Alopecia : it is either patchy ((localized hair loss)) or diffuse.
1-Patchy hair loss Either scarring or non-scarring : Non scaring and it's causes are (can induce hair growth by Rx):
Neonatal. Occur in the 1st 3 months of life, It is transient physiological condition usually occipital hair affected due to Estrogen withdrawal , Trauma of labor or Friction with pillow, Recover happen spontaneously after period of the time without Rx
Alopecia areata .
Pyogenic infection: Infection of scalp in form of folliculitis or boil cause localized hair loss in form of bald area. it lasts far days or wks, then hair re-growth within mths, unless its deep or scarring will form.
Taenia captis: Common among children in Iraq (not seen in adult life) so any scaly scalp with patchy hair loss =T. capitis unless proved other wise. O/E the skin appears abnormal scaly, crusted and hair is not shiny at area of hair loss
traumatic alopecia include 3 groups:
Traction alopecia mean Continuous excessive pulling of hair cause patchy hair loss, appears on the site of traction depending on hair style . hair will re-grow spontaneously when stopping traction, its usually associated with follicutitis.
Lichen simplex (Neurodermatiti): disease of adult due to the habit of scratching, itching localized area due to psychological tension. Rx by reassurance to stop hair scratching so Hx is important and missed in Dx
Trichotillomania: in children and young adults ♀ are more affected, caused by the habit of pulling hair (Moustache in male. Eye brows and eye lashes in female) during psychological cause or tension called”obsessive compulsive neurosis” and patients deny pulling hair.
Affected area in the scalp that the hair was cutting by scissor and hair broken at the surface of the skin.
Others: Connective tissue disease (SLE, DLE) lichen planus In DLE, the area of hair loss appears erythematous and may end with scarring
Scaring patchy alopecia Complete destruction of hair follicle and no hope of hair growth with Rx. (absence of hair follicle) and it' causes are :
Cysts :hair over the cyst will be lost
fungal kerion favus.
Bacterial pyogenic infection as in T.B. of the scalp.
Phyysical causes :
Mechanical trauma. most common.
Scleroderma and dermatomyositis
Neoplasms:- SCC ,BCC , Syringoma
Dermatitis of unknown origin: include lichen planus , sarcoidosis
Alopecia and its causes are :-
Physiological (Male pattern or Female pattern): Normally around 100 hairs fall/ day
Neonatal: after 3 mths, patchy or diffused
Baldness after the age of 40, usually males is affected more than females
Congenital: epidermal dysplasia.
Alopecia areata : telogen alopecia.
Telogen efflurium: affecting all age especially children and young adults , Hair growth will be arrested causing hair fall ,Its transient condition with less recurrence , Rx by placebo.
All these causes arrest hair growth at telogen phase: 1 post operative, 2 post severe syst.disease, 3 post delivery,4 post psychological trauma
Iron diffeciency anemia even in the absence of anemia.
Endocrine: Rx by treating the underlying causes.
Thyroid “hypo or hyper” pan hypopitutarism, DM, pregnancy can be an endocrine causes
Severe skin conditions: Exfoliative skin diseases
Sever chronic illness. lymphoma, lenkemia
Simple trauma: affect hair and cause fragile hair shaft
Drugs and chemicals:
Cytotoxic agents affect hair matrix and stop hair growth at anagen phase and the effect occurs after few wks from receiving cytotoxic drugs. Cytotoxic inhibition of mitosis in hair papilla lead to narrowing and fractures of hair called angen alopecia could be prevented by ice packs to induce vasoconstrictions half hr before receive chemotherapy and prevents reaching of cytotoxic drug to scalp.These will lead to inhibition of mitosis in hair papilla which leads to narrowing and fractureing of the hair and could be prevented by ice packs.
Colchicene anagen alopecia 1-12wks.
Anticoagulants as heparin and cumarin after (3-20)wks.
Diseases affects the shaft with unknown cause
Hair shaft abnormalities, pts have fragile hair shaft and any simple trauma
داء الغزال او داء الثعلب الخاصه البقعيه
A common disease, 70-80% of cases has it appear between 5-40 yrs, can affect any age ♀: ♂ ratio is equal, but in ♀s may be more due to the use of cosmetics. Usually these patients have genetic bases and +Ve family hx of alopecia areata is found in 30% of pts.
Genetic factors 10-24% with +ve family Hx.
T cell dysfunction.
Associated autoimmune diseases as vetligo and thyroid diseases.
Physiological and Psychological causes
Old theory: eye retraction and tooth
Recently: C.M.V infection
Sometimes it proceeded by itching and burning and parasthesia before onset of alopecia areata but usually asymptomatic and noticed by relative. Characterized by rapid and complete hair loss. Present as single or multiple patchy hair loss, Skin at the area of hair loss look apparently normal.
Broken hair which is characterized by a specific feature called ”Exclamation mark”.
Complete hair loss on scalp ⇒ Alopecia totalis.
Complete hair loss on occipital margin of scalp ⇒ alopecia ophiasis.
Complete hair loss on whole body ⇒ A. universalis
T- cell lymphocytes cause damaged hair follicle and the hair follicle will stop from growth and change from anagen into telogen like, normally the proximal part of hair is thicker than distal part while in Alopecia Areata because there is damage to the hair follicle become thinner proximally and thicker distally.
T- lymphocytes infiltrated and aggregation around the hair follicle that damage the matrix of the follicle and hair root causing the loss of hair broken hair is normal but damaged by immune factor so hair bulb form no more hair. So presence of normal and abnormal segments and old segment ⇒ broken hair ⇒short hair.
Other changes:Associated with alopecia areata
Nail changes:because it is systemic disease it affects nails: Pitting, ridging, dystrophy, complete nail destruction which is temporary, koilonychic like picture.
Pigmentary hair changes:
1- Premature grayness of hair.
2- Patchy grayness of hair.
3- After Rx hair grows white
Pt who had grayness when affected by AA=only the pigmented hair will be affected while white & gray one will remain.
Course and prognosis:
Recovery rate is high and recurrence high so the course is unpredictable.No cure from AA, recovery may take mths, yrs or life time.
Bad prognostic signs:
1- Sever condition (Totalis, Universalis) from the start.
2- Associated with nail changes.
3- +Ve family Hx and personal or family Hx of atopy.
4- Chronically, especially when started in early childhood.
5- +Ve family Hx of AA.
6- Site: affect margin (ophiasis) seen pre-pubertal Children and hair loss seen in occipital and retro auricular regions.
A- Topical Rx:
* Spontaneous recovery is not uncommon, but may take mths or yrs without Rx. So therapy to decrease the time of recovery.
* many irritants (phenol, plants extract, garlic, onions) induce dermatitis locally disturbing the already disturbed immunity in the area and prevent the damage to the hair follicles by T-lymphocyte and autoantibody ⇒ hair re-growth.
* DNCP (other irritant) mutagenic, so not used.DCP is the new one and salicylic acid.
4- Short anagen phase (2 months or 2 weeks) with long
telogen phase, but the hair follicle never die & always
Androgen hormone: in ♀s; excessive and rogen from
ovaries or adrenals, in ♂s; castration (deprivation of
aman from his testes befor puberty ⇒ No baldness.
25-30 years in endocrinal normal female metabolism of
The hair follicles contain the enzyme 5α- deduct ase, which is responsible for converting testosterone into dihydro testosterone (which is the active from), if the level or the activity of this enzyme is increased, this may lead to baldness.
Clincal features :
“Affect all individuals”
1- Both sexes are affected, but less in females, because of
the protecting hormones (oestrogen).
2- In males it occurs between the ages of 15-16 *, when
the growth of hair at the fronto vertical region becomes
slow, with sbortening of anagen phase and hair fall, the
hair becomes dry curly light in colour and there will be
telogen hair losslester less called trichorickes.
*: The early onset & usual site is fonto vertical hair ranely
sides of scalp
1- Topical: all treatments use placebo topically, but there are other topical remedies that are worth less. e.g. Topical steroid & minoxidil.
2- Systemic: useful in females usually and they are all
antiandrogen: (act on androgen receptors & stop affect
of it reduce hair groeth)
3- Syrgery: mainly in males, hair graft:
Excessive Hair Growth
Growth of hair at any site which coarser, longer and more profuse than normal for age, sex and race (e.g. eastern like (Iraqis, Indians) have excessive hair growth while (Japanese) have minimal growth).
Excessive hair growth in non-hormonal (androgen) dependent areas (in both sexes), it has different types and the causes of of hypertrichosis include:-
Causes of hypertrichosis:-
1- Congenital hypertrichosis Lanugenosa:- Many children are born with long silky hair covering the neck, limbs and face. It may be fine and fire hair, this is normal condition.
2- Acquired hypertrichosis:- lanugenoza: Excessive hair growth of silkyhair and become coarse pigmented and remained later in life. It has a sudden onset of appearance. it is associated with malignancy, e.g. GI tumor, lymphoma, leukemia, breast carcinoma. It may be fine yellowish (blond) hair.
Navoid Hypertrichosis:- Coarse pigmented hair appears at site of naevi. It is marker of spina bifida if it is in the lower back, appears like a Taft of hair. So, Naievoid structure appeared and covered by hair, like in congenital nevus (circumscribed hypertrichosis, Melanocytes Naevi, Faur-tailNevus and also Becker's Naevi). (Becker's naevi is common in both sexes, it appear in childhood as a pigmented patch and get larger until age of 20 year then stop progression, it usually around the chest and shoulder on one side, associated with excessive hair growth (coarse) present for life , no treatment apart from surgery "laser").
-Symptomatic hypertrichosis:-Hereditary disease, it appears as symptoms of many diseases, with hypernevus (porphyria) mainly on the cheeks, associated with many variants of porphyria (Erythropoietic proto porphyria, P. cutanea trada, P. Variegate, Hepatic porphyria).
Endocrine disorder:- as hypothyroidism in children and hyperthyroidism in adults, Peritibial myxoedema with coarse hair on the legs, also in case of early maturation, lipodystrophy.
Diencephalic or pituitary mechanism:- in children after encephalitis or mumps and after 1-3 months of head injury especially in children.
Malnutrition:- either (primary or secondary) or (anorexia nervosa in which the patient eat and vomiting causes excessive weight loss and if treated and nourished the excessive hair will fall).
Epidermolysis bullosa dystrophica:- which lead to increase hair growth at diseased area.
Fetal alcoholic syndrome:- if the mother consumes alcohol during pregnancy, fetal hypertrichosis will develop with capillary haemangioma and mental retardation of infants.
Iatrogenic (drug not related to androgen) if we stop them, hair will regress. e.g:
Phenytion (for epilepsy)
Streptomycin , cortisone, pencillamine,
PUVA(for treatment of skin problem).
minoxidil and cyclosporinesand benoxaprofen. (immune suppressive agent).
Excessive hair growth in the female in androgen dependent hair as a course terminal hair in part or in the whole body. (male pattern in female).
It is a very common problem; about 55% of Iraqi women have it in different distribution.
Age usually start after puberty around age of menarch (14 year) and increase in severity and remain for life.
Forms of androgen in females:-
1- Testosterone: 99% is bound (inactive) and 1% is free (active).
2- Androstenedione: from ovaries.
3- Dihydrotestosterone (DHT):- which is the main source of androgen in females and converted to androstenedion in the skin.
4- Others (DHA).
And for the bound testosteron
80% of bound testosterone is bound to sex hormone binding globulin (SHBG).
20% is bound to albumin and corticosteroid binding globulin.
Causes of hirsutism:-
Idiopathic :racial (undetermined):common among some races like Arab ,Kurd ,Turkmen, Indian and other races in the middle east and common in welsh people in england. It is now arare cause.
Ovarian:- Virulized ovarian tumor and polycystic ovary. (This is the most common causes with or without endocrine causes).
Congenital adrenal hyperplasia,
Virilizing adrenal tumor
borderline adrenal dysfunction.
Combined ovarian and adrenal causes.
Pituitary:- Acromegaly, microadenoma (Increase prolactin) and Cushing syndrome
Iatrogenic:- Drugs (phenytion and steroids).
Stress:- lack of peace of mind is both as a cause & a result of hair suitism. *Emotional Tension may intiate or exacerbate
hairsuitism ,more stress more hirsutism
Ectopic Virulizing tumor:- Bronchogenic carcinoma or
*Undetermined Hirsutism((idiopathic)).:- In which the cause cannot be identified by the available investigations (it occur in genetically susceptible people).
It is widely used term but with no universally accepted definition.
To some hair suitism without an obvious clinical causes.
Whilst others define it as hair suitism without any discernible biochemical cause but abnormalities of androgen metabolism are probably demonstrable in all cases.
So probably there is no idiopathic ;but they are heterogenous groups of cases with negative investigations.
* Causes of undetermined Hirsutism:-
1- Genetic causes:- It runs in families.
2- Minor adrenal dysfunction.
3- Active (5-alpha reductase enzyme)in the skin causes increases DHA.
Androgen receptors in the target organs either high in
number or over sensitive to normal testosterone in
Pathogenesis of Hair suitism:-
1- Genetic causes (family history).
2- Testosterone: overproduction of androstenedion from ovary or adrenal.
3-Target organ (hair follicle) abnormality (over sensation to testosterone, in some patients the target organs have the ability to change testosterone into much more active androgen which is called (Dihydrotestosterone(DHT)) and this explain why in some cases hairsutism occur with normal hormone level.
1- Common problem among *Iraqi females.
2- Usually start after puberty (15-16 years old) and might increase in severity after years.
3- Androgenic syndrome:- which is hirsutism, female baldness and acne vulgaris caused by androgen excess, it is rare in Iraq and the age of onset is around 14, while the age of presentation is around 21.
* It could involve one area or multiple areas.
* Male sexual pattern:- chin (91%), moustache (31.3%), chest (35.2%), side of face (30.3%), neck (4.4%), nipples and breast (39.2%), Linea Alba, above umbilicus or thigh.
* May have a complete beard like a man.
* Linea Alba below the umbilicus is usually normal.
* In Iraq commonly on the area around the chin, nipple and mustache .
5- Many hairsutism patients have irregular period or sterility as a part of polycystic ovaries, but other may have pregnancy and normal children.
6- Positive family history in 30% of cases.
*incidence of hairsutism in Iraqi female :
82% of females.
Chin 12/82 =14.6%.
Side of the face 9/82=10.9%.
Linea alba and above the umbilicus=19.5%.
Rarely needed and they are very costly and may be negative in high percentage.
Serum hormones:- FSH, LH, Prolactin, Progesterone and Testosterone (recently measure free testosterone from saliva).
24 hour urine collection for steroids.
Ultrasound of ovary, skull X-ray or CT scan to see the pituitary gland.
Sex hormone binding globulin(SHBG).and also chek for other secondary causes in suspected cases.
No effective treatment, because if it is stopped, we may have relapse , but it helps to decrease the progression of the condition.
And keep in mind that wedge dissection of the polycystic ovary the hairsuitism not changed. And we keep the pt. like that with or without Rx.
The pills for 21 day from the 5thday of period + dexamethason one (0.5) daily at night.
If stop treatment we may have relapse.
If the woman is married with infertility this is dangerous complication, So Don't continue on treatment.
2- Cyproterone Acetate:- 50 mg/day for 10 days from 5th day of cycle, help electrolysis, May causes irregular period, so it is given with ethinyl estradiol((high dose and low dose.)), it is an effective treatment but with high relapse rate, some may have complete cure. This type of treatment should be uses with caution with unmarried women((they don’t prefer it)). because it causes menstrual disturbance and may lead to no pregnancy.
3- Cimitidine (Antiandrogen).
4- Spironolactone (Antiandrogen).
5- Flutamide (Antiandrogen).
6- Ketoconazole (Antiandrogen).
7- Fine strides (5-alpha reductase inhibitor).
1- Hair bleaching:- with 20 vol. H2O2 will break the hair.
2- Waxing:- plugging creams as Thioglycollate or calcium hydroxide.
3- Abrasive as pumice:- rub the hair away from the surface (note that continuous hair epilation may cause permanent damage to the hair bulb so it will lead to no more hair, also it may be associated with pseudofolliculitis.
Hair diathermy:-Electrolysis,Hair cautry it is the most effective done in private clinics, it is expensive and needs time (many sittings) and high skills, the idea is to kill the hair root mainly papillae, it has many side effect (it needs many sitting this may causes swelling and eryhthema which lead to infections and pigmentations which lead to *scaring but they are all temporary).
The scaring is usually temporary especially superficial and it is disappear with time usually within a year and scaring of the face is better than scaring of mind.
5- Laser therapy:- effective, but very expensive.
1- Mention the causes of undetermined Hirsutism.(2 times).
2- Mention the causes of Hirsutism in Iraqi females.
3- Mention the factors involved in pathogenesis of Hirsutism.