Use of Moisturizers in Atopic Dermatitis

Use of Moisturizers in Atopic Dermatitis

Dr. MOH. IFNUDIN. SpKK.

INTRODUCTION

Atopic dermatitis (AD) is one of the many terms used to describe the form of a skin disorder that often occurs. The word comes from Greek atopy atopos which means out of place. DA is also known as atopic eczema, infantile eczema, disseminated neurodermatitis and prurigo diasthique. In 1930 Hill and Sulzberg is a scholar who introduced the term to describe atopic dermatitis skin condition characterized by chronicity of the disease, the superficial location, the presence of inflammatory reactions and itchy.

Atopic dermatitis occurs in 15% of the population of children - children and associated with high levels of IgE in these patients so that suspected immunological factors play a role in DA. DA Sufferers usually have a family history of allergy or atopy, but it got too manifestation of atopic diseases such as: Asthma, Hay fever or rhinitis allergica. DA lesions can get worse in cold weather and dry conditions. The number of people with AD in the United States reached 15 million people, of which 60% of which occurred in under 12 years of age. DA is very rare in old age (over 50 years). DA can occur in infants, the young age of these infants suffer, then the manifestation of DA that appears in the form of patches - red spots that can occur at all and usually on the face, scalp and folding legs that can be accompanied by the formation of crust.

Atopic dermatitis have a close connection with immunological factors. In AD patients there is a high-IgE levels than in normal people, and the patient's blood smear was obtained peninggkatan number of eosinophils. Jam factor immunology, DA is also influenced by genetic factors. Ueahara study on 270 patients with DA showed 60% of DA on DA panderit these offspring.

In DA there is a change characteristic of normal skin. DA manifestations may include: pruritus which is the main complaint people with DA, xerosis (dry skin), keratosis pilaris, ichthosis vulgaris, pityriasis alba and Dannie morgan skinfold. DA apart people with dry skin are also susceptible to virus infection, bateria and fungi. This situation can occur because of the DA occurs ganggua barrier function (barrier) skin. Disorder is caused partly by sweating dysfunction, the occurrence of Trans Epidermal Water Loss (TEWL) and skin fat changes.

The management of DA to the form of systemic treatment and medication that is topical.Systemic therapy with use: antihistamines, corticosteroids, interferon, cyclporin, tacrolimus, antibiotics, and phototherapy. Baiasanya topical therapies are intended to overcome the skin manifestation that occurs in the form of moisturizers and topical corticosteroids.

Dry skin condition on the DA will increase the itching and the skin becomes vulnerable to infection, so that one of the therapy of atopic dermatitis should also aim to overcome these skin dryness. Giving moisturizing skin is expected to overcome the drought that occurred so that buffer to reduce complaints and skin complications are common.

Writing scientific papers will address the dry skin condition that occurs in atopic dermatitis, DA treatment in general and the provision of moisturizer as one form of therapy on DA.

ON SYSTEM skin barrier of atopic dermatitis

The outermost layer of skin is a layer as thick as approximately 10-15 corneum which serves as a barrier against excessive water discharge. Corneum layer is the top layer of skin barrier and a top layer composed of corneocytes are arranged like a braid, on the sidelines - there is webbing between intercellular fat, the skin under normal conditions depending on the 2 factors and environmental conditions of the skin condition itself.Damage from koerneum layer will increase water loss from the skin so the skin will become dry as it did in the DA.

Corneum layer buffer diganbarkan as the composition of the brick wall where brick marupakan corneocytes and intercellular lipid mixture resembles cement. In the corneocytes are natural moisturizing factor (NMF), which bind water so that the corneocytes become "bloated" this prevents the occurrence of fissures or cracks in between the corneocytes. Elasticity of skin depends on the content of the water, healthy skin has a high water content.

Extracellular fat in a layer of corneum is an important factor in maintaining the water content. Fats are composed of over 40% of ceramide, about 25% fatty acids and 20% cholesterol. Ganngguan the three components of the intercellular fat dapart cause skin barrier dysfunction. For example, the provision of lovastatin which is a cholesterol synthesis inhibitor when given topically will disturb the skin barrier function. There is no one single type of fat that secra can maintain skin barrier function, so that normal levels of each - each type of fat ekstraeluler is vital to maintaining skin barrier function. In DA disruption in the lining corneum barrier function.

Dry skin (xerosis) is one of the symptoms of DA caused a decrease ole corneum water content in layers that can cause deskuamasi of corneocytes. Rawling and his colleagues showed that patients with abnormally dry skin, where an increase in fat-free adam and decreased levels of Ceramide. Several studies have shown that the incidence of dry skin on the DA because there is a change levels of ceramide. Other research has shown that the ability to maintain kadae definisis water is not followed by the definition of ceramide. Xerosis on DA may be caused by changes in intercellular lipid lamellar structure in the corneum layer resulting in increased evaporation of water through a layer of corneum or known by TEWL. Reduced water content causes the corneocytes shrink, forming a gap of which can serve as the entrance for substance - and elergen irritant.

Shafer and Kragballe trying to find out the relationship between the definition of intercellular fat in the corneum layer and the occurrence of dry skin, both graduate research shows that in AD patients corneum layer decreased ceramide levels are real.Based on this, the definition of ceramide regarded as an important factor for the occurrence of dry skin in AD patients. This is in line with research conducted by Baradesca and Maicbach which showed an increase in TEWL and decreased water binding capacity corneum layer caused by changes in intracellular lipid content.

GENERAL TREATMENT atopic dermatitis

DA pengbatan success requires a systemic approach that eliputi sticking the skin, topical corticosteroids and find and stop the trigger factors such as irritants, allergens, infectious agents and stresoe emotional. Many factors such as the extent of lesions, trigger factor, which can cause symptoms of atopic dermatitis to be complex, so that treatment in each patient is different - different. In patients who can not be treated with conventional medicine, alternative anti-inflammatory and immunomodulatory can be used.

Skin hydration

DA Patients mostly have dry skin which can increase the severity of the disease with the onset of skin fissures or cracks. Use a moisturizer for dry skin in atopic dermatitis is necessary, this will be discussed further.

Topical glucocorticoid treatment

Topical Glucocorticoids through his work as an anti-inflammatory treatment is the basis eksematosa lesions. Patients should be given an explanation of its consumer and side effects. The use of high potency glucocorticoids should be avoided in advance, genetalia and intertriginous areas, in the area - this area is recommended to use a low potency glucocorticoid. Initial treatment consisted of 1% hydrocortisone ointment applied 2 times per day on the lesions on the face and folding.

Glucocorticoids potential is very high (ultrahigh-potency) is only used in areas that occur likenifikasi and in the short term, should not be on the face or folding. The potential is to be used for long-term regional body and extremities.

Side effects of topical glucocorticoids depending on the level of potency and duration of use. It is important to remember that the higher the higher the potential side effects. To minimize side effects of topical glucocorticoid use, things - the following important consideration: age, place of lesion, extent of lesion, type of preparations and methods of application.

● Age

For children - children with mild to moderate eczema can be used hydrocortisone 1%.Hydrocortisone 1% does not cause systemic side effects through absorption. Stronger preparations are not recommended for infants at the beginning of nursing. In older children potency topical steroids are necessary to shorten the usage. In adults, mild potency topical corticosteroid use is usually not cause systemic or local side effects.Preparations with a potentially strong and powerful should be used in a short time.

● Location

Absorption of corticosteroids will increase the region face daily newspaper. Side effects caused a permanent telangiectasia, so that the area - this area is recommended hydrocortisone 1%. The use of topical steroids that long on the area around the eyes can cause glaucoma, so must be careful - careful especially in patients who have a family history or herself suffering from glaucoma. In young adults also need to be careful - careful in the use of topical steroids are more potent because it may cause strie atrophicae in areas - areas such as breasts, adomen, upper arm and thigh.

● The extent of lesion

The potential for systemic absorption increased at a widespread eczema. The main risk is the pituitary adrenal axis suppression that can affect growth in children - children. It is important to monitor the number, strength, and size of the tube every time the patient control, so there is no excessive doses or deficiency.

● Types of Preparations

generally ointment (ointment) is better than the cream. Absorption ointment is better, and the incidence of irritant and hypersensitivity little more, because the material - there are more preservatives in creams.

● Method of application

treatment should not be more than twice a day, the preparations that are new or have never used once daily is recommended oiled first. The amount used varies between individuals, it is recommended to use the size of a fingertip in which patients equated to 0.5 g.

Identification and Elimination factor triggers

DA sufferers are more susceptible to irritants than normal individuals, so it is important to identify and eliminate factors - factors that triggers that can cause itching, such as soap or detergent, materials - chemicals, tobacco, exposure to light and humidity.

Food and aeroalergen such as house dust, fungi and plant extracts can be causing exacerbation of DA. Avoidance of material - the material could heal skin lesions. Infants and children - more children meliki food allergies, while in adults more allergic to aeroallergen.

Although emotional stress does not directly cause the DA, but can cause exacerbation of the disease. DA sufferers often experience frustration or stress which can increase itching and scratching. Psychological evaluation or counseling should be given to people who mempnyai difficulty overcoming emotional triggers.

Antibiotics against staphylococci can help treat patients infected with S. aureus is a common pathogen. Macrodile erythromycin and azithromycin and clarithromycin new as is usually useful in patients that do not contain S. aureus resistant. For this type of macrodile resisiten S.aureus which can be given dicloxacilin, oxacillin, or cloxacillin. The first-generation cephalosporins are also effective for staphylosporins and streptococci.Mupicorin used topically for treatment of lesions - lesions of impetigo bleak, even in patients with secondary infection panggunaan more widely used systemic antibiotics.

Pruritus

Treatment of itching in the DA should know basic disease. To reduce inflammation and skin dryness given glikokortikoid topical and skin hydration which can reduce the itching. Allergen should be eliminated. Systemic antihistamines may be given as hydroxyzine hydrochloride and hyphenhydramine, but this therapy is not effective without the other DA therapy. hydrochloride which has the effect of tricyclic and inhibit receptor antidepresen H and H with a dose of 10-75 mg orally at night in adult patients can be given if the itching that is especially. Topical antihistamines are not recommended on the DA because it can cause skin sensitization.

Wet compress

Hydrate skin with wet compresses can increase transepidermal penetration of drugs - topical medications. Compress ekskoriasi can accelerate wound healing. The use of excessive compression will cause maceration and can lead to secondary infections.Wet compress and soak it can cause dryness and fissures of the skin if not given a moisturizer. So can compress to control the DA but should be under the supervision of a physician.

Systemic glucocorticoids

Short-term systemic glucocorticoids can be given to the DA who experience acute exacerbations. Although clinical recovery of DA that were treated with systemic glucocorticoids is very fast but often a rebound effect if treatment is stopped. If systemic glucocorticoids are given, it is very important to reduce the dose and provided skin care with topical glucocorticoids followed by use of a moisturizer to prevent a rebound effect on DA.

Ultraviolet Rays

Ultraviolet A (UV-A), UV-B or a combination of both, psoralen + UV-A (PUVA), UV-B 1 (narrow band UV-B) can be used. Short-wave UVB can be used for additional therapy at the recalcitrant DA. Phototherapy with PUVA can be given to people with extensive and severe DA who failed with topical glucocorticoids and topical glucocorticoids avoid side effects if given in large lesions. Side effects which occur widely in Ultraviolet light therapy is usually in the form of erythema, itching or pigmentation, whereas long-term effects of premature aging skin dar, skin malignancy. The recommended maintenance dose 1-2 times per month.

Several other drugs such as azathioprine, cyclosporine, tacrolimus, Chinese herbal medicine and immunomodulator such as interferon and thympetin been reported effective in the treatment of DA but still needs further study. Hepatotoxic effects have been reported on the provision so that patients with Chinese herbal medicine Chinese herbal liver function tests should be done regularly.

IN MOISTURIZING Dermatitis

Moisturizer (moisturizer) is a complex material made with the aim to maintain the water content in the corneum layer between 10-30%. Research on the moisturizer developed in about 1950, when it balnk showed that dry skin is caused by low water content. If there is damage to the skin barrier layer corneum's water content will also be reduced, and water content can be returned in normal condition only when the evaporation of water through the corneum layer is reduced. The purpose of the use of moisturizers is to maintain the water levels in the corneum layer temporarily until the damaged skin barrier system is restored.

There are some terms that often are associated with a moisturizer, namely: emollient and moisturizer. Each - each term is often equated by dermatologists, although in fact each - each term has a special meaning. Emollient is a material used to cover the surface of the corneum layer that can hold water in the corneum layer tersebut.sedangkan moisturizer (moisturizer) is a material that can increase the water content of the skin or to bind water in the corneum layer. The term emollient and moisturizer often equated because amolien also have the ability to increase the water content in the corneum layer.

Use a moisturizer should be combined with a soak (Bathing) because soak therapy can increase the effects of moisturizers or corticosteroid penetration, some combination therapy and the use of soak anatar pelembaba have records as follows:

• Treatment soak in the DA will clean the skin that can reduce the number of bacteria.

• Pemeberian soak therapy in combination with the use of moisturizers can add moisture to strengthen corneum layer.

• Provision of therapy can increase the absorption of corticosteroids used in the treatment of DA.

Moisturizers usually an emulation of oil in water (oil in water) such as lotions or water in oil emulsion (water in oil) like cream. Main types of moisturizers are good standing of both types.

Occlusive Material

Moisturizers this group serves to occlusive or form a layer that has kamampuan to replace natural hydrophilic layer thus reducing TEWL, usually group is also known by the term emollient because this material also has the ability as an emollient in addition to reducing TEWL.

Occlusive materials available at this time were mostly petrolatum and mineral oil. Which includes this golonga material other than petrolatum and mineral oil are:

• Paraffin

• Squalene

• Dimethcone

• Propytlene glycol

• Lanolin

DA treatment using the emollient can increase the water content at corneum layer thus put in to prevent dry skin (xeroxis) which is the cause of itching in atopic dermatitis.Emollient will form an oily layer on the surface of the corneum layer that will prevent water evaporation (TEWL). The water will evaporate will be hampered by the emollient so that water will fill the gap - a blank gap between corneocytes addition emollient will also seep into the corneum layer upon layer so as to resemble the function of intercellular fat which in DA levels berkuran. In addition to functioning as retaining water, emollient has indirect effects as an anti-inflammatory that is useful to overcome the DA.

Should be given after a bath emollient, because at this moment corneum layer of water content on high-up to when given the membrane greasy emollient emollient may prevent the evaporation of water whose levels are increased setealah bath. Emollient given at least 2 times a day, when administered to the entire body is usually in children - a child needs approximately 250-500 grams of emollient a week.

That many types of emollient use is petrolatum which is a mixture of several hydrocarbons, this substance is in use since 1872. petrolatum emollient dinaggap as standard preparations. The advantage of petrolatum is not cause allergic reactions which usually exacerbates kondisa DA. Disadvantage is its use of petrolatum, giving rise to an adult berimnyak oelh uncomfortable because it is often combined with other substances that can reduce the oily taste. The other type of emollient is lanolin that sheep sebaceous gland secretion berasaldari, lanolin it contains cholesterol, which is interselluler komponene from fat. Laonolin often cause allergies, so in general right now does not contain lanolin emollient.

Some studies suggest a complete emollient treatment consisting of emollient ointment / cream, emlien bath oil, and use of emollient soap. The effectiveness of the use of emollient can be improved by using the wet wrapping. Cork menunjukkna improvement in skin condition atopic dermatitis after the use of emlien regularly after 28 days. The applicability of emolie n regularly can reduce the symptoms of itching and to reduce the use of topical corticosteroids. Evaluation of the use of emollient can be made of them by observation / complaint civilization of the skin and decrease itching. Lucky and his friends - friends show that can act as an emollient cream seteroid - sparring in the treatment of atopic dermatitis children, emollient which dberikan with hydrocortisone cream 2.5%, respectively - each once a day turned out to have the same effectiveness with the provision of 2.5% hydrocortisone twice a day.

Humketan

Humektan is a material that is soluble in water and has a high kemempuan absorb water. Hmektan can absorb water from around and beneath the epidermis layer of the corneum. Humektan ability to absorb water from the surroundings can only be done if the surrounding environment kelebaban mncapai 80%. We recommend the use of emollient humektan combined premises so as to achieve maximum effect. Therefore humektan have the ability to absorb water then a layer of corneum become a bit "swollen", this change will give the sensation of smooth skin is not wrinkled. Some examples are benyak humektan used are:

• Glycerin

• Sorbitol

• Sodium hyaluronate

• Urea

• Propylene glycol

• Hydroxy acid

Glycerin is a strong humektan and has the ability to absorb water hampr same as natural moisturizing factor (NMF) which is a natural water-binding in the corneocytes.What type of moisturizing glycerin membandngkan others on 394 patients with dry skin manunjukkan better results in patients who used glycerin moisturizer mamakai compared with the other. Glycerin is normal to dry skin back like Nirmal and able to maintain normal conditions is much longer than other moisturizers.

Humektan other types are urea which is a component of the NMF. Urea is widely used as a hand cream since the 1940s. Apart from being humektan urea also has kemampuan.sebagai antipruritus, it is advantageous to use on DA. TEWL can be lowered with the use of 10% urea cream. Penetration of urea can be increased when combined with hydrocortisone. Use a moisturizer that contains urea is recommended only used when the skin is moist (after a bath) to avoid irritation. In AD patients there is a lack of skin in urea up to 85% so that the use of urea in atopic dermatitis diaharapkan can improve these factors. Pigatto and friends - friends using urea cream 10% with vehikulum vaseline, paraffin, and glycol propelin in his research. After giving two meals a day for 15 days in patients with atopic dermatitis, ceramide levels increase by 30% and clinical improvement occurred in the form of reduced xerosis, pruritus and erythema.

Humektan which is a lot of other used-hydrocy acids (AHAs), which is a class of organic acids and can also serve as the substance ekfoliatif. Several substances including AHAs group are: glycolic acid (glicilic acid), lactic acid (lactic acid) and malic acid (malic acid). Humektan class propylene glycol is an odorless liquid that can function as well humektan occlusive material.

Materials that are important for treatment humketana DA is lactic acid. As is known in patients with decreased levels of ceramide DA which is a component of intercellular fat so that an increase in TEWL, whereas from studies in vitro and in vivo is known that administration of lactic acid can increase the production of ceramide which improves the conditions in pnederita DA.penelitian corneum layer made by Rogers and friends - friends getting results that lotio lactic acid 5% given twice daily for two weeks can reduce the severity of xerosis, although better results obtained by using ammonium lactate 12%.

SUMMARY

Atopic dermatitis is a skin disease characterized by itching and dry skin (xerosis) usually found in infants and children. Some factors that have a close connection with atopic sermatitis include immunological factors and genetic factors. In atopic dermatitis there is a change in skin khususya the corneum layer which is the skin barrier system.Normally corneum layer is composed of corneocytes and intercellular fat consisting of: ceramide, fatty acids and cholesterol. The main function is to prevent the corneum layer waters trasnipedermal loss (TEW) so the skin moisture content can be maintained under normal circumstances. What happens in atopic dermatitis adala changes in the structure of corneocytes and intercellular fat so that an increase in TEWL leading to atopic skin becomes dry.

One modality of treatment of atopic dermatitis is by giving a moisturizer that aims to mengmbalikan water levels become normal again. Moisturizers are used to form occlusive ingredients that make up the veil on the skin surface to reduce TEWL or humketan binding water. Treatment of atopic dermatitis by using a moisturizer is often combined with the use of corticosteroids to achieve optimal results.

Use moisturizer on the DA can improve skin barrier, reducing TEWL and can relieve itching and to reduce the provision of topical steroids.

Literature

1. Moreno JC. Atopic Dermatitis. Alergol Immunol Clin 2000; 15: 279-95.

2. Atopic Dermatitis, Eczema, and noninfectious Imonudeficiency Disorders. In: Odom RB, James WD, Berger TG, editors. Disease of the skin. 9 Ed. Philadelphia: WB Saunders Company; 2000.p. 69-94.

3. Rebecca J. Atopic dermatitis. Primary Care: Clinics in Office Practice 2000; 27: 1-11.

4. Rajka G. Emollient therapy in atopic dermatitis. J Dermatol Treat 1997; 8: S19-S21.

Correale CE, Walker C, Murphy L, Graig TJ. Atopic Dermatitis: A Review of Diagnosis and Treatment og. Am Fam Physician 1999; 60: 1191-210.

Edting By: EnongXp

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Review literature Management pitiriasis versicolor

Review literature

Management pitiriasis versicolor

dr. MOH. IFNUDIN. SpKK.

INTRODUCTION

Pitiriasis versicolor is a chronic superficial fungal disease in stratumkorneum the skin caused by a yeast called Malassezia furfur lifofilik (Pityrosporum ovale or Pityrosporum orbiculare). Synonyms is Tinea versicolor, dermatomikosis fururasea, kromifitosis, tinea flava, liver spots.

Mushrooms are part of the normal flora of human skin with the largest colony in the scalp area, ektremitas top and folding of the body and can not attack the hair, nails and mucosa.

The disease was first recognized in 1846 by Eichtedt and Sluyter in 1847 which states that the disorder is caused by the fungus Malassezia in 1889 called Malassezia furfur fungus is the cause which is the proper name for the fungi that cause disease.Synonyms Pityrosporum orbiculare and Pityrosporum ovale is a variant of breeding M.furfur. The term tinea versicolor is a misnomer because the disease is first suspected to be caused by dermatofita.

Clinical symptoms pitiriasis versicolor is very easy to diagnose lesions premises color depending on the individuals affected by abnormal pigmentation. There are two clinical forms that can be found in the form of macular and papular forms.

In the form of macular derived from multiple small lesions, which continues to expand with skuama thin on top. Some lesions may merge into one large shape. While the form of papular usually around hair follicles (follicular fairy).

Martin AG dividing M. infection furfur in 3 clinical symptoms namely papolosquamosa lesions, folliculitis and tinea versicolor inversa

The main complaint because the patient usually a cosmetic problem, where in the fungus infected skin color changes occur because of disorders of pigmentation.

Disorders of pigmentation disebabka because of fungus or product that can filter out the sunlight and affect the process of melanin formation.

Pitiriasis versicolor can attack almost any age, especially in adolescents, most aged 16-40 years. There is no difference between men and women. The disease is spread throughout the world, especially in subtropical and tropical regions, including Indonesia.The incidence of pityriasis versicolor in Indonesia, an accurate yet exist. Diperkirakana Only 50% of the population in tropical countries affected by this disease.

DIAGNOSIS

To determine pitiriasis versicolor diagnosis based on typical clinical symptoms, Wood's lamp examination and direct examination of preparations from scrapings of the lesion.In the Wood lamp examination pitiriasis versicolor lesions appear golden brown. The advantages of using wood lamps can also determine the lesion boundary is not clearly visible on naked eye examination.

Examination preparation done directly with 10-30% KOH solution is mixed premises superkrom parker ink permanent blue-black with a ratio of 9:1 will give a picture of blue mold element. Taking keroken materials by using scalpel and glass objects and glass cover, or can use also an easier method that is transparent cellulose tape and attached to the lesion suspected of being infected. M.furfur. A positive result if found elements - elements that mold the form of short and thick hyphae and spores clustered large image resembles dermatofita diagnosis of infection and candida, a negative microscopic examination can rule out the diagnosis.

M. furfur is not easy to be left in artificial media, so this procedure is not a routine procedure performed. Can be cultured with a medium fat (Sabouroud Dextrose for coated olive oil) or Tween media.

Diagnosis APPEAL

Dermtitis Seborroik

In this disease yellowish red lesions skuama premises which are soft and oily on the area - an area predisposition (Sebooroik area).

Pitiriasis rosea

Symptoms are more acute with the rapid spread and there is a larger initial lesion ("Herald spots").

Syphilis Stage II

Stage syphilis lesion is more pale with a diameter of less than 1 cm with a spread on the chest, legs and extremities of the flexor. It was also found enlarged lymph comprehensive and serological tests for syphilis are positive.

Morbus Hensen Type BB

In the lesions there is a section that is misbehaving taste (hypo or anesthesia), nerve enlargement also occurs edge.

Eritrasma

Can be very similar to pitirasis versicolor and may also occur simultaneously. Wood's lamp examination premises appear red brick ("Congo red").

Vitiligo

Vitiligo lesions in white like chalk or milk with varying shapes and sizes. The distribution of lesions is usually symmetrical. With found mildew causes on examination keroken can get rid of this disorder.

MANAGEMENT

Management pitirisasis versicolor can be topically or systemically. Can also be preventive treatment for patients with recurrence rate is as high as about 60% in one year and 80% in two years. For topical treatment can be given:

1. Selenium sulfide suspension

Used at a concentration of 2.5% with topically once daily on the affected areas, left for 10 minutes and rinsed with a bunch of water immediately afterwards. This method is repeated every day for 7 days. Disadvantages of this treatment is the presence of strong smelling and feeling the heat so the skin after topical drug treatment should sihindarkan lesions in the genital area. Sanchez et al. found 17% of the 52 patients who smeared pitiriasis versicolor selenium sulfide shampoo experience side effects such as contact dermatitis.

2. Zinc Pyrithione

A material that has the effect of anti-fungal and anti bacterial which are usually present in a mixture of shampoo, proved very effective for such lipophilic yeast M.furfur. shampoos containing these ingredients is applied to the skin lesions once a day, allowed to stand for 5 minutes, then rinsed and siulang every day for 2 weeks.

3. Sodium hiposulfit 20-25%

Applied 2 times daily for 2-4 weeks. Can also be used Tinver lotion containing 25% sodium thiosulfit salsilat acid 1% and 10% alcohol in the same way

4. Propyleneglicol 50% in aqua

Applied to the lesion 2 times a day forever 2 weeks. Can be used on an extensive body lesions degan risk of skin irritation is mild with good results and low prices.

5. Materials keratolik

Can be used in the form of cream, ointment, or a mixture lotio shampoos with acid concentrations between 3-6% salsilat eg Whitfield ointment, ointment 3-10. Applied twice daily for 2 weeks. It can also be used soap containing salicylic acid.

6. Antifungal drug

Used in a cream or solusio, which includes all classes imidasol, alllamines, siklopiroks, halloprogin and tolnaftate / tolsiklat. Applied twice daily for 2-4 weeks to eliminate pitiriasis versicolor lesions, but at a cost of more expensive and no more effective than other materials. Imidasol Group is a topical 2 times a day that is klotrimasol, mikonasol, Ekonasol and some are applied only once a day that is Tiokonasol, Ketokonasol, Bifonasol, Okdikonasol.

7. Retinoic acid cream

Applied twice daily for 2 weeks to recover. This material is good for pitiriasis versicolor lesions are dark in color because mempuyai mangambat freezing effect of melanin, so good for people who are very ashamed of the lesion pitiriasis versikoler.

Faergement advise in choosing a topical treatment pitiriasis versicolor, especially with large lesions should be used solusio form or shampoo because it is more easily applied than cream or ointment form. In addition to topical treatment, management of pitiriasis versicolor can also be a systemic treatment. Indications versicolor is a systemic treatment:

1. Lesions P. versicolor resistant to topical treatment.

2. Patients who frequently relapse

3. Pitiriasis versicolor lesions are extensive.

Systemic drugs used were:

1. Ketoconzole

Is an oral antifungal medication is effective and has a broad spectrum antifungal. With a dose of 200 mg daily for 5 days - 5 weeks (- average 10 days) has a cure rate to 90%.Many other regimens that are used with a higher cure rate, but using larger doses and longer periods. With that brief treatment of the risk effect of drugs on the liver have a low risk.

2. Itraconazole

Is a new azole derivative effective in the treatment pitiriasis versicolor. The recommended dose is 200 mg once daily for 5 days. Mikrologis healing can be seen after 3-4 weeks.

In patients who have lesions that have important depigmentasi lesions are reminded that it will persist for several months after treatment was stopped, so the patient does not feel that the treatment failed. Changes in the nature M.furfur from saprophyte to pathogen depends on several predisposing factors that are difficult kekronisan eliminated that cause this disease. For such patients can be considered prophylactic treatment to prevent recurrence. The recommended way is to use a tablet ketokonazole with a dose of 200 mg for three consecutive days - joined every month or 400 mg once every month for one year.

SUMMARY

Pitiriasis versicolor is a superficial fungal disease is chronic in the skin caused strarumkorneum dimorphic lipophilic yeast called Malassezia furfur.

Diagnosis of this disorder based on clinical symptoms, Wood's lamp examination, and inspection microscope with 10-30% KOH plus Parker ink superkhrom permanent blue-black lesions on keroken material.

The management of this disorder can by using materials and topical or system. Need treatment of prevention in patients who frequently relapse.

Literature

1. Rippon JW. Medical mycology: Superficial infection. 3rd ed. Philadelpia: WB Sauders Co., 1988: 154-9

2. Hay RJ. Robert SOB, McKenzie DWR. Mycology. In Champion RH, et a, eds. Texs Book of Dermatology. London: Blackwell Scietific Publication, 1992:1176-86.

3. Martin AG, Kobayasi YS. Yeat infection: Candidiasis, pityriasis (Tinea) versicolor In: Fitzpatrick TB, Eisen AZ, Wolff K, et al, eds. Dermatology in General Medicine. McGraw Hill Inc, 1993: 2452-65.

4. Arndt K. Manual of Dermatology theapeutics with essential of diagnosis. 5th ed.Boston: Little Brown and Company, 1995: 84-6.

5. Parto Suwiryo S, Danukusuma The topic, pitiriasis versicolor. In: Budimulja U, Kuswadji, Basuki S, et al, eds. Diagnosis and conduct implementation dermatokismosis, Jakarta: BP FKUI, 1992: 65-9

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Fotokemoterapi on hypopigmentation Post Infalmasi

Fotokemoterapi on hypopigmentation Post Infalmasi

Dr. MOH. IFNUDIN. SpKK.

INTRODUCTION

Infalamsi on skin patches often cause hyperpigmentation on penymbuhan process.Although it can be caused by various kerafdangan skin, the most serig usually caused by chronic dermatitis. However, in individuals with dark skin color, psca manifestation of this inflammation can cause patches of hypopigmentation. This disorder can last long after the inflammatory process pentmbuhan, even spotting in to settle.

Post-inflammatory hypopigmentation on melanosom transfer. Diagnosis based on history or observation of other skin diseases. When the diagnosis is difficult, a biopsy of the lesion may show a picture histology hipomelanotik basic disease of skin disorders.

Usually when the doctor managed to cure the primary disease in a patient with post-inflammatory hypopigmentation and get the doctor will feel successful in providing therapy, but patients still arise feeling worried about the disorders that exist, even extension - sometimes people find the former arising from this is a problem and really become pikran of the primary lesion itself so that the desire to mengobat I to disappear.

Treatment of post-inflammatory hypopigmentation is usually not specific. Many doctors advise sufferers to use emollient and menuggu until there is improvement pigment spontaneously, while some other doctors emberikan prescription topical corticosteroid in the hopes of a change. PUVA is one of the effective treatment of post-inflammatory hypopigmentation disorders.

POST-inflammatory hypopigmentation

A number of inflammatory skin diseases may be accompanied or leave hipomelanosis spots on the affected area. It is often found in atopic dermatitis, proriasis, and allergic dermatitis, and more rarely on perapsoriasis, pitiriasis likenoides chronic, mycosis fungoides, Liken planus, discoid lupus erythematosus and seborrheic dermatitis.

Clinically, the majority of post-inflammatory hipomelanosis look similar, not depending on the type of skin inflammation that occurs earlier. Spots are usually white with no clear boundaries and is always associated with the location of the preceding eruption. These patches appear immediately after the process of the disease in remission and started to fade within a few weeks to months, especially in areas exposed to sunlight.

The disorder is thought to occur due to transfer melanosom barriers, where the eczema it is in because of the edema. While in psoriasis increased epidermal turnover held responsible. In T cell lymphomas have degenerative changes in melanocytes and melanosom. In post-inflammatory hypopigmentation clinicopathologic loss is among groups that melanopenik where erjadi disorders because of the failure in the functioning of melanocytes or epidermal melanin unit.

Diagnosis based on observation or a history of abnormalities that accompany dermatosis. If the diagnosis is difficult to enforce, a biopsy of the lesion histology hipomelanosis pnaykit bias reveal the underlying picture.

Normally, treatment is aimed at basic abnormalities. When the inflammatory process has been improved, constitutive skin color is slowly coming back. This can be accelerated by exposure to sunlight, but in the long-standing inflammatory process of skin color can not be normal.

FOTOKEMOTERAPI

Definition

Phototherapy

Is the use of electromagnetic radiation that is not etrisonasi daalm treatment of disease.Electromagnetic radiation is energy that has a spectrum of different wavelengths.Wavelengths over 100 nm referred to as non-ionizing radiation does not cause kaena photon ionization of atoms erkena. Phototherapy is usually used with ultraviolet B therapy as a chromophore in this therapy is endegon, particularly deoxyribonucleic acid.While the definition fotokemoterapi is a treatment that uses radiation elktromagnetik are not ionized by a combination of exogenous chromophore. Treatment that is already known is PUVA arrives consisting of A and psoralen ultraviolet radiation.

History

Sunlight is the main source of physical heat. Light, energy and the source of life since ancient revered and worshiped by the belief of the Egyptians, Persians and Greeks. In the second century BC, who is the father Helioterapi Hedrodotus stressed the importance of sun exposure to improve health. At the end of the eighteenth century 'Dark Ages' end to this practice when the sun has the effect in curing rickets.

In 1890, Neil Finsen received the Nobel Prize because of karbonarc pnggunaan sunlight on kutis tuberkuolusis treatment. The popularity of UV phototherapy menigkat view hot discovery of smoke mercury lamp in the early 20th century. From 1920 to 1970, the UV source is most often digunakandalam dematologi practice.

The use of topical material derived from extracts of growing - plants, seeds or other plant parts that contain psoralen followed by irradiation of natural sunlight premises have been used by ancient Egyptian and Indian medicine man in 1000 years ago as a therapy vitiligon. In modern medicine, clinical research regarding the provision of topical and oral psoralen in vitiligo first dilaorkan by El Mofty in 1948 and later by Lerner and friends - friends. In 1974, the use of 8-metoksipsoralen (MOP) orally and then given artificial UVA radiation is very effective in the treatment of psoriasis, which is a new concept in terms terapuetik fotokemoterapi or PUVA.

PUVA Therapy Principle

Electromagnetic radiation is a form of energy spectrum yamg have different wavelengths. Wavelengths over 100 nm referred to as non-ionizing radiation from atomic affected. The basis of PUVA therapy is to stimulate remission of various skin diseases with a controlled reaction fototoksik and repetitive. This reaction occurs only when psoralen activated by UVA.

Psoralen

Psoralen is a tricyclic furocoumarin are naturally present in plants, but some psoralen synthesis are also available. Psoralen the most frequently used orally and to soak the 8-MOP (methoxalen, xanthotoxin), which comes from plants but also present in the form of synthesis that is less fototoksik on oral usage, but rather on the use of a berebdam fototoksik. Also 5-MOP (bergapten) in therapeutic effect on the use of oral and bath, less eritemogenik on the use of oral use does not cause allergic reactions.

Topical

Psoralen can be used topically on the provision of certain areas or to lace. The advantage of using a topical psoralen are the absence of systemic side effects. While the losses:

- Fototoksik more severe due to high psoralen concentrations in the skin.

- Limited area except dgnan soaking treatment.

- Expensive in pengguanaan ririskiky bath.

Oral

Crystalline 8-MOP (meladinine) is usually given at a dose of 0.6 mg / kg given 2 h before irradiation performed. Determination of the body surface dose (25mg / m) showed the concentration of psoralen is more evenly distributed in the plasma. 8-MOP in liquid form in soft gelatin capsules, is usually more expensive and difficult to obtain. 5-MOP (Bergaptan) diberiakn with a dose of 1.2 mg / kg because penterapannya difficult.Use of member benefits orally simple procedures. But there are also losses of the gastrointestinal side effects such as nausea and vomiting. This problem can be reduced by administration with food.

Giving antimetik can also use a half hour before giving treatment. In patients who were intolerant of these side effects are advised to change treatment. In addition, patients are advised to use protective goggles rays up to 12 hours after the penmberian therapy or during therapy. Although there are no reports of increased incidence of cataracts in fotokemoterapi PUVA.

UVA radiation

UVA is most often used for PUVA therapy are fluorescent lamps or high-pressure metal halide lamp. Typical, on PUVA fluorescent lamp, having peak emission at 352 nm and pancarabn about 0.5% in the UVB range. UVA dose is given in J / cm, usually photometer measurements performed with a sensitivity maximum at 350-360 nm.

Fotosintesitifitas Securities PUVA

PUVA therapy produces an inflammatory response with erythema fototoksik manifestation of delayed type. This reaction depends on drug dose and UVA as well as individual sensitivity to the reaction fototoksik. Pigmentation is the second important effect of PUVA, clinically erythema can occur without incident, especially in the delivery of 5-MOP or TMP is given orally, especially in the treatment of vitiligo and as preventive therapy in fotodermatosis teetentu. In normal skin, PUVA pigmentation because the maximum occurs in about 7 days after the exposure and can last several weeks to several months.

Fotokemoterapi working Mekanismee PUVA

Mechanism of action of fotokemoterapi definite yet on exactly understood. A variety of diseases with pathogenesis are not the same premises can be treated either at fotokemoterapi raises suspicion about the different reactions that occur fotobiologi.various alleged mechanism of action is happening:

1. Inhibits DNA synthesis

Absorption of photons from ultraviolet radiation with psoralen photochemical bond lead to a pyrimidine base. The first known pharmacological effects of PUVA is inhibited DNA synthesis.

2. Immunomodulatory effects

a. Immunosuppression

Inhibit the reaction of radiation delayed type hypersensitivity by inhibiting and reducing the function of Langerhans cells, which is the main skin cell antigen presenters.

b. Effects on cell antigen presenters

Epidermal Langerhans cells are an antigen presenter cells that play a role in the early immunologic reaction, the numbers decreased in PUVA irradiation premises, which result in disturbances in the function antige presentation.

c. Produsi factor in the immunological process

Keratinocytes to produce various cytokines and chemokines pre-inflammatory. PUVA improving production and spending a few factors that can inhibit the destruction of this immunological reaction

d. Eefk on lymphocytes

In PUVA irradiation causes changes in lymphocyte cell populations at the edge of the blood vessels that cause the migration of lymphocytes toward kemoreaktan munujukkan inhibited and decreased production of IL-2 in spleen in vivo in experiments conducted on mice.

e. Pressing Mast cells

PUVA suppress mast cell degranulation and histamine from mast cells expenditure

3. Melanogenesis

Enhances the formation of melanin and melanocyte stimulating.

4. Phototolerance

Cause thickening of the epidermis and also the color of brown on the skin. This effect makes the skin become more resistant erhadap rays.

PUVA on melanogenesis

PUVA therapy in vitiligo that causes healing have long been known. PUVA effects on melanogenesis suspected cause:

1. Mitosis and proliferation of melanocytes

2. Activation and increased synthesis of tyrosinase

3. Enhances the formation of melanin from melanosom

4. Improve melanosome transfer to keratinocytes.

Indications and contraindications

Indications PUVA

Fotokemterapi PUVA is more advisable to:

1. The disease is responsive to PUVA

2. Considered for treatment with maintenance doses.

The disease is responsive to PUVA

Some diseases that respond well to PUVA treatment include:

1. Abnormalities hiperproliferatif

Psoriasis

Cutaneous T cell lymphoma

Papulosis limfomatoid

Pitiriasis rubra pilaris

2. Inflammation

Atopic dermatitis

Hand dermatitis and chronic leg

Postulosis palmoplantar

Liken planus

Alopecia areata

Cutaneous graft versus host disease

Pitiriasi likenoid et variosiform acute

3. Abnormalities of melanocytes

Vitiligo

Hypopigmentation post infalamasi

4. Mast cell disorders

Uritkaria pigmentosa

5. Photosensitive disorders

Poplymorphous light reaction

Aknitik chronic dermatosis

Contraindications

A literature states there is no absolute contraindication to fotokemoterapi, that there is a relative contraindication, namely:

1. Younger age, less than 12 years

2. Low intelligence

3. Pregnancy or breastfeeding

4. Vesiko bullous disease due to autoimmune disorders

5. Patients who do not cooperate

6. History of premalignant skin tumors or malilgna.

Another source states that pregnancy, hepatic and renal disfunction weight, and disease which is exacerbated or stimulated by exposure to UVA as lupus erythematosus, porphyria, xeroderma pigmentosum is an absolute contraindication to PUVA. Cataract and afakia not an absolute contraindication if the protective pad Amata performed adequately. It should be noted also that patients with bulous pemfigoid pemfigus and relapse may occur with the provision of PUVA, patients with a history of skin Keener at risk for the occurrence of new cancers. While patients with immune system disorders should not receive PUVA, although not yet clearly defined.

Acute Side Effects Fotokemoterapi

An array of side effects may occur acutely at fotokemoterapi namely:

1. Erythema to severe burns with a bull.

2. Allergic reactions to psoralen.

3. Persistent pruritus during therapy and pain like the sting parasaan can spread to surrounding areas where radiation. This mechanism is not known, and not respond on providing antihstamina.

4. Side effects of psoralen, such as nausea and vomiting.

5. Tanning.

Long-Term Side Effects Fotokemoterapi

Use the old libertine fotokemoterapi can also cause various side effects, such as:

1. Photodamaged skin

- Lentigenes: frekles form of the disorder that gives a clear picture of skin damage from radiation. This occurs because of repeated and long-term terapu, resulting in cumulative doses of UVA and the large dose. Patients with lentigenesis should watch out for his place of skin malignancy.

- Keratosis: These lesions are most common in lower ektremitas. Can be removed by cryotherapy

2. Incidence of malignancy

Depending on the cumulative dose of UVA. Although the incidence is lower in Asian people who get this etrapi. PUVA therapy in patients with risk of squamous cell carcinoma, but not of basal cell carcinoma.

3. Effects on the eye

Although the research on animals, citing the risk of premature cataract, but the clinical evaluation showed no increase in cataracts than in patients who did not get good protection. Most of the prospective study did not report increased incidence of lens opacities in patients who use eye protection for psoralen administration. It is clear there is no risk in giving psoralen when given topically or soak.

Phototherapy PROTOCOL AND FOTOKEMOTERAPI

There are 3 important components of the protocol of ultraviolet radiation (UVR).

Initial Dose

For successful treatment, it is important determining the correct dose beginning. Low doses will produce a faster treatment in curing diseases caused due to tanning effect, causing the skin to be more tolerant to light. With larger doses will lead to feelings of pain due to burning rays. There are 2 ways in the beginning of Neutron dose.

a. This type of skin that react to sunlight this system introduced by Fitzpatrick in 1970 to determine the dose at the beginning of fotokemoterapi PUVA. System in bedasarkan adanay terbaakr history and tanning rays after the exposure to sunlight. There are 6 skin types:

This type of dose administration

1. I always burn, never tan

2. II always burn, sometimes tan

3. III mostly tan, sometimes burn

4. IV always tans, rarely burns

5. V keclokatan

6. Black VI 0.5 j / m

1 j / m

1.5 j / m

2 j / m

2.5 j / m

3 j / m

There are some weaknesses of this system, as there are some people that the history can not be inserted into the skin type above. Is because some of them that can not remember the changes that occur when the sun, because there are few places where the sun is less popular as in Asia. Also this mnujukkan that UVB or PUVA erythema sensitivity can not be expected based on skin type. Therefore, the most common type of skin dianjurklan for each type of skin is lower than it should be given to avoid feeling pain due to burns.

b. Fototes

This method was introduced by Wolff in the beginning of the dose determination. This method can be well received and is the best method in determining the sensitivity of UVB or PUVA erythema. But this method requires more time and sometimes - sometimes very difficult. Principle of fototes is to give exposure to a small area of ​​skin to determine the dose of ultraviolet. Even though the most sensitive areas are the buttocks, this is difficult in doing fototes in this aera. Tests are usually done on the back or inner arm. Dosage should be initiated approximately 70% of the minimal erythema dose (lowest dose that can cause erythema) or fototoksik dose (lowest dose that can cause erythema with phptpsensitizer).

The recommended dose for fototes

To fotokemoterapi PUVA

White skin (skin types I, II): 1,2,, 4,5,6,8,11,12 j / cm

Dark skin (skin type III, IV): 2,4,6,8,11,12,16 j / cm

Dose fototoksik minimal public within 72 hours after irradiation.

Frequency of treatment

Treatment provided more often will give more effective results. Erythema caused by radiation is a limiting factor for therapy control. Treatment should not diberiakn if erythema has not been lost on previous treatment.

PUVA erythema caused by slower. There were no less than 48 hours and can occur 72 hours after irradiation. Therefore, PUVA should be given at least at intervals of 48 to 72 hours.

Peniggakatan dose

Fotokemoterapi diving, tanning and skin thickening of the skin mebuat become less sensitive to UV radiation. Although the distance and duration of adaptation to cause the skin is not known. For skin inflammation penigkatan dose should be more aggressive to menggulangi in the adjustment of the skin.

Fotokemoterapi on post-inflammatory hypopigmentation

Before doing fotokemoterapi, there are several selection criteria should be established:

1. Patients without contraindications to undergo systemic fotokemoterapi.

2. Primary disease is not a contraindication to PUVA therapy.

3. Essentially disease must be cured first before PUVA therapy.

4. Patients are educated, so meraka can understand the complications of treatment and to inform them that complications and side effects of treatment on the doctor.

5. Failed therapy with other means, and is a difficult case.

6. Patients who are willing.

While the standard contraindications are contraindicated for systemic fotokemoterapi.As an example of systemic PUVA for post-inflammatory hypopigmentation from tinea versicolor infection yangdibuktikan with positive KOH examination and then make ppengobatan tinea versicolor for 3 weeks, then re-examination of KOH after receiving treatment, hsilnya negative. Dapun interval KOH examination and began PUVA treatment about 60 days. During this period the patient is only using the emollient. But with 8-MOP (dose 0.6 mg / kg) given 2 hours before the previous irradiation. UVA illuminates on the affected area, with a dose of 50% MPD. Exposure beginning given 3 times a week, if the patient does not show adverse effects, the dose may be increased by 0.5 j / cm every 2-3 treatment until there is improvement, then considered to reduce the frequency of treatment. Evaluation during treatment in the occurrence of pigmentation.

The result, 90% of patients have improvement memuaskna (80-100% occurred pigmentation) and 10% of patients obtained a good result (60-80% occur pigmentation).

As for side effects that occur are nausea, dizziness, erythema, and tingling. Although fotokemoterapi effective in post-inflammatory hypopigmentation but not the first choice of treatment, may be an option after the treatment of other forms of therapy fail.Fotokemoterapi into consideration the difficult and chronic cases that have failed on conventional therapy. Therefore fotokemoterapi is time-consuming treatment, this requires good patient preparation so that the therapy process runs smoothly and well established cooperation between doctor and patient.

Literature

1. Johnson LB Elder ED, Clark Jr.. Disorder of pigmentation. In: Bondi EE, Jegashoty BV, Lazarus GS, editors. Dermatology, Dianosis and Therapy. New Jersey: Appleton & Lange; 1991.p.188-205

2. Jirot Sindhvananda MD. Photochemoterapy of postinflammatory hypopigmentation.Manual for work shop in photodermatology. Pre-Congress Teaching Course the 12th regional conference of dermatology (Asian - Australia). 1996

3. Mosher BD, Fitzpatrick TB, Ortone JP, Hori Y. Hypomelanoses and hypermelanoses.In: Freedberg IM, Eisen AZ, Wolff K, Goldsmith LA, Klatz SI, et al, editors. Dermatology in General Medicine. 5th ed New York McGraw-Hill Inc; 1999.p.945-1017

4. Morison WL. Phototherapy and Photochemoterapy of skin disea. 2nd ed. New York: Raven Press; 1991

5. Anavaj Sakunthabhai MD. Principle of Phototherapy and Photochemoterapy. Manual for workshop inphoto-dermatology. Pre - Congress Teaching Course The 12 regional conterence of dermatology (Asia - Australia). 1996

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