hair grows at a rate of about 0.3 mm per
pathogenesis of the alopecias involves a range of genetic, day, or 1 cm per month. The maximum attainable hair
endocrine, immune, and inflammatory processes, each of length depends on the duration of the anagen phase. A
which calls for its own form of treatment. brief transitional (catagen) phase follows, and then a
rest (telogen) phase lasting 2–4 months, after which the
►Cite this as:
hair falls out (2).
Wolff H, Fischer TW, Blume-Peytavi U:
Normally, the ca. 100 000 hairs on a person’s head
The diagnosis and treatment of hair and scalp diseases.
grow independently of one another. Intrinsic or extrin-
Dtsch Arztebl Int 2016; 113: 377–86.
sic factors can synchronize the hair follicles by in-
DOI: 10.3238/arztebl.2016.0377
ducing a premature transition from the anagen to the
telogen phase, leading to noticeable hair loss 2–4
months later (2). These factors include hormones,
growth factors, drugs, and the seasons (2, 3).

Department of Dermatology and Allergology, Ludwig-Maximilians-Universität

München: Prof. Dr. med. Wolff
Department of Dermatology, Allergology and Venerology, University Medical
Hair growth cycle
Center Schleswig-Holstein: University of Lübeck: PD Dr. med. Fischer Each of the ca. 100 000 hairs on the head
Department of Dermatology, Venerology and Allergology, Charité – independently goes through a growth cycle
Universitätsmedizin Berlin: Prof. Dr. med. Blume-Peytavi
consisting of three phases: anagen (3–6 years),
catagen (1–2 weeks), and telogen (2–4
months).

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Figure 1: Physical examination

Androgenetic Inspection of the scalp (capillitium) reveals whether
alopecia, there is a visible reduction of the amount of hair (alope-
female type,
cia) and, if so, in what pattern. Any inflammatory redness
Ludwig grade I
or scaling should be noted, as psoriasis and eczema can
cause effluvium (e3). Dermatoscopic examination of the
scalp is helpful as well (5).
A clinical hair-pull test is supplemented by a
tricho(rhizo)gram, in which 20–50 hairs are epilated
with a rubber-shod artery clamp and then analyzed
under a microscope. The differently formed roots in
each of the growth phases can then be counted. A per-
centage of hairs in the telogen phase that exceeds 20%
indicates increased hair shedding (6, e4). A non-
invasive phototrichogram can also yield an estimate of
the anagen-to-telogen ratio (e5) but cannot reveal root
anomalies such as dystrophic hairs.

Laboratory tests for diffuse effluvium

In patients with effluvium of unknown cause, labora-
tory testing should be performed to exclude, in particu-
lar, the following:
● Iron deficiency (ferritin) (7)
● Thyroid dysfunction (TSH, T3, T4)
History-taking in a patient with hair loss ● Stage II syphilis (TPPA test).
A complaint of “hair loss” may refer to either of two Syphilis is very rarely detected, but omitting to take
things: an increased amount of hair falling out daily (ef- the relevant history or to perform the TPPA test in a
fluvium) or visible hairlessness (alopecia). Up to 100 patient with hair loss can have serious consequences for
hairs normally fall out every day (3). It is important to the patient, and for the physician as well, if
ask patients about the drugs they are taking. While neurosyphilis should later develop.
“hair loss” is listed as a possible side effect on practi-
cally all package inserts, only a few drugs are truly rel- Androgenetic alopecia
evant (e1). For example, hair loss 2–4 months after the Androgenetic alopecia is the most common type of
administration of multiple heparin injections is not at hair loss, affecting up to 70% of men and 40% of
all rare (e2). Women should be asked about gynecologi- women (8). Histological examination reveals dimin-
cal factors such as the initiation or discontinuation of ished size of terminal hair follicles in genetically pre-
hormonal contraceptive drugs. Transient postpartum disposed areas of the scalp, shortening of hair growth
effluvium is normal: the stress of delivery, and the hor- phases, and decreased thickness of hair shafts (8). The
monal changes afterward, cause many hair follicles to pattern of hair loss is characteristic: in men, receding
undergo a transition from the anagen to the telogen temporal hairlines and hair loss in the region of the
phase, so that hair loss is seen 2–4 months later (2). whorl at the back of the head (Norwood–Hamilton
Highly toxic factors such as chemotherapeutic drugs type); in women, diffuse midline thinning on the top of
can induce severe follicular damage, causing hairs to the scalp (Ludwig type) (Figure 1).
break off in their follicles within one to three weeks. As Androgenetic alopecia in men is ascribed to genetic
a consolation, patients can be told that this process syn- variants of the androgen receptor (8, 9). Dihydrotestos-
chronizes the growth phases of the follicles, so that the terone (DHT), generated from testosterone through the
hair, once it has grown back, is often thicker than be- activity of the enzyme 5α-reductase, plays a key role
fore. Structural changes can occur in which originally (10). There is no association of male-pattern baldness
straight hair regrows as curly hair, or vice versa (4). and androgen levels in the blood; rather, the condition

Nomenclature Trichogram
Increased daily hair loss is called “effluvium”; A trichogram yields an estimate of the percent-
visible hairlessness is called “alopecia.” ages of actively growing (anagen) hairs and
resting (telogen) hairs: the normal values are
>80% and <20%, respectively.

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TABLE

Treatment options for androgenetic alopecia and the evidence supporting them*

Treatment Evidence Efficacy in Efficacy in Safety Practicality Practicality

level preventing improving for the patient for the physician
progression manifestations
Finasteride (men) 1 +++ ++ +++ ++++ ++
Minoxidil 5% (men) 1 +++ ++ ++++ +/++ +++
Minoxidil 2% (women) 1 +++ ++ ++++ + +++
Oral hormones (for women) 3
- with hyperandrogenism + + + +++ ++
- with normal hormonal status +/– +/– + +++ ++
Hair transplantation 4 – +++ (men) ++ + procedure +
(men und women) ++ (women) +++ long-term effect
Various other treatments insufficient inadequately +/– unknown + +
(aloe vera, aminexil, ginkgo, evidence studied in
food supplements, etc.) clinical trials

*Adapted from (12), Blumeyer et al.: J Dtsch Dermatol Ges 2011; for a complete list of all randomized trials, cf. “Guideline Androgenetic Alopecia” at the Internet address
www.euroderm.org/edf/index.php/edf-guidelines/; global rating from − to ++++ .

is thought to reflect a genetically variable sensitivity of Treatment

hair follicles in the affected areas to normal levels of The evidence-based European guideline for the
circulating androgen. Multiple genes are apparently in- diagnostic evaluation and treatment of androgenetic
volved (9). The gene for the androgen receptor lies on alopecia recently became available (12). The main
the X chromosome; thus, a man’s tendency to develop goal is to stop hair loss and, if possible, reverse the
androgenetic alopecia in later life can be inherited in shrinking of hair follicles, in order to promote the re-
the maternal line (e6). sumption of hair growth (12). The success or failure
The data on androgenetic alopecia in women are of treatment should be objectively documented with
sparse, but here, too, there is clear evidence of a genetic standardized photographic documentation and,
predisposition (e7). optionally, a phototrichogram.
The appropriate diagnostic evaluation of andro- Two drugs are now recognized as effective
genetic alopecia, including a diagnostic algorithm, against androgenetic alopecia: topical minoxidil
was presented in a European consensus statement in solution (for women and men) and finasteride
2011 (11), with the following main conclusions: tablets, 1 mg (for men only).
● Men with a typical balding pattern need no
further laboratory evaluation. The diagnosis can Topical treatment with minoxidil
be made on clinical grounds alone. Minoxidil, a calcium channel opener, has been
● Women should undergo further laboratory approved as a 2% solution for women (13, 14) and a
testing depending on the history and physical 5% solution or foam for men (15) and can be bought
examination. A gynecologic-endocrinological in a pharmacy without a prescription in most parts of
evaluation is indicated if there is evidence of the world. A 5% minoxidil foam to be used once
hormone dysregulation (acne, hirsutism). daily by women would simplify the treatment and is

Androgenetic alopecia Topical treatment with minoxidil

Androgenetic alopecia, the most common type of The topical application of minoxidil is an effective
alopecia, is caused by a genetic predisposition treatment for androgenetic alopecia in both men
and reflects the sensitivity of hair follicles to and women.
circulating androgens.

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Figure 2: 12). It is relatively well tolerated, with a mildly

Alopecia areata: elevated rate of reversible loss of libido and erectile
sharply demarcated dysfunction (appr. 2%) as well as a mildly elevated
hairless areas
incidence of gynecomastia (10). The notion, which
appears in some Internet fora, that finasteride might
increase the risk of prostate cancer, breast cancer, or
infertility has made patient education about this drug
increasingly difficult but is not supported by valid
scientific evidence (16, e8).
Finasteride is not approved for use by women, as
it can cause developmental genital defects in male fe-
tuses (10) and is ineffective against androgenetic
alopecia in postmenopausal women (17).
Dutasteride, a dual (type I and type II) inhibitor of
5α-reductase, is currently approved in Germany only
for the treatment of benign prostatic hyperplasia.
Therefore, we advise against its off-label use to treat
alopecia (18).

Topical or systemic treatment with hormones

There is as yet inadequate evidence for the topical
use of natural estrogens, progesterone, or anti-
androgens to treat androgenetic alopecia in women
who do not have hormonal dysregulation (Table)
(12).
Nor is there adequate evidence to support the use
of systemic antiandrogens in women with andro-
genetic alopecia whose menstrual cycles are nor-
mal, other than a proof-of-principle study in which
expected to be approved in Germany in 2016. these hormones were given at very high doses (19).
Minoxidil solution is the only topically applied drug In women who do have hormonal dysregulation,
against androgenetic alopecia whose efficacy has androgenetic alopecia can be treated with anti-
been documented by high-level (level 1) evidence androgens such as cyproterone acetate, chlor-
(12). It was found, in large-scale studies, to stop hair madinone acetate, or dienogest (level 3 evidence)
loss in 80–90% of persons treated; hair became (Table) (19).
visibly thicker in about 50% (13–15). Its side effects
include redness and scaling of the scalp; rarely, con- Surgical treatment
tact dermatitis; and hypertrichosis in women—mostly Autologous hair transplantation is a supplementary
at the temples. treatment for advanced androgenetic alopecia. Hair
is removed from the occipital (androgen-insensitive)
Systemic treatment with finasteride scalp and transplanted into the affected areas. Hair
Finasteride, a type II inhibitor of 5α-reductase, was follicle transplantation can thicken the hair not only
approved in Germany in 1999 for use by men aged in men with androgenetic alopecia, but also in
18–41 at a dose of 1 mg po qd (10). Level 1 evidence women (level 4 evidence). A further measure—the
documents its efficacy against androgenetic alopecia easiest of all, and one that affected persons can carry
(12). out for themselves—is the comb-over, i.e., appropri-
Like minoxidil solution, finasteride at a dose of ate hair styling to cover up areas of androgenetic
1 mg per day stops hair loss in 80–90% of persons alopecia. If restyling cannot achieve the desired
treated and visibly thickens hair in about 50% (10, effect, a toupee or wig can be worn.

Systemic treatment with finasteride Androgenetic alopecia in women

Finasteride 1 mg po qd can be given to men for There is as yet inadequate evidence for the
the systemic treatment of androgenetic alopecia. topical use of natural estrogens, progesterone,
Antiandrogens (EL 4) can be helpful for women or antiandrogens to treat androgenetic alope-
with hyperandrogenemia. cia in women.

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Alopecia areata Figure 3:

Alopecia areata (“baldness in a circle”) often arises Folliculitis
suddenly; it usually affects a round patch of scalp at decalvans:
scarring alopecia
first, then spreads in a centrifugal or multilocular pat-
with inflammatory
tern (Figure 2). This disorder has a genetic component papules, pustules,
(e9). Alopecia areata affecting the entire scalp is called crusts, and tufted
alopecia areata totalis; that affecting the entire body is hairs
called alopecia areata universalis. Acute alopecia area-
ta begins with marked, diffuse hair loss (20). Alopecia
areata has a lifelong incidence of 1–2% and is the third
most common type of hair loss after androgenetic and
diffuse alopecia (31).
This condition is associated with other inflamma-
tory and autoimmune diseases including atopic ecze-
ma, Hashimoto’s thyroiditis, Graves’ disease, and
vitiligo.
The following factors imply a worse prognosis (20):
● Onset in childhood (21)
● Extensive involvement and long duration
● Ophiasis type (nuchal involvement)
● Nail involvement (pitting; sandpaper nails)
● Atopic dermatitis and autoimmune disease
● Positive family history. ● Multiple large foci, often confluent, that can
The condition is thought to be due to an autoimmune persist for years
reaction, because scalp biopsies from patients with ● Total hair loss that persists for decades.
alopecia areata have revealed dense infiltration of One-third of patients have a spontaneous
lymphocytes and other immune cells in the deepest part remission within six months of the initial manifes-
of the hair follicles (bulb and dermal hair papilla). The tation; 50–80% are asymptomatic after one year
hair follicles are reversibly damaged, mainly by cyto- (23).
toxic T lymphocytes and cytokines (interferon-γ, inter-
leukin-2, and interleukin-15 receptor β); in conse- Treatment
quence, the hair falls out (22). The treatment of alopecia areata depends on the
It remains unclear why and when alopecia areata severity of involvement (23). If the disorder is mild
arises, why the hair a few centimeters away from an and does not cause the patient very much distress,
area of alopecia grows normally, and how spon- waiting for a spontaneous remission is a sensible op-
taneous remission comes about. Emotional and physi- tion. Treatment with zinc as a putative immune
cal stress are thought to precipitate alopecia areata, modulator generally has no side effects and is there-
but this has not been scientifically confirmed. The fore suitable for use in children (e10). Topical corti-
condition does not seem to be explicable as the costeroids can be applied for several weeks without
product of an infection or a toxic environmental in- risk, but their efficacy against alopecia areata has
fluence. not been established (20). A clear benefit was seen in
Alopecia areata takes a highly variable course, a double-blind trial of a high-dose steroid foam with
manifesting itself clinically in any of the following an intrapatient control (right vs. left side of the head)
ways: (24).
● A single small focus that resolves sponta- Alternatively, alopecia areata can be treated by
neously the intralesional injection of triamcinolone crystals.
● Multiple simultaneously present areas of alope- This can be tried if the patient has only a few, stable
cia, including some with regrowth of hair, and foci of baldness. In rare cases, systemic cortico-
others newly arising steroids are helpful (25).

Alopecia areata Spontaneous remission of alopecia areata

Alopecia areata is an autoimmune disease in If the disorder is mild and does not cause the
which T lymphocytes and other immune cells patient very much distress, waiting for a
reversibly “paralyze” the hair follicles. spontaneous remission is a sensible option.

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Figure 4: ● Folliculitis decalvans

Lichen planus ● Folliculitis et perifolliculitis capitis abscedens
follicularis: et suffodiens
atrophizing alopecia
with peripilar
● Chronic discoid lupus erythematosus
erythema and
● Lichen planus follicularis (lichen planopilaris)
collar-like scaling ● Postmenopausal frontal fibrosing alopecia
(Kossard)
● Brocq’s pseudopelade.
Most of these types of alopecia are easily recogniz-
able from their clinical appearance, although they
may be hard to distinguish from one another in early
stages. If necessary, a biopsy taken from the edge of
the lesion where there is still hair can help establish
the diagnosis (e12).

Folliculitis decalvans
Folliculitis decalvans, which affects both men and
The most effective treatment (level 2 evidence) is women, is one of the most difficult scalp diseases to
topical immune therapy with diphenylcyclo- treat (26, 27). It manifests itself as intense granulocytic
propenone or squaric acid dibutylester (23). The inflammation that destroys both the hair follicles and
mechanism of action is competitive inhibition of the the skin of the scalp. Staphylococcal organisms and an
responsible T lymphocytes by the induction of type excessive inflammatory response are involved in the
IV allergy to whichever of these two substances is pathogenesis of this disease. Inspection reveals scarred
used; both of them are obligate chemical allergens and atrophic areas with a red, inflamed margin (Figure
not normally present in the environment. Once an 3). Hair tufts, consisting of 5–20 hairs, are often found
allergic dermatitis has been induced in this way, the at the edges of lesions; they are the portal of entry for
hair may grow back in 3–6 months. The response staphylococci and thus play a role in the progression of
rate varies from 30 to 80% depending on the base- the inflammation (27).
line findings, i.e., the total surface area of the lesions The treatment of folliculitis decalvans is long and
and the length of time that they have been present difficult. Basic treatment consists of daily antimicrobial
(20). shampooing to lessen the load of staphylococci.
Various other therapeutic approaches will not be Systemic antibiotic treatment with clarithromycin or
discussed here for lack of space and scientific doxycycline for 4–8 weeks often leads to improvement,
evidence, e.g.: stimulation with dithranol, psoralen- but recurrences are common.
UVA turban therapy, 308 nm excimer laser, The most effective antibiotic treatment, a combi-
methotrexate/prednisolone and sulfasalazine (20, nation of clindamycin 300 mg po bid with rifampicin
23, 25). 300 mg po bid for 6 to 12 weeks, renders nearly all pa-
Modern biologic agents, e.g., TNF-α antagonists, tients asymptomatic, sometimes for many months (27,
are surprisingly ineffective and can even induce 28). About half, however, have recurrent disease
alopecia areata; thus, they are not recommended requiring further treatment. In a small fraction of pa-
(22, 23). It is hoped that Janus kinase inhibitors tients (1 in 17), gastrointestinal side effects necessitate
(mainly for topical use) will be found to have a the discontinuation of treatment (28).
positive effect (e11). Dapsone 50 mg po bid for several months or years
can likewise keep the inflammatory activity under con-
Scarring and atrophizing alopecias trol (e13, e14).
The scarring (cicatricial) and atrophizing alopecias To prevent recurrences, all tufted hair follicles
are a heterogeneous group of diseases that destroy should be surgically removed from the scalp. Once the
hair follicles irreversibly (26). They include the fol- disease process has been arrested, larger areas of
lowing: scarring can be surgically reduced.

Effective treatment for alopecia areata Folliculitis decalvans

The most effective treatment (level 2 evidence) Folliculitis decalvans is a chronic, destructive,
is topical immune therapy with diphenylcyclo- scarring alopecia. Its pathogenesis is not entirely
propenone or squaric acid dibutylester. clear; staphylococcal organisms and an excessive
inflammatory response in the scalp are involved.

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Folliculitis et perifolliculitis capitis abscedens et suffodiens Figure 5:

This disease affects men almost exclusively. It Frontal fibrosing
manifests itself initially with hemispherical, lividly alopecia of Kossard
with perifollicular
inflamed, hairless lesions on the hair-bearing scalp
erythema in a
that are soft and fluctuant to palpation. The bloody 66-year-old
exudate that can be aspirated from them is gen- woman. Total eye-
erally microbiologically sterile. In the extreme brow loss, covered
case, the entire scalp is undermined by confluent up in this case with
inflammatory exudate (29). permanent make-
If there are only a few fluctuating nodules, the up
initial treatment can consist of fluid aspiration
followed by the injection of a triamcinolone crystal
suspension (10 mg/mL) through the same needle.
Marked inflammation can be treated with a
combination of systemic glucocorticoids (e.g.,
methylprednisolone, 1 mg/kg body weight) and
isotretinoin (0.5 mg/kg BW) or else with a combi-
nation of dapsone and isotretinoin (30). This being
a rare disease, there are no guidelines on how to or IV corticosteroids, which have a favorable side-
treat it, and the therapeutic recommendations given effect profile (31).
here are only the authors’ expert opinions (level 5 Systemic corticosteroids are not used to treat this
evidence). condition because of the serious adverse effects of
their long-term use. The use of the retinoid acitretin
Lichen planus follicularis (lichen planopilaris) is limited by the cutaneous and mucosal dryness
In lichen planus of the scalp, a dense collection of that arises in more than 80% of patients who take
T lymphocytes appears under the epidermal and it, as well as other side effects. The best-tolerated
follicular basal membrane zone (31). systemic treatment seems to be with hydroxychlo-
The pathogenesis of this condition is thought to roquine 200 mg po bid (level 4 evidence) (31).
involve a misdirected cellular immune response to
an unknown antigen in the basal membrane zone. Frontal fibrosing alopecia of Kossard
The T lymphocytes destroy the follicular stem cells In 1994, the Australian physician Steven Kossard
in the bulge area of the hair follicle, leading to described a disease that he called “postmenopausal
irreversible hair loss (e14). frontal fibrosing alopecia” (32). This condition,
The characteristic clinical finding is that of small considered a variant of lichen planopilaris, arises
patches of alopecia with peripheral follicular hy- nearly exclusively in elderly women; it does, how-
perkeratosis. The hairs at the edge of an affected ever, affect a small number of premenopausal
area seem to possess a tight-fitting white collar women and even men (33), and we therefore omit
surrounded by perifollicular erythema (Figure 4). the word “postmenopausal” from its name. The pat-
Lichen planus of the scalp is usually asymptomatic tern of hair loss resembles at first glance that of an-
and is often present for years before it is noticed. drogenetic alopecia in men (Figure 5).
Further lichen planus lesions are only rarely seen Perifollicular erythema and hyperkeratoses can
elsewhere on the patient’s body. Lassueur–Gra- often be seen at the affected hairline. The condition
ham-Little–Piccardi syndrome consists of lichen is often restricted to the frontal region, although
planus follicularis that involves the scalp and the there are also temporal, occipital, and even cen-
body and is accompanied by dystrophic changes of tripetal distribution patterns. The eyebrows are
the fingernails and toenails (31). nearly always thinned or completely lost.
To arrest or at least slow the gradual inflamma- Asymptomatic loss of hair follicles can be seen
tory destruction of the hair follicles, we prefer to on the body as well (33). The treatment is analo-
use topically applied foam preparations of class III gous to that of lichen planus (33–36).

Preventing recurrence of folliculitis decalvans Lichen planus follicularis

To prevent recurrences, all tufted hair follicles In the autoimmune disease lichen planus the hair
should be surgically removed from the scalp. follicles are destroyed by T lymphocytes, yielding
Once the disease process has been arrested, an irreversible, atrophizing alopecia usually
larger areas of scarring can be surgically reduced. consisting of small bald patches on the scalp.

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Conflict of interest statement 14. van Zuuren EJ, Fedorowicz Z, Carter B: Evidence-based treat-
Prof. Wolff has received lecture honoraria from the MSD Sharp & Dohme, ments for female pattern hair loss: a summary of a Cochrane sys-
Johnson & Johnson, Pierre Fabre, Grünenthal, and Bayer companies. tematic review. Br J Dermatol 2012; 167: 995–1010.
Dr. Fischer has received lecture honoraria from, and has served as a paid con- 15. Olsen EA, Dunlap FE, Funicella T, et al.: A randomized clinical
sultant for, the following companies: MSD Sharp & Dohme, Johnson & Johnson, trial of 5% topical minoxidil versus 2% topical minoxidil and placebo
Galderma, Pierre Fabre, ASATONA, ISDIN, Dr. Kurt Wolff, HairDreams, and Bayer. in the treatment of androgenetic alopecia in men. J Am Acad
Prof. Blume-Peytavi has received lecture honoraria from, and has served as a Dermatol 2002; 47: 377–85.
paid consultant for, the following companies: Almirall, Johnson & Johnson, 16. Mella JM, Perret MC, Manzotti M, Catalano HN, Guyatt G:
Galderma, Pierre Fabre, Procter & Gamble, and Bayer. Efficacy and safety of finasteride therapy for androgenetic alopecia:
a systematic review. Arch Dermatol 2010; 146: 1141–50.
Manuscript submitted on 24 July 2015, revised version accepted on 17. Price V, Roberts JL, Hordinsky M: Lack of efficacy of finasteride in
5 April 2016. postmenopausal women with androgenetic alopecia. J Am Acad
Dermatol 2000; 43: 768–76.
Translated from the original German by Ethan Taub, M.D.
18. Gubelin Harcha W, Barboza Martinez J, Tsai TF, et al.: A randomized,
active- and placebo-controlled study of the efficacy and safety of
different doses of dutasteride versus placebo and finasteride in
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the growth and shedding of hair. Br J Dermatol 1996; 134: 47–54. immunerkrankung. Hautarzt 2003; 54: 713–22.
4. Lindner J, Hillmann K, Blume-Peytavi U, et al.: Hair shaft abnor- 21. Tosti A, Bellavista S, Iorizzo M: Alopecia areata: a long term follow-
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23. Messenger AG, McKillop J, Farrant P, McDonagh AJ, Sladden M:
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British Association of Dermatologists’ guidelines for the manage-
6. Whiting DA: Chronic telogen effluvium: increased scalp hair ment of alopecia areata 2012. Br J Dermatol 2012; 166: 916–26.
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25. Fischer TW: Alopezien – Diagnostisches und therapeutisches
8. Blume-Peytavi U, Blumeyer A, Tosti A, et al.: S1 guideline for diag- Management. Akt Dermatol 2008; 34: 209–25.
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adolescents. Br J Dermatol 2011; 164: 5–15. 26. Trüeb RM: Vernarbende Alopezien. Hautarzt 2013; 64: 810–9.
9. Heilmann S, Brockschmidt FF, Hillmer AM, et al.: Evidence for a 27. Powell JJ, Dawber RPR, Gatter K: Folliculitis decalvans including
polygenic contribution to androgenetic alopecia. Br J Dermatol tufted folliculitis: clinical, histological and therapeutic findings. Br J
2013; 169: 927–30. Dermatol 1999; 140: 328–33.
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(5-year) multinational experience with finasteride 1 mg in the tis decalvans – Behandlung mit einer systemischen Rifampicin-
treatment of men with androgenetic alopecia. Eur J Dermatol Clindamycin-Kombinationstherapie bei 17 Patienten. Akt Dermatol
2002; 12: 38–49. 2001; 27: 361–3.
11. Blume-Peytavi U, Vogt A: Current standards in the diagnostics and 29. Bolz S, Jappe U, Hartschuh W: Successful treatment of perifolli-
therapy of hair diseases—hair consultation. J Dtsch Dermatol Ges culitis capitis abscedens et suffodiens with combined isotretinoin
2011; 9: 394–410. and dapsone. J Dtsch Dermatol Ges 2008; 6: 44–7.
12. Blumeyer A, Tosti A, Messenger A, et al.: Evidence-based (S3) 30. Scerri L, Williams HC, Allen BR: Dissecting cellulitis of the scalp:
guideline for the treatment of androgenetic alopecia in women and response to isotretinoin. Br J Dermatol 1996; 134: 1105–8.
in men. J Dtsch Dermatol Ges 2011; 9 (Suppl 6): 1–57. 31. Le Cleach L, Chosidow O: Clinical practice. Lichen planus. N Engl
13. Lucky AW, Piacquadio DJ, Ditre CM, et al.: A randomized, placebo- J Med 2012; 366: 723–32.
controlled trial of 5% and 2% topical minoxidil solutions in the 32. Kossard S: Postmenopausal frontal fibrosing alopecia. Scarring
treatment of female pattern hair loss. J Am Acad Dermatol 2004; alopecia in a pattern distribution. Arch Dermatol 1994; 130:
50: 541–53. 770–4.

Frontal fibrosing alopecia

The pattern of hair loss resembles that of
androgenetic alopecia in men. Perifollicular
erythema and hyperkeratoses can often be
seen at the hairline. The condition is not always
restricted to the frontal region.

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 MEDICINE

33. Vano-Galvan S, Molina-Ruiz AM, Serrano-Falcon C, et al.: Frontal

Further information on CME
fibrosing alopecia: a multicenter review of 355 patients. J Am
Acad Dermatol 2014; 70: 670–8.
This article has been certified by the North Rhine Academy
34. Manousaridis I, Manousaridis K, Peitsch WK, Schneider SW: Indi-
vidualisierte Behandlung und Therapiewahl bei Lichen planus: ein for Postgraduate and Continuing Medical Education.
schrittweiser Ansatz. J Dtsch Dermatol Ges 2013: 981–91. Deutsches Ärzteblatt provides certified continuing medical
35. Racz E, Gho C, Moorman PW, Noordhoek Hegt V, Neumann HA: education (CME) in accordance with the requirements of
Treatment of frontal fibrosing alopecia and lichen planopilaris: a the Medical Associations of the German federal states
systematic review. J Eur Acad Dermatol Venereol 2013; 27: (Länder). CME points of the Medical Associations can be
1461–70.
acquired only through the Internet, not by mail or fax, by
36. Harries MJ, Messenger A: Treatment of frontal fibrosing alopecia the use of the German version of the CME questionnaire.
and lichen planopilaris. J Eur Acad Dermatol Venereol 2014; 28:
1404–5. See the following website: cme.aerzteblatt.de
Participants in the CME program can manage their CME
Corresponding author
Prof. Dr. med. Hans Wolff
points with their 15-digit “uniform CME number” (einheit-
Klinik und Poliklinik für Dermatologie und Allergologie liche Fortbildungsnummer, EFN). The EFN must be
Ludwig-Maximilians-Universität München entered in the appropriate field in the cme.aerzteblatt.de
Frauenlobstr. 9–11
D-80337 Munich, Germany website under “meine Daten” (“my data”), or upon registra-
[email protected] tion. The EFN appears on each participant’s CME certifi-
cate.
This CME unit can be accessed until 21 August 2016, and
earlier CME units until the dates indicated:
– “Alcohol Dependence and Harmful Use of Alcohol”
(Issue 17/2016) until 24 July 2016,
– “Acute Lumbar Back Pain” (Issue 13/2016) until 26 June
2016,
– “Evidence-Based Hernia Treatment in Adults” (Issue
@ Supplementary material
For eReferences please refer to:
www.aerzteblatt-international.de/ref2116
9/2016) until 29 May 2016.

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MEDICINE

Please answer the following questions to participate in our certified Continuing Medical Education
program. Only one answer is possible per question. Please select the most appropriate answer.

Question 1 Question 6
What is the name of the resting phase that lasts two to Which of the following factors implies a worse prognosis for
four months before a hair falls out? alopecia areata?
a) catagen a) onset in adulthood
b) telogen b) nail involvement (pitting; sandpaper nails)
c) anagen phase c) female sex
d) anaphase d) location on the top of the head
e) miophase e) limited involvement

Question 2 Question 7
How long is the growth phase of a hair follicle on the What is a possible side effect of minoxidil treatment in women
scalp? with androgenetic alopecia?
a) about 48 hours a) irregular menstrual cycles
b) about 6 months b) acne
c) 2–6 years c) loss of libido
d) 12–18 years d) hypertrichosis
e) a lifetime e) infertility

Question 3 Question 8
In effluvium of unknown cause, which of the following What measure can lessen the likelihood of recurrent folliculitis
should be ruled out by laboratory testing? decalvans?
a) vitamin C deficiency a) use of a shampoo that contains caffeine
b) vitamin B deficiency b) weekly scalp baths in basic salt solution
c) iron deficiency c) at least 6 months of treatment with TNF-α antagonists after all the
d) zinc deficiency affected areas have healed
e) calcium deficiency d) surgical removal of all tufted hair follicles from the scalp
e) UVB irradiation of the affected scalp areas

Question 4 Question 9
What is the most common type of hair loss? Which of the following types of alopecia is reversible?
a) frontal fibrosing alopecia a) lichen planopilaris
b) lichen planus follicularis b) alopecia areata
c) folliculitis decalvans c) Brocq’s pseudopelade
d) alopecia areata d) chronic discoid lupus erythematosus
e) androgenetic alopecia e) folliculitis decalvans

Question 5 Question 10
A 23-year-old male student complains of marked hair In what type of alopecia do staphylococci play an important
loss over a period of four weeks, and this is confirmed pathogenetic role?
by a trichogram. Which of the following tests must not a) lichen planopilaris
be omitted in the further work-up? b) alopecia areata
a) blood sugar profile over the course of the day c) frontal fibrosing alopecia of Kossard
b) serum zinc level d) chronic discoid lupus erythematosus
c) urinary protein e) folliculitis decalvans
d) syphilis test
e) ECG

386 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2016; 113: 377–86
 MEDICINE

Additional material to:

The Diagnosis and Treatment of Hair and Scalp Diseases
by Hans Wolff, Tobias W. Fischer, and Ulrike Blume-Peytavi
Dtsch Arztebl Int 2016; 113: 377–86. DOI: 10.3238/arztebl.2016.0377

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