Simple notes on alopecia

1. DEFINITION
Alopecia is defined as excessive or abnormal loss of hairs.
2. PHYSIOLOGY
Natural hair loss is a physiological phenomenon. It is not a disease. Only when the loss is excessive or when the pattern of loss is abnormal, then it is pathological. Before one talks about the causes of alopecia, one has to understand the physiology of hair growth (Diagram 1).
Diagram 1: Hair Cycle
2-6 years
Anagen ---------------------------------------» Catagen
| |
Hair shedding «---------------------------------Telogen
100 days
90% of our terminal hairs are at anagen phase which is the growing phase. It lasts for 2-6 years. The scalp hair on average grows at the rate of 0.37 mm per day.
Catagen is a transient period. Hair matrix cells stop dividing. As a result, there is no hair growth.
Less than 10% of our hairs should be in telogen phase which lasts for 100 days (about 3 months). Since on average, each person has about 100,000 hairs. Therefore, less than 10,000 should be in telogen phase and on each day less than 100 hairs fall off physiologically.

3. SPECIAL POINTS TO LOOK FOR
When examining patients with alopecia the following points are worth paying attention to:
1) Pattern of alopecia
a) Diffuse alopecia is usually due to telogen effluvium, systemic disorder (e.g. hypothyroidism, Fe deficiency, secondary syphilis), drugs.
b) Patchy alopecia is typically seen in alopecia areata, scarring alopecia.
c) Marginal alopecia affects the hair margin only. It occurs in alopecia areata or due to hair styling.
d) Frontal and bitemporal alopecia is typical of male-type baldness.
2) Sign of scalp inflammation indicates alopecia may be secondary to inflammatory dermatosis (e.g. tinea capitis)
3) Presence of scarring together with alopecia will switch the differential diagnosis towards the cause of scarring alopecia (e.g. DLE, Lichen Planus).
4) Other than the scalp, see if hairs in other areas are also affected (e.g. axillary, pubic regions, eyebrow, eyelashes etc.).
5) Detailed drug history and history of past health are important.
4. CAUSES OF DIFFUSE ALOPECIA WITH NO SIGN OF INFLAMMATION NOR SCARRING
1) Telogen Effluvium
a) Post-Partum
b) Severe Illness
c) Major Operations
d) Malnutrition
2) Anagen Effluvium e.g. chemotherapy
3) Male Pattern Baldness
4) Female Pattern Baldness
5) Diffuse Alopecia Areata
6) Drugs e.g. heparin, antithyroid drugs, etretinate, isotretinoin
7) Systemic Disease e.g. Fe deficiency, thyroid disease, secondary syphilis, SLE
8) Ageing: usually causes thinning of hairs
4.1. Telogen Effluvium
When a severe insult striking our bodies (severe infection, delivery, major operation) the anagen hairs (> 90% of hair population) will all simultaneously shift to telogen phase. As a result, about 3 months after the insult, more than 90% of the hairs will fall off at the same time giving rise to the condition which is called telogen effluvium.
The diagnosis can be made from a detailed history of the past health. In case when the diagnosis is in doubt, it can be confirmed by the telogen hair count test. It is done by plucking a bundle of hairs and counting for the percentage of telogen hairs present. Normally, the telogen hair count should not exceed 10% of the total hair count. Unfortunately, this test is not available in most centres.
For telogen effluvium, no specific treatment is needed since spontaneous remission is the rule.

4.2. Anagen Effluvium
Chemotherapy attacks the rapidly dividing cells i.e. anagen hairs. As a result, more than 90% of hairs fall off soon after chemotherapy. Usually, there is no problem with the diagnosis since it is obvious from the history.
4.3. Male Pattern Baldness (Androgenetic Alopecia)
4.3.1. Pathogenesis
Even though the exact aetiology is unknown, there are proofs that genetic factor, as evidenced by frequent positive family history, and androgen play an important role in the development of the disease. Eunuchs and castrated males never develop baldness. Under the influence of androgen in a genetically predisposed person, the terminal hairs are gradually transforming into vellus hairs and they eventually fall off.
4.3.2. Clinical Features
Typically, it starts off with bitemporal recession and subsequently, thinning or complete loss of hair at the crown. Hair on the occiput and around the sides of the scalp is seldom affected and it seems that hair in those areas are more resistant to the effect of androgen. The diagnosis can often be made by the characteristic pattern of hair loss and the frequently presence of a positive family history.
4.3.3. Treatment
1.No good treatment is available at present.
2.Topical minoxidil may be useful in minority of cases but the effect disappears soon after stopping the treatment and yet it is expensive. It is the only FDA approved drug at presence for the treatment of androgenetic alopecia.
3.Topical ether-in-spirit: the effect is no better than placebo.
4.Hair Transplant: based on donor dominance theory which states that hairs from growing areas will survive and grow when transplanted to bald areas. The operation is tedious and requires expertise.
5.Wigs: quite practical if it is acceptable by the patient.
4.4. Female Pattern Baldness
It is characterized by thinning of hairs at the crown or a diffuse hair loss. Unlike male pattern baldness, there is no bitemporal and frontal recession. If female pattern baldness occurring in a young female, especially with the presence of menstrual disturbance, signs of hirsutism or virilization, excessive androgen activity needs to be excluded e.g. androgen-secreting tumour. Treatment is difficult but one may try cyproterone acetate which is an anti-androgen.
5. CAUSES OF PATCHY ALOPECIA WITHOUT SCARRING
Alopecia areata/totalis/universalis
Trichotillomania
Traction alopecia
Tinea capitis (excluding favus)
5.1. Alopecia Areata/Totalis/Universalis
These 3 conditions all belong to a spectrum of the same disease. They only differ in the degree of severity. When all the scalp hair is lost, it is called alopecia totalis. If both scalp and body hair are involved, it becomes alopecia universalis.
Alopecia areata is the commonest cause of patchy alopecia.
5.1.1. Aetiology
The exact aetiology is unknown. Genetic factor and atopy play some role as some patients may have positive family history or history of atopy. It is considered as a kind of autoimmune disease since it has an association with other organ-specific autoimmune disease (e.g. Vitiligo, Hashimoto thyroiditis). The incidence of alopecia areata is high in patients with Down's syndrome and those who are under stress.
5.1.2. Clinical Features
The disease affects male and female equally at all age. It is presented as discrete patches of baldness with no scarring and no sign of inflammation. Broken hairs with tapering shafts (i.e. exclamation mark hairs) are diagnostic. Nail pitting may also be present.
5.1.3. Treatment
1.Local Steroid
a) Topical Steroid e.g. 0.025% fluocinolone, halometasone
b) Intralesional Steroid e.g. triamcinolone
These treatment modalities may be useful in dealing with localized disease.
2.Irritants or Contact Sensitizers e.g. dithranol, diphencyprone. DNCB is no longer recommended because of its carcinogenic potential.
3.PUVA/UVB: May show response in some cases but need many treatment sessions. The actual beneficial effect is controversial.
4.Topical minoxidil: effect is doubtful.
5.Oral prednisolone: it is effective in some cases but has to be reserved for resistant or severe cases (e.g. alopecia universalis or alopecia totalis) because of its potential side effects.
6.Wigs wearing: last solution.
5.1.4. Prognosis
The prognosis is usually good since 75% of patients with alopecia areata have spontaneous remission eventually.
Signs of Poor Prognosis:
Multiple patches
Ophiasis (extensive hair loss at occipital area)
Eyebrows and eyelashes involvement
Alopecia totalis/universalis
Young age of onset
Presence of atopic disease
Frequent recurrent attacks
Nail involvement
Down's syndrome
5.2. Trichotillomania
5.2.1. Cause
The hair loss is due to self-induced twisting and pulling of hairs. It usually occurs in children or adolescents. It may be due to a bad habit, attention seeking or a manifestation of psychological problem.
5.2.2. Clinical Features
Patches of alopecia with no sign of inflammation are seen. Unlike alopecia areata, the margin of the lesion is less well defined and there is no exclamation mark hairs. The hair loss is never complete. Short broken hairs of varying length are characteristic.
5.2.3. Diagnosis
The disease can be diagnosed clinically. A detailed social and psychological history are essential.
5.2.4. Treatment
Often, the disease is self-limiting upon reassurance. Parents have to be interviewed so that the problem can be addressed. Sometimes, referring patient to clinical psychologist or psychiatrist may be helpful.
5.3. Traction Alopecia
Alopecia secondary to hair styling, hot-combing to straighten kinky hair.
It is rare in Hong Kong.
5.4. Tinea Capitis
Tinea capitis must be considered as one of differential diagnosis as a cause of patchy alopecia in children. The infected hair are brittle and are easily broken. It is associated with inflammation i.e. redness, scaling. Even though for most of the time, the lesion heal without scarring, in severe cases (e.g. kerion), scarring alopecia can occur. Please refer to the chapter on skin infection for details.
6. CAUSES OF DISCRETE PATCHY ALOPECIA WITH SCARRING
1.Congenital e.g. aplasia cutis, naevus sebaceus
2.Post-trauma e.g. burn, injury, radiotherapy
3.Post-infection e.g. kerion, herpes zoster
4.Inflammatory dermatosis e.g. DLE, lichen planus, morphoea: common cause of scarring alopecia
5.Neoplasm e.g. squamous cell carcinoma of skin
6.Idiopathic
6.1. Aplasia Cutis
This is a very rare congenital disease and the alopecia is present since birth.
6.2. Naevus Sebaceus
It is a kind of epidermal naevus which presents at birth as a yellowish hairless plaque on the scalp. It becomes more warty after puberty. The diagnosis can be confirmed by skin biopsy. It has potential of undergoing malignant change (e.g. basal cell carcinoma). For this reason, excision of the lesion after puberty is recommended.
6.3. Inflammatory Dermatosis Causing Alopecia
DLE, lichen planus and morphoea are common causes of patchy scarring alopecia. Sometimes, clinically, it is difficult to differentiate them one from another. One should examine the rest of the body to look for any sign that are related to each of these 3 diseases. Of course, skin biopsy of the lesion on scalp is usually helpful.
6.4. Idiopathic Scarring Alopecia (Pseudopelade)
Occasionally, despite thorough examination and investigation, no cause can be attributed to patient's scarring alopecia. If the disease is still active, topical steroid can be tried.

(Social Hygiene Handbook - 2nd Edition )