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

Edting By: EnongXp