CHAPTER 48

 
Hair is derived from the epidermis . It develops about the third or fourth month of the fetal life. After birth the hair follicles distributed on the scalp or other parts of the body become stable and no more hair follicles are developed after that. Meanwhile hair follicles may be modified or decreased in number by age or due to different factors . 

There are two types of skin, the glabrous type, which is covered by hair, and non-glabrous, which is the smooth skin, not covered by hair even after puberty.

Newborn babies skin is covered by fine light colored hair known as lanugo hairs, which tend to be most dense on the face, limbs and trunk. Lanugo hair is shed during the first months of life to be replaced by vellus hair.

It is fine hair, lightly pigmented, which covers most of the whole skin surface except palms, soles and the red surface of the lip near the mucocutaneous junction.

This is fine hair, usually light colored and is characteristically seen on children face and limbs. The vellus hair usually covers the female skin .

This is coarse, thick and pigmented hair. The hair follicle may produce a vellus hair at the beginning where later, under certain factors it 7 is transformed into terminal hair.

The type of hair varies according to the site, sex, race, age and other factors mainly the sex hormones.

Hair follicles appear first in the regions of the eyebrows, upper lip and chin at about 9 weeks of embryonic development, and in other regions in the fourth month . Hair follicles of the scalp are established after about six months after birth.

The total number of follicles in an adult man has been estimated at about 5 million, of which about 1 million are in the head (face, eyebrows, moustache area, eyelids).

The growth of hair occurs in cycles. Hair does not continue to grow indefinitely. Hair follicles grow in a repetitive sequence called hair cycle. Hair growth is present in different stages and in special balance in normal individuals, where the growing hairs constitute the majority.

1. Anagen (growing phase):

   This is the growing phase which takes about 3 months or more depending on the site. The follicular cells grow, divided and become keratinized to form growing hair. The base of the hair shaft is moist and soft where a darkly pigmented portion is evident just above the hair bulb. The growing hair in normal individuals constitutes about 90% of the total hair . 

2. Telogen (resting phase):

   Telogen hairs are in a state of resting (for about 3 months)where part of the growing hair (about 10 % )passes in this stage before falling .

   Telogen hair is also known the “club hair“ that is shed when a new hair grows. 

3. Catagen (transition phase):

   Catagen hairs undergo transition from growing to the resting phase where growth ceases with the formation of club hair .

   When the hair approaches the end of its growing phase  different changes occur in the follicle.

   Under normal conditions most of the hair is in the growing phase , others in the resting phase, and a small percentage of hair is in the catagen or falling phase.

   Normal scalp has approximately 100,000 follicles. Scalp hair growth is 0.35 mm/ day.

   The growing period of the scalp hair is about six months.

   The growing phase is much altered by different factors, mainly hormonal, generalized debilitating diseases, stress, pregnancy, lactation and other factors. In such conditions the growing phase is shortened and most of the hair pass in the resting phase.

   The scalp hair normally looses from 100-120 hairs / day . The lost hair is compensated later on.

   In contrast to the belief by some individuals, mainly females, that baldness is expected because she looses that number of hair daily. The convincing answer is that if this is the case and falling hairs are not replaced by new hair, all human beings are bald.

   Resting hair is exposed to falling easily because, they are less firmly anchored .

   Scalp hair differs in that its growth does not require any androgenic stimulus, in contrast increased circulating androgens may lead to hair falling.

The hair is composed of :

Hair shaft or stem which forms at the lower end; the hair papilla. The hair shaft is made up of keratinized cells. The hair shaft consists of the sheath or cuticle, the cortex and the medulla. The medulla begins at some distance from the tip and ends near the bulb. The hair follicle may in fetal life produce lanugo hair and in the adult life the terminal hair .

The hair root or matrix that is the intrafollicular portion of the bulb.

Outside the hair root is the hair cuticle . The inner root sheath is made up of the cuticle and additional two layers of cells , the Huxley and the Henele layer . The outer root sheath extends from the epidermis to the hair bulb. It is thickened near the epidermis and becomes attenuated in its lower portion. The sebaceous gland is derived from it .

The hair bulb is an expanded mass of epithelial cells, which gives to different types of keratinized cells. The bulb and part of the shaft are contained in the hair follicle

Hair color depends on the degree of melanin synthesis in the matrix fibers and the intervening spaces between the fibers.

Melanin synthesis begins in the matrix fibers. Melanin in the hair follicle is produced in the cytoplasm of melanocytes .

The pigment in dark and gray color of the hair is composed of tyrosine - melanin while the blond and red hair, the pigment is phenoalanin.

Black hair color - In this type the melanocytes contain dense melanosomes.

Brown hair : melanocytes are smaller.

Light brown hair : consists of mixture of the melanosomes of the dark hair and the incomplete melanosomes of the dark hair.

Red hair :contains iron pigment. Melanin deposit is incomplete on the matrix fibers

Grey hair : Melanogenic activity is decreased.

Melanocytes and melanosomes are decreased.

Loss of tyrosinase activity.

Age

Metabolic changes : such as in porphyrias and kwashiorkor disease .

Drugs: chloroquine therapy for a long time may cause depigmentation of hair. Chloroquine interferes with phaeomelanin synthesis. The reaction is usually reversible where the color returns back to normal within few months after stopping the drug .

Topical preparations: Dithranol and chrysarobin stain light colored or gray hair mahogany brown. Resorcin formerly used a great deal in a variety of skin diseases, colors black or white hair yellow or yellowish-brown.

Mephenesin, glycerol ether used for diseases with muscle spasms, causes pigmentary loss in dark-haired people .

Triparanol, an anticholesterolaemic drug and fluorobutyrophenone, an antipsychotic drug can cause change in the hair color.

Minoxidil and diazoxide, two potent anti hypertensive agents, both cause hypertrichosis and darkening of hair.

Diazoxide causes reddish hair discoloration, whilst Minoxidil darkens hair mainly by converting vellus hair to terminal hair.

Hydroquinone and phenylthiourea interfere with tyrosine activity, causing hypopigmentation of skin and hair .

In this chapter short notes are mainly applied to the most common diseases and abnormalities of hair in infants and children ,where some of these diseases and changes may be the same as in older age groups.

The patches are oval or round where at the periphery there is loose hair were given the term “exclamation mark.” When pulled shows an atrophic hair bulb. The scalp surface of the area is usually smooth.

The hair loss may continue spreading peripherally forming new areas free of hair, or regeneration may occur later on. The new growing hair is downy, light or even white in color devoid of pigment.

In long standing cases of alopecia, fingernails stibbling may occur.

Local infection of the scalp  such as folliculitis , Tinea capitis and favus.

1. Skin diseases: Lichen planus, discoid lupus erythematosus.

2. Focal infection :

3. Chronic tonsillitis, sinusitis and septic foci have blamed as a causative for alopecia.

4. Dental abnormalities :

   Infections of teeth

   Dental caries in children, errors of refractions and impacted wisdom tooth in older age groups are some of the different causes of alopecia areata .

5. Stress, nervous tension and psychic trauma are also considered important causes of alopecia areata.

                                                                                                    

                                                                                                  Fig.410b. Alopecia and nail dystrophy

   Majority cases of alopecia areata we face in our practice in children are due to dental caries , psychic trauma, septic foci in the tonsils or sinuses and due to immunological factors.

2. Pressure Alopecia :

   This may be noticed in babies who sleep most of the time on the occipital region where by continuous pressure on the occipital area, localized patch free of hair develops.

3. Alopecia in the course of febrile diseases

   Alopecia may develop during systemic diseases such as fevers and chronic recurrent bacterial infections.

4. Telogen effluvium (Disturbances of hair cycle)

   Telogen effluvium is the early and excessive loss of normal hairs from normal follicles of the scalp. This type of hair loss is most common in females that may occur in the postpartum period, post febrile, postnatal , post surgery and post-traumatic conditions.

   Increased shedding of hair is clearly related to the stressful episode that preceded hair falling by 6-16 weeks.

Marasmus: is due to protein-calorie deficiency, usually in the first year of life. The hair is fine and dry; the diameter of the hair bulbs is reduced to a third of normal and almost all follicles are in telogen state.

Kwashiorkor disease: occurs during the second year of life in children suddenly weaned to a diet very low in protein and high in carbohydrate. The hair changes are grossly similar to those in marasmus, but there are more anagen follicles although most are atrophic. In both states the hair is brittled, falls easily where partial or complete alopecia may occur. The hair is lusterless and if normally black, may assume a reddish tinge. Many hair shafts may show constrictions, which increase susceptibility to mild trauma leading to hair shedding.

Iron deficiency: is occasionally associated with diffuse alopecia, even in the absence of anemia.

Zinc deficiency: resulting from a failure in absorption gives rise to alopecia and cutaneous changes as in acrodermatitis enteropathica and prenatal zinc deficiency. Zinc deficiency may present with erythema, scaling, bullae and hair loss.

Parental iron deficiency may also cause deficiency of essential fatty acids. This results in erythema, scaling of the scalp and eyebrows and diffuse alopecia. 

6. Metabolic Alopecia

   In homocystinuria, which is an inborn error in the metabolic pathways of methionin, the hair is sparse, fine and fair.

   In hereditary aciduria , which is a rare inborn error of pyrimidine metabolism, characterized by retarded physical and mental development, macrocytic anemia, the hair is fine, short and sparse.

   Histidine, tyrosine and arginine errors of metabolism : The hair is dry, lusterless, tightly curled hair. 

8. Endocrinologic alopecia: occurs in the course of hypothyroidism and hyper thyroidism. 
    

9. Alopecia marginalis usually this type occurs in dark races where there is loss of hair from the margins. 

Fig.417b. Alopecia marginalis                                                                                                                                         Alopecia universalis

8. Trichotillomania

   This type is seen in neurotic children who pull the scalp hair and the eyelids or eyebrows hair. 

   

   Fig.417b. Trichotellomania

    

9. Drug induced alopecia

   Different types of drugs may induce hair loss . Methotrexate in cancer therapy,Thallium, Colchicine, cytotoxic drugs, prolonged vitamin A intake may cause alopecia.

   Corticosteroids may induce diffuse alopecia of the scalp together with lanugo hair formation elsewhere.

   Anti-coagulants : heparin and coumarin may cause alopecia.

10. Hypervitaminosis A

    Excessive consumption of vitamin A gives rises to a variable syndrome in which the principal features are dryness, irritability and sometimes pigmentation of the skin, and slowly progressive thinning of scalp, body hair, eyebrows and eyelashes. Loss of weight, fatigues, anemia and bone pain.

    Liver and spleen are sometimes enlarged.

11. Genetic alopecia

    This is an autosomal dominant type of alopecia where racial factors play also an important role.

12. Alopecia areata with auto-immunity

    Different auto-immune diseases may be associated with alopecia mainly:

    Alopecia is associated with thyroid diseases.

    The association of vitiligo with alopecia

15. Pseudopelade

    The term pseudopelade is used to designate a slowly progressive cicatricial alopecia, without clinically an evident folliculitis and no any marked inflammation.

    The condition may occur in childhood . Pseudopelade is therefore generally regarded as a clinical syndrome that may be the end result of any one of a number of different pathological processes.

    Lichen planus and lupus erythematosus can produce a very similar clinical lesion . 

    The affected patches are smooth, soft and slightly depressed. At an early stage in the development of any individual patch there may be some erythema. The patches tend to be small and round or oval, but irregular bald patches may be formed by confluence of many lesions .The hair in uninvolved scalp is normal. 

16. Alopecia due to Physical Agents

    Burns or deep X-ray causes this type of alopecia .

17. Cosmetic Alopecia

    Chemicals in cosmetic preparations as strong alkaline shampoos, different topical applications of the scalp, hair gels and dyes.

    Hydrogen peroxide or other chemicals in hair dyes .

    Excessive use of hot combs or chessoirs.

    Straightening of hair. 

18. Androgenic Alopecia

    Androgenetic alopecia (or male pattern baldness) begins with recession of the frontal hairline. This is followed by thinning over the vertex and then, eventually, complete loss of hair over the crown. It is partially mediated by circulating and locally produced androgens, including testosterone and 5-dihydrotestosterone, combined with a genetic susceptibility, possibly inherited in an autosomal dominant fashion with variable penetrance.  Men who have been castrated before puberty and homozygotes for 5-reductase type II deficiency do not develop androgenetic alopecia.   5-Reductase is the enzyme that converts testosterone to 5-dihydrotestosterone. On the scalp of patients who are predisposed to the condition, androgens lead to miniaturisation, a switch from terminal to vellus or vellus-like follicles, and a reduction in the duration of anagen.   The concentration of androgen receptor and 5-reductase activities in frontal hair follicles is greater than in occipital follicles . Higher activities of aromatase, a bifunctional enzyme involved in converting testosterone to oestradiol, are found in occipital hair follicles.  This may explain the loss of hair in the frontal area in androgenetic alopecia, while occipital hair is retained. In women, in whom androgenetic alopecia expression is less severe and often spares the frontal hair line, lower concentrations of androgen receptors and 5-reductase activities are found in the frontal hair follicles, and aromatase activities are higher.

    Partial baldness is sometimes first apparent on the vertex, but the most frequent presentation of androgenic alopecia in women is a diffuse hair loss.

    Replacement of terminal hairs by progressively finer hairs, which are eventually short and virtually un pigmented.

    Vellus hairs are interspersed with hairs that are still normal and others are only slightly reduced in diameter.

The side effects of anti-androgens preclude their use in men. In women, there is some scientific evidence for regrowing of hair with cyproterone acetate, but in general this drug, in doses of 50-100 mg/ day with ethinyl oestradiol, may be said to prevent further progression of hair falling.

Finasteride is a 5-reductase inhibitor. Its use results in decreased circulating and scalp concentrations of 5-dihydrotestosterone and a compensatory rise in testosterone and gonadotrophin values.  The androgen receptor is not affected by finasteride  Further hair loss is prevented in most patients treated with finasteride. About half of men achieve some regrowth, and in about a third, after two years of continuous use, this is considered cosmetically important  To date, studies have examined the effect only at the vertex, where the benefit is greatest. Less clinically dramatic but statistically significant improvement in hair counts also occur at the frontotemporal scalp margin, indicating that the progression of hair loss in this region may at least be prevented.  Although regrowth may be seen as early as three months, patients should be encouraged to take finasteride for two years before evaluation. The prevention of further loss and the likelihood of regrowth do not seem to correlate with the grade of androgenetic alopecia. If treatment is successful it should be continued indefinitely, as the balding process continues when it is stopped. 

The most common side effects, which occur in less than 2% of men, are erectile dysfunction, diminished libido, and decreased ejaculate volume. These effects are reversible and tend to be less of a problem over time if the patient continues taking the drug.   To date, this agent has not be shown to be effective in treating female androgenetic alopecia. ^{(Recent advances in dermatology).}

Topical preparations

Minoxidil : Minoxidil 2% -5% solution (Regain) is a topical preparation used for treatment of hair fall . It is a piperidinopyrimidine derivative and a potent vasodilator that is effective orally for severe hypertension.

The medication should be used twice daily for a long period not less than 8 months.

When applied topically containing 10% propylene glycol, Minoxidil has shown conversion of vellus to terminal hair in up to 30% of individuals.

19. Total Alopecia

    An autosomal recessive gene usually determines total alopecia as an apparently isolated defect. Many isolated cases may be associated with other ectodermal dysplasia.

    The scalp hair is often normal at birth but is shed between the first and sixth months, afterwhich, no further growth occurs.

Loss of the scalp and whole body hair . The problem may develop suddenly or within few days or months .

In some cases the scalp has been totally hairless at birth where the child lives with permanent alopecia .

Eyebrows, eyelashes and body hair may also be absent.

Teeth and nails are normal and general health, intelligence and expectation of life are unimpaired. 

20. Circumscribed alopecia of congenital origin

    Congenital alopecia

    This type is usually associated with other ectodermal defects.

Aplasia: of all layers of the skin gives rise to a congenital defect. There is usually a circular or a linear area of scarring somewhat depressed below the scalp surface commonly appears on the vertex.

Pseudopelade may develop during early infancy in association with certain hereditary syndromes, e.g. incontinentia pigmenti and Conradi‘s syndrome.

Circumscribed non-cicatricial alopecia: is uncommon. It is the result of hypoplasia or aplasia of a group of follicles. The scalp patches may develop between the third and sixth months. This type may present with different types mainly :

Vertical alopecia: a small and often irregular patch of alopecia is present on the vertex at birth.

Sutural alopecia : multiple patches overlie the cranial sutures.

Triangular alopecia: a triangular area overlying the fronto-temporal suture just inside the anterior hairline, and with its base directed forwards.

Seborrheic alopecia: occurs with severe state of seborrhea where the hair loss may be localized or diffuse.

Trichorerhexis nodosa: this is britling of the hair due to follicular dysfunction, which produces nodal swelling along the fibers leading to hair fiber fracture and alopecia.

Menke‘s kinky hair disease

The hair becomes sparse, kinky and short due to fiber fracture.

Physical and mental abnormalities where the condition may be fatal.

Diagnosis: serum copper is decreased and copper accumulation in all body cells.

SYNDROMES ASSOCIATED WITH ALOPECIA

1. Universal alopecia

   This syndrome is characterized by:

   Congenital deafness

   Spiny hyperkeratosis

   Universal alopecia

   Gastrointestinal polyposis manifests with vomiting , diarrhea and abdominal pain .

2. Papillon-Lefevre syndrome

   Clinical Features

   Hyperkeratosis of palms and soles

   Hyperhidrosis

   Alopecia

3. Cartilage hair hypoplasia

   Clinical Manifestations

   Abnormal fine and sparse hair in children .

   Limb dwarfism

   Recurrent respiratory tract infection.

4. Marinesco-Sjogren syndrome

   Clinical Manifestations

   Congenital cataract

   Mental retardation

   Cerebellar ataxia

   Mental retardation

   Thin brittled, sparse hair.

5. Hallman -Streif syndrome

   Clinical Features

   Hypotrichosis

   Birdlike faces

   Microcephalus

   Micrognathia

   Congenital cataract

6. Lipodematous alopecia

   Alopecia

   Joint hyperlaxity and hyperelasticity .

7. PROGERIA

   Failure of development normally after the first year of life .

   Clinical Features

   Premature senility .

   Large bald head and absent eyelids and eyelashes .

   Skin : wrinkled , pigmented and atrophied .

   Subcutaneous fat is decreased or absent .

8. Turner‘s syndrome

   Clinical Features

   Alopecia of the frontal area of the scalp.

   Low hairline on the back.

   Typical webbing.

   Short stature.

   Prominent ears.

   Increased carrying angle.

   Cubitus vulgaris.

   Cutix laxa.

   Webbing of the neck.

   Coaractation of the aorta.

9. Noonan‘s syndrome

   The clinical manifestations are the same as Turner‘s syndrome without aortic coaractation.

10. Klippel-Feil syndrome

    Occurs mainly in girls.

    Clinical Features

    Low posterior hairline.

    Short neck .

    Fused cervical vertebrae.

    Strabismus, nystagmus .

    Cleft palate.

    Bifed uvula.

11. Werner‘s syndrome

    Clinical Manifestations

    Alopecia.

    Premature hair graying.

    Short stature.

    Atrophy of muscles and subcutaneous tissue .

    Spindle extremities due to bone atrophy and osteoporosis .

    Cataract.

    Skin changes : poikeloderma , diffuse hyperpigmentation with dark gray and hyperkeratosis.

    Hypogonadism.

12. Graham -Little syndrome

    Occurs mostly after puberty and is characterized by:

    Cicatricial alopecia of the scalp.

    Non cicatricial alopecia of the axilla and pubic hair.

    Lichen planopiliaris.

    Pseudopalade.

Treatment of Alopecia Areata

General

Correction of the predisposing factors such as anemia , emotional factors, infections and others.

Usually the condition is reversible. Hair may begin to regrow in the bald area in a short or long time without treatment.

Topical preparations

Minoxidil preparations: These may give good results if are used for a long time (6-8 months).

Corticosteroids: These may give results, if used for a long time.

Topical corticosteroids:

Local infiltration by triamcinolone (Leddercort ) by syringe or dermojet. Much care must be considered to use diluted steroid preparations in order not to cause skin atrophy or hypopigmentation, which may result from the concentrated corticosteroids during infiltration of the area.

Systemic medications are rarely needed . Severe cases of alopecia my need prednisone tablets or Depot medrol injections once weekly for 1-2 months.

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