dysmenorrhea part 1..

Hampir 2 jam saya terkapar dengan nyeri yang terus menggila. Uterus seperti sedang teremas garang, berusaha untuk tidur dan akhirnya memang tertidur juga, karena dysmenorrhea saya obatnya cuma tidur. Alhamdulillah saat bangun nyeri sudah berkurang. dan bangganya saya tidak minum analgetik lo :). Mengurangi kebiasaan terhadap ketergantungan dengan analgetik, untuk meningkatkan ketahanan terhadap nyeri.

Apa sih dysmenorrhea? Orang awam bilangnya nyeri saat haid. Nyeri haid dalam istilah kedokteran disebut dysmenorrhea dan dalam praktik diartikan sebagai nyeri saat haid Berdasarkan pencarian di mbah google, saya menemukan bahwa dysmenorrhea berasal dari bahasa yunani yaitu dys, yang berarti nyeri/abnormal, meno, berarti bulan, dan rrhea, berarti aliran. Pinsonneault dkk, menyatakan bahwa nyeri saat haid yang paling umum, berhubungan dengan keluhan ginekologis yang sering dialami wanita. Penatalaksanaan yang optimal tergantung pada penyakit yang mendasarinya.

Kebanyakan wanita tidak merasakan gejala- gejala pada waktu haid, tetapi sebagian kecil merasa berat dipanggul atau merasa nyeri. sedangkan sepertiga dari wanita muda mengalami gejala yang parah. Keluhan itu sering terkait dengan penyebab absensi kerja, sekolah, ataupun aktivitas-aktivitas lain. Meskipun frekuensi dan beratnya nyeri saat haid sering terjadi, tetapi sebagian besar wanita tidak mencari perawatan medis. Contohnya saya, tapi semoga bukan apa-apa. Amin :

Pemeriksaan pada pasien dysmenorrhea harus dilakukan secara sistematis. Rasa tidak enak pada pelvik secara normal terjadi pada kebanyakan wanita dari berbagai tingkatan selama periode menstruasi, walaupun tidak terjadi pada semua wanita dan insidensinya bervariasi tergantung populasi dan kultur. Keadaan ini ditandai dengan nyeri perut bagian bawah, nyeri punggung, dan nyeri yang menjalar ke paha dengan disertai mual, muntah, diare, dan nyeri kepala. Biasanya manifestasi timbul kembali secara siklik berhubungan dengan menstruasi, dimulai bersamaan dengan terjadinya perdarahan atau beberapa jam sebelumnya dan berlanjut selama periode waktu yang bervariasi pada masa menstruasi sendiri. Keadaan ini biasanya didahului oleh sindroma pramenstruasi dan tampaknya hampir selalu terjadi pada siklus ovulasi saja.

Dysmenorrhea terbagi menjadi dua yaitu primer (spasmodic) dan sekunder ((kongestif). Dysmenorrhea primer didefinisikan sebagai nyeri menstruasi yang tidak berhubungan dengan kelainan makroskopis di daerah pelvis (tidak ada penyakit pada pelvis). Sering terjadi pada tahun-tahun awal setelah menarche dan hampir 50% terjadi pada wanita postpubertas. Dysmenorrhea sekunder didefinisikan sebagai nyeri menstruasi dengan kelainan anatomi dan makroskopis pelvis, terjadi pada wanita dengan endometriosis atau PID (pelvic inflammatory disease). Kondisi ini sering ditemukan pada wanita berumur antara 30-45 tahun.

Diagnosis banding yang penting ditandai oleh terjadinya onset. Rasa nyeri saat haid tidak diketahui secara pasti kaitannya dengan penyebabnya, namun diduga faktor ketidakseimbangan hormon dan faktor psikologis dapat mempengaruhi rasa nyeri tersebut baik itu berupa gangguan primer maupun sekunder. Nyeri saat haid yang disebabkan gangguan primer sering kali terjadi. Penelitian yang dilakukan oleh Andersh pada tahun 1982 di Swedia menyatakan bahwa sekitar 72% dari 596 gadis umur 19 tahun menderita nyeri haid primer dan 15% diantaranya sangat berat sehingga memerlukan pengobatan untuk menghilangakan rasa nyeri tersebut. Nyeri haid primer biasanya timbul setelah dimulainya menstruasi pertama dan seringkali berkurang atau bahkan hilang setelah kehamilan atau melahirkan anak pertama.

Faktor resiko yang terjadinya dismennorhea dihubungkan dengan tingkat keparahan

1.      usia terlalu dini saat menarche

2.      periode menstruasi yang lama

3.      aliran menstruasi yang banyak/deras

4.      perokok

5.      adanya riwayat keluarga

Faktor lain yang juga mempengaruhi obesitas dan pengkonsumsi alkohol ( tetapi tidak pada semua kasus). Aktivitas fisik dan siklus menstruasi tidak ditemukan punya hubungan dengan nyeri menstruasi.

Patofisiologi

Etiologi dan patofisiologi dyemenorrhea tidak sepenuhnya dijelaskan.

dysmenorrhea primer

Berdasarkan evidence saat ini menyatakan bahwa patogenesis dari dysmenorrhea primer adalah prostaglandin F2 alfa (PGF2alpha), vasokonstriktor dan stimulant miometrium poten, yang disekresikan oleh endometrium. Respon terhadap inhibitor prostaglandin pada dengan dysmenorrhea menunjukkan dengan jelas bahwa dysmenorrhea dimediasi oleh prostaglandin. Evidence substansi menghubungkan dysmenorrhea dengan kontraksi uterus yang prolong dan penurunan aliran darah ke myometrium.

Peningkatan level prostaglandin ditemukan pada cairan endometrium wanita dengan dysmenorrhea dan berhubungan dengan tingkatan nyeri. Peningkatan 3 kali lipat prostaglandin endomentrial terjadi dari fase folikular samapi pada fase luteal, dan peningkatan lebih jauh lagi selama menstruasi. Peningkatan prostaglandin di endometrium yang mengikuti saat terjadi penurunan jumlah progesteron pada akhir fase luteal  menghasilkan peningkatan tonus myometrial dan kontraksi uterus yang juga meningkata tajam.

Leukotrin telah diketahui sensitive terhadap serabut nyeri di uterus. Sejumlah leukotrin yang cukup signifikan telah didemonstrasikan pada endometrium wanita dengan dysmenorrhea primer  tidak respon terhadap prostaglandin antagonis. Hipotesis neural juga menjadi dasar patogenesis pada dp. Saraf nyeri tipe c distimulasi oleh metabolit anaerob yang disebabkan endometrium yang iskemik.

Dysmenorrhea primer juga dipengaruhi faktor kebiasaan dan psikologi. Meskipun factor tersebut belum secara jelas disimpulkan akan tetapi bila terjadi kegagalan treatmen medical faktor penyebab tersebut dapat dipertimbnagkan.

dysmenorrhea sekunder

Sejumlah faktor yang mempengaruhi patogenesis dysmenorrhea sekunder. Berikut beberapa kondisi yang menyebabkan dysmenorrhea sekunder :

·         Endometriosis

·         Pelvic inflammatory disease

·         Tumor dan kista ovarium

·         Oklusi atau stenosis servik

·         Adenomyosis

·         Fibroids

·         Polip uterus

·         Adhesi intrauterin

·         Congenital malformations (eg, bicornate uterus, subseptate uterus)

·         Intrauterine contraceptive device

·         Transverse vaginal septum

·         Pelvic congestion syndrome

·         Allen-Masters syndrome

Hampir semua proses yang mempengaruhi viscera pelvic dapat menyebabkan siklus nyeri pelvis. 

Referensi

1. Calis , Dysmenorrhea available from http://emedicine.medscape.com/article/253812-overview 

2. Rahmatika I, Perbandingan dysmenorrhea pada wanita yang sudah menikah antara yang sudah pernah melahirkan dan yang belum pernah melahirkan. 2009. available from etd.eprints.ums.ac.id/6590/1/J500050050.pdf  

tentang vitiligo

Ini paper waktu stase bahasa inggris. *sedikit aneh memang, masa ada stase bahasa inggris?? ga juga sih, stase ini jadi pengganti program KKN*

Padahal sih asli nya saya lebih suka KKN tapi apa daya ga ada teman, dan bukankah menunda hal yang besar untuk hal yang lebih besar lagi ;)

pada tau Michael Jackson kan ? beliau salah satu penderita vitiligo dan bukan hanya beliau. Ada pesohor dunia lain yang juga menderita vitiligo seperti Amitabh Bachchan, Asifa Bhutto Zardari dan masih ada lagi (berdasarkan berita yang saya baca di wikipedia)

this is english version (lebih enak buat paper pake english ya, ga capek translate, hee :P)

Introduction

Vitiligo is a disorder in which white patches of skin appear on different parts of body. Common, worldwide, affect up to 1% of the population. All races are affected and both sexes are equally afflicted. A female preponderance has been reported but the discrepancy has been attributed to a presumed increase in reporting of cosmetic concern by female patients.

The disease can have devastating consequences on an individual’s relationships with others and internal feelings of self-worth. Approximately 20 percent of patients with vitiligo have at least one first degree relative with vitiligo, and relative risk for first degree relatives of vitiligo patients is increased by 7- to 10- fold. The disease  can have devastating consequences on an individual’s relationships with others and internal feelings of self-worth. Additionally, in regions where leprosy is endemic, individuals with vitiligo are stigmatized due to similarities in appearance between the two diseases. Fortunately, advances in our understanding and management of vitiligo are reducing its effect on the millions of individuals

Definition

Vitiligo is a skin disease that causes patients to develop white lesions on the skin that vary in size and location. It is an acquired idiopathic disorder of melanogenesis. These often appear symmetrically, usually in the face, but also on the nape, axillae, elbows, hands, knees and genitals. Vitiligo usually occurs in a localized or generalized pattern, as well as rarely in a dermatome. Vitiligo can run a rapidly progressive course or remain stationary. Epidermal and mucosal variants occur.

Prevalence

            Vitiligo occurs worldwide, with a prevalence of 0.1 percent to 2.0 percent. In the United States, the estimated incidence is 1 percent. Vitiligo commonly begin in childhood or young adulthood, with peak onset of 10 to 30 years but it may occur at any age. Fifty percent of vitiligo patients experience disease onset before the age of 18 when they are most concerned about their appearance, and self-image is the most fragile.

 

Etiology and Pathogenesis

The cause of vitiligo is not yet fully understood. Vitiligo is a multifactorial polygenic disorder with a complex pathogenesis. Although several theories have been proposed to explain the loss of epidermal melanocytes in vitiligo, the precise cause remains unknown. Considerable progress has been made, however, over the last two decades. Theories include autoimmune, cytotoxic, biochemical, oxidant-antioxidant, neural, and viral mechanism for destruction of epidermal melanocytes. Several studies also point to a significant role of genetic susceptibility to vitiligo. Several theory are of particular importance :

   1. Genetic of vitiligo

Vitiligo is characterized by incomplete penetrance, multiple suspectibility loci, and genetic heterogeneity. The inheritance of vitiligo may involve genes associated with melanin biosynthesis, response to oxidative, and regulation of autoimmunity. The frequent association of vitiligo with autoimmune diseases prompted investigations of possible HLA association in vitiligo. HLA types associated with vitiligo in more than one study include A2, DR4, DR7, and Cw6.

   2. Autoimmune theory and Humoral immune response

One of the most important and well known theories is the “autoimmune theory”. It is based on the observation that several autoimmune diseases (e.g. autoimmune thyroid disease, type I diabetes mellitus) often appear along with vitiligo. Further, vitiligo patients often display elevated serum levels of antibodies towards melanocytic antigens (e.g. tyrosinase, tyrosinase-related proteins 1 and 2).The association of vitiligo with autoimmune conditions is well established.

Thyroid disorders, particularly Hashimoto thyroiditis and graves disease, are commonly associated with vitiligo, along with other endocrinopathies such as Addison disease and diabetes mellitus. Alopecia areata, pernicious anemia, systemic lupus erymathosus, inflammatory bowel disease, rheumatoid arthritis, psoriasis, and autoimmune polyglandular syndrome are other associated disorders, but the significance of some of these associations is debated. The most convincing evidence of an autoimmune pathogenesis is the demonstration of circulating autoantibodies in patients with vitiligo.

            The question has been raised whether vitiligo antibodies are present as a result of pigment cell destruction, as an epiphenomenon, or if these antibodies cause destruction of pigment cells. Support for the latter possibility comes from animal studies in which pigment cell antibodies appear before the onset of pigment loss.

  3. Disturbance in the oxidant-antioxidant system in vitiligo

Oxidant stress may also play an important pathogenic role in vitiligo. Several studies validate a possible oxidant stress theory, which suggest that accumulation of free radicals toxic to melanocytes leads to their destruction. Increased nitric oxide levels have been demonstrated in cultured melanocytes and in the serum of patients with the vitiligo, suggesting that nitric oxide could lead to auto destruction of melanocytes.

  4. Neural theory

Segmental vitiligo frequently occurs in a dermatomal pattern, leading to a neural hypothesis that proposes certain chemical mediators released from nerve endings cause decreased melanin production.

Clinical findings

Patients with vitiligo present with one to several amelanotic macules that appear chalk- or milk-white in color. The lesions are usually well-demarcated, but the margins may be scalloped. They are accentuated an wood`s lamp examination. Lesions enlarge centrifugally at an unpredictable rate and can appear on any body site, including mucous membranes. However, initial lesions occur most frequently on the hand, forearms, feet and face. When vitiligo occurs on the face, it often a perioral and periocular distribution.

Classification of vitiligo

Vitiligo is classified as segmental, acrofacial, generalized and universal or by pattern of involvement as focal, mixed, and mucosal types.

-          Focal vitiligo: usually a solitary macule in one area, most commonly in the distribution of the trigeminal nerve, although the neck and trunk are also commonly involved.

-          Segmental vitiligo: unilateral macules in a dermatomal or quasi-dermatomal distribution. This tends to have an early age of onset and, unlike the other types, is not associated with thyroid disease or other autoimmune disease. This type occurs more commonly in children. Alteration of neural peptides has been implicated in the pathogenesis of this type. More than one-half of the patients with segmental vitiligo have patches of white hair, known as voliosis.

-          Acrofacial vitiligo: depigmentation of the distal fingers and periorficial areas.

-          Generalized vitiligo: also termed vitiligo vulgaris, the most common pattern. Depigmented patches are widely and usually symmetrically distributed.

-          Universal vitiligo : depigmented macules and patches over most of the body, often associated with multiple endocrinopathy syndrome.

-          Mucosal vitiligo : involvement of the mucous membrane sites only.

Koebnerization commonly occurs in vitiligo. Lesions frequently develop at sites of trauma, such as mild friction from clothes, or from a cut, burn, or abrasion. Depending on ethnic color, vitiligo is more or less conspicuous.

  

Differential diagnosis

     Related physical findings

Vitiligo is frequently associated with disorder of autoimmune origin. The most prevalent associated endocrinopathy is thyroid dysfunction, either hyperthyroidism (Graves disease) or hypothyroidism (hashimoto thyroiditis). Vitiligo usually precedes the onset of thyroid dysfunction. Addison disease, pernicious anemia, alopecia areata, and diabetes mellitus also occur with increased frequently in patients with vitiligo. Patient with autoimmune polyendocrinopathy candidiasis-ectodermal dystrophy have an increased prevalence of vitiligo. Mutation of the AIRE (autoimmune regulator) gene has been identified in this syndrome. Patients should be questioned about symptoms for these disorders.

Vitiligo may affect active melanocytes throughout the body, including pigment cells present in hair, the inner ear, and the retina. Poliosis (leukotrichia) occurs in many patient. Premature graying has been reported in vitiligo patients and in their close relatives. Auditory and visual disturbances are present in some patients.

Vitiligo like depigmentation can occur in patients with malignant melanoma and is believed to result from a T-cell-mediated reaction to antigenic melanoma cells, with cross reaction to normal melanocytes. Such depigmentation has also been observed during the course of autologous T-cell- based immunotherapy of melanoma. Depigmentation in this setting may portend a better prognosis. Amelanosis around primary tumors may resemble a halo nevus, but vitiligo like depigmentation can also occur at sites remote from the melanoma. 

Laboratory examination

The diagnosis of vitiligo is primarily based on clinical examination. However, given the association between vitiligo and autoimmune diseases, several screening laboratory tests are helpful, including thyroid stimulating hormone level, antinuclear antibody, and complete blood count. Clinicians should be consider investigation for serum antithyroglobulin and antithyroid peroxidase antibodies, particulary when patients have sign and symptoms of thyroid disease. Antithyroid peroxidase antibodies, in particular, are regarded as a sensitive and specific marker of autoimmune thyroid disorders.

1.      Wood Lamp examination

This examination is required to evaluate macules, particularly in lighter skin types and to identify macules in sun-protected areas in all but the darkest skin types.

2.      Dermatopathology

In certain difficult cases. A skin biopsy may be required. Established vitiligo macules show normal skin except for an absence of melanocytes. Use special  stains to identify melanocytes. There may be a mild lymphocytic response.

3.      Electron Microscopy

Absence of melanocytes and of melanosomes in keratinocytes, also changes in keratinocytes. Lymphocytes have been seen in the epidermis.

Treatment

There are many different treatment options available for patients with vitiligo. Most therapies are intended to restore pigment to the skin. All approaches have advantages and disadvantages and none is appropriate for every patient with vitiligo.

Topical therapy

1. Sunscreens

Sunscreens help prevent sunburn and thus may lessen photodamage as well as the chance that a Koebner phenomenon will occur. Sunscreens also decrease tanning of the uninvolved skin and therefore lessen the contrast with vitiligous lesions.

2. Cosmetics

Many patients, especially patients with focal vitiligo, find cosmetic cover-ups to be valuable treatment option. Area of leukoderma, especially on the face, neck or hands can be covered with conventional make-up, self tanning, product or other topical dyes. Cosmetics offer limited cost, minimal side effect, and the ease of application. As well, many of the cover-ups can be individualized to obtain an exact color match to the patient`s normal skin.

3. Topical corticosteroids

Topical corticosteroids are indicated for the treatments of limited areas of vitiligo and are often the first line of therapy for children. Although most experience in anecdotal. Lesion on the face appear to have the best response to topical corticosteroids, lesion on the neck and extremities (with the exception of the fingers and toes) also have a favorable response. It is not known why lesions on the face have a better response rate. Possible explanation include a high permeability of the facial skin to the corticosteroids, a larger number of residual melanocytes in the uninvolved facial skin, greater follicular reservoirs, or melanocyte damage that is more easily reversed. Lesions on the face often repigment diffusely whereas a dot-like follicular pattern of repigmentation is more common elsewhere. 

Localized lesions can be treated with a high-potency fluorinated corticosteroid for 1 to 2 months, after which prudence dictates that therapy is gradually tapered to a lower-potency corticosteroid. In children and patients with larger lesions, a medium potency non-flourinated corticosteroid is often used. Caution must be used at the expense of efficacy. Caution must be used when using topical steroids on and around the cyclids, as their use can increase intraocular pressure and exacerbate glaucoma.

Wood`s lamp examination can be used to monitor response to treatment. If no response is seen by 3 months, therapy should be discontinued. Maximum repigmentation may take 4 months or longer ( there is a 30 percent to 40 percent response rate with 6 months of corticosteroid use). More darkly pigmented patients often have a more favorable response to topical corticosteroids than those with lighter complexions. The ease of application, high rate of compliance and limited cost are the benefits of topical corticosteroid for treating limited vitiligo. Recurrence after cessation of treatment and corticosteroid side effect (skin atrophy, telangiectases, striae, and rarely, contact dermatitis) are the lilmiting factors. All patient, particularly children, should be monitored closely, for these potential side effects.

4. Topical immunomodulators

Topical tacrolimus ointment 0.03 percent to 0.1 percent is effective in repigmentation of vitiligo when applied twice daily in patients with localized disease, particularly on the face and neck. It is reported to be more effective when combined with ultraviolet B (UVB)or eximer (308nm) laser therapy. Tacrolimus ointment is generally considered safer for children than topical steroids.

5. Topical calcipotriol

Topical calcipotriol 0.005 percent produces cosmetically acceptable repigmentation in some patients with vitiligo. It can be combined with topical corticosteroids in adults and childrean to give possibly faster onset of repigmentation with better stability of achieved pigmentation.

6. Depigmentation

Monobenzeyl either of hydroquinone (Monobenzone) is the only agent available in the United States and Europe for depigmenting residual normal skin in patients with extensive vitiligo. Monobenzone is a phenolic toxin that destroys epidermal melanocytes after protracted use. Monobenzone can therefore produce a uniform depigmented state that is cosmetically more acceptable for many patients than the contrast between normal and affected skin. Monobenzone is available as a 20 percent cream and can be formulated at concentrations up to 40 percent. The individual using monobenzone should avoid direct contact with others for 1 hour after application, as contact may cause depigmentation of others skin. Monobenzone may also be irritating and allergic sensitization may occur.

Systemic therapies

Systemic immunosuppressive drugs have many potential side effect that are difficult to justify for a disease such as vitiligo. However, systemic corticosteroids have been used as pulse therapy with variable results and may prevent rapid depigmentation in active disease.

Phototherapy therapies

1. Psoralen and ultraviolet A therapy

Topical or oral 8-methoxypsoralen combined with UVA (320 to 400 nm) irradiation (PUVA) is effective for treatment vitiligo, although frequent treatments over many months are required. After exposure to UVA, psoralens covalently bind to DNA and inhibit cell replication. How this then leads to repigmentation of vitiligo areas is not well understood. PUVA stimulates tyurosinase activity (an essential enzyme in melanin synthesis) and melanogenesis in unaffected skin. PUVA is also locally immunosuppressive, and decreased melanocyte antigens has been reported.

In vitiligo, melanocytes in the bulb and infundibulum of the hair follicle are often destroyed, but the lower and middle portions of the follicle as well as the outer root sheath are spared. PUVA stimulates follicular melanocytes to migrate into the epidermis and repopulate the surrounding depigmented skin, possibly as a result off the release of cytokines and chemotactants from the epidermal keratinocytes.  

Topical PUVA is sometimes used in patients whose vitiligo involves less than 20 percent of the body surface area. However, unwanted side effects are common and include cosmetically displeasing hyperpigmentation of skin surrounding vitiligo areas due to inadvertent psoralen application, severe phototoxicity reactions, intense pruritus. Oral psoralen are use to patients with more extensive involvement or in patient who do not response with topical PUVA.

It is important to select vitiligo patients carefully for PUVA therapy. Although 70 percent to 80 percent of patients experience some repigmentation with PUVA, fewer 20 percent of patients totally re-pigment. In general, vitiligo on the trunk, proximal extremities, and face response well to PUVA, but lesions on the distal extremities respond poorly. As with corticosteroid, patients with a darker complexion tend to respond better to PUVA, possibly because they tolerate higher PUVA exposure.

2. Narrowband ultraviolet B radiation

NB (311 nm)-UVB irradiation is another option for patients with vitiligo and is considered by many to be the first choice for most patients. In patients with extensive generalized vitiligo, NB-UVB therapy was more effective than topical PUVA (67 percent versus 46 percent response rate, respectively). If no improvement is seen within 6 months of treatment, NB-UVB therapy should be abandoned. In one study, 53 percent of children experienced more than 75 percent repigmentation after NB-UVB therapy and 6 percent showed complete repigmentation. Again, better pigmentation was achieved on the face, trunk, and proximal extremities than with the distal extremities than with the distal extremities and groin.

3. Excimer laser

Excimer (308 nm) laser has been recently studied in several trials for its efficacy in treating vitiligo. It has been found to be most effective when treatment are given three times weekly, with treatment periods of more than 12 weeks necessary to obtain satisfactory repigmentation. The initial dose is 50 to 100 mJ/cm2. As with standard phototherapy, excimer laser produces the best treatment results on the face; the least responsive areas are the hands and feet.

Surgical Therapy

1. Autologous thin thiersch grafting

Thin split-thickness grafts in the treatment of vitiligo are obtained using scalpel or dermatome and are placed onto recipient sites prepared in similar manner or by dermabrasion. Achromic areas ranging in size from 6 to 100 cm2 can be treated. Recently, the technique of thin split-thickness grafts by mechanical dermatome, which shown excellent results. This technique has also been used to successfully treat vitiligo of the lip. The advantage of this technique is that it allows the grafting of large areas in a relatively short time. However, this must be weighed against the need for general anesthesia and the risk of hyperthrophic scaring of both donor and recipient sites.

2. Suction blister grafts

Separation of viable epidermis from dermis can be accomplished through the production of suction blisters that separate skin immediately above the dermal-epidermal junction. This is adapted to the treatment of vitiligo pigmented epidermis is harvested by this technique and is used to cover achromic areas that have been prepared by denuding them with liquid nitrogen blisters. Melanocytes are contained within the epidermal root of 3.0 to 3.5 cm suction blisters. The tops of these blisters are removed and are directly applied to denuded area of achromic skin. Pigmentation usually develops in 3 to 6 months. There may be areas of achromic fissures between grafts in the recipient areas. An advantage of suction blister grafts is that scarring is minimal, as the dermis is left intact in both donor and recipient sites. However, physicians do not have the mechanical apparatus needed for the production of the blisters at the donor site.

3. Autologous mini-punch grafts

The autologous mini-punch grafts technique uses 1.20 to 1.25 nm full-thickness punch grafts placed 4 to 5 mm apart onto comparably sized recipient site. This graft size was found to minimize both the cobblestoning(trap door) effect and the cosmetic damage to donor site that is especially prominent with larger-sized grafts, yet it also contained enough melanocyte sources to stimulate the spotty perifollicular repigmentation.

4. Transplantation of cultured autologous melanocytes

The technique of transplanting melanocyte-containing cultures of cells has the theoretic advantage of potentially treating large areas using cells harvested from a small piece of donor skin by expanding the melanocyte population in vitro. Its major disadvantage lies in the complexities and cost of culture systems. As well, there is concern about what, if any, effect the additives required for culturing the cells have on the melanocytes and subsequently, on the patient. Melanocytes can be cultured more readily in the presence of keratinocytes, and co-cultured can be used to re-pigment areas of skin depigmented by disease or injuries. In the United States, these techniques now require that the cultures be performed using good manufacturing practices very regulated and expensive approach available at very few academic centers.

Prognosis

The prognosis and course of vitiligo are unpredictable. Initial clinical subtype of vitiligo does not predict future anatomical sites of involvement or activity of disease. 

Hampir seluruh isi paper ini saya copy dari Fitzpatrick, tapi ga langsung paste soalnya ebooknya ga bisa ;P

References

1. Flitzpatrick TB, Johnson RA, Wolf K. Polano et al. Color Atlas and Synopsis of Clinical Dermatology. United States: The McGraw-Hill Companies ; 1997. p. 335-41.
2. Halder RM, Taliaferro SJ. Vitiligo. In : Wolf K, Goldsmith LA, Katz SI, et al editors. Fitzpatrick`s Dermatology in general medicine. 7^th ed United States: The McGraw-Hill Companies; 2008. p. 616-22.
3. Forschner T, Buchholtz S, Stockfleth E.  Current state of vitiligo therapy – evidence-based analysis of the literature. Journal compilation JDDG 2007. [online 2010 februari 2]. Available from URL: http://www3.interscience.wiley.com
4. Huggins RH, Schwartz RA, Janniger CK. Vitiligo.  Acta Dermatoven APA Volume 14, 2005. [online]. [cited 2010 februari 2]. Available from URL: http://ibmi.mf.uni-lj.si/acta-apa/acta-apa-05-4/2
5. National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). What Is Vitiligo?. [online]. [cited 2010 Februari 2]. Available from URL: http://www.niams.nih.gov