Chronic telogen effluvium:

A study of 5 patients over 7 years

Rodney Sinclair, MBBS, FACD
Melbourne, Australia

Chronic telogen effluvium is said to be self-limiting in the long run; the natural history of this condition,
however, has not been investigated prospectively. Four women, aged between 18 and 64 years and
diagnosed with chronic telogen effluvium between 1996 and 1997, were followed up prospectively for
a minimum of 7 years. One (previously reported) woman diagnosed in 1998 developed female pattern hair
loss confirmed on biopsy specimen within 18 months that was partially reversed by spironolactone. The
remaining 4 women continued to experience chronic diffuse telogen hair shedding that fluctuated in
severity. However, serial photography demonstrated no visible reduction in hair density, and serial scalp
biopsy specimen showed no follicular miniaturization. Although 4 out of 5 of our patients showed no
tendency toward development of female pattern hair loss or to spontaneous improvement, further work is
required to define the natural history of chronic telogen effluvium and the relative risk of developing
female pattern hair loss. ( J Am Acad Dermatol 2005;52:S12-6.)

C hronic telogen effluvium (CTE) was de-
scribed as a primary idiopathic disease entity
in 1996.1 Women present with an abrupt
onset of generalized shedding of telogen hairs from
the scalp, with or without an identifiable trigger, that
persists more than 6 months. The hair may come out
in handfuls. The shedding is frequently accompanied
by bitemporal recession. Importantly there is no
frontoparietal hair loss with widening of the central
part and these women characteristically present with
a full, thick head of hair. Important differential
diagnoses include female pattern hair loss (FPHL),
thyroid disease, drug-induced hair loss, systemic
lupus erythematosus, and nutritional deficiency.2
FPHL is the preferred term for female androgenetic
alopecia. CTE can be differentiated from early FPHL
histologically using a horizontally sectioned 4-mm
punch biopsy specimen taken from the vertex scalp.
At the midisthmus level, a ratio of terminal to vellus
hairs (T:V) of less than 4:1 is considered diagnostic of
This supplement is made possible through the gener-
ous support of Stiefel Laboratories for the American
Academy of Dermatology.
From the Department of Dermatology, University of Melbourne.
Funding sources: None.
Conflicts of interest: None identified.
Reprint requests: Rodney Sinclair, MBBS, FACD, University of
Melbourne Department of Dermatology, St Vincent’s Hospital,
41 Victoria Parade, Fitzroy, 3065, Melbourne, Victoria, Australia.
E-mail: sinclair@svhm.org.au.
0190-9622/$30.00
ª 2005 by the American Academy of Dermatology, Inc.
doi:10.1016/j.jaad.2004.05.040
FPHL, whereas a ratio greater than 8:1 indicates
CTE.3 A single biopsy specimen may underestimate
FPHL due to inadequate sampling.4 Multiple punch
biopsy specimens from immediately adjacent skin on
the scalp increases the diagnostic reliability from 79%
for a single biopsy specimen to 98% when 3 biopsy
specimens are taken.5 The natural history of CTE has
not been studied prospectively; however, it has been
suggested that the hair shedding is self-limiting and
that women with this condition do not go bald.1
There is limited evidence to support the use of
oral antiandrogen therapy in the management of
FPHL.6,7 Scalp biopsy may, therefore, be useful to
identify women most likely to respond to this
treatment and to exclude women not likely to
benefit.
CASE 1
A 54-year-old woman presented in 1995 with an
18-month history of continuous excessive hair shed-
ding. The hair shedding began suddenly and she was
able to collect between 40 and 150 hairs per day (Fig
1). She estimated the thickness of her ponytail had
decreased by 50% during the preceding 18 months.
Her father had died at the age of 40 but was Hamilton
stage IV at the time of his death. There was no other
family history of FPHL; however, her sister had
experienced a single patch of alopecia areata that
had regrown spontaneously. Her history included
Hashimoto’s thyroiditis; she was, however, being
treated with thyroxine and was euthyroid. She was
postmenopausal and not on hormone replacement
therapy.

S12
J AM ACAD DERMATOL
VOLUME 52, NUMBER 2
Fig 1. Patient brought in a bag full of hair at her initial
presentation. Each bundle corresponds to the amount she
shed in 1 day.
On examination she had shoulder length hair,
with moderate bitemporal recession. There was no
widening of the central part, and she appeared to
have a normal head of hair (Fig 2). There was
a positive hair pull of telogen hairs over the entire
scalp. Iron studies, serum zinc, thyroid function tests,
free androgen index, and dihydroepiandostendione
levels were all normal and antinuclear antibody was
negative. As CTE had not been described, a pre-
sumptive diagnosis of FPHL was made. Cyproterone
acetate (100 mg daily) for 10 days each month was
started in combination with ethinyl estradiol (0.0625
mg) and reviewed at 6-month intervals. During the
next 18 months there was no reduction in daily hair
shedding, and in 1997 a scalp biopsy was performed
to determine whether she had FPHL or CTE.
The histology was consistent with a diagnosis of
CTE (Table I). The cyproterone acetate and ethinyl
estradiol were ceased and topical minoxidil was
started.
Twelve months later, in 1998, the hair shedding
had continued unabated, although there was still no
reduction in hair density over the midfrontal or
vertex scalp. She was counting the number of hairs
she shed each day and kept a diary. She reported
losing 150 hairs per day and 400 hairs when she
shampooed. The hair pull test was positive. The
topical minoxidil was ceased and a repeated scalp
biopsy specimen showed 32 follicles on horizontal
section, of which none were miniaturized. Three
were in telogen. Repeated blood tests all revealed
normal findings.
Twelve months later, in 1999, the hair shedding
was continuing. The hair pull test was positive.
Standardized scalp photography was performed
with her head placed in a stereotactic device
(Fig 3). A repeated biopsy specimen sectioned
horizontally showed 52 follicles of which 7 were
vellus. Two catagen/telogen hairs were seen. The
T:V was 9:1.
Sinclair S13
Fig 2. Hair at initial presentation.
On review in 2000 and again in 2001, the hair
shedding was continuing at a rate of between 50 and
150 hairs per day and the hair pull test was positive;
however, serial scalp photography showed no dis-
cernible reduction in hair density over the midfrontal
(Fig 3) or vertex scalp. To reduce the possibility of
underestimating FPHL through limited sampling, in
2001 three 4-mm punch biopsy specimens were
taken from her midfrontal scalp and all were
sectioned horizontally. The T:Vs were 13:1, 8:1, and
6:1, which again was consistent with CTE.
On review in 2002, in spite of continuing hair
shedding, the photos showed no loss of hair volume,
and a biopsy was not performed. At the most recent
review in 2003, the hair shedding continues. The hair
pull test remains positive. She appears to have a full
head of hair. Scalp photographs show no reduction
in hair density, however, the bitemporal recession
is largely unchanged (Fig 4). Repeated biopsy
specimens sectioned horizontally showed no evi-
dence of FPHL almost 10 years after her initial
presentation and after 8 years of formal clinical,
photographic, and histologic follow-up.
CASE 2
A 64-year-old woman presented with a 6-month
history of diffuse hair shedding. She had collected
450 hairs in a single day. The loss was increased with
S14 Sinclair J AM ACAD DERMATOL
FEBRUARY 2005

Fig 3. Case 1, standardized serial midfrontal scalp photography with head positioned in
stereotactic device, from 1999 until 2003, and lateral photography to monitor bitemporal
recession.

Table I. The ratio of terminal to vellus hair follicles on scalp biopsy specimen for patients 1 to 5 at various time
intervals from baseline to year 7
Second biopsy Third biopsy Fourth biopsy Fifth biopsy
Patient Initial biopsy A B C A B C A B C A B C
1 ‘ (34:0) ‘ (32:0) 9:1 13:1 8:1 6:1 9:1 7:1 7:1
2 16.5:1 9:1 13.3:1 16:1 24:1 8.6:1 8.3:1 31:1
3 7.2:1 8.2:1 8.2 8:1 5.2:1 8.2:1
4 31:1 14:1 8:1 5.2:1 6.5:1 18:1 5.5:1 6:1
5 15:1 1:1 2.6:1 1.9:1

hair washing, and consequently she now only
washed her hair once every 2 weeks. There was no
family history of androgenetic alopecia. She had
a history of hyperthyroidism treated with radioactive
iodine. She subsequently developed hypothyroid-
ism and has been on thyroxine replacement therapy
for more than 25 years. Investigation by her referring
doctor revealed low T4 and elevated thyrotropin.
Her thyroxine dose was increased from 100 g to 150
g. At the time of presentation, she had been
euthyroid for 4 months. Iron studies and hormone
levels all revealed normal findings. Her only other
medication was sinvastatin. Scalp biopsy specimen
was consistent with a diagnosis of telogen effluvium
(Table I). The sinvastatin was ceased and topical
minoxidil (2%) was started. Six months later there
had been no improvement and she continued to
shed up to 400 hairs per day. The patient was
reviewed regularly, and serial standardized photog-
raphy was begun in 1999. On review, 4 years after
initial presentation, the hair shedding continued.
Repeated biopsy specimen was consistent with CTE.
On further review 8 years after initial diagnosis, she
was still shedding 50 to 150 hairs per day, however,
scalp photography (Fig 4) showed no loss of hair
volume and scalp biopsy specimen showed no
decrease in follicle T:V.
CASE 3
A 19-year-old woman presented with an 8-month
history of chronic diffuse hair shedding, reduction
in the volume of her ponytail, bitemporal recession,
but no widening of her central part. The hair shed-
ding had started suddenly; no precipitant event was
identified on questioning. Thyroid function tests,
iron studies, and hormone parameters all revealed
normal findings. She took no medications. Scalp
biopsy specimen was consistent with CTE (Table I).
On review at 6 months, 12 months, 2 years, 4 years,
and 8 years, the hair shedding had continued, but
J AM ACAD DERMATOL
VOLUME 52, NUMBER 2
Fig 4. Patients 2 to 5, standardized serial midfrontal scalp photography with head positioned in
stereotactic device.
the magnitude fluctuated between 50 and 300 hairs
per day. The shedding seemed worse in spring and
autumn. Repeated biopsy specimen at 12 months, 24
months, and 8 years revealed no decrease in follicle
T:V to suggest androgenetic alopecia, and serial
scalp photography begun in 1999 showed no re-
duction in hair density (Fig 4).
CASE 4
A 27-year-old woman presented with a 4-year
history of increased hair shedding, loss of volume of
her ponytail, bitemporal recession, but no widening
of her central part. No trigger for the hair shedding
was identified on history. Thyroid function tests, iron
studies, and hormone parameters all revealed nor-
mal findings. Scalp biopsy specimen was consistent
with CTE (Table I). On review at 6 months, 12
months, 2 years, 4 years, and 8 years, the hair
shedding had continued, but the magnitude fluctu-
ated between 50 and 300 hairs per day. The shedding
Sinclair S15
seemed worse in spring and autumn. Repeated
biopsy specimen at 12 months, 4 years, and 8 years
revealed no decrease in the follicle T:V to suggest
androgenetic alopecia. Serial scalp photography
from 1999 onward showed no reduction in hair
density (Fig 4).
CASE 5
This case has been previously reported.4 A 16-
year-old girl presented with a 12-month history of
generalized hair shedding from the scalp. The onset
of the shedding coincided with the development of
Hashimoto’s thyroiditis and iron deficiency. At the
time of initial presentation, the Hashimoto’s thyroid-
itis had been treated with neomercazole and she was
euthyroid. The iron stores were still low with a ferritin
of 13 g/L and because she was a vegetarian, oral iron
replacement therapy was commenced. Hair shed-
ding fluctuated in intensity during the course of the
year. On follow-up 6 months later, her iron stores
S16 Sinclair
were normal (ferritin 36 g/L). However, the hair
shedding continued. On examination there was
a positive hair pull test from both the vertex of the
scalp and the occipital scalp. There was mild bi-
temporal recession but no widening of the central
part and she appeared to have a full, thick head of
hair. Additional investigations at that time revealed
normal thyroid function and negative antinuclear
antibody and syphilis serology. She was on no
medication other than the neomercazole.
Serum testosterone, dihydroepiandosterone, and
sex hormone binding globulin levels were all nor-
mal. As the hair shedding was continuing, two 4-mm
punch biopsy specimens were taken from the vertex
of the scalp, and one sectioned horizontally and the
other vertically. The histology was consistent with
CTE (Table I) with a T:V of 15:1. No treatment was
recommended.
At follow-up 12 months later, the hair loss has
progressed with widening of the central part (Fig 4).
Repeated blood tests showed normal iron studies,
thyroid function, and hormone parameters. Three
4-mm punch biopsy specimens were taken from the
vertex of the scalp and sectioned horizontally. The
T:V was now 1:1, 2.6:1, and 1.9:1. A diagnosis of
androgenetic alopecia was made and oral spi-
ronolactone (200 mg/d) was started. There was
a substantial response to the spironolactone with
reduction in hair shedding and a marked increase in
hair density.
DISCUSSION
Although most women who present with chronic
diffuse telogen hair shedding with no visible re-
duction in scalp hair density will be found on biopsy
specimen to have FPHL, approximately 40% will
have normal scalp biopsy specimen and be diag-
nosed with CTE.5
The pathogenesis of CTE is unknown, but it is
theorized that CTE is caused by a reduction in the
duration of the anagen growth phase without hair
follicle miniaturization.1,8 A reduction in the duration
of anagen also occurs in FPHL, and it has been argued
that CTE is merely the earliest stages of FPHL,9 in an
analogous way to acquired progressive kinking.10
Long-term follow-up in 4 of these 5 patients identi-
fied no evidence of evolution into FPHL. This
suggests that CTE is a distinct clinical and histologic
entity, with a natural history different from that of
FPHL, although even longer follow-up will be re-
quired to confirm this.
With respect to the fifth patient, the very rapid
clinical transition makes it likely that a sampling error
J AM ACAD DERMATOL
FEBRUARY 2005
failed to detect miniaturization and led to misdiag-
nosis of CTE. We subsequently demonstrated that
biopsy specimens from immediately adjacent areas
can show sufficient variation in T:V ratio to cause
misdiagnosis and that diagnostic accuracy is im-
proved by taking 3 punch biopsy specimens side
by side.4 There is limited evidence to suggest that
oral antiandrogens such as spironolactone or cyprot-
erone acetate can be used to treat FPHL.6,7 In
contrast, there is no evidence to support the use of
antiandrogens in CTE. Therefore, in women who
present with increased hair shedding but no visible
reduction in scalp hair density, horizontally sec-
tioned scalp biopsy specimen is indicated to distin-
guish CTE from FPHL.
As the population prevalence of FPHL among
women in their 60s is at least 25%,11 some women
with CTE will develop FPHL coincidentally. Further
studies are required to estimate the relative risk of
developing FPHL among women with CTE.
The authors would like to acknowledge Dr Jill Magee
from Dorovitch Mayne pathology for taking the photomi-
crography, and Ms Rebecca Davies for taking the clinical
photographs.
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