HAIR DISORDERS GROUP 5 Objectives Describe the normal hair growth cycle Discuss the etiology, clinical features and management of androgenetic alopecia and alopecia areata. Discuss drug induced alopecia Discuss vitamins which are beneficial for healthy hair. HAIR STRUCTURE Hair is composed of strong structural protein called keratin. This is the same kind of protein that makes up the nails and the outer layer of skin. Each strand of hair consists of 3 layers. Cont’d An innermost layer or medulla which is only present in large thick hairs. The middle layer known as the cortex. The cortex provides strength and both the color and the texture of hair. The outermost layer is known as the cuticle. The cuticle is thin and colorless and serves as a protector of the cortex. STRUCTURE OF HAIR ROOT Below the surface of the skin is the hair root, which is enclosed within a hair follicle. At the base of the hair follicle is the dermal papilla. The dermal papilla is feed by the bloodstream which carries nourishment to produce new hair. Cont’d The dermal papilla is a structure very important to hair growth because it contains receptors for male hormones and androgens. Androgens regulate hair growth and in scalp hair Androgens may cause the hair follicle to get progressively smaller and the hairs to become finer in individuals who are genetically predisposed to this type of hair loss. THE HAIR GROWTH CYCLE Hair follicles grow in repeated cycles. One cycle can be broken down into three phases. Anagen - Growth Phase Catagen - Transitional phase Telogen - Resting Phase Each hair passes through the phases independent of the neighboring hairs. ANAGEN PHASE – GROWTH PHASE Approximately 85% of all hairs are in the growing phase at any one time. The growing phase of the normal hair growth cycle is responsible for producing new hair and for allowing the continued lengthening of that new hair. The Anagen phase or growth phase can vary from two to six years. ANAGEN PHASE In this cycle hair is produced at the root and growth is maintained through the blood vessels, which feed the hair strand its nourishment. Hair grows approximately 10cm per year and any individual hair is unlikely to grow more than one meter long. CATAGEN PHASE – TRASITIONAL PHASE At the end of the Anagen phase the hairs enters into a Catagen phase which lasts about one or two weeks. During the Catagen phase the hair follicle shrinks to about 1/6 of the normal length. The lower part is destroyed and the dermal papilla breaks away to rest below. TELOGEN PHASE – RESTING PHASE The resting phase follows the catagen phase and normally lasts about 5-6 weeks. During this time the hair does not grow but stays attached to the follicle while the dermal papilla stays in a resting phase below. Approximately 10-15 percent of all hairs are in this phase at any one time. TELOGEN PHASE cont’d At the end of the Telogen phase the hair follicle re-enters the Anagen phase. The dermal papilla and the base of the follicle join together again and a new hair begins to form. If the old hair has not already been shed the new hair pushes the old one out and the growth cycle starts all over again. Each day anywhere from 50 to 100 hair strands are shed during the normal process of this phase. This is also the phase that is most associated with baldness. If a person is suffering from alopecia or hair loss they will first notice an abnormally high rate of shedding. At first this excessive hair loss will result in hair thinning but the end result could be baldness. Abnormal hair loss or shedding is defined as the loss of more than 150 hair strands each day for an extended period of time. HAIR HEALTH Slow hair growth, brittle and/or damaged hair may be due to nutritional deficiencies. Certain vitamins and supplements can boost hair growth and encourage healthy hair. Vitamin B-complex - 50 mg. of the major B- vitamins (including folate, biotin and inositol) Vitamin B-6 - 50 mg. Vitamin C with bioflavonoids – 1-2 grams daily. Vitamin E - 400 to 800 IU daily. Beta-Carotene - 10,000 to 15,000 IU daily. One recommended daily dose of magnesium, sulfur, zinc. Flaxseed oil - one tbsp daily or one tablet. ANDROGENETIC ALOPECIA A genetically determined, patterned, progressive loss of hair from the scalp. Hair loss is caused by androgen- mediated follicular miniaturization that leads to fine, short, non-pigmented, vellus hair formation. It affects both men and women at a similar prevalence of approximately 40%. Men present with gradual thinning in the temporal areas, producing a characteristic M shape with gradual extension to the crown (vertex) area. Women usually present with diffuse thinning on the crown area while maintaining a frontal hairline. AETIOLOGY The condition is generally considered to be a dominantly inherited disorder. In women, autosomal-dominant inheritance and a link to polycystic ovary syndrome have been found. PATHOPHYSIOLOGY Androgenic alopecia is characterized by progressive shortening of the Anagen growth phase with each hair cycle associated with increased Telogen and catagen hair transformation. This process leads to follicular miniaturization with conversion of long, terminal hairs to short and fine vellus hairs. CLINICAL FEATURES Progressive thinning of hair in women, over the frontal area, over a period of years. Progressively receding hairline in males. Thinning of hair on top of head in males. MANAGEMENT In men –Topical Minoxidil or Oral Finasteride. In women - Topical Minoxidil or Anti- androgenic therapy with spironolactone or cyproterone. TOPICAL MINOXIDIL Minoxidil is the currently preferred treatment for androgenetic alopecia and is topically administered as 2 percent Minoxidil. Its also available in 5% formulations. Cont’d The exact mechanism by which Minoxidil works is not known, but the treatment appears to affect the hair follicle in three ways. It increases the span of time follicles spend in Anagen, it rouses follicles that are in catagen and it enlarges the actual follicles. Cont’d In effect, vellus hairs enlarge and are converted to terminal hairs, and shedding is reduced. Earlier, exogenous estrogen was used to treat androgenetic alopecia, but this treatment is used less often now, because of the efficacy of Minoxidil. Hypertrichosis may occur with use of Minoxidil. FINASTERIDE Finasteride has been shown to be effective in men with alopecia. The agent should not be used in women of childbearing age, because 5a-reductase inhibitors may cause abnormalities of the external genitalia in the male fetus. Cont’d Additionally, Finasteride has not been shown to be useful in postmenopausal women with androgenetic alopecia. When hair loss is extensive, wigs may be worn. Hair transplantation, an accepted (but expensive) treatment for male balding, is increasingly being used in female hair loss. ALOPECIA AREATA Alopecia areata (AA) is an autoimmune disease that affects almost 2% of the population. Inflammatory cells target the hair follicle, thus preventing hair growth. Typically, a small round patch of hair is noticed. This patchy hair loss may regrow spontaneously. (Patchy alopecia areata) In other cases there can be extensive hair loss - Alopecia totalis, indicating total loss of scalp hair In rare cases there is loss of all scalp and body hair (alopecia areata universalis). ALOPECIA AREATA ALOPECIA UNIVERSALIS ALOPECIA AREATA TOTALIS AETIOLOGY The aetiology of AA has not been determined. However, it is hypothesized to be an organ-specific autoimmune disease mediated by T lymphocytes directed at hair follicles. PATHOPHYSIOLOGY As in many other autoimmune diseases, there is a strong association of AA with human leukocyte antigen (HLA) class II alleles. There also appears to be a link between AA and Down’s syndrome suggesting that chromosome 21 may also be involved. CLINICAL FEATURES Hair loss. Balding. Bald patches. Nails may have pitting or trachyonychia. Exclamation point hairs. MANAGEMENT Corticosteroids Corticosteroid therapies can include intralesional injections or topical application. Intralesional steroids are the first-line treatment in localized conditions. Hair growth may persist for 6-9 months after a single injection. Adverse effects mostly include pain during injection. Injections are administered every 4-6 weeks. TOPICAL STEROIDS Fluocinolone acetonide cream 0.2% (Synalar HP) twice per day. Betamethasone dipropionate cream 0.05% (Diprosone). Treatment must be continued for a minimum of 3 months before regrowth can be expected, and maintenance therapy often is necessary. TOPICAL IMMUNOTHERAPY Topical immunotherapy is defined as the induction and periodic elicitation of an allergic contact dermatitis by topical application of potent contact allergens. Commonly used agents for immunotherapy include squaric acid dibutylester (SADBE) and diphencyprone (DPCP) Topical immunotherapy has been used for almost 20 years; no serious adverse effects have been reported. The most common side effect, which is desired, is a mild contact dermatitis (redness, scaling, itching). Both SADBE and DPCP appear to be equally effective. The mechanism of action of topical immunotherapy is unknown. Antigenic competition has been hypothesized. That is, the introduction of a second antigen can initiate a new infiltrate containing T-suppressor cells and suppressor macrophages that may modify the preexisting infiltrate and allow regrowth. MINOXIDIL Minoxidil appears to be effective in the treatment of alopecia areata in patients with extensive disease (50- 99% hair loss). The 5% solution appears to be more effective. No more than 25 drops are applied twice per day regardless of the extent of the affected area. Initial regrowth can be seen within 12 weeks, but continued application is needed to achieve cosmetically acceptable regrowth. Minoxidil usually is well tolerated. Adverse effects include distant Hypertrichosis and irritation. DRUG INDUCED ALOPECIA This may be partial or complete and can involve sites other than the scalp, although the scalp is commonly affected. Medications can lead to two types of hair loss: Telogen effluvium and Anagen effluvium. TELOGEN EFFLUVIUM Telogen effluvium is the most common form of drug-induced hair loss. It usually appears within two to four months after taking the drug. This condition causes the hair follicles to go into their resting phase (Telogen) and fall out too early. People with Telogen effluvium usually shed between 100 and 150 hairs a day. ANAGEN EFFLUVIUM Anagen effluvium is hair loss that occurs during the Anagen phase of the hair cycle, when the hairs are actively growing. It prevents the matrix cells, which produce new hairs, from dividing normally. This type of hair loss usually occurs within a few days to weeks after taking the medication. It's most common in people who are taking chemotherapy drugs and is often severe, causing people to lose most or all of the hair on their head, as well as their eyebrows, eyelashes, and other body hairs. DRUGS CAUSING ALOPECIA Anticoagulants Anticonvulsants Antithyroid drugs Beta-blockers Withdrawal of oral contraceptives Cytotoxic drugs Gold salts Interferon's Lithium Retinoid Sodium valproate PIGMENTATION DISORDERS Hyperpigmentation Hypopigmentation HYPERPIGMENTATION o Also known as Hypermelanosis o Due to an increased number of pigment cells (melanocytes) or from increased production of melanin. o Hormones that stimulate melanin synthesis, such as melanocyte- stimulating hormone (MSH), are frequently elevated. TYPES Darker skin patches Post- inflammatory (trauma, burns, skin disease) Purpura Urticaria Melanoma Pigmented purpura Mastocytosis Chloasma (melasma) Freckles Chloasma Also known as melasma – a blotchy, brownish pigmentation on the face that develops slowly and fades with time. The pigmentation is due to overproduction of melanin by the pigment cells, melanocytes. Often found in pregnant women Causes Genetic predisposition to melasma. Pregnancy – the pigment often fades a few months after delivery. Hormonal contraceptives, including oral contraceptive pills and injected progesterone Sun exposure Scented or deodorant soaps, toiletries and cosmetics – a phototoxic reaction Unknown factors, when it arises in apparently healthy, normal, non- pregnant women Clinical features Melasma usually affects women; only one in twenty affected individuals are male. Starts between the age of 30 and 40. Common in people that tan well or have naturally dark skin compared with those who have fair skin. Affects the forehead, cheeks and upper lips resulting in macules (freckle-like spots) and larger patches. Clinical features Type Clinical features Epidermal Well-defined border Dark brown color Appears more obvious under black light Responds well to treatment Dermal Ill-defined border Light brown color Unchanged under black light Responds poorly to treatment Mixed Combination of light and brown patches Partial improvement with treatment MANAGEMENT Response to treatment very slow. Start gently – Sensitive skin. Harsh treatments may result in an irritant contact dermatitis, and this can result in postinflammatory pigmentation. Discontinuing hormonal contraception. Year-round sun protection. Use a broad-spectrum very high protection factor sunscreen of reflectant type and apply it to the whole face. E.g Aquasun SPF4 Lotion(Octyl methosycinnamate 3, butyl methoxydibenzoylmethane 1.5%, Zinc oxide 5% Titanium dioxide 3%). Alternatively, use a make-up containing sunscreen. Use of a mild cleanser, and if the skin is dry, a light moisturiser. Preventing new pigment formation. Bleaching creams inhibit the formation of melanin by the melanocytes. They include: Hydroquinone 2-4%, for 2 to 4 months. This sometimes causes stinging and redness. Azelaic acid can be used longterm, and is safe even in pregnancy. It may sting. Kojic acid Topical corticosteroid such as hydrocortisone works quickly to fade the colour and has an additional benefit of reducing the likelihood of a contact dermatitis caused by other agents. Hydrocortisone 0.5-2.5% (DermAid Cream/Soft Cream and Lotion-HC 1%) Peeling off the pigment. Salicylic acid creams Topical alpha hydroxyacids including glycolic acid and lactic acid, as creams or as repeated superficial chemical peels. Topical retinoids, such as tretinoin, works in several ways to improve skin color, but can be hard to tolerate and might cause dermatiits. Not to be used during pregnancy. Dermabrasion(is a cosmetic medical procedure in which the surface of the epidermis of the skin(the stratum corneum) is removed by abrasion (sanding). Microdermabrasion (a cosmetic procedue in which the stratum corneum (dead outermost surface of the skin) is partially or completely removed by light abrasion, to remove sun-damaged skin and to remove or lessen scars and dark spots on the skin. damage to the melanocytes may increase pigment production and darken the melasma. Laser resurfacing – results may be unpredictable. Newer fractional lasers may prove safer. Destroying the pigment with pigment laser or intense pulsed light device – this is possibly the best treatment for a quick result but several treatments may be necessary. Applying cosmetic camouflage (make-up). Results take time and the above measures are rarely completely successful. About 30% of patients can achieve complete clearance with a prescription agent that contains a combination of hydroquinone, tretinoin and a topical corticosteroid. Unfortunately, even in those that get a good result from treatment, pigmentation may reappear on exposure to summer sun and/or because of hormonal factors. HYPOPIGMENTATION Generalized reduction in pigmentation of the skin. It is caused by melanocyte depletion i.e. a decrease in the amino acid tyrosine, which is used by melanocytes to make melanin Localized hypopigmentation may be due to partial or complete loss of melanin Types of hypopigmentation Albinism Bleaching creams Chemical leukoderma Leprosy Vitiligo VITILIGO Vitiligo is an autoimmune disease in which pigment cells (melanocytes) are destroyed resulting in irregularly shaped white patches on the skin. Any part of the body may be affected but common sites are face, neck, eyes, nostrils, nipples, navel, genitalia), body folds (armpits, groin), sites of injury (cuts, scrapes, burns) and around pigmented moles TYPES OF VITILIGO TypeA-include all cases of vitiligo not in type B. Can occur at any age. New depigmented patches continue to appear through out patients lives. Type B -depigment patches are confined to a defined dermatome in the same manner as herpes zoster virus. generally affect youngsters. activity ceased after one year following rapid spread over the dermatomal areas. CAUSES Melanin is the pigment that determines the color of skin, hair, and eyes. It is produced in cells called melanocytes. If melanocytes cannot form melanin or if their number decreases, skin color will become progressively lighter. The cause of vitiligo is not known. It sometimes follows physical injury such as sunburn, or emotional stress. There are three theories on the cause of vitiligo: The pigment cells are injured by abnormally functioning nerve cells. MANAGEMENT Topical steroid e.g. cortisol cream. Calciniurin inhibitors like topical pimecrolimus and tacrolimus.(safe and effective to use on face and neck where strong steroid cream can cause skin thinning). There may be an autoimmune reaction against the pigment cells (the body may destroy its own tissue, which it perceives as foreign). Autotoxic theory - the pigment cells are self-destructive. Narrowband UVB phototherapy(helpful particularly in combination with calcineurin inhibitors, and perhaps with calcipotriol cream PUVA- form of light treatment requires the patient to take a psoralen medicine and then be exposed to ultraviolet . Gradual but partial repigmentation may results light (UVA). When the treatment is stopped, some of the pigment disappears again. PUVA takes less than five minutes twice weekly, and is continued for up to two years. PUVA is unsuitable for children or very fair skinned people. Surgical treatment- Experimentally some centres are removing the top layer of skin by various techniques (including dermabrasion or sandpapering) and replacing it with skin with normal pigmentation from another site. Sun protection. Protection from injury. DEPIGMENTATION THERAPY If a dark skinned person has vitiligo affecting a large part of the exposed areas, he or she may wish to undergo depigmentation. A cream containing monobenzyl ether of hydroquinone is applied to the skin. This causes all the skin to lose its pigment. Its effect is usually permanent. ALBINISM Hypopigmentary congenital disorder characterized by a partial (in hypomelanism, also known as hypomelanosis) or total (amelanism or amelanosis) lack of melanin pigment in the eyes, skin and hair (or more rarely the eyes alone). Albinism results from inheritance of recessive alleles. CLINICAL FEATURES Nystagmus. Photophobia. reduced visual acuity. a lack of stereopsis. MANAGEMENT No specific medical treatment is available. For occular ablinism, Refractive errors should be corrected, and some patients benefit from bifocal lenses. If visual acuity is severely impaired, these patients can be helped with telescopic and other low-vision devices. The most promising treatment for nystagmus is the eye muscle surgery that reduces the movement of the eyes but vision may not improve in all cases due to other associated eye abnormalities. For photophobia the eye doctors prescribe dark glasses that shield the eyes from bright light. ophthalmologists prefer to treat the infants at the age of six months before the function of their eyes has developed fully. They may recommend that parents patch one eye to promote the use of the non-preferred eye. It is vital that people with albinism use sunscreen when exposed to sunlight to prevent premature skin aging or skin cancer. Special UV-proof clothing and swimsuits are available and are a good alternative to excessive use of sunscreen. REFERENCES http:\Alopecia Areata Treatment & Medication - eMedicine Dermatology.mht Http:\American Hair Loss Association - Drug Induced Hair Loss.htm Http:\[Drug-induced alopecia review of the literature] [Therapie_ 1995 Mar-Apr] - PubMed result.mht http://www.hairlossexpert.co.uk/WhatIsNor malCycleHairLossReGrowth.html http://bestpractice.bmj.com/best- practice/monograph/222/basics/classif ication.html http://www.dermnet.org.nz/hair-nails- sweat/female-pattern-hairloss.html Walker,R., CLINICAL PHARMACY AND THERAPEUTICS 4th Edition. AMH 2008 http://www.medindia.net/patients/patie ntinfo/Albinism-Treatment.htm http://health.nytimes.com/health/guide s/disease/albinism/overview.html http://www.antivitiligo.com/ http://www.medicinenet.com/vitiligo/art icle.htm http://health.hpathy.com/chloasma- melasma-symptoms-treatment- cure.asp APPENDIX DRUG PIGMENTATION Amiodarone Blue - grey Anticonvulsants Brown Antimalarials Blue - grey Beta - blockers Brown Imatinib Hypo/hyperpigmentation Imipramine Blue - grey Methyldopa Brown Oral contraceptives Brown spots/patches Phenothiazines Brown / blue - grey Tetracyclines Blue - black Methoxsalen Brown HYPERTRICHOSIS Hypertrichosis is excessive hair growth over and above the normal for the age, sex and race of an individual (in contrast to hirsutism, which is excess hair growth in women). Hypertrichosis can develop all over the body or can be isolated to small patches. Hypertrichosis may be congenital (present at birth) or acquired (arises later in life). The causes mat be genetic, metabolic, or due to drugs. QUESTIONS Describe the different phases of the hair growth cycle. Differentiate between alopecia areata and androgenetic alopecia. Which vitamins are good for hair? Give 3 examples of hyperpigmentation and hypopigmentation. Discuss the causes of Vitiligo and Chloasma.
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