ALOPECIA

PRACHI DESHMUKH T.Y.BAMS ROLL NO. 6

Sr. no. | Topic | Page No. | Remark | 1 | Normal hair growth | 1-2 | | 2 | Alopecia i. Classification ii. Causes iii. Telogen Effluvium iv. Tinea Capitis | 3-6 | | 3 | Alopecia Areata i. Classification ii. Causes iii. Signs and symptoms iv. Diagnosis v. Treatment a. Medicinal b. Surgical c. Other treatment | 7-14 | | INDEX

NORMAL HAIR GROWTH In human beings, hairs serve for protection on a primary level, but they are all-important for personal adornment. These hairs are of two types: 1) Lanugo (Vellus) hairs- very fine hairs present all over the body. 2) Terminal hairs- coarse, thick and pigmented hairs which are best developed on the face, scalp and extremities. The hairs are mostly found on all external body parts, except that of nail, palms, soles, lips, eyelids. Hairs are naturally present as eyebrows, eyelashes as also on scalp. But the development of hairs on forearms, legs, and other body parts is dependent on “adrenal androgen”. The adrenal androgens causes rise in plasma testosterone level that leads to growth of hair on forearm and legs called ambisexual hair as they are present in both sexes. At puberty, with further rise in plasma testosterone level hairs start appearing in axillary and pubic region. With further advanced puberty, males develop hair on face and trunk, termed as sexual hair as they are present only in males (present in females in case of disorder such as hirsutism). Hair growth consists of following phases under normal conditions: * Anagen (Growing Phase) -about 75% of the hair remain in this phase for about 3 years. * Catagen (involution) -about 5% of the hair remains in this phase for about 3 weeks. * Telogen (Resting Phase) –about 20% of the hair remains in this phase for about 3 month.

ALOPECIA

Alopecia means loss of hair in areas where ordinarily hair would be found. Generally this means loss of terminal hair in any region of the body.

Classification of alopecia I. The two major forms of alopecia are: SCARRING | NON-SCARRING | 1) It is associated with inflammation, fibrosis and destruction of the hair of hair follicles. | 1) Hair shafts are gone but the hair follicles are preserved | 2) Alopecia is permanent. | 2) Alopecia is temporary and reversible. | 3) It is due to primary skin disorders such as lichen planus or systemic diseases such as lupus erythematosis, etc. | 3) The common causes are- telogen effluvium, androgenetic alopecia, alopecia areata, tinea capitis and some cases of traumatic alopecia, etc. |

II. 1) Androgenic alopecia- it occurs in women and is due to elevated plasma levels of androgens. Other manifestations are menstrual abnormalities, hirsutism, acne and infertility. The treatment is that of hyper androgenenism. 2) Androgenetic alopecia- it is hereditary disorder due to excessive conversion of testosterone to DHT in the scalp skin in genetically susceptible men and women. The miniaturized hair of various lengths and diameters are the hallmark of this condition. Recession of anterior scalp line is seen on men n some women. In this condition there is increased sensitivity of affected hairs to the effects of testosterone and in women there is an increased level of circulating androgens. 3) Alopecia areata 4) Drug induced

Causes of alopecia I. Scarring type:- a. Physical trauma – e.g. overdose of X-ray, burns, long term traction on hair.
b. Infection – i) bacterial= leprosy, TB, late secondary and tertiary syphilis, folliculitis decalvans, dissecting folliculitis, carbuncles ii) Dermatophytosis=e.g. zoophilic fungi iii) Viral=e.g. herpes zoster, recurrent herpes simplex.
II. Non scarring type:- 1) Post partum alopecia – The hairs are actually thicker during pregnancy due to increased circulating estrogens, but after the birth of baby, the estrogen levels falls back to normal pre-pregnancy levels, and additional hair foliage drops out. Similar situation occurs in women taking the fertility-stimulating drug “clomiphene”. 2) Infection - dermatophytes, bacterial and spirochaetal. 3) Chemicals and drugs - Any that affect the body’s hormone balance have pronounced effect: this includes the contraceptive pill, hormonal replacement therapy, steroids and acne medications, chemotherapy, etc. Alopecia is a side effect of the following drugs-warfarin, heparin, carbimazole, lithium, beta blocker, colchicines and amphetamines. 4) Physical trauma- traction alopecia (continuous pull on hairs with excessive force seen in people with ponytails, comrows), trichotillomania ( compulsive pulling and bending of hairs) 5) Endocrinopathy- hypo- and hyperthyroidism, hypopituitarism, hypo- and hyperparathyroidism. 6) Serious systemic diseases- SLE, dermatomyositis, lymphoma. 7) Deficiency of protein, iron, biotin, and zinc and hypervitaminosis A. 8) Primary cutaneous disorders- Telogen effluvium, androgenetic alopecia, alopecia areata, tinea capitis, traumatic alopecia.

III. Miscellaneous causes 1) Congenital alopecia 2) Hair shaft abnormalities- e.g. monilethrix, pili annulati wooly hair.

Telogen effluvium - It refers to the shedding of an abnormally large quantity of morphologically normal club hairs.
There is premature conversion of normal anagen hair follicles into catagen and then into telogen phase and about 3 months later they shed in bulk causing alopecia.
Causes –stress is main cause, other causes include- acute febrile illness, or severe emotional or physical trauma, surgery, pregnancy.

Tinea capitis- It is characterized by scaling with minimal hair loss to discrete patches with “black dots” (broken hairs) to boggy plaque with pustules (kerion).
Pathogenesis – invasion of hairs by dermatophytes, most commonly Trichophyton tonsurans

Diagnosis a) The pull test helps to evaluate diffuse scalp hair loss. Gentle traction is exerted on a group of hairs (about 40–60) on three different areas of the scalp. The number of extracted hairs is counted and examined under a microscope. Normally, fewer than three hairs per area should come out with each pull. If more than ten hairs are obtained, the pull test is considered positive

b) The pluck test is conducted by pulling hair out "by the roots". The root of the plucked hair is examined under a microscope to determine the phase of growth, and is used to diagnose a defect of telogen, anagen, or systemic disease. Telogen hairs have tiny bulbs without sheaths at their roots. Telogen effluvium shows an increased percentage of hairs upon examination. Anagen hairs have sheaths attached to their roots. Anagen effluvium shows a decrease in telogen-phase hairs and an increased number of broken hairs.

c) Daily hair counts are normally done when the pull test is negative. It is done by counting the number of hairs lost. The hair from the first morning combing or during washing should be counted. The hair is collected in a clear plastic bag for 14 days. The strands are recorded. If the hair count is >100/day, it is considered abnormal except after shampooing, where hair counts will be up to 250 and be normal.

d) Scalp biopsy is used when the diagnosis is unsure; a biopsy allows for differing between scarring and nonscarring forms. Hair samples are taken from areas of inflammation, usually around the border of the bald patch. Occasionally, in inactive AA, no inflammatory infiltrates are found. Other helpful findings include pigment incontinence in the hair bulb and follicular stelae, and a shift in the anagen-to-telogen ratio towards telogen.

e) Trichoscopy is a noninvasive method of examining hair and scalp. The test may be performed with the use of a handheld dermoscope or a video dermoscope. Trichoscopy may aid differential diagnosis. In AA, trichoscopy shows regularly distributed "yellow dots" (hyperkerotic plugs), small exclamation-mark hairs, and "black dots" (destroyed hairs in the hair follicle opening). It allows differential diagnosis of hair loss in most cases.

Treatment
If the affected region is small, it is reasonable just to observe the progression of the illness, as the problem often spontaneously regresses and the hair may grow back, but in case of severe hair fall treatment is needed. | Treatment | Telogen effluvium | Observation; discontinue any drugs that have alopecia as a side effect, must exclude underlying metabolic causes, e.g. hypo- or hyperthyroidism. | Androgenetic alopecia | If no evidence of hyper androgen state, then topical minoxidil, finasteride, hairs transplant. | Alopecia areata | Topical anthralin, intralesional glucocorticoids, topical contact sensitizers | Traumatic alopecia | Discontinuation of offending hairstyle or chemical treatments, trichotillomania may require hair clipping and observation of shaved hairs or biopsy for diagnosis, followed by psychotherapy | Tinea capitis | Oral griseofulvin or terbinafine plus 2.5% selenium sulfide or ketoconazole shampoo; examine family members |

Medicines
Three medications have evidence to support their use in male pattern hair loss: finasteride, dutasteride and minoxidil. They typically work better to prevent further hair loss than to regrow lost hair. 1. Finasteride ((brand names Proscar and Propecia) - It is a type II 5α-reductase inhibitor. 5α-reductase is an enzyme that converts testosterone to dihydrotestosterone (DHT). Dose- 1 mg of finasteride daily Side effects - depression or gynecomastia Contraindicated- in women (strictly) 2. Dutasteride (trademark name Avodart, manufactured by GlaxoSmithKline)- same as finasteride. 3. Minoxidil - Minoxidil is an antihypertensive vasodilator medication. It also slows or stops hailoss and promotes hair regrowth. Minoxidil is marketed under many trade names, including Avogain, Rogaine, Regaine, and Lipogaine. This drug promotes follicular DNA synthesis. It is used as a 5%solution
Use-In a liquid or foam; it is rubbed on the scalp twice a day.
Frequent side effects- are mild scalp irritation, allergic contact dermatitis, and increased facial hair.

Other medicines are:- 1) For small patches on the beard or head, suppression with topical tacrolimus ointments, such as “Protopic”, are possible. Symptoms may remain suppressed until aggravated by stress or other factors. 2) Anthralin- This agent is used as a non specific immuno-modulating medication 3) Hormonal modulators (oral contraceptives or antiandrogens such as “spironolactone” and “flutamide”) can be used for female-pattern hair loss associated with hyperandrogenemia. 4) Topical immunotherapy cyclosporine, Dinitrochlorobenzine (DNCB), Squaric Acid (SADBE) and Diphenylcyclopropenone 5) Steroid injections are commonly used in sites where the areas of hair loss on the head are small or especially where eyebrow hair has been lost. Whether they are effective is uncertain. 6) Corticosteroids- Topical corticosteroids frequently fail to enter the skin deeply enough to affect the hair bulbs, which are the treatment target, and small lesions typically also regrow spontaneously. Oral corticosteroids decrease the hair loss, but only for the period during which they are taken, and these drugs have serious adverse side effects. 7) Photo chemotherapy (PUVA) - This is used to modify T-cell function and antigen preservation in the hair. 8) Cyclosporine - Use of this agent is controversial due to its high side effect incidence and overall efficacy.