HAIR DISORDERS

Biology of Hair growth

Anagen phase of normal active growth
Telogen - resting phase
Catagen brief transitionphase ( between abagen and telogen) during which hair growth stops.
Duration of anagen phase is different ( varing at differents body sites, in different dividuals and
age groups). On the scalp the anagen phase lasts for about 3 years and more, the catagen phase
for about 2-3 weeks and the telogen phase about 3 months. At any time 80-90% of scalp hair is
in the anagen phase and 10-20% is in the telogen phase, thus acciunting for a normal sheeding
rate of 25 to 100 hairs per day.
Disorders characterized by hair loss are classified into non-cicatrical alopecia, where clinically
there is no sign of tissue inflammation, scarring 0r atrophy of the skin, and cicatrical alopecia,
where evidence of tissue destruction such as inflammation, atrophy, scarring is apparent.

Non-scarring alopcia:
-

Telogen Effuluvium
Androgenic Alopecia
Trichotillomania
Alopecia Areata
Loose Anagen Syndrome

Telogen Effluluvium
Marked emotionally or physiogically stressful events may result in an alteration of the
normal hair cycle and diffuse hair loss. The dcalp is made up of a mosaic of anagen and
telogen hairs. Telogen Effuluvium is characterized by excessive and early entry of hairs into
telogen phase. Causes of telogen effluvium include high fever, childbirth, chronic ilness,
major surgery, anemia, severe emotiomal disorders, crash diets, hypothyroidism, drugs such
as birth control pills ( staring, stopping or changing), heparin, varfarin, beta-blockers,
imdometacin, lithium, angiotensin-converting enzyme inhibitors, retinoids.
Hair loss occurs 2-4 months after the physical or mental strss. Most patients are women. The
patient has diffuse thinning of the hair, the scalp is normal, there is scarring or erythema.
Gentle pilling of the hair will show an excessive hair shedding ( normally fever than three
hairs are pulled by grasping a small lock of hair and applying gentle traction from the base to
tip of the hair lock).
In stress-induced telogen hair loss the number of telogen hairs is increased from a normal
percentage of 10-20% to more than 25%.
This condition is usually a self-limiting, reversible problem that resolves within 2 6
months, but it may be prolonged if the underlying stress continues.

Androgenic alopecia
Occures more often in genetically predisposed persons. Androgenic alopecia represents
postpubertal replacement of terminal hairs by miniaturized hairs and eventually complitely
atrophic follicles. It occures in genetically predisposed both male and female. Clinically this is
non-scaring disorder and involves the vertex and frontotemporal regions of the scalp. Among
Caucasians it takes approximately 100% but age at onset is highly variable. Patterned hair
thinning occurs in approximately 50% of women aged over 40 years. In the areas of baldness
thick and more dark termimal hairs are replaced by finer, miniturized ( vellus- like) hair, which
then become atrophic, leaving a smooth, shiny scalp with bareky visible follicular orifices. The
number of follicles remains unchanged. Baldness characteristically occurs in a distinctive pattern

that spares the posterior and lateral margins of the scalp, in men the process begins with
bitemporal recession, followed by balding of the vertex. In women the process is mainly
manifested by diffuse thinnung over the top of the scalp ( the crown ) and by the intact frontal
hairline.
LOOSE ANAGEN SYNDROME
Background: Loose anagen syndrome was first described in 1984. It is a hair disorder characterized
by anagen hairs of abnormal morphology that are easily and painlessly pulled or plucked from the
scalp. Hair is thinned in appearance and typically does not grow beyond the nape of the neck.
Pathophysiology: The precise pathogenesis of loose anagen syndrome is not known, but theories
postulating an abnormality in the hair's anchoring mechanism predominate.
The inner root sheath is thought to play an integral role in anchoring the hair shaft within the
follicle. In loose anagen syndrome, mutations in genes coding for cytokeratins have been identified
in some cases and are thought to result in abnormal keratinization of the inner root sheath. This
faulty keratinization leads to impaired adherence of the deformed hair shafts to their follicles. The
impaired attachment may result in premature cessation of the anagen phase and account for reduced
hair length. One author has also reported reduced follicle size due to delayed maturation. This may
be responsible for sparse hair growth.
Frequency:

In the US: The prevalence of loose anagen syndrome is unknown. Although recently
described, loose anagen syndrome may actually be rather common. It is undoubtedly often
misdiagnosed as alopecia areata or trichotillomania. It has likely been both underdiagnosed
and underreported to date.

Mortality/Morbidity: The diffuse hair loss that occurs in loose anagen syndrome often raises
considerable concern among patients, parents, and clinicians. Although no treatment is currently
available, the condition is of cosmetic significance only, and symptoms generally improve over
time.
Race: Loose anagen syndrome has been reported only in white persons.
Sex: The syndrome is more common in females than in males.
Age: The classic patient with loose anagen syndrome is a girl aged 2-5 years with blonde hair;
however, cases of loose anagen syndrome in boys, in adults, and in individuals with dark hair have
also been reported.
History:

Parents often report that the child's hair is thinning and that haircuts are never needed or are
needed only very infrequently.

Parents may have noticed that hair traction, either accidental during playing or intentional, yields clu
painlessly removed hair.

Many parents complain that hair is unmanageable, lusterless, dry, dull, or matted.

Parents or siblings occasionally have a history of similar symptoms.

Children who are affected are healthy and free from underlying nutritional deficiencies or
other illnesses.

Growth and development are normal.

Physical:

Physical examination reveals sparse growth of thin, fine hair and diffuse or patchy alopecia
without inflammation or scarring.

Gentle traction results in hair that is painlessly removed; however, hair is not fragile or
easily breakable.

Hair may be of varying lengths and may have an unkempt, lackluster appearance.In
particular, hair overlying the occiput tends to be rough or sticky and does not lie flat
No scalp inflammation or scarring is present.
Eyebrows, eyelashes, and body hair are rarely involved.
Other structures of ectodermal origin (eg, skin, teeth, nails) are not affected.

Causes: Although its occurrence is typically sporadic, familial cases of loose anagen syndrome
have been observed. Inheritance appears to be in an autosomal dominant pattern with variable
penetrance. Loose anagen syndrome has not been consistently associated with any other disorder;
however, individual cases associated with the following syndromes have been reported. These
associations were most likely coincidental.

Noonan syndrome
Ocular coloboma syndrome
Trichorhinophalangeal syndrome
Nail-patella syndrome
Hypohidrotic ectodermal dysplasia and ectrodactyly-ectodermal dysplasia-clefting syndrome
Acquired immunodeficiency syndrome
Woolly hair
Alopecia areata
Loose anagen syndrome with features resembling uncombable hair syndrome
Colobomas and dysmorphic features including low-set ears, hypertelorism, left
microphthalmia, frontal bossing, a thin upper lip, a simple philtrum, and slight left facial
hypoplasia
Noonan-like syndrome characterized by short stature, a distinctive facial phenotype,
macrocephaly, enlarged cerebral spinal fluid spaces, a short neck with redundant skin, severe
growth hormone deficiency, mild psychomotor delay with attention deficit/hyperactivity
disorder, and increased skin pigmentation

Other Problems to be Considered:

Lichen planopilaris
Traction alopecia
Hypothyroidism
Hyperthyroidism
Iron deficiency anemia
Medication-induced hair loss (most commonly from chemotherapeutic agents, gout medications,

vitamin A, oral contraceptives, and antidepressants)