sign in sign up
<<
Home , Hot comb, Pseudopelade of Brocq, Traction alopecia

Diseases of Diseases of hair

Normal human can be classified according to cyclical phases of growth into:- • Anagen hairs are growing hairs lasting about 3 years (1000 days). • Catagen hairs: it is transitional phase lasting 1-2 weeks in which all growth activity ceases with the formation of club hair. • Telogen hairs : also club hairs are resting hairs which continue for 3-4 months ( about 100 days) before they are pushed out of the hair follicles by the hairs growing underneath them or pulled out by a hair brush or any mechanical means. Diseases of hair

• 85%- 90% of scalp hairs are an anagen hairs and 10-15 % are catagen or telegen. • The scalp normally contains 100,000 hairs • The average number of hair shed daily is 100-150 , neither nor menstruation has any effect on the hair growth rate . Diseases of hair

Human hair is also designated as • hair: - fine hair present on the body of fetus which is then replaced by the vellous and . • Vellous hair s are fine colored and characteristically seen on the children face and arms. • Terminal hairs: are course, thick and dark except in blonder. present on the men's face , chest and abdomen, • Hairs present on all parts of the body except palms, sole, and glance. • Hair disorder divided into; alopecia, , • • Alopecia classified into; • • I. non cicatricial alopecia in which there is no clinical sign of tissue , scarring or atrophy of the skin which is of two types; • • A. Focal (patchy, localized) • oduction decline which is either triangular alopecia or androgenetic alopecia • Hair breakage include , , infection ( tinae capitis ) , primary or acquired hair shaft abnormalities • Unruly hair ( difficult to keep tidy) • Abnormality of cycling like , syphilis • B. diffuse hair loss • Failure of follicle production • Hair shaft abnormality • Abnormality of cycling ( shedding ) like T. effluvium , , alopecia areata , • • II. Cicatricial alopecia; evidence of tissue destruction, such as inflammation, atrophy and scarring is apparent which is either • 1. Primary; mainly SLE, lichen planopilaris, , others like dissecting , folliculitis decalvance , keloidalis nuchae • 2. Secondary cicatricial alopecia • 3. Congenital cicatricial alopecia Alopecia areata

• A disorder characterized by rapid and complete loss of hair in one or more often several round or oval uninflamed , not scaly patches , usually occurs on scalp, area , , eye lashes, ranges from 1-5 cm in diameter , at the periphery of the bald patch . are loose hairs that may be broken off near the scalp leaving short stumps and when the are pulled out a tapered attenuated bulb is seen as a result of atrophy of that portion what we called exclamation marks. There may be • complete loss of scalp hair () • involve the whole body region (). • Loss of hair may occur along the temporal and occipital scalp () • on the entire scalp except for this area sisiapho.

Alopecia areata

Etiology • Most evidence points have documented that: 1. An autoimmune disease mediated by cellular arm and modified by genetic factors. 2. Genetic susptibility suggested by human leukocyte antigens HLA class 2 association. 3. 25% have positive family history. Alopecia areata

Histology • In early disease there is helper T cell dominant lymphocytic infiltration and peribulber area of anagen or early catagen follicles. The follicle enters in abnormal catagen phase followed by persistent Telogen structures. In the phase of recovery T suppressor cell predominate. Alopecia areata

Differential diagnosis • Tinea capitis. • Early lupus erthymatosus. • Trichotellomania. • Traction alopecia. • Syphilis. • Congenital triangular alopecia. Alopecia areata Treatment • Patient with first or minor attach can be reassured about the prospect for regrowth without treatment. • Intralesional steroid injection for localized cosmetically conspicuous patches such as those in eye brew. • High strength topical steroid cream. • Topical anthralin1% cream for 15 – 20 minutes in resistant cases. • Topical minoxidil may be combined with other treatment. • For extensive disease resistant to treatment induction of contact sensitivity to dinitrochlorobenze, topical and oral methoxsalen, and PUVA (ultra violet therapy). • Oral prednisolon in high dose in rapidly progressive wide spread disease. Alopecia areata

Prognosis • Poor prognostic factors ➢ early childhood onset ➢ Association with atopic dermatitis, down syndrome and other autoimmune disease. ➢ Wide spread involvement. ➢ Positive family history. ➢ Ophiasis, onychodystrophy. ➢ Duration more than five years. Androgenic ALOPECIA

• Define as gradual lose of hair chiefly from the vertex and frontotemporal regions during twenties or early thirties. • The anterior hair line recedes on each side so the forehead become high eventually the scalp devoid of hair. • The most frequent pattern is the biparietal recession with loss of hair on the vertex. The parietal and occipital areas are usually spared permanently. • Androgenic ALOPECIA

• Etiology ➢Inherited factor (polygenic inheritance). ➢Adequate androgen stimulation at a particular age of individual. ➢Increase in 5 α reductase enzyme inn bald area. Androgenic ALOPECIA

• Pathogenesis • Lengthening of Telogen phase and shorting of anagen phase, eventually the follicles become short and small with sclerosis of the dermis ands miniaturization of the hair Androgenic ALOPECIA

• Treatment • 2-5% topical minoxidil solution, success depend on early cases , less than 10 years duration and limited extend less than 10 cm and pretreatment hair density more than 20 hairs in cm. • Fenstride (type 2 5 α reductase inhibiter) giving as 1 mg tablet daily, it lower the dihydrotestosteron in scalp and serum of treated patient given for 6 -12 months. • Hair transplantation, minigraft from occipital to anterior scalp given excellent cosmetic result. • Androgenetic alopecia in women

• Definition : diffuse hair loss through out the midscalp sparing the frontal hair line except for slight recession, begin as thinning of midline part (Christmas tree pattern of hair loss) Androgenetic alopecia in women

• Causes • Genetic preposition excessive androgen response even though levels of circulatory testosterone not elevated. • Increase free testosterone level as in PCOS, and this could be associated with other sign of androgen excess such as hirsutism , acne. Androgenetic alopecia in women

• Treatment – Fenstride: but it is contraindicated in women of childbearing potential.

– Topical minoxidil may limit hair loss.

– Wigs may give quite satisfactory cosmetic result. Other forms of alopecia:

➢ Trichotellomania. Neurotic breaking of the hair from the scalp or eye lashes mostly in female under 10 years of age. ➢ Hot comb alopecia mostly in black women who straitening their hair with hot comb. ➢ Traction alopecia, prolong tension on hair. ➢ Pressure alopecia in babies lying on their backs. ➢ alopecia syphliticum ➢ Inflammatory alopecia as in lichen simplex chronicus, DLE, . ➢ Neurologic alopecia in lower extremities in diabetes mellitus. ➢ Endocrinologic alopecia such as in hypothyroidism. ➢ Tumour alopecia.

➢ Congenital alopecia.

• Excessive loss of normal club hairs from normal

resting follicles from scalp Telogen effluvium

• This result from traumatization of the normal hair by some stimulus such as: – surgery – parturition – fever – drugs ( such as metoprolol, captopril , propranolol and bromocriptin ) – traction which precipitate the anagen into catagen and telogen phase, clinically the patient notice a lots of hairs coming out by roots. Telogen effluvium

• Management: • 1- Reassurance, as the majority of the cases will stop spontaneously and hair will regrow. – 5% minoxidil solution plus cyproteron acetate 50 mg from 5-15 day of cycle combined with ethinyl estradoil 0.035 mg per day in premenopausal women. – Cyproteron acetate 50 mg daily in post menopausal woman. – Spironolactone 50-100 mg per day. – Flutamide 125- 250 mg per day.

• • Frequently following the administration of chemotherapeutic agents such as antimetabolite and cyclophosphmide , so loss of anagen hair become apparent after 1-2 months this reversible after stop the drug within few weeks because the drug dose not destroy the hair , so pressure culff applied around the scalp during chemotherapy and scalp hypothermia and topical minoxidil. Hirsutism

• Excess of terminal hair growth in women in a pattern more typical of men involve androgen sensitive area which include upper lip , cheek , chin, central breast, breast , lower and midline abdomen, inner thigh and lower back.

• Pathogenesis • In women the androgen biosynthesis occurs only in adrenal and ovary, potent androgen testosterone and androgen a precursor androstenedoin are secreted by the ovary , adrenal androgen are dehydro epiandrostenedoin ( DHEA), dehydroepiandrostenedoin sulphate ( DHEA sulphate) and androstenedoin , all these require peripheral conversion in the skin to testosterone which then converted to dihydrotestosteron by the action of 5 α reductase enzyme . 99% of testosterone are bound to carrier molecule so 1% unbound testosterone is the active part which reflect clinical androgen excess. • Causes: 1. PCOS (stienleventhal syndrome) characterized by menstrual irregularity in the form of oligomenorrhea, secondary amenorrhea or polymenorrhae , clinical or biochemical increase in androgen level manifested as acne , hirsutism , androgenetic alopecia and ultra sound appearance of PCOS. 2. Ovarian tumor benign and malignant example unilateral microadenoma , androplastoma , leydij cell tumor , granular cell tumor. 3. Adrenal causes: includes congenital adrenal hyperplasia, adrenal adenoma, and adrenal carcinoma which cause virilizm. 4. Pituitary causes include Cushing disease, acromegaly and prolactin secreting tumor. 5. Systemic causes: hypothyrodism , hepatorenal failure. 6. Drugs intake: phenothiazine , high progestin . Birth control pills. 7. End organs hyper sensitivity. 8. Racial variation, women of middle eastern Russia and European country have facial , abdominal and thigh hairs , where as Asian , Indian have little terminal hair growth . Diagnosis – Careful history focus on onset and progression, menstrual history, virilization and family racial background. – Physical examination may reveal signs of Cushing disease or acromegally , galactorrhoea , voice depth. – Investigation: ➢Total testosterone level and DHEA sulphate level in mild hirsutism. ➢ Overnight dexamethason suppression test for Cushing disease. ➢LH/FSH ratio for screening of suspected case of PCOS. ➢Prolactin level for prolactin secreting tumors. ➢If signs of virilization is present, Deepings of vice, muscular body, sever hirsutism and clitoral hypertrophy then an androgen secreting tumor is suspected. ➢17 hydroxy progesterone and ACTH stimulation test will screen for the late onset congenital adrenal hyperplasia. ➢Pelvic sonography for PCOS suspected cases and computed tomography of adrenal gland, MRI and CT scan in suspected cases. Hirsutism

• Treatment I. medical treatment: • Antiandrogen includes: – Cimetidine, which has weak antiandrogenic effects. – Ketoconazole (side effect hepatic toxicity). – Cyproteron acetate combined with ethinyl estradoil. – Spironolactone ( stronger antiestrogen in dose of 75-200 mg daily has a side effect of metroraghia so combined with oral contraceptive to limit menstrual irregularities and prevent conception). – Flutamide in dose of 25 mg daily (same efficacy of Spironolactone). – Fenstride ( 5 α reductase inhibiter ) given as 5 mg daily the side effect is feminization of male fetus if used during pregnancy. – Gonadotropins releasing hormone agonist. All above treatment must be used with strict contraception • Hirsutism

II. Surgical treatment – Laser . – Shaving wax depilatories. – Chemical depilatories. – Bleaching of the hairs with hydrogen peroxide. – Electrolysis. – X-ray therapy. Hypertrichosis

• It is an over growth of hair not localized to the androgen depended area of the skin • • Types: • 1/ localized acquired hypertrichosis caused by local cause like smooth muscle hamartoma, meningioma, Becker's nevus, topical steroid and eczema or systemic cause like porphyria or Pretibial myxodema. • 2/ localized congenital hypertrichosis appear during infancy and regress during adolescent (lanugo hair), it is either familial or due to congenital nevocytic nevi, anti cervical hypertrichosis. • 3/ generalized congenital hypertrichosis, this is an x linked dominant triad, the entire body covered with fine villous hair 2-10 cm long scalp hair is normal palm and sole not involved. • Causes: fetal hydantoin syndrome, fetal alcohol syndrome, pregnant women used minoxidil. • 4/ generalized acquired hypertrichosis : either caused by acquired hypertrichosis lanuginosa or secondary to drug intake ( minoxidil , cyclosporine , danazol , corticosteroid , topical androgen or associated with syndrome lipotrophic diabetes , Robenstien taybi syndrome .