Acute and Chronic Telogen Effluvium

Abstract

The human hair cycle has four recognised phases - anagen, catagen, telogen, and exogen - with the duration of each phase being site specific. In scalp hair, telogen lasts for around 12 weeks, following which the telogen hair is shed, a process instigated by unknown factors in the exogen phase. Any disturbance to the hair cycle will induce a relative change in the equilibrium between growth and rest, initiating an acute telogen effluvium. It is essential therefore to identify the inducing factor so as to consider if any intervention is required; reassurance is frequently all that is needed. However, if the increase in hair shedding persists for 6 months or more (chronic telogen effluvium), then biochemical investigations are required. Frequently hair loss induces changes in the patient’s hair care and grooming routines resulting in an artificial increase in the observed shedding; understanding this potential exacerbating factor is essential. Finally, increased hair shedding can initially occur in patients in whom reduced hair density (hair per cm2) will ensue; diagnostic and treatment options will only be briefly discussed in such situations.

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Chapter Title Acute and Chronic Telogen Effluvium
Copyright Year 2015
Copyright Holder Springer-Verlag Berlin Heidelberg
Corresponding Author Family Name Rushton
Particle
Given Name D. Hugh
Suffix
Degrees BA, PhD, DSc
Division
Organization/University School of Pharmacy &
Biomedical Sciences, University
of Portsmouth
City Portsmouth
State Hants
Postcode PO1 2DT
Country UK
Email rushton@btinternet.com
Abstract The human hair cycle has four recognised phases – anagen, catagen,
telogen, and exogen – with the duration of each phase being site
specific. In scalp hair, telogen lasts for around 12 weeks, following
which the telogen hair is shed, a process instigated by unknown
factors in the exogen phase. Any disturbance to the hair cycle will
induce a relative change in the equilibrium between growth and
rest, initiating an acute telogen effluvium. It is essential therefore
to identify the inducing factor so as to consider if any intervention
is required; reassurance is frequently all that is needed. However,
if the increase in hair shedding persists for 6 months or more
(chronic telogen effluvium), then biochemical investigations are
required. Frequently hair loss induces changes in the patient’s hair
care and grooming routines resulting in an artificial increase in the
observed shedding; understanding this potential exacerbating factor
is essential. Finally, increased hair shedding can initially occur in
patients in whom reduced hair density (hair per cm2) will ensue;
diagnostic and treatment options will only be briefly discussed in
such situations.
Keywords (separated by “ - “) Hair loss - Telogen effluvium - Hair shedding - Chronic telogen
effluvium
Q1

A. Katsambas et al. (eds.), European Handbook of Dermatological Treatments,
DOI 10.1007/978-3-662-45139-7_96, © Springer-Verlag Berlin Heidelberg 2015
Introduction
Hair is considered to be a major component of an
individual’s general appearance. Throughout his-
tory, and in most (although not all) civilisations,
scalp hair has been associated with positive sig-
nals such as beauty and power. Baldness or hair
loss on the other hand has a negative attribute.
The psychological impact of hair loss results
in a measurably detrimental change in self-
esteem and is associated with images of reduced
worth. It is not surprising that both men and
women find hair loss a stressful experience even
in conditions where a complete recovery can be
expected. Yet the distress, even by a temporary
loss of hair, profoundly affects an individual’s
self-confidence and quality of life. This can result
in the sufferer seeking help from unscrupulous
organisations selling useless, ineffective lotions
and potions for large sums of money.
Compounding matters, many sufferers will, upon
D.H. Rushton, BA, PhD, DSc
School of Pharmacy & Biomedical Sciences,
University of Portsmouth, Portsmouth,
Hants PO1 2DT, UK
e-mail: rushton@btinternet.com
96
Acute and Chronic Telogen
Effluvium
D. Hugh Rushton
[AU1]
Key Points
s Hair loss is distressing to many patients.
s In telogen effluvium (TE), once the ini-
tiating factor is identified, reassurance is
often all that is required. However, the
physician should be aware of a possible
underlying issue if the increased hair
shedding does not resolve.
s At the initial consultation, time must be
given to evaluate all possible factors that
might have affected the individual up to
4 months prior to the patient becoming
aware of an increase in hair shedding.
s Frequently hair loss induces changes in
the patient’s hair care and grooming
routines, which can result in an artificial
increase in the observed shedding.
Patients should be advised to maintain
their normal hair care routine.
s If nutritionally induced hair loss has been
identified, either a change in dietary hab-
its or taking the appropriate or stopping
the inappropriate supplement should
address this problem. The physician also
needs to explain the time lag between
correcting the imbalance and the patient
seeing a reduction in hair loss. In long-
standing chronic TE (CTE), many
months are required to return the long
hair volume to its former status.
s In conditions that result in hair density
changes, increased hair shedding is
often the first indication of an impend-
ing problem and a modified unit area
trichogram will aid diagnosis.
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seeing an increase in hair shedding, change their
hair care and grooming habits, thus adversely
affecting the aesthetic appearances and inducing
an apparent increase in the perceived hair loss. In
addition, there may also be a relative increase in
sebaceous matter and scaling due to ineffective
and inefficient shampooing, which can also
exacerbate the loss of hair.
In this chapter we focus on commonly pre-
senting causes leading to acute and chronic telo-
gen effluvium without any change in hair density
(parting width unchanged). However, in severe
acute or persistent chronic conditions where
increased hair shedding is occurring, the possi-
bility of a lag phase issue should be considered.
Although increased hair shedding may be present
in conditions where there is reduced hair density
(Rushton 1993), these will only be briefly dis-
cussed. Conditions that involve a delay in the ini-
tiation of the new anagen cycle (a lag phase issue)
that results in a reduction in the relative number
of visible hairs, i.e. reduced hair per cm2, will not
be fully covered. The reader should consult the
endocrine literature in such cases for an in-depth
guide to the appropriate investigations and treat-
ment options.
Identifying and Classifying Hair
Variables Involved in Telogen
Effluvium
Three hair variables define the aesthetic profile of
an individual, (a) the number of hairs per cm2, (b)
hair diameter, and (c) the length of the anagen
growth phase and related subsequent release of
the telogen hair. In a normal healthy individual in
whom there is no underlying scalp scaling
malady, these variables exist in a steady state.
Only when there is an alteration to one or a
combination of these variables are the aesthetic
hair profile change and hair loss observed.
In telogen effluvium (TE), there is generally
no change in the number of hairs per cm2 nor is
there a change in hair diameter; however, an
increase in the number of telogen hairs, with a
corresponding relative decrease in the number of
growing hairs, affects the observed hair when
combing and shampooing. Many physicians like
to undertake a ‘pull test’ to confirm hair loss is
occurring. This is unnecessary in TE since the
patient already knows more hair than normal is
falling out. Not only is extracting a large amount
of hair from the scalp in a single ‘pull’ painful, it
can cause further distress to an individual already
anxious about losing hair. Furthermore, the ‘pull
test’ provides no objective data or useful infor-
mation about the cause of the hair loss.
If the effluvium is severe or there is a delay in
the initiation of the new anagen cycle, there can
be a temporary reduction in hair density. In the
majority of telogen effluvium cases, no change in
hair density occurs. Figure 96.1 illustrates the
impact of a decrease in the anagen phase and the
resulting relative increase in daily hair shedding
for a given total scalp hair density. For example,
with a total hair density of 150,000 hairs and an
anagen duration of 7 years, the individual would
lose 59 hairs per day; however, if the anagen
duration was to reduce to 5 years, then the daily
hair loss would rise to 82, an increase of 39 %. If
the TE lasts only for a few weeks, most indi-
viduals would be unaware of any increase in hair
shedding, but when shedding is observed, it can
set off an adverse sequence of events. For example,
[AU2]
450
Hair density & anagen duration
400
350 Daily shed (150k)
Daily shed (100k)
300
250
200
150
100
50
012345
Years
Hairs per day
678910
Fig. 96.1 Projected daily hair shedding for an individual
with a total hair density of 150,000 or 100,000 hairs with
anagen durations from 1 to 10 years
D.H. Rushton
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if an individual shampooed every 2 days but as a
consequence of seeing an increase in hair shed-
ding they then reduce their shampooing fre-
quency, this would result in an apparent increase in
hair lost on subsequent shampoos. This induced
change is of course not a true increase but an
observed difference in their hair shedding due to
the relative change of their hair care routine.
It is frequently quoted that 100 hairs are lost
each day; from Fig. 96.1, this corresponds to
4-year anagen duration for a total hair density of
150,000 and approximately 3 years for a total
hair density of 100,000. Assuming an average
monthly growth rate of 1.2 cm, such individuals
would respectively be able to grow their hair to
58 cm or 43 cm in length. Obviously not all of the
hair would have grown to these lengths because
for 3 months, 9,000 hairs are in telogen, repre-
senting respective telogen values of 6 and 9 %.
Quoting a general daily hair shedding amount or
giving specific percentages for anagen or telogen
hair is meaningless. Individuals have their own
parameters for these variables and it is the rela-
tive change for them, which is the critical factor.
Causes of Telogen Effluvium (TE)
A change in the anagen/telogen (A/T) equilib-
rium can occur from many events, and it is impor-
tant to try to identify any alteration to the patient’s
medical history, hair care routine, scaling mala-
dies, and lifestyle changes. Common events
include changes in medication dosages, starting
or stopping a medication (oral contraceptive),
childbirth (postnatal), fever, illness, miscarriage,
menstrual dysfunction, excessive vitamin A
intake, weight loss (crash dieting), and surgery
involving a general anaesthetic.
Diagnosis
The Initial Consultation
It is of paramount importance to spend time tak-
ing a full and complete history of the events that
occurred 4 months before the patient became
aware of increased hair shedding. Often the cause
can be identified and the appropriate reassurance
and guidance given. In many cases no further
action is required and reassurance alone is suffi-
cient to ease the patient’s fear that they will not
become bald. It is also important to explain the
time delay involved before they will see a reduc-
tion in the amount of hair being shed. When TE
is linked to a prescription medication, whether an
alternative preparation could be prescribed
requires careful consideration. A sympathetic
understanding is often needed, as many patients
are more worried about their hair loss than the
underlying medical issue. Simply dismissing the
patient’s hair loss concerns as unimportant can
cause unnecessary distress.
Drug and patient information leaflets fre-
quently list alopecia as a reported side effect but
the association is often tenuous; where proven
the frequency is relatively rare. However, there
are groups of drugs which in all family members
cause hair loss (a relative alteration to the anagen/
telogen ratio); for example, anticoagulants (hepa-
rin, heparinoids, and coumarins) and many cyto-
static agents induce an anagen effluvium. Dawber
and Van Neste and Van Neste and Rushton publi-
cations give a comprehensive list of drugs that
can cause hair loss.
When hair loss is a reported side effect, this is
often stated as alopecia. However, the very word
alopecia to the layperson is often taken to mean
they will go bald. Explaining the various types of
alopecia requires skill to allay any unfounded
fears of the patient becoming bald. It should also
be remembered that the published data proving
drug-induced hair loss is somewhat limited.
Demonstrating cause and effect is particularly
difficult in medication-induced TE. Establishing
a positive causative link usually requires re-
challenging the patient with the drug once the
hair loss has abated, but patients are often unwill-
ing to restart a medication they believe caused
their hair loss.
The recently identified role of the exogen
phase in hair shedding could explain synchro-
nised hair moults in animals and the non-
synchronised hair shedding in humans. How the
hair is released in exogen is still unknown but
[AU3]
[AU4]
96 Acute and Chronic Telogen Effluvium
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some medications appear to induce a premature
telogen effluvium by activating the exogen path-
ways. It is not unusual to discover a patient
observing increased hair shedding within 4 weeks
of starting a prescribed medication. The hair
morphology of the shed hair is that of a telogen
bulb indicating the premature release of the telo-
gen hair. Examination of the shed hairs distin-
guishes the hair from an anagen effluvium, as
would occur with chemotherapy, from a true telo-
gen effluvium. Whether an altered exogen phase
continues to operate during drug therapy is the
subject of ongoing research.
Since TE only becomes evident if the distur-
bance to the anagen/telogen balance lasts long
enough to induce an observed increase in hair
shedding, it is important to recognise that the
underlying cause may not be immediately obvi-
ous and should alert the physician to consider
undertaking some biochemical investigations.
This situation is usually encountered if the
cause(s) does not self-correct and the hair
shedding has been present for 6 months or more;
in this situation chronic telogen effluvium is the
diagnosis.
Chronic Telogen Effluvium
Chronic telogen effluvium (CTE) occurs where
there is a relative decrease in the proportion of
growing hair (anagen) and an increase in telogen
hair, which has persisted for at least 6 months.
This results in a reduction in the long hair volume
(less hair to clip up or tie back in the ponytail;
Fig. 96.2) and a frequent complaint seen in der-
matological clinics. In addition, compared with
the normal hair growth situation (Fig. 96.3), there
is a relative increase in the incoming new hair
(Fig. 96.4).
In the absence of an obvious cause for persis-
tent increased hair shedding, biochemical investi-
gations frequently reveal no apparent problem.
This situation is compounded by current labora-
tory practice where the lower female reference
ranges for some haematological variables (hae-
moglobin [Hb], red blood cell count [RBC], and
serum ferritin) were derived from arbitrarily
assigned parameters. Unfortunately these studies
contained a significant number of iron-deficient
females. The significance of this can be seen
when a male presenting with a Hb of 125 g/L
(12.5 g/dL) would be considered anaemic and
investigated, yet such a value in the female is
deemed normal with no further action considered;
this situation also applies for RBC and serum fer-
ritin. Given that in non-human mammals there is
no sex difference for Hb or RBC concentrations
(veterinarians do not evaluate ferritin), I would
recommend employing the lower male reference
ranges for Hb, RBC, and serum ferritin until the
appropriate studies in proven iron-replete women
[AU5]
[AU7]
Fig. 96.2 Hair samples presented at consultation by a
patient complaining of unexplained chronic telogen efflu-
vium over a 7-year period. Her mother obtained the sam-
ple on the right at the age of 18 years, a family tradition in
her culture (the hair in females is traditionally left uncut
from birth until their 18th birthday). The left sample was
cut when aged 27 due to the distress of persistent unex-
plained increased hair shedding for the previous 5 years;
the hair had not been cut since her 18th birthday and
weighs 30 % less than the right sample
D.H. Rushton
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have been undertaken. With regard to the cur-
rently cited parameters for other micronutrients
and various vitamins, conflicting reference range
values are widespread and objective evidence
supporting specific parameters is lacking.
The role of nutrition in hair growth is well
established in severe malnutrition, anaemia, and
anorexia nervosa. However in the absence of an
underlying pathology, nutritional effects are
poorly understood. Investigating chronic telogen
effluvium in apparently healthy individuals and,
in particular women, requires a different approach.
Employing reference ranges constructed to define
the limits of illness must be interrupted in relation
to the fact that most individuals complaining of
CTE are apparently healthy. Consequently, opti-
mising blood variables for the non-essential tis-
sues often requires higher concentrations than
those used to define illness.
Studies have shown that CTE arises from a
nutritional imbalance and iron deficiency appears
to be the most frequent cause. While 34 % of pre-
menopausal females have CTE, it is well recog-
nised that while there is widespread iron
deficiency in menstruating females, many do not
experience increased hair loss. The recently iden-
tified iron-regulating hormone hepcidin is
involved in hair follicle iron metabolism and hae-
mochromatosis where there is variable pene-
trance; a similar situation might operate in CTE.
Data from 200 apparently healthy women
complaining of CTE showed depleted iron stores
(as assessed by serum ferritin) as the main find-
ing. Sixty-five per cent failed to achieve the lower
reference level for males (40 ng/ml), while 95 %
had a serum ferritin level below (70 ng/ml), the
99 % confidence limit for iron staining in the
bone marrow; the accepted ‘gold standard’ for
being iron replete. Total iron binding capacity
(TIBC) values not only reflect the iron transport
status; they also indicate protein insufficiency.
TIBC levels in the lower half of the reference
range, indicating an adequate iron status, were
found in women with low serum ferritins. These
findings suggest that a large number of women
with CTE might also have a suboptimal intake of
first-class proteins. Normally, TIBC increases in
response to iron deficiency with concentrations
above or in the upper half of the reference range.
Furthermore, 28.5 % of this group had a raised
serum folic acid level suggesting excessive vita-
min supplementation, which was probably taken
to treat their excessive hair shedding.
Despite the accumulating publications linking
unexplained chronic telogen effluvium and low
serum ferritin concentrations in women, some
dermatologists still believe there is no association
at all or that the link is tenuous. These views,
based on five subjects with no objective follow-
up hair data or serum ferritin values or with
[AU8]
[AU9]
Fig. 96.3 The normal presentation of scalp hair from an
individual being studied during the establishment of nor-
mal parameters for hair variables in females (Rushton,
PhD Thesis 1988)
[AU6]
Fig. 96.4 Typical presentation of chronic telogen efflu-
vium (CTE) in a 28-year-old female patient complaining
of unexplained increased hair shedding for over 2 years.
Note the abnormal number of short hair compared with
the presentation found in a normal 28-year-old female
(Fig. 96.3)
96 Acute and Chronic Telogen Effluvium
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confounding and contradicting issues, were sub-
sequently criticised. Despite these shortcomings,
both are still widely cited. It is noteworthy that
the homozygous ‘Mask’ mouse (a hepcidin
knockout mutant that inhibits iron absorption)
fed on a normal mouse diet develops a gradual
loss of body but not facial hair leading to almost
complete trunk nudity within 4 weeks. In addi-
tion, they become iron deficient and anaemic and
the females are infertile. However following iron
supplementation to their normal diet, all symp-
toms completely resolve.
Excessive intake of vitamin A causes hair
loss, as can vitamin A deficiency. Low serum
zinc (Zn) is frequently cited to cause hair loss,
but with the exception of acrodermatitis entero-
pathica, there is little evidence to support this
widespread belief. However both low vitamin A
and Zn have been linked to increased skin exfo-
liation and scaling, which if present on the scalp
can induce hair loss. Recently low vitamin D
concentrations <20 nmol/L (8 ng/ml; 2.5 nmol/L,
equals 1 ng/ml) have been associated with
increased hair shedding, but further work is
needed to confirm the role of low vitamin D con-
centrations and hair loss.
Acute and Chronic Telogen
Effluvium in Patients
with Impending or Exhibiting
Reduced Hair Density
The possibility of increased hair shedding in
patients with reduced hair density, particularly in
women, needs to be considered. While the previous
sections detailed how to investigate acute and
chronic telogen effluvium without a change in
hair density, sometimes telogen effluvium occurs
initially in patients in whom reduced hair density
will become a future problem; in these cases a
hormonal imbalance should be considered. In
those presenting with reduced hair density, the
possibility of coexisting factors, as described
above, should be considered.
When the clinical history is unhelpful in iden-
tifying a possible cause for reduced hair density,
how do you proceed? Understanding tissue sensi-
tivity is an important concept in the absence of
any gross pathology (hyperandrogenism; acne
and/or hirsutism); you have to consider tissue
sensitivity in a patient with a normal androgen
status. This situation is challenging in a busy
clinical environment since such patients require
additional time to identify a potential problem. In
these cases such patients would benefit from
undergoing a hair analysis. The ideal test is the
modified unit area trichogram, which evaluates
two variables that are diagnostic for male and
female pattern hair loss that is actively progress-
ing and is much more sensitive than a ‘pull test’
or a scalp biopsy. In the modified unit area tricho-
gram, a sample of at least 50 hairs is required.
The individual hairs are epilated in the direction
of hair growth from the area under investigation
and then placed onto a microscope slide with
double-sided tape. The percentages of telogen
≤30 mm in length and vellus hair (hair ≤40 μm in
diameter ≤30 mm in length) are determined. If
the per cent of telogen hair ≤30 mm is above
6.1 % in males or 7.2 % in females (Rushton
et al. 1990) or the per cent of vellus hair is
>10.2 in males or >13.0 in females, then an active
androgenic drive must be considered. When both
variables are elevated, treatment should not be
delayed.
In males, finasteride 1 mg (Propecia) a
5α-reductase inhibitor has proven effective in
around 40 % of men by preventing the conversion
of testosterone to dihydrotestosterone (DHT) via
the 5α-reductase pathway. Dutasteride, a type I
and type II 5α-reductase inhibitor, has yet to
undergo formal evaluation for use in male pattern
hair loss. While minoxidil does not appear to
affect the 5α-reductase pathway, it can prolong
the anagen phase, thereby limiting the number of
transitions into telogen and delaying the progres-
sion of male pattern hair loss.
Figure 96.5 lists the treatment options for hair
loss in women with respect to likely outcomes,
but help in enabling the patient to achieve an
acceptable aesthetic appearance often requires
addressing the hair care as well as the medical
needs.
D.H. Rushton
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Hair loss in women
Partially reversible Non-reversible
Androgen-dependent alopecia
also known as: -
Androgenetic alopecia
Androgenic alopecia
Common baldness
Diffuse hair loss
Female baldness
Female pattern hair loss
Genetic hair loss
Acute & chronic
telogen effluvium
Post-natal, Drugs,
Iron, Fever,
Thyroid,
Alopecia areata,
Anagen effluvium
Cosmetic treatments.
Potential Treatments
Options limited: -
Can be self-limiting,
Poor prognosis.
?
Anti-androgens: -
Cyproterone acetate
Spironolactone
Flutamide
5 alpha reductase inhibitors
Finasteride, Dutasteride
Others :-
Minoxidil,
Prostaglandin analogs?
Diazoxide?
Self-correcting
but some require
specific
interventions.
Common conditions
Scarring Alopecia
Outcomes
Reversible
Fig. 96.5 Flow chart for common hair loss conditions in women
96 Acute and Chronic Telogen Effluvium

Conclusions
Hair loss is distressing to many patients and
simply dismissing their concerns is both irre-
sponsible and unethical. Too often the patient
is dismissed because hair loss is non-life
threatening.
In TE once the initiating factor is identified,
reassurance is often all that is required.
However, the physician should be aware of a
possible underlying issue if the increased hair
shedding does not abate.
At the initial consultation, time must be given
to evaluate all possible factors that might have
affected the individual up to 4 months prior to
the patient becoming aware of an increase in
hair shedding.
Frequently hair loss induces changes in the
patient’s hair care and grooming routines,
which can result in an artificial increase in the
observed shedding. Patients should be advised
to maintain their normal hair care routine.
If nutritionally induced hair loss has been
identified, either a change in dietary habits
or taking the appropriate or stopping the
inappropriate supplement should address
this problem. The physician also needs to
explain the time lag between correcting the
imbalance and the patient seeing a reduction
in hair loss. In long-standing CTE, many
months are required to return the long hair
volume to its former status.
In conditions that result in hair density
changes, increased hair shedding is often the
first indication of an impending problem.
Undertaking a modified unit area trichogram
will identify an active androgen-mediated
condition.
References
Rushton DH. Management of hair loss in women.
Dermatol Clin. 1993;11:47–53.
Rushton DH, Ramsay ID, James KC, Norris MJ, Gilkes
JJ. Biochemical and trichological characterization of
diffuse alopecia in women. Br J Dermatol.
1990;123(2):187–97.
Further Reading
Cash TF. The psychological effects of androgenetic alope-
cia in men. J Am Acad Dermatol. 1992;26(6):926–31.
Dawber RPR, Van Neste D. Hair and scalp disorders,
common presenting signs differential diagnosis and
treatment. London: Martin Dunitz; 1995. 262 p.
Deloche C, Bastien P, Chadoutaud S, Galan P, Bertrais S,
Hercberg S, et al. Low iron stores: a risk factor for
excessive hair loss in non-menopausal women. Eur J
Dermatol. 2007;17(6):507–12.
Du X, She E, Gelbart T, Truksa J, Lee P, Xia Y, et al. The
serine protease TMPRSS6 is required to sense iron
deficiency. Science. 2008;320(5879):1088–92.
Hård S. Non-anemic iron deficiency as an etiological fac-
tor in diffuse loss of hair of the scalp in women. Acta
Derm Venereol. 1963;43:562–9.
Holler PD, Cotsarelis G. Retinoids putting the “a” in alo-
pecia. J Invest Dermatol. 2013;133(2):285–6.
Kantor J, Kessler LJ, Brooks DG, Cotsarelis G. Decreased
serum ferritin is associated with alopecia in women.
J Invest Dermatol. 2003;121(5):985–8.
Kingsley DH. The development and validation of a qual-
ity of life measure for the impact of androgen-
dependent alopecia [PhD]. Portsmouth: University of
Portsmouth, School of Pharmacy & Biomedical
Sciences; 1999.
Olsen EA, Reed KB, Cacchio PB, Caudill L. Iron defi-
ciency in female pattern hair loss, chronic telogen
effluvium, and control groups. J Am Acad Dermatol.
2010;63(6):991–9.
Park SY, Na SY, Kim JH, Cho S, Lee JH. Iron plays a
certain role in patterned hair loss. J Korean Med Sci.
2013;28(6):934–8.
Puolakka J. Serum ferritin in the evaluation of iron status
in young healthy women. Acta Obstet Gynecol Scand.
1980;95(Suppl):35–41.
Rasheed H, Mahgoub D, Hegazy R, El-Komy M, Abdel
Hay R, Hamid MA, et al. Serum ferritin and vitamin d
in female hair loss: do they play a role? Skin Pharmacol
Physiol. 2013;26(2):101–7.
Rook A, Dawber RPR. In diseases of the hair and scalp.
Oxford: Blackwell Scientific Press; 1982.
Rushton DH. Investigating and managing hair loss in
apparently healthy women. Can J Dermatol. 1993;
5:455–61.
Rushton DH. Nutritional factors and hair loss. Clin Exp
Dermatol. 2002;27(5):396–404.
Rushton DH, Barth JH. What is the evidence for gender
differences in ferritin and haemoglobin? Crit Rev
Oncol Hematol. 2010;73(1):1–9.
Rushton H, James KC, Mortimer CH. The unit area
trichogram in the assessment of androgen-dependent
alopecia. Br J Dermatol. 1983;109(4):429–37.
Rushton DH, Ramsay ID, Norris MJ, Gilkes JJ. Natural
progression of male pattern baldness in young men.
Clin Exp Dermatol. 1991;16(3):188–92.
D.H. Rushton
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490
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Rushton DH, Dover R, Sainsbury AW, Norris MJ, Gilkes
JJ, Ramsay ID. Reference limits for haemoglobin and
ferritin. BMJ. 2001;323:806–7.
Rushton DH, Dover R, Sainsbury AW, Norris MJ, Gilkes
JJ, Ramsay ID. Iron deficiency is neglected in wom-
en’s health. BMJ. 2002;325:1176–7.
Rushton DH, Norris MJ, Dover R, Busuttil N. Causes of
hair loss and the developments in hair rejuvenation. Int
J Cos Sci. 2002;24:17–23.
Rushton DH, Dover R, Norris MJ. Is there really no clear
association between low serum ferritin and chronic
diffuse telogen hair loss? Br J Dermatol. 2003;148(6):
1282–4.
Rushton DH, Ramsay ID, Gilkes JJH, editors. The use of
placebo or untreated controls in male pattern hair loss
leads to a significant and permanent loss of hair.
London: Dermatology; 2006.
Rushton DH, Bergfeld WF, Gilkes JJ, Van Neste D. Iron
deficiency and hair loss-nothing new? J Am Acad
Dermatol. 2011;65(1):203–4; author reply 204–6.
Rushton DH, editor. Hepcidin, the iron-regulating peptide –
what you need to know about its role in hair loss and, in
particular, chronic telogen effluvium (CTE). Proceedings
of the 7th World Congress for Hair Research. Edinburgh:
J Investigative Dermatology. 2013.
Sinclair R. There is no clear association between low
serum ferritin and chronic diffuse telogen hair loss. Br
J Dermatol. 2002;147(5):982–4.
St. Pierre SA, Vercellotti GM, Donovan JC, Hordinsky
M. Iron deficiency and diffuse nonscarring scalp alo-
pecia in women: more pieces to the puzzle. J Am Acad
Dermatol. 2010;63(6):1070–6.
Trost LB, Bergfeld WF, Calogeras E. The diagnosis and
treatment of iron deficiency and its potential relation-
ship to hair loss. J Am Acad Dermatol.
2006;54(5):824–44.
Van Neste DJ, Rushton DH. Hair problems in women.
Clin Dermatol. 1997;15(1):113–25.
Va n Ne s t e D , L e r oy T, C o n i l S . Exogen hair characterization
in human scalp. Skin Res Technol. 2007;13(4):436–43.
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