Hair Problems
Types of hair: Hairs are classified into three main types.
1 Lanugo hairs. Fine long hairs covering the fetus before birth.
2 Vellus hairs. Fine short hairs covering much of the body surface.
3 Terminal hairs. Coarse long hairs e.g. scalp or pubic hair.
The hair cycle:There are three phases of follicular activity.
1 Anagen: The active phase of hair production.
2 Catagen: short phase of conversion from active to resting phase.
Growth stops, and the end of the hair becomes club-shaped.
3 Telogen: resting phase at the end of which the club hair is shed.
On the scalp anagen lasts 3 years (6 months in eyebrows and chest hair),
catagen 3 weeks, and telogen 3 months. It is estimated that 85% of scalp
hairs are normally in anagen and 15% in the telogen phase. Scalp contains an
average of 100 000 hairs, and shed about 100 hairs/day as a normal
consequence of cycling. Hair growth rate is 1 cm/month.
Alopecia
The term means loss of hair. It has many causes and patterns. It is important
to decide whether or not the hair follicles have been replaced by scar tissue; if
they have, regrowth cannot occur. The presence of any disease of the skin
itself should also be noted.
Alopecia is conveniently divided into localized (patchy) and diffuse types.
Each in turn is divided into scarring and non-scaring types.
Scarring Alopecia
Hair follicles can be damaged in many ways. If the follicular openings can no
longer be seen with a lens, regrowth of hair cannot be expected. Sometimes
the cause is obvious: trauma (most commonly), a severe burn,
radiodermatitis, a carbuncle or an episode of inflammatory scalp ringworm.
Discoid lupus erythematosus, lichen planus and morphoea can also lead to
scarring alopecia. Epidermal warts, congenital naevi, Cysts and neoplasms
are of the causes. The term ‘pseudopelade’ is applied to a slowly progressive
non-inflamed type of scarring which leads to irregular areas of hair loss
without any apparent preceding skin disease. If inflammation is present, a
biopsy may help to establish the diagnosis.
Non scarring Alopecia
Some of the most common types are listed below; only a few can be dealt with
in detail.
1-Alopecia areata: discussed later.
2-Androgenetic alopecia: may present as a localized or a diffuse alopecia.
(Discussed later).
3-Neonatal alopecia: is a transient, physiological event that occurs in the first
3 months of life, probably due to estrogen withdrawal or trauma of labor. It
present mostly as patchy occipital hair loss (friction with the pillow) or
sometimes as a diffuse hair loss, that recover spontaneously (after a period)
and needs no treatment.
4-Pyogenic infection: folliculitis or boil of the scalp may cause transient
localized non-scarring alopecia, followed by spontaneous regrowth that may
last months. History of previous infection will suggest the diagnosis; otherwise,
it may be confused with alopecia areata.
5-Tinea capitis (human): a common cause of localized alopecia among
children in Iraq. The classical scalp ringworm derived from human sources
causes areas of scaling with broken hairs.
6-Traumatic hair loss: 4 groups
A-Traction alopecia: Affects usually girls and young women due to
excessive continuous pulling of hair. The pattern of hair loss is determined by
the cosmetic procedure in use, hair being lost where there is maximal tug. The
bald areas show short broken hairs, folliculitis and sometimes scarring.
Patients are often slow to accept that they are responsible for the hair loss, or
to alter their cosmetic practices. Even if they do, regrowth is often
disappointingly incomplete.
B- Hair-pulling habit (Trichotillomania): Is a minor comfort habit in
children or young adults. The hair is twisted and pulled continuously especially
during psychological tension. The bald areas are irregular in outline and hair
loss is never complete. Those hairs that remain are bent or broken, and of
variable length. The bald areas do not show the exclamation-mark hairs of
alopecia areata, or the scaling and inflammation of scalp ringworm or the
hyperpigmentation of neurodermatitis. Common sites are mustache in males,
eyebrows and lashes in females, and scalp hair in both. The patient usually
deny the habit and some parents do not know what is going on.
C- Neurodermatitis: is a disease of adults, with a habit of scratching a
localized area under psychological tension. In hairy areas this will result in
alopecia with broken hair and hyperpigmented thick lichenified skin.
D- Massage alopecia: by massaging the hair.
Alopecia Areata
A common disease, affects 2% skin clinics' patients. It affects any age group,
mostly 5-40 years with equal male to female ratio.
Cause: An immunological basis is suspected because of an association with
thyroid disease, vitiligo and atopy. Histologically, T lymphocytes cluster like a
swarm of bees around affected hair bulbs, having been attracted and made to
divide by cytokines from the dermal papilla. Alopecia areata is probably
inherited as a complex genetic trait, with a positive family history in 30% of
cases. The existence of trigger factors, such as stress, fits with this idea.
Presentation: Rapid and almost complete hair loss in patchy area(s). usually
asymptomatic and discovered by others, although uncommonly preceeded by
itching and burning sensation. A typical patch is uninflamed, with no scaling,
but with easily seen empty hair follicles. Pathognomonic
‘exclamation-mark’
hairs may be seen around the edge of enlarging areas. They are broken off
about 4 mm from the scalp, and are narrowed and less pigmented proximally.
Patches are most common in the scalp and beard but other areas, especially
the eyelashes and eyebrows, can be affected too. An uncommon diffuse
pattern is recognized, with exclamation-mark hairs scattered widely over a
diffusely thinned scalp. Up to 50% of patients show fine pitting or wrinkling of
the nails.
Course: The outcome is unpredictable. In a first attack, regrowth is usual
within a few months. New hairs appear in the centre of patches as fine pale
down, and gradually regain their normal thickness and color, although the new
hair may remain white in older patients. Subsequent episodes tend to be more
extensive and regrowth is slower. Hair loss in some areas may coexist with
regrowth in others. A few patients lose all the hair from their heads (alopecia
totalis) or from the whole skin surface (alopecia universalis).
Prognosis: the following suggest a poor prognosis.
1 Onset before puberty.
2
Association with atopy or Down’s syndrome.
3 Unusually widespread alopecia, (totalis, universalis).
4 Involvement of the scalp margin (ophiasiform type), especially at the nape of
the neck.
5 Positive family history.
6 Association with nail changes.
Differential diagnosis
1-Patches are not scaly, in contrast to ringworm.
2-Patches are usually uninflamed, in contrast to lupus erythematosus and
lichen planus.
3-In the hair-pulling habit of children, and in traction alopecia, broken hairs
may be seen but true exclamation-mark hairs are absent.
4-Secondary syphilis can also cause
a ‘moth-eaten’ patchy hair loss (excluded
with serological tests if necessary).
Treatment
1- A patient with a first or minor attack can be reassured about the prospects
for regrowth. Tranquillizers may be helpful at the start.
2- Topical irritants (dithranol, phenol, salicylic acid, plant extract, garlic, onion)
and contact sensitizers (e.g. diphencyprone DNCP) are often used to
induce dermatitis that disturb the already disturbed immunity hoping for
hair regrowth.
3- Topical steroid lotions and creams.
4- Intradermal injection of steroid leads to localized tufts of regrowth while not
affecting the overall outcome. This may be useful to re-establish eyebrows
or to stimulate hope.
5- Ultraviolet radiation or even psoralen with ultraviolet A (PUVA) therapy may
help extensive cases.
6- Topical immunosuppressive agents (e.g. tacrolimus).
7- Systemic therapy: in sever conditions such as systemic steroid, psoralen,
oral zinc sulphate and immunomodulation with BCG vaccination.
Diffuse Alopecia
Hair is lost evenly from the whole scalp; this may, or may not, be
accompanied by a thinning visible to others. Some of the most common
causes are listed below, but often a simple explanation cannot be found.
1-Physiological
A- Normally 100-hair fall/day, a common cause.
B- Neonatal, 3 months after birth.
C-Baldness, after age of 40years is a normal event in the life
of every male or female.
2- Androgenetic alopecia: discussed later.
3- Diffuse type of alopecia areata
4-Congenital causes: eg. The hypohidrotic ectodermal dysplasias are a group
of rare inherited disorders characterized by sparse hair, scanty sweat glands,
and poor development of the nails and teeth.
5-Telogen effluvium: can be triggered by any severe illness, particularly those
with bouts of fever or haemorrhage, by childbirth and by severe dieting. All of
these synchronize catagen so that, later on, large numbers of hairs are lost at
the same time. The diffuse hair fall, 2
–3 months after the provoking illness,
can be mild or severe. Regrowth, not always complete, usually occurs within a
few months. This condition is unaffected by therapy, but patients can be
reassured that their hair fall will be temporary.
6-Deficiency state: iron, zinc, marasmus and kwashiorkor.
7-Endocrine
causes:
hypopituitarism,
hypo-
or
hyperthyroidism,
hypoparathyroidism.
8- Severe skin condition: such as exfoliative dermatitis.
9-Severe chronic illness: lymphoma, leukemia.
10-Drugs and chemicals: especialy antimitotic agents that stop the hair growth
at the anagen phase causing diffuse har loss few weeks later (anagen
effluvium). Local ice pack application during therapy may prevent it. Of the
other drugs are anticoagulants, vitamin A excess, oral contraceptives,
colchicin.
11-Hair shaft abnormalities that result in fragile hair shaft fractured on simple
trauma.
12-Idiopathic: it is true to say that often no cause for diffuse alopecia can be
found.
The causes mentioned should be considered, However,.
Androgenetic Alopecia
Physiologic process with increased follicle sensitivity to androgens leading to
change from terminal to vellus hair follicles with distinct patterns of alopecia.
Cause: Clearly familial. Polygenic inheritance with variable penetrance seems
more likely, but it runs as autosomal dominant in some families. The hair
follicles have increased androgen receptors as increased activity of 5-
α-
reductase type II (that change testosterone to the active form,
dihydrotestosterone) leading to increased androgen sensitivity. In females,
androgenetic alopecia, with normal circulating androgen levels, is seen only in
those who are strongly predisposed genetically.
Presentation: Thinning of hair without scalp disease, In bald areas, terminal
hairs are replaced by finer vellus ones. There are two classic patterns
1-
“Male pattern”: The common pattern in men is the loss of hair first from the
temples, and then from the crown.
2-
“Female pattern”: the hair loss may be much more diffuse, particularly over
the crown.
Clinical course: Hair loss is relentless, tending to follow the family pattern
with some losing hair quickly and others more slowly. The diffuse pattern seen
in women tends to progress slowly.
Differential diagnosis
The diagnosis is usually obvious in men, but other causes of diffuse hair loss
have to be considered in women (p. 168).
Investigations
None are usually needed. In women, virilization may have to be excluded.
Treatment
Scalp surgery, hair transplants and wigs are welcomed by some.
Topical application of minoxidil lotion may slow early hair loss and even
stimulate new growth of hair in a few cases. Small and recently acquired
patches respond best. When minoxidil treatment stops, the new hairs fall out
after about 3 months.
Anti-androgens help some women with the diffuse type of androgenetic
alopecia.
Finasteride, an inhibitor of human 5-α-reductase type II, reduces levels of
dihydrotestosterone. It may increase hair counts and so lead to a noticeable
improvement in scalp hair. However, the beneficial effects slowly reverse once
treatment has stopped.
Excessive Hair Growth
Growth of hairs that are longer, thicker or more numerous than the location,
age, and racial background of the patient would predict.
Hirsutism
Increased growth of terminal hairs in androgen-dependent areas, producing
male-like hair growth pattern in women. It is a common problem among Iraqi
females. Family history is positive in third of cases. Areas of androgen
dependence may be affected singly or in combination, these are chin, sides of
face, moustache, neck, chest presternally, breast especially around the
nipples, upper back and shoulders, linea alba above the umbilicus.
Virilization is the association of hirsutism with other signs of male
development, such as voice deepening, clitoral enlargement, increased
muscles, loss of breast tissue, acne, and androgenetic alopecia.
Causes:
1- Physiologic: Some degree of hirsutism may be a racial or familial trait
constituting most cases of hirsutism. Minor facial hirsutism is common after
the menopause
2- Idiopathic: Some patients without a family background of hirsutism become
hirsute in the absence of any demonstrable hormonal cause. Probable
indemonstrable causes are:
A-Minor ovarian or adrenal dysfunction,
B-
local increased 5α reductase activity, or
C-Increased number of androgen receptors at hair follicles.
D-Increased sensitivity of androgen receptors at hair follicles.
3-
Iatrogenic:
Phenytoin,
androgens,
corticosteroids,
contraceptives
(progesterone has androgen action)
4- Symptomatic: Some patients with hirsutism will have one of the following
disorders
A- Ovarian: Polycystic ovary disease, virilizing tumors.
B- Adrenal:Congenital adrenal hyperplasia virilizing tumors.
C- Pituitary: Cushing disease, acromegaly, prolactinoma
D-Ectopic virilizing broncogenic or GIT carcinomas.
Investigations
Women with a normal menstrual cycle and no signs of virilization are unlikely
to have a significant endocrine cause for their hirsutism. Investigation is
needed if these symptoms are present. Tests might include: blood levels of
LH, FSH, testosterone, prolactin; urinary free cortisol; CT scan of suprarenal
areas; pelvic ultrasound, Skull X-ray..etc
Therapy
Often unsatisfactory and needs continuous use, usually with relapse after
treatment discontinuation.
A-Treat underlying disease.
B-Removal of hairs:
1-Shaving, wax epilation, thread epilation, chemical epilation.
2-Bleaching (6
–10% hydrogen peroxide in water).
3-Destruction of individual hair follicles by electrolysis or thermolysis.
4-Photoepilation (with lasers or intense pulsed light source);
much faster and more effective.
5-Eflornithine (topical) effective but only as long as used; expensive.
C-Systemic therapy:
1-Primary antiandrogen: Flutamide, Cyproterone acetate.
2-Agents with secondary antiandrogen activity: Spironolactone.
3-GRH agonists: leoprolide and nafarelin.
4- 5-
α-Reductase inhibitor: Finasteride 2.5-5 mg daily.
5-Combination therapy.
Hypertrichosis
Excessive growth of terminal hair that does not follow an androgen-dependant
pattern.
A- Hypertrichosis lanuginosa
1-Hypertrichosis lanuginosa congenita:
Uncommon genodermatosis in which newborn is covered by long lanugo
hairs, which are not shed and replaced, but continue to grow. Patient typically
winds up with a silvery coat of hairs 10 cm long.
2-Hypertrichosis lanuginosa acquisita:
The sudden profuse covering of the skin by white lanugo hairs is a reliable
marker of internal malignancy (e.g. lung, colon, or breast, as well as others)
B- Generalized Hypertrichosis
The entire body seems affected with regional differences. There are many
causes for diffuse excess numbers of terminal hairs:
1-Hereditary: Porphyria cutanea tarda, mucopolysaccharidoses, chromosome
abnormalities (trisomy 18).
2-Endocrine: Pituitary and thyroid disorders.
3-Eating disorders: (especially anorexia nervosa), malabsorption, fetal alcohol
syndrome.
4-Medications: Cyclosporine, minoxidil, phenytoin are most common
C- Localized (nevoid) hypertrichosis
1-Becker nevus: Localized mosaic area of increased melanin and increased
hair growth.
2- Faun tail nevus: Localized hair growth over sacrum; a serious marker for
potential underlying spinal cord defects or spina bifida. Neurological and
radiological work-up mandatory.
3-Hair nevus: localized area with excess hair follicles and no other
abnormalities; Uncommon.