Approach to a case of diffuse hair loss in females . Anagen effluvium- (a)Dystrophic (b)Loose anagen hair 2. Telogen effluvium – (a)acute telogen effluvium (b)Chronic telogen effluvium 3. Female pattern hair loss Primary CTE –represents a primary disorder and is a diagnosis of exclusion. Secondary CTE- secondary to variety of systemic disorders. Iron deficiency Other deficiency –protein calorie malnutrition ,zinc deficiency Thyroid diseases Metabolic diseases-chronic liver or renal failure, advanced malignancy, pancreatic disease and upper GI disorder with malabsorption SLE and other connective tissue disorders. HIV infection Drug induced

1. Moderator
Dr Puneet Bhargava

2. INTRODUCTION
 Women presenting with diffuse hair loss is a very common
and challenging problem for dermatologists.
 Telogen effluvium (TE) is the most common
cause, followed by female pattern hair loss (FPHL) and
chronic telogen effluvium (CTE); the rest of the causes are
not so common and can be relatively easily diagnosed
through history and examination.
 The problem arises in differentiating between
TE, FPHL, and CTE, which account for the majority of
diffuse alopecia cases in females.

4. Hair follicle cycling
 Hair follicle is subjected to constant turn over.
 Different phases of hair cycle are-
ANAGENphase of active hair growth
Responsible for final length of hair
80-90% of scalp hair at any one time
3 year or more in scalp
1-3 month in other area
2. CATAGEN At the end of anagen, the follicle enters an involutionary
phase known as catagen.
1.
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



5.  phase of regression
 Proximal end of hair shaft keratinizes to form club shaped
structure
 The lower part of follicle involutes by apoptosis
 Base of follicle, together with its dermal papilla move
upwards to lie just below the level of arrector pili
 Lasts about 3 weeks.
 Approximately 2% of hair of scalp
3. TELOGEN resting phase
 period between completion of follicular regression & onset
of next anagen phase
 The club hair lies within an epithelial sac to which it is
attached by tricholemmal keratin
 Lasts about 3 months
 8 to 10% of scalp hair

6. 4. EXOGEN –
It is a highly controlled active process of shedding of the
hair fiber ,unlike the previous assumption that the newly
formed hair fiber pushes the resting shaft outward to effect
shedding.
5. KENOGENThe interval of hair cycle in which the hair follicle remains
empty after the telogen hair has been extruded and before
a new anagen hair emerges.

7. `

8. PATHOLOGIC DYNAMICS OF HAIR
LOSS
Dystrophic anagen effluvium
 Results from a direct insult to the rapidly dividing bulb
matrix cells.
 Abrupt cessation of mitotic activity leads to weakening of
the partially keratinized, proximal portion of the hair
shaft, its narrowing, and subsequent breakage within the
hair canal.
 Thus Shedding of the hair from anagen phase of growth.
 Morphological consequence- tapered proximal end and
lack of root sheeth.

9. Telogen effluvium
 Headington proposed classification of telogen effluvium
into 5 functional types1. Immediate anagen release
 the follicle that would normally complete a longer
cycle by remaining in anagen, prematurely enters
telogen.
 Most common type.
 Occurs after periods of physiological stress, fever etc.
 Shedding is dependent on transition from anagen
through catagen and telogen, with subsequent release
of telogen hair, hair loss occurs 3-4 months after the
inciting event.

10. 2. Delayed anagen release


Hair follicle remain in prolonged anagen rather than
cycling into telogen.
When finally release from anagen ,clinical sign of
increased shedding of telogen hair is found.
Seen in post partum hair loss
3. Immediate telogen release Hair follicle normally programmed for release of the
club hair after an interval of usually 100 days after the
end of anagen, are prematurely stimulated to cycle
into anagen.
 Premature teloptesis.
 Seen in initiation of therapy with topical minoxidil.

11. 4. Delayed telogen release hair follicle remain in prolonged telogen rather than
being shed and recycled into anagen, when finally
teloptesis sets in, increased shedding of club hair is
observed.
 Seen in moutling in mammals.
5. Short anagen phase Slight but persistent telogen effluvium in association
with decrease hair length.
 Seen in androgenetic alopecia or female pattern hair
loss.

12. Causes of diffuse hair loss in
females
1. Anagen effluvium(a)Dystrophic
(b)Loose anagen hair
2. Telogen effluvium –
(a)acute telogen effluvium
(b)Chronic telogen effluvium
3. Female pattern hair loss

13. Loose anagen hair
 This condition features anagen hairs that are loosely




anchored and easily pulled from the scalp .
The majority of cases are fairhaired children, aged 2–9
years, mostly girls.
Autosomal dominant inheritance.
They typically have slightly unruly hair, which is of uneven
length and patchy in quality.
Hair is usually easily and painlessly plucked with the hairpull test.

14.  There have been isolated reports of loose anagen syndrome
associated with hypohidrotic ectodermal dysplasia and
ocular coloboma.
 Histological examination shows premature keratinization
of the inner root sheath layers of Huxley and Henle.
 Trichograms show 98–100% anagen hairs.

15. Dystrophic Anagen effluvium
 It is the hair loss that result from the shedding of large
number of hairs from anagen phase of growth.
 Causes-
Anti neoplastic drugs (chemotherapy induced alopecia).
2. Radiation (radiation induced alopecia).
3. Toxins (toxic alopecia).
1.

16. chemotherapy induced alopecia
 Begins at 1-3wks and is complete at 1-2 month after






initiation of chemotherapy.
Normally upto 90% of scalp hairs are in anagen ,hair loss is
usually copious and the resulting alopecia is quite obvious.
Drugs are(a) antimicrotubule agents eg paclitaxel
(b)topoisomerase inhibitors eg doxorubicin
(c) alkylators eg cyclophosphamide
(d) antimetabolites eg 5 fluorouracil plus leucovorin

17.  This type of alopecia is usually reversible with hair
regrowth typically occurring after a delay of 2-3 months.
 In some patients the regrown hair shows changes in colour
,structure and texture.
Radiation induced alopecia
 May be reversible or permanent
 Permanent alopecia occurs with >30gy of deep x rays or
>50gy of soft x rays.

18. Toxic alopecia
 Occurs from occupational exposure to hazardous
chemicals
 Many heavy metals are capable of disrupting the formation
of the hair shaft through covalent binding with the
sulfhydryl groups in keratin : thallium ,mercury, arsenic
,copper , cadmium and bismuth.

19. TELOGEN EFFLUVIUM
 TE is characterized by an abrupt onset, and




rapid, diffuse, self-limited, excessive shedding of normal
club hairs, usually seen 2-3 months after a triggering event.
In one-third of cases, no trigger can be identified.
Premature termination of anagen into catagen and telogen
hair follicle is the main mechanism behind TE.
Acute TE or classical TE is a self-limiting condition lasting
for about 3-6 months
if the stimulus/event that causes diffuse shedding persists
beyond six months, then the condition becomes chronic.

21. Diagnostic features of telogen
effluvium
Abrupt onset, rapid diffuse generalized shedding of
hairs, usually seen 2-3 months after a triggering event.
Nearly 100-1000 hairs/day may be lost.
2. HAIR PULL TEST- Strongly positive
 Usually more than 10% of the total hairs pulled are easily
extracted from any part of the scalp in the acute phase of
TE, if the patient has not shampooed the hairs for more
than 24 hours.
 Approximately, 60 hairs are grasped between the thumb
and the index and middle fingers and gently pulled.
 A negative test (≤6 hairs obtained) indicates normal
shedding, whereas a positive test (>6 hairs obtained)
indicates active hair shedding.
1.

22. 3. A trichogram (forcible complete hair pluck of 40-60 hairs)
showing significant reduction in anagen:telogen ratio.
 Usually, >25% of the plucked hairs are telogen hairs in
acute phase.
4. Videodermoscopy will show large number of short-tip
pointed regrowing hairs in the absence of hair diameter
variability.
5. Biopsy shows normal histology except for an increase in
the telogen follicles.
 The proportion of normal telogen follicles in excess of
15% is considered suggestive of TE.
 while a level of 25% or more is considered definitive.
 Normal telogen counts are typically in the range of 613%.

23. Chronic Telogen Effluvium
 CTE is an idiopathic distinct entity characterized by an
excessive alarming diffuse shedding of hairs in females
aged 30-60 years, with a prolong fluctuating course and
near-normal histology.
 The exact pathogenesis of CTE is not known, but it is
theorized that it is due to reduction in the duration of
anagen growth phase without miniaturization of hair
follicles.
 Also, the etiology of CTE is unclear and it is diagnosed
after excluding other causes of chronic diffuse hair loss.

24.  Primary CTE –represents a primary disorder and is a diagnosis
of exclusion.
 Secondary CTE- secondary to variety of systemic disorders.
1. Iron deficiency
2. Other deficiency –protein calorie malnutrition ,zinc
deficiency
3. Thyroid diseases
4. Metabolic diseases-chronic liver or renal failure, advanced
malignancy, pancreatic disease and upper GI disorder with
malabsorption
5. SLE and other connective tissue disorders.
6. HIV infection
7. Drug induced

25.  History and examination will generally suggest the cause of
TE
 if not, then a minimum battery of laboratory tests, which
includes complete blood count (CBC), routine urine, serum
ferritin, and T3, T4, and TSH should be performed.
 Iron deficiency anemia and thyroid hormone disorders are
the two common conditions associated with TE .

26. Diagnostic features of chronic
telogen effluvium
 History of abrupt, excessive, alarming, diffuse, generalized
shedding of hair from a normal looking head is the main
feature of CTE. Chunks of hair are seen in the bathroom
(may block the drain), pillow, brush and comb.
 Obvious diffuse thinning is not a feature of CTE, though
many of these women do notice 50% reduction in the
volume of their ponytail thickness.
 Moderate to severe bitemporal recession may also be seen.
 A positive pull test at all sites of scalp (vertex, occipit, and
sides) is seen in active phase.

27.  Absence of widening of central parting and
miniaturization of hairs
 Absence of any underlying cause for chronic diffuse hair
loss.
 Counting of total number of telogen hairs and vellus hairs
shed during standardized shampooing (wash test) has
been reported as a good tool to differentiate between CTE
and FPHL.
 Ten percent or more of vellus hairs is considered enough to
diagnose FPHL.
 Normal histological picture except for a slight increase in
the telogen hair follicles.

28. Female Pattern Hair Loss
 FPHL is a gradual onset, slowly progressive nonscarring
alopecia, which can be seen any time after menarche, but is
most common in females aged 20-40 years.
 It results from a progressive reduction of successive hair
cycle time leading to miniaturization of hair follicles.
 These changes are mediated through interaction between
androgens, their respective receptors and enzymes like 5a
reductase and p450 aromatase.

29. Three types of FPHL patterns have been described.
1.
Diffuse central thinning (Ludwig type): The diffuse hair
loss is concentrated over frontoparietal region leading to
thinning/rarefaction over central scalp with intact frontal
hair line .

Ludwig graded it into three stages depending upon
whether the central thinning is mild (stage I), moderate
(stage II), or severe, that is, near-complete baldness of
the crown (stage III).

31. 2. Frontal accentuation (Olsen type): It leads to widening of
central parting line and thereafter to chrismas-tree pattern.
3. Frontotemporal recession/vertex loss (male
pattern/Hamilton type): It leads to recession of
frontotemporal hairline or bitemporal recession and/or
thinning at vertex.

33. Causes
i.
ii.
Genetic Predisposition,
Androgen excess,
Ovarian cause- Polycystic ovarian syndrome,
- Other ovarian tumor,
. Unilateral benign
microadenoma.
. Leydig cell tumor
. Hilar cell tumor.

34.  Adrenal cause
- Congenital adrenal hyperplasia (androgenital
syndrome) due to deficiency of –
21 hydroxylase (most common)
11-β hygroxylase.
3-β hydroxysteroid dehydrogenase.
- Tumor
Adrenal adenoma
Carcinoma.

35.  Hyperandrogenism is seen in <40% of cases and may
manifest through hirsutism, severe or recalcitrant
acne, oligomenorrhea, infertility, acanthosis nigricans, and
galactorrhea.
 Hormonal screening is indicated in cases with features of
hyperandrogenism as well as in women in whom FPHL is
abrupt, rapidly progressive, severe, or associated with
severe bitemporal recession, to rule out any underlying
cause for androgen excess like polycystic ovarian disease
(PCOD), and ovarian or adrenal tumors.
 complete screening panel for hyperandrogenism consists of
free and total testosterone, DHEAS, LH, FSH, T3, T4, TSH, prolactin, and ultrasound for
ovaries and adrenal glands.

36. Diagnostic features of female
pattern hair loss
 Gradual onset, slowly progressive hair loss, which is often
diffuse, and predominantly affects the frontoparietal region
leading to central thinning with intact frontal hair line, or
widening of central parting line.
 Rare cases may show frontotemporal or bitemporal
recession with or without hair loss at vertex.
 Presence of miniaturized/vellus hairs (short thin hairs <3
cm and a shaft diameter of .03 mm) at the frontoparietal
region is an important diagnostic feature of androgenetic
alopecia.

37.  DERMOSCOPY -Hair shaft diameter diversity(HDD)

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


>20% has been reported to be an early sign of female
pattern hair loss.
In addition, peripilar halos and peripilar atrophy can also
be seen during dermoscopy in a few patients.
Shedding may or may not be present, and if present, it is
mild and never profound as noticed in TE/CTE.
HAIR PULL TEST is usually negative.
HISTOPATHOLOGICAL EXAMINATION reveals
miniaturization of hair follicles, which is the histological
hallmark of FPHL, and leads to significant reduction of
terminal to vellus hair ratio.
The T:V ratio is reduced from a normal of 8:1 to 2.2:1 in
FPHL and any ratio <4:1 is diagnostic of FPHL.

38.  In addition, a slight increase in telogen hair count, 1520%, predominantly lymphohistiocytic perifollicular
infiltrate, perifollicular fibroses, and follicular streamers
may also be seen.

40. Management of Diffuse Hair Loss
A. General measures
Identification and treatment of underlying cause: High
fever, severe infection, or any other disease which could
be the reason behind acute/chronic telogen hair loss
should be identified and treated.
 Similarly, patients of FPHL with suspected androgen
excess need hormonal assessment and treatment/referral
to gynecologist/endocrinologist.
2. Reassurance and explanation: The patient should be
explained that TE or CTE represents excessive hair
shedding rather than actual hair loss, all the hair lost
would be replaced by regrowth and does not lead to
baldness.TE generally ceases within 3-6 months if the
stimulus is removed, while CTE may take 3-10 years.
1.

41. 
Even in FPHL the picture is not gloomy. Baldness, unlike
in males, is not a feature of FPHL.
 It only leads to thinning of hair, which can be prevented
and to some extent regrowth of hair is possible through
drugs like minoxidil.
3. Assessment and treatment of iron deficiency and thyroid
hormone disorders:
4. Monthly assessment of the case: A resolving TE is
characterized by absence of shedding, a negative hair pull
test, and synchronized hair growth. Any unresolved TE
with shedding of hairs beyond six months needs further
evaluation.
 Numerous methods (biopsy, trichogram, unit area
trichogram, phototrichogram, trichoscan, and
videodermoscopy) are used to assess the hair growth
variables (hair density, diameter, growth, anagen:telogen
ratio, etc.) and to study the treatment response to various
therapeutic modalities.

42. 5. Optimize the diet and avoid drugs associated with hair
loss: Vitamin A, vitamin A containing preparations like
antioxidants, etetrinate, acitretin, and high dose
OCP/HRT, etc. should be stopped or replaced with suitable
substitutes.

43. B. Specific treatment
Telogen effluvium
 TE does not require specific drugs as the condition is selflimiting and usually resolves in 3-6 months if the trigger
is removed.
 Complete recovery may take one year.
Female pattern hair loss
 Minoxidil topical solution 2% - for mild to moderate FPHL
(Ludwig stage I and II) without hyperandrogenism.
 Minoxidil 2% plus antiandrogens/finestride - for mild to
moderate FPHL (Ludwig stage I and II) with
hyperandrogenism.


44.  Hair prosthesis (wig, hair extension, hairpiece) and hair
cosmetics (tinted powders, lotions sprays) - for severe
FPHL (Ludwig stage III) and as adjuvant to medical therapy
in mild to moderate cases.
 Hair transplantation - ideal candidate for hair
transplantation are moderate cases of FPHL (Ludwig stage
II) who have high-density donor hair (>40 follicular
unit/cm 2 ) in some areas and extensive loss or thinning at
frontal or mid frontal scalp only.

45. Chronic telogen effluvium
 There are no specific drugs for CTE.
 Empiric use of topical minoxidil 2% has been suggested in
anticipation that it will prolong anagen growth.
 It is said that CTE is a self-limiting process, which may
resolve spontaneously in 3-10 years.

46. Pull test
positive
Negative
Trichogram
Telogen effuvium
Dystrophic anagen effuvium
<6month:
Acute telogen effuvium
Patient history
Chemotherapy
Radiation exposure
Negative
Patient histroy:
•Fever
•Postpartum
•Crash diet
>6 month:
Chronic telogen
effuvium(CTE)
Patient histroy and laboratory
investigations
Secondary CTE
Negative:
Primary CTE
Negative
Occupational exposure
Environmental
exposure
Dermoscopy and/or biopsy for D/D:
Toxicological studies:
•Diffuse alopecia areata
•Heavy metals
•Androgenetic alopecia
•Plant toxin
•Drugs
•Iron deficiency
•Thyroid dysfunction
•Other

47. THANKS