Pendahuluan

Alopecia areata is an autoimmune disorder of hair follicles causing loss of hair in sharply defined areas of skin. 4 Alopecia areata is a common disease that causes loss of hair on the scalp and elsewhere. Alopecia areata may cause patchy hair loss over vast portions of the scalp. Any hairbearing area on the body may be affected. Alopecia areata occurs at all ages although children are affected most often and the disease affects males and females equally. Patients with alopecia areata are otherwise healthy, although they may have a higher incidence of atopic conditions such as atopic eczema, allergic rhinitis and asthma. The condition is not contagious. 6 Alopecia areata can be localized (<50% involvement) or extensive (>50% involvement). Hair loss can be diffuse over whole scalp patchily (diffuse alopecia areata), involve one spot (alopecia areata unilocularis) or many spots (alopecia areata multilocularis), involve beard only (alopecia areata barbae), be complete over the scalp (alopecia areata totalis) or complete over whole of body (AA universalis). 5

Epidemiologi At any given time, approximately 0.2 percent of the population has alopecia areata and approximately 1.7 percent of the population experiences an episode of alopecia areata during their lifetime. However, there are great geographic and ethnic variations in the incidence and prevalence of the disease. this is also seen with respect to the immunogenetic background of patients with alopecia areata. In most patients, the onset is within the first three decades of life although alopecia areata can start at any age. The sex incidence is probably equal. 2

Etiologi

It is not possible to attribute all or indeed any case of AA to a single cause. Among many factors. which appear to be implicated in at least a portion of cases, are the patient's genetic constitution. the atopic state, non-specific immune and organ- specific autoimmune reactions and possibly emotional stress. 6

Patogenesis T-lymphocyte interaction with follicular antigens (autoantigens) has been implicated in alopecia areata. The importance of T cells in this disease has been demonstrated by several investigators. Sections of scalp skin from patients with alopecia areata will grow hair when engrafted onto congenitally athymic nude mice, and it is possible to transfer alopecia areata to human skin explants on SCID mice by the injection of scalp infiltrating lymphocytes (both CD4+ and CD8+ T cells are required), but not with non-follicular scalp homogenates. Melanocyte-associated antigens recognized by T cells might also function as possible autoantigens. 7 Normal anagen hair follicle keratinocytes typically lack expression of class I and class II major histocompatibility (MHC) antigens, suggesting immunologic privilege of the human hair follicle bulb. In alopecia areata, human leukocyte antigens (HLA-A, -B, -C, DR) become expressed by the hair follicle, allowing an interaction of cytotoxic T lymphocytes with hair matrix cells. Additional evidence for a primary role of T cells in the pathogenesis of alopecia areata comes from clinical experience and data demonstrating the successful use of immunosuppressive agents such as glucocorticoids or cyclosporine in the management of this disease. 7

Manifestasi Klinik Alopecia areata (In French, pelade) is characterized by rapid and complete loss of hair in one or more round or oval patches, usually on the scalp, bearded area (Fig. 33-I), eyebrows, eyelashes, and less commonly, on other hairy areas of the body. Often the patches are from 1 to 5 cm in diameter. A few resting hairs may be found within the

patches. Early in the course there may be sparing of gray hair, and white hairs are rarely affected. Sudden whitening of hair may represent widespread alopecia areata in a patient with salt and pepper hair. In about 10% of cases of alopecia areata, especially in long-standing cases with extensive involvement, the nails develop uniform pits that may form transverse or longitudinal lines. Trachyonychia, onychomadesis, and red or spotted lunulae occur, but less commonly. Complete loss of scalp hair is referred to as alopecia totalis, and complete loss of all hair as alopecia universals. In most cases, hair loss is confined to the scalp and is patchy in distribution. Loss may occur confluent along the temporal and occipital scalp (ophiasis) or on the entire scalp except for this area (sisaipho). Rarely, alopecia areata may present in a diffuse pattern that may mimic pattern alopecia. Clues to the correct diagnosis include a history of periodic regrowth, nail pitting, and the presence of tapered fractures or exclamation point hairs. Alopecia areata generally presents as an anagen effluvium, with an inflammatory insult to the hair matrix resulting in tapering of the hair shaft, and resulting in fracture of anagen nails. As the hair miniaturizes or converts from anagen to telogen, the remaining lower portion of the hair rises above the level of the scalp, producing the exclamation point hair. Alopecia areata is associated with a higher incidence than usual of atopic dermatitis, Down syndrome, lichen planus, and autoimmune diseases, such as systemic lupus erythematosus, thyroiditis, diabetes meIlitus, myasthenia gravis and vitiligo. However, most cases of alopecia areata occur without associated disease, and routine screening for these disorders is of little value unless prompted by signs or symptoms. Migratory poliosis of the scalp may represent a forme fruste of alopecia areata. Patients with this disorder present with migrating circular patches of white hair, but never loose hair.The histology resembles alopecia areata. 3

Figure 18.3 Small, discrete areas of hair loss in alopecia areata. 4

Figure 18.5 A large patch of alopecia areata showing regrowth of non-pigmented hair. 4

Diagnosis Diagnosis Alopesia areata berdasarkan gambaran insfeksi klinis atas pola mosaik alopesia atau alopesia yang secara klinis berkembang progresis. Didukung adanya trikodistrofi, efluvium anagen, atau telogen yang luas, dan perubahan pada gambaran

histopatologi. Pada stadium akut ditemukan distrofi rambut anagen yang disertai rambut tanda seru (exclamation mark hair) pada bagian proksimal, sedangkan pada stadium kronik akan didapatkan peningkatan jumlah rambut telogen. Perubahan lain meliputi berkurangnya diameter serabut rambut, miniaturisasi, pigmentasi yang tidak teratur. Tes menarik rambut pada bagian tepi lesi yang positif menunjukkan keaktifan penyakit." 8 Biopsi pada tempat yang terserang menunjukkan peradangan limfostik peribulbar pada sekitar folikel anagen atau katagen disertai meningkatnya eosinofil atau sel mast. 8

Diagnosa Banding
In children the main sources of difficulty are tinea capitis and trichotillomania. Tinea capitis should always be considered in children presenting with patchy hair loss. There is usually evidence of scalp inflammation but this may be limited to mild scaling. The hair loss in trichotillomania may be asymmetrical or occur in artificial shapes. Broken hairs are usually present across the areas of hair loss, giving a bristly texture and, unlike exclamation mark hairs, are firmly anchored in the scalp. In most cases the true diagnosis will become evident with time; a biopsy is useful when doubt remains. Occasionally, the early stages of scarring alopecia can resemble alopecia areata. The diffuse form of alopecia areata is perhaps the most difficult to identify. A history of previous episodes of hair loss, nail dystrophy and the usually rapid progression may provide clues, but other causes of diffuse hair loss, such as SLE, may need to be excluded by appropriate serological tests and a scalp biopsy. Secondary syphilis sometimes presents with diffuse or patchy hair loss.1

Penatalaksanaan A number of treatments can induce hair growth in alopecia areata, but none has been shown to alter the course of the disease. The high rate of spontaneous remission makes it difficult to assess efficacy, particularly in mild forms of the disease. Some trials have been limited to patients with severe alopecia areata where spontaneous remission is unlikely. However, these patients tend to be resistant to all forms of treatment and the

failure of a treatment in this setting does not exclude efficacy in mild alopecia areata. Few treatments have been subjected to randomized controlled trials and, except for contact immunotherapy, there are few published data on longterm outcomes. These difficulties mean that counselling of the patient and, where relevant, of their family, are of paramount importance. This should include discussion of the nature of the disease and its natural history, the treatments available and their chances of success. Some patients have great difficulty coping with alopecia areata and require considerable support. Sources of support may include the physician, other patients, formal patients support groups and, in some circumstances, professional counselling services. 1

Pengobatan Since alopecia areata is a benign condition, treatment is not mandatory. Moreover treatment also depends on the extent of the illness since spontaneous remission rate is high in those with less than 40% scalp hair loss (making treatment less mandatory) and low in those with greater than 40% involvement. 5 Topical Treatment Corticosteroids: Such therapy includes intralesional injections or topical application. Intralesional steroids are the first-line treatment in localized conditions. Injections using a 3-mL syringe and a 30-gauge needle are administered intradermally. Triamcinolone acetonide is used most commonly. A concentration of 5 mg/mL is usually sufficient on the scalp. Less than 0.1 mL is injected per site. Injections are administered every 4-6 weeks. In responsive patients regrowth usually is seen within 4-6 weeks. Hair growth may persist for 6-9 months after a single injection. Treatment with topical steroids can be useful in children not tolerating injections and include fluocinolone acetonide cream and betamethasone dipropionate cream.

Minoxidil: Minoxidil 5% solution has been found to be effective in the treatment of AA in patients with extensive disease.

Immunotherapy: Topical immunotherapy using pollen allergens like squaric acid dibutylester and diphencyprone acts by eliciting an allergic contact dermatitis. In patients with severe alopecia areata (>50% involvement) acceptable regrowth varies from 22-68%.

Anhralin: So far studies with topical anthralin have shown less efficacy and more toxicity. Systemic Treatment

PUVA: Both systemic and topical Psoralen and UV-A have been used but were not found to be an effective long term therapy due to a high relapse rate.

Steroids: Systemic prednisone is not considered an agent of choice due to adverse effects.

Cyclosporine: Though useful, it has not found favor due to its high recurrence rate and adverse effect profile.

Other agents like tacrolimus, dapsone, methotrexate and interferon have been tried but are not yet approved.

Other Treatment Modalities: include biological agents (like adalimumab, etanercept), nitrogen mustard, acupuncture, nonpharmacologic methods (dermatography, hair pieces). 5

Prognosis Spontaneous remission can be expected in the majority of cases where hair loss is limited to a few small patches (possibly, up to approximately 80 percent within 1 year), although most patients experience recurrences at some stage. The prognosis in extensive alopecia areata, particularly alopecia totalis and universalis, is less favorable

and fewer than 10 percent of patients in the latter two groups recover spontaneously. The ophiasis pattern of alopecia also tends to be recalcitrant. Other features pointing to a poor prognosis include onset in childhood, loss of body hair, nail involvement, atopy, and a positive family history for alopecia areata. 2

Daftar Pustaka

1. Rooks Textbook of Dermatology, Seventh Edition 63.36 2. Fitzpatrick-Dermatology 800 3. Andrew's Disease of The Skin, Clinical Dermatology 10th 760 4. Roxburgh's Common Skin Disease, 17th ed. 2003 271 5. Alopecia Areata, Shehzad Ahmed Khan MD 6. Alopecia_areata_3 7. BOLOGNA 2 EDITION 8. Alopesia Areata - dr imam budi fitra