Journal College Mirror |
Vol 19 No. 4 Oct/ Dec 1993 APPROACH TO HAIR LOSS
Most hair problems in presenting patients are that of alopecia. The three major points in this challenging problem are to: a) Make an accurate diagnosis based on sound knowledge of anatomy and pathophysiology of hair, and its affected phase of growth. b) Exclude systemic disease. c) Investigate and effectively manage.
ANATOMY: OVERVIEW There are about 100,000 to 150, 000 hair follicles on the scalp. About 90% are in active growth (anagen). 10% go into an inactive retiring phase (telogen). Thus the anagen: telogen ratio is 90%: 10%. Hair grows at about 0.4 mm a day. The follicular density (number of hair follicles/ cm2) decreases from 1135/ cm2 at birth to 435/ cm2 by 70-80 years of age. Thus older people have less hair. The growing area is the bulb which shows a bulbous club and with a firm hair sheath, compared to a telogen hair with a small bulb.
PRACTICAI, GUIDELINES TO HAIRLOSS On average 50-100 hairs will be shed each day. Loss of more then the daily average of 100 hairs is abnormal. Basically, check the hair and scalp and categorize into two groups: - If the hair is affected, but the scalp is normal and non-scarred. - If the hair and scalp is affected and scarred. I. Non-scarring localised alopecia For patchy alopecia:
Non-scarring generalised or diffuse alopecia:
II Scarring alopecia: scar seen. - common: discoid or systemic lupus erythematosus (hair follicular plugs, telangiectasia, with active red edges seen and lesions on the face and body) and morphea (ivory yellow plaque). - uncommon: fungal abscess as in kerion, with short broken shafts.
INVESTIGATION After deciding on the possible diagnosis, a few useful tests are
is increased to 30-40%. the hair shaft. A hair culture for fungus may be taken.
SOME COMMON SCALP CONDITIONS Non-Scarring Alopecia Androgenetic Alopecia Androgenetic alopecia or male pattern baldness commonly can affect about 40% of men and women, over the ageof40. It is genetically inherited but the expression is variable. In severe cases, the family history is pronounced and the hair fall begins early, at the late teens. In males, there is a bitemporal recession and also vertex hair loss. The hair miniaturises and becomes small vellus hair, which will also fall and baldness sets in. The degree of loss is classified by Hamilton's grades I to VII. In women, the hair loss is over the vertex and is classified by Ludwigs I to 111. At menopause, the hair fall is accelerated, but they do not bald completely. Treatment presently is with topical minoxidil (piperidinopyrimidine) which may have an effect on the proliferation of the hair bulb and matrix of the hair. Used daily, results are seen in 30-40% only after 4 to 6 months, with a maximum possibly 2.5 times of regrowth but not to full density. It plateaus out after a year. Continued use is necessary. An uncommon side effect is allergic dermatitis. Cost is a major factor, as a bottle / month costs about $60-$80.
This appears in 50% of persons before the age of 20. This may be localised hut can be widespread. In 80% of cases, type I alopecia areata, they appear as patches. They have no history of atopy and endocrine (e.g. thyroid) problems and have a good prognosis. In type II alopecia areata, about 10% there is a history of asthma, allergic rhinitis and atopic dermatitis and this hairloss lasts longer and recurs. In type III alopecia areata, there is a family history of hypertersion, the hairfall is chronic and can go on to alopecia universalis. The last group, Type IV alopecia areata, have endocrine (thyroid) problems, are present over the age of 40, and often have it over the occiput (ophiasis pattern).
Treatment : Often treatment is better in children, and when the disease is present for a shorter period. It may last up to 6-8 months. Topical steroids: Synalar gel may be used with occlusion. Intralesional triamcinolone is to be given just below the epidermis, and not beyond mid-dermis. Not preferred in large areas of alopecia. Oral steroids: between 20-40 mg for children to adults and later saner. It may he advantageous to combine with intralesional triamcinolone. The side-effects of steroids have to be monitored. Isoprinosine potentiates T-lymphocyte and phagocyte function. Doses of 50 mg/kg tds for 6 months may be tried. Others tried are Minoxidil 2%, topical chemical sensitisers like DNCB, squaric acid ester and diphencyprone.
The hairloss occurs about 2 months after the event. This could be hormonal, nutritional factors, iron deficiency, psychological stress, drugs, illnesses, major surgery hair grooming procedures, thyroid diseases (hyper or hypothyroidism), pregnancy, infections with high fever, chronic illness like leukemia, carcinoma, ulcerative colitis, syphilis, and a number of drugs like antihypertensives, allopurinol and anti-cholesterolaemie drugs. The prognosis is goodcomplete regrowlh of hair is the rule.
Some hair shaft problems in Congenital Hairloss Hair shaft defects are related to (a) fractures of hair leading to hair fragility and breakage (b) twisting and curling of the hair shaft (c) indentation and grooves (d) irregularities
Some more common and simple examples are:
Scarring Alopecia This is uncommon but permanent and frustrating. Often a biopsy of the scalp is required to exclude lupus erythematosus, lichen planus, tinea capitis and infections. The above are the inflammatory causes; non-inflammatory causes include developmental, hereditary and neoplastic conditions. Lupus Erythematosus: This accounts for about 40C. of scarring alopecia, often in females, in adults. Systemic features may not be present. The lesions are discoid, scarred, with keratin plugs. A biopsy is confirmatory. Lichen Planus: This accounts for another 3040% of scarring alopecia. Features are like lupus erythematosus and a biopsy is mandatory. Folliculitis: may be scarred and flat, from staph aureus, or bulging due to dissecting cellulitis, often associated with acne conglobate and hidradenitis suppurativa. These are boggy plaques and the sides may exude pus. Surgical intervention gives a permanent cure.
This is mainly for advanced stages of androgenetic alopecia. Older techniques include punch grafting and scalp reduction. Newer techniques give improved cosmetic features and include strip harvesting of hair follicles, use of minigrafts, use of Ultraplus CO2, hair implants, tissue expansion preceding scalp reduction. Scars of cicatrical alopecia are excised by a combination of techniques.
More Pics - Androgenetic alopecia , Tinea capitis, etc |