NEW CONCEPT seborrheic dermatitis AND DANDRUFF

NEW CONCEPT seborrheic dermatitis

AND DANDRUFF

Dr. MOH. IFNUDIN. SpKK.

Dandruff is always discussed with seborrheic dermatitis (DS) because clinical gamabaran skuama steamy soft on the scalp and the relationship between the two trigger kontrofersi long ago. Some researchers menebut DS as severe Dandruff dandruff while others refer to as flaking of the scalp or dandruff whatever the cause is a mild clinical picture ayng DS because both clinical penyalit is indeed a unity, even a few other researchers mention dandruff as kondis DS is not beradang. From the data that there is much to conclude that the DS and the dandruff is a disease that has different clinical manifestation of the same disease.

Some factors suggested as contributor to the incidence of DS including impaired immune system conditions such as HIV / AIDS infection. Factor - factor causing the DS include seborrhea, microbial effect, kerentana individual drugs - certain drugs, physical factors neurotransmitter abnormalities, nutritional disorders of emotional stress, and hormonal imbalances.

At first the role of fungal genus Malassezia in the pathogenesis of DS a lot of controversy, but now many who agree with these opinions after the several drugs both topical and systemic antifungal proven to reduce symptoms and improve klisnis DS.Among them are topical antifungal like terbinafine, butenafine, Ciclopirox and immunomodulatory (pimecrolimus and tacrolimus). Even tea tree oil, honey, and cinnamic acid after investigation also has an antifungal effect against Malassezia sp. In the case of a widespread Ds can be considered giving oral antifungal preparations such as ketoconazole, itraconazole, and erbinafin. Antifungal therapy in various preparations such as creams, shampoos, and oral formulations can reduce the number of Malassezia that will lead to clinical improvement as well as safe and effective for the treatment of DS.

Successful treatment using a class of azole DS premises such as ketoconazole are more widely known to new horizons membka DS treatment had previously only known keratolitik and kortrikostroid. Especially after the investigation that ketoconazole has anti-inflammatory effect that can be used as a therapy that tends to chronic recurrent DS.

Seborrheic dermatitis PERSPEFKTIF HISTORY AND DANDRUFF

Historical perspective and dandruff DS diseases through the long period since more than a century ago, teptnya Rivolta in 1873 when first discovered that he got from Pityrosporum round scaly lesions on her neck smooth own. 1874 malassez discovered fungus called "le champignon du pityriasis simple" on the scalp da other areas of the body smooth scaly. Unna in 1887 invented the term "seborrhoeic eczema" for either form of dandruff skin lesions and abnormalities in the form of scales or crusting on the scalp. In 1904 his discovery that sabouraud mangumumkan pityrosporm ovale is a fungus that is often associated with the onset of DS. These findings continue to be developed by McLeod and Dowling 1928 and Moore et al in 1936, but there are still many who doubt these hiphotesis.

After the second world war, corticosteroids began to be used for the treatment of DS and give a satisfactory result. Next DS clarified as one eksematous disease. Beginning in the 1970s kligman et la stated that the DS and dandruff are 2 different diseases, where the DS through the process of inflammation, whereas dandruff is the result of epidermal and P. hiperproliferasi oval secondary role in the pathogenesis of DS.

Scenario again changed about 100 years after the discovery of the term "seborrhoeic eczema". In 1984 Shuster concluded that P.ovale role as the primary factor in the pathogenesis of DS as well as dandruff, where both conditions are the same disease, differing only tingakt severity. This Opinion msih used by most dermatologists throughout the world especially after ketoconazole proven cure dapt DSi.

Taxonomy of fungi that play an important role on the DS and dandruff changing premises of the new discoveries, old keputakaan menybutk \ her as Pityrosporum ovale in accordance teksonomi keputakaan issued a long while after the 1990s to replace a malasszia accordance with the new taxonomy. Called Malassezia according to a new taxonomy for the genus name that formally could not accept the second phase of growth, both forms of yeast (Pityrosporum) or mycelium (Malassezia). Until now all spsesies malasseziamasih regarded as M. furfur by klininisi and epidemiologists. Fitzpatrick latest literature in 2008 also menybut M. sebgai furfur fungus that plays on the DS and dandruff, although some researchers like Gueho and Gulilliot since 1996 has found many new spsesies of the genus malassezi. Among them is often associated premises DS and dandruff namely M. globosa, M. restricta and M. slooffiea.

Epidemiology

DS prevalence in immunocompetent adults of 1-3% and found more bnyak in men than in women. While dandruff about 50-10% of the population. The incidence of DS in patients imunokompromais (HIV / AIDS) was found higher at around 30-85%. DS is one of the manifestations of skin disease most commonly found in people with systems for HIV Infectioon and Disea in Adult and Adolescens in 2005, then the DS the most common HIV padapenderita stage II. Other literature mentions that the DS was found at 15% in patients with CD4 levels> 200 cells / ml and experience penigkatan up to 58% in patients premises CD4 levels <200 cells / ml.

Etiology and pathogenesis

Immune factors have an important role in the Ds. Presumably not just caused by the fungus Malassezia tunbuhnya excessive, but rather is caused by an abnormal host response against this fungus on the skin. The failure of cell mediated immunity (CMI) can cause mildew better able to survive on the skin. Faergemann et al detected an increase in natural killer (NK) 1 + and cells - CD16 + cells by activation of complement.Also found increased activated lymphocytes (human leucocyte antigen - HLA) - DR4 in large quantities.

Although many factors are known as the cause of DS, but only got 3 main factors namely the secretion of sebaceous glands (seborrhea), fungus Malassezia keberasan microbes (microbial effect) and keretanan individuals.

• Saborrhea

Sebum that is produced depends on the control of sex hormones. DS and dandruff have a strong correlation between the activity of sebaceous glands and umu rpenderita. In the newborn in getting sebum that comes from maternal hormones and the Malassezia colonization was found on cradle cap. Furthermore, the amount of sebum decreases until puberty, active since the influence of maternal hormones and then decreased again.

The incidence of DS is higher in the newborn is equivalent to the size and activity of the sebaceous glands. A newborn has a large sebaceous glands with sebum secretion of High Renata sam aorang nearly adult. At adulthood, seborrhea is no longer associated premises DS, because the activity of sebaceous glands mancapai peak in early puberty, but the disease first appeared in a few decades later.

• effects of microbial

In DS infantile often found Candida albicans but not at all related to pathogenesisnya, Staphylococcus aureus was found in patients with skin lesions 20 & Ds, and these bacteria are rarely found on the skin of healthy people. Propionybacterium acnes are found only in small quantities only, meaning only found a little free fatty acid (FFA) in skin lesions of patients with DS.

Lipophilic fungus Malassezia furfur dietmukan exaggerated, as many as 922.000/cm on normal people. This finding supports the opinion of many close hubunganayng between Malassezia furfur with DS, as evidenced by three things: the discovery of this fungus in large amounts in the lesions, giving an antifungal preparations to give a satisfactory treatment outcomes and actions will lead to lesions of reinfection DS or dandruff.

• Individual Kerantanan

Kerantanan individuals against dandruff seems to be caused by differences in the ability of skin to prevent fatty acid berrier malakukan penetration. Oleic acid, one of the main components of the fatty acid in human sebum are known to induce a similar deskuamasi dandruff. Interestingly oleic acid with the same dose given to subjects who do not suffer from dandruff was not able to induce lesions. This may explain individual susceptibility problems in people with DS or dandruff.

Factor - Another fakor causing DS:

• Physical Factors

Blood flow and skin temperature distribution is estimated to be responsible towards the DS. Temperature in the fall season dingain hand and low humidity also erndah at room warmed ayng known to worsen the condition of patients with DS.

• nutritional disorders

Zinc deficiency usually occurs in patients acrodematitis enteropathica. Often this disease found similar skin lesions on the DS was not obtained wajah.setalah studied zinc deficiency and supplementation on the DS lesion. DS infatil defisinsi biotin linked premises which are secondary, due to primary deficiencies of enzimholocarboxylase or biotinidase.

• Drugs

Several types of drugs reported to cause skin lesions that resemble the appearance of DS, including: arsenic, gold, metildopa, cimetidine, and drugs - neuroleptics drugs.

• neurotransmitter abnormalities

DS often diakitkan deanga various neurological disorders which confirms the possibility of influence sisetm nerve. Neurological conditions in include Parkinson's, epilepsy, supraorbital injury, paralysis, facial, unilateral injury to the ganglion gasseri, poliomyelitis, siringomielia, and quadriplegia.

Cowley et al found an excessive amount of sebum in patients with neurological disorders. Excessive amount of sebum in a good media for growth of fungus Malassezia.

• Emotional Stress

Ever found a high incidence of DS at the soldiers during the war.

• Hormonal Imbalance

Hormone which is estimated to affect is hoemon androgens. It is estimated that the effect of androgens on the unit Horon pilosebasea gland gives rise to the DS. There may be oengingkatan levels of androgen hormones occur Arau hypersensitivity to normal androgen levels that underlie the emergence of the DS.

• epidermal proliferation

Increased epidermal Poliefrasi in Ds such as psoriasis may explains why sitostatica therapy can improve this condition. DS or dandruff is a disease that is not only about koerneum stratum, but also significant changes in the epidermis with the discovery hiperprofilerasi, intercellular and intracellular lipids excessive and parakeratosis.

• Genetic factors

Recent findings mention any damage to the zinc finger protein genes in patients with DS.

Pathogenesis of DS based on several things:

• sebaceous gland activity

Sebum production in the era's biggest lump of skin, face, chest and back. Its production is controlled by hormones, such as in infants, sebaceous glands androgwn activated by hormones from the mother. Sebum complex consists of triglycerides, fatty acids, waks esters, sterol esters, cholesterol, cholesterol esters and skualen. At the time of primary Seara secreted sebum content consists of trigliresida and ester by microbes in the skin komensal premises lipase will help in breaking into diglycerides, monoglycerides and free fatty acids. The existence of specific fatty acids generated a new human sebum terliaht after metabolized by the fungus Malassezia.

• Metabolites produced by Malassezia

Malassezia require lipid as a source makana to grow and proliferate. These fungi degrade sebum with the aid of lipase into various fatty acids mainly from trigleserida.However Malassezia mengkonsimsi only a very specific fatty acids, namely saturated fatty acids for its growth, sedangakn unsaturated fatty acids left on the skin surface.Metabolites of unsaturated fatty acids form most often found is around oleic acid, and this metabolite is thought to play a role in the formation of skuama DS.

• Sensitivity of the individual against Malassezia fungal metabolite

The existence of permeability of the skin barrier deficiency due to penetration of materials - materials that diekresi glandulan sebaceous (especially oleic acid) will cause damage to the skin barrier function, causing inflammation, irritation and the appearance of skuama. These metabolites can penetrate the stratum corneum barrier because it has a low molecular weight (probably <1 -2 kDa) and soluble in fat.metabolite in question here is a toxin produced by the fungus Malassezia. This pathological mechanism does not support the previous hypothesis Diman inadequate immune response against Malassezia will menybabkan emergence DS.

Other literature also explains the same thing that is hiperproliferasi epidermis is the result of the FFA which induces damage to the scalp bearrier. Malassezia are lipid-dependent function, the fungus requires the FFA produced by the sebaceous gland triglycerides from. Malassezia is a non-specific lipase to produce FFAs of sebum. They took the fatty acids which required, and FFAs to penetrate the stratum corneum and scalp damage the skin barrier. Skin barrier is damaged ayng indicated by increased trans epidermal water loss in patients with DS. Barrier broken play an important role directly to the clinical picture of DS, such as the emergence of itching, scales, and erythema.

• Immunological Mechanisms

In patients with HIV is estimated to occur changes in cytokine levels that lead to the DS.Levels of interferon alpha and tumor necrosis factor is increased in HIV disease. These cytokines result in changes in lipid metabolism, increase levels of triglycerides and cholesterol in serum. Changes in metabolism were allegedly dapt lipd increase sensitivity to inflammatory mediators that dihsilkan Malassezia.

Excessive growth of Malassezia furfur will cause inflammation, not only due to product metabolite of the fungus in the epidermis or the presence of fungal cells on the skin surface. The mechanism of onset of inflammation is through activation of Langerhans cells and T lymphocytes by Malassezia or products. When Malassezia furfur associated with serum binding activates the complement malalui tersbut direct and alternative pathways.

MANIFESTAISKLINIS

DS referred to as seborrhoeic eczema or pityriasi simplex. DS papolosquamous loss is among the class of chronic dermatosis that can be easily identified. Can be found at the age of infants and adults, often associated with pengingkatan production of sebum (seborrhea) of the scalp and sebaceous follicles on the face and body.

In infants the disease is commonly known as infantile DS. The disease is predominant in the first month of 1 month (usually the third and fourth weeks), at most the first 3 months and will disappear spontaneously without treatment by age 8 to 12 months. DS infantile primary on the scalp and intertriginous areas skuama view oily and crusting.There are others who terkana is the center of the chest face and neck. Scalp affected are the frontal part and periteal covered by crust that is very oily, thick, often seems broken - broken and is called cradle cap. Complications of Infantile DS is arythoderma desquanmativum found by Leiner in 1908. Patients usually look sick anemia, vomiting, and generally common bacterial infection of the skin lesions.

In adults the disease is often found in the fourth to seventh decades of age and have berfariasi levels from mild to severe, including lesions that resemble the pattern psoriasi or pitiriasi and aretroderma.

Dandruff is usually considered a mild clinical form of the DS, characterized premises skin flakes off white and dry. Excessive Skuama on the scalp is often accompanied by itching and sometimes - sometimes get a mild inflammation. White dandruff is symptomatic of the scalp is often referred to as pityriasis sicca.

Patchy classic DS yangdisebut with seborrheic dermatitis, known as a chronic lesion rekunen. Predeleksinya in the area of ​​the scalp, forehead, folds, naso-labial, the inside of the eyebrows and glabella, external ear canal retroaurikuler folds and the area shaped 'V' on the chest and back. Called pityriasi steatoides when skin lesions appear yellow, accompanied by mild to severe erythema, infiltrate beradang mild, greasy, scaly thick, and berkrusta. Kebanyakn patients often complain of intense itching, especially on the scalp and ear holes.

DS clinical manifestation in patients with HIV are more extensive, severe and usually more difficult to treat. Patients often complain of itching. The lesions on the face look as macula ertematous that eterdistribusi like picture butterfly - butterfly, so menyarupai pasa lupus rash. In other parts of colored kunig skuama berkrusta above oily and erythematous skin plaques mild to very red, sometimes accompanied by non-scaring alopecia is more severe.

MANAGEMENT

In general, DS and dandruff treatment are to:

• reduce and clean up of scales and crusting

• inhibit fungal colonization

• prevent secondary infection

• mangurangi erythema and itching

DS Infantil

For the scalp, when found in a thick crust can be reduced by providing:

• Salicylic acid 3% in olive oil or in water-soluble base.

• Apply warm olive oil.

• hydrocortisone cream or lotion 1% within a few days.

• Topical Antifungal such as imidazole groups in the form of shampoos

• baby shampoo that is mild.

• Proper skin care for babies in the form of emollient, cream or a soft paste.

For areas of intertrigo should mengguanakan dry lotion such as zinc oil from 0.2 to 0.5%, or imidazole (eg ketoconazole 2% in shape of soft ayng pasta, cream, or lotion)

Topical antifungal therapy is proven to have positive effects on healing infantile DS because it can inhibit the growth of the fungus Malassezia furfur. In addition, the effect of anti-inflamasinya general cleaning results that are equivalent to hydrocortisone 1%.

 

Adult DS

• Topical

For DS lesions on the scalp is recommended for frequent shampooing with a shampoo that mengadung sulfide, 1 to 2.5%, 2% zinc pyrithione ketoconazol, benzoy peroxide, salicylic acid, coal tar or juniper tar. Use of tincture, alcohol solution, hair tonic or hair care type should be avoided because it can aggravate the inflammation.

Topical preparations are effective for the DS are:

1. Corticosteroids

Crusting or skuama same practice can be reduced with the provision of topical corticosteroids or salicylic acid in water-soluble base. Topical corticosteroids can be prescribed to reduce inflammation and lesions aritemasi DS. The use of preparations kortikosterois old numbers will give side effects such as skin or telangiektasia. Even the usage of the type kortikkosteroid stronger in a longer time could result in a rebound phenomenon, contact dermatitis or rosacea-like lesions.

For face and body areas should be avoided dosage form of oil or ointment, soap pengguanaan, ayng fluid containing alcohol or aftershave lotion. Low potency glucocorticoids such as hydrocortisone 1% may help overcome the DS.

2. Antifungal

Unlike corticosteroids, topical antifungal menyababkan rare side effects. Topical antifungal that memeberi benefit in most patients is imidazole group. Clinical studies reported satisfactory results between 63% - 90% 4 weeks after the administration of premises using preparations itraconazole, miconazole, fluconazole, econazole, bifonazole, climbazole, coclopirox, and xiclopiroxolamine. Among the imidazole class of antifungal preparations most widely used is ketoconazole. Ketoconazole 2% cream given to the lesions twice one heart and akn provide healing within 2-4 weeks. For the case of DS-resistant cream ketoconazole 2% can be supplied with hydrocortisone cream 1% at the time of going to bed. For the use of ketoconazole 2% shampoo is given 2-3 times a week with the way left on the scalp to 10 or 15 minutes just to rinse.

Giving oral antifungal indeed give a satisfactory result, but some researchers do not justify the provision of oral therapy in DS due to various reasons. The first reason because the DS is a chronic recurrent disease that requires repeated treatment in a long time. The second reason for the lesions DS only bounded strictly and only on a restricted area, means the DS is only on certain body areas and do not need to receive systemic treatment.

3. Metronidazole

The formulation used is in the form of base cream 1-2% or a commercial product such as gel / cream / lotion 0.7% or 1% cream used once or twice a day.

4. Lithium

Lithium succinate and lithium gluconate which has the effect of the antifungal.

5. Calcineurin inhibitors

Tacrolimus and pimecrolimus, both have the effect of anti - inflammatory and has no significant side effects when used long term.

6. Vitamin D3 analogue

Vitamin D3 analogues such as calcipotriol cream or lotion dosage or tacalcitol calcitiol ointment can be used for the treatment of DS, kaerna have the effect of anti-inflammatory and antifungal.

• Oral

1. Antifungal

Although there are opinions that are not approved systemic antifungal, should be considered indications for the DS case is very heavy or widespread as in people with HIV / AIDS. Can be given ketoconazole 200 -400 mg / day forever 2 weeks or itraconazole 200 mg / day for 7 days. Itraconazole has a high affinity on kerati networks, such as skin, hair, and nails, could settle for 2 -24 weeks and resevior therapeutic effect.Terbinafin included in the group that is broad-spectrum allylamine against dermatofir, molds, dimorphic fungi and yeast. Preparations are effective for the treatment of both topical and systemic DS with a dose of 250 mg / day. Topical dosage forms have anti-inflammatory effect, while the oral form is not.

2. Isotretinoin

Can diberiakn in low doses from 0.05 to 0.10 mg / kg setiapa day for several months, especially for the case of the DS is difficult to recover.

• phototherapy

Use of phototherapy narrow-band ultraviolet B is effective and safe pangobatan for severe cases of DS. Therapy with psoralen and ultraviolet A rays also give good results for the case eritrodemi for DS.

Need further explanation regarding the state of illness in patients and families. DS infantile prognosis good results, because the condition was not severe and can heal itself. In adults need to be notified when the disease is chronic and therapy cenderungbesifat aims to better control the disease rather than cure. Ketoconazole was found in 1976 and began to be used extensively in the 1980's. Ketocinazole has five ring structure containing two nitrogen atoms.

Ketoconazole including the imidazole group. Other azole class are miconazole, clotrimazole, econazole, and tioconazole. In addition to the antifungal ketoconazole also has a broad spectrum antikimiakrobial effects, which can eliminate bekteri gram positive such as Staphylococcus aureus, S. epidermidis and enterococcal stertococci.

The morphology and biochemistry, ketoconazole primary work in cell membranes of fungi. When cholesterol is a major component of mammalian cell membrane, ergosterol is the main component in the yeast cells. Ketoconazole works by blocking enzymes that disrupt cytochrom P450 ergosterol biosynthesis. Next will cause the accumulation 14alfa-methyl sterols like lanosterol which can not replace the function of ergosterol in the yeast cells. 14alfa-methyl sterols accumulation along with reduced ergosterol in fungal cell membrane will cause an unstable situation and disrupt membrane function, growth and viability of yeast cells.

Ketoconazole has 2 ways of working, fungistatik by inhibiting ergosterol biosynthesis, namely when administered with a concentration of 0.001 mg / L and fungicidal when administered with a concentration of 1 mg / L which can cause damage to cell membranes. In ketoconazol topical note absorbs percutaneous problems and systemic effects, particularly when used in a long time as a chronic kondis DS.

A study was conducted to determine the effects of ketoconazole 2% cream in the face of the DS patients with moderate to severe for 2 weeks to 3 months. Obtained results of percutaneous absorption is greater in the facial skin because these areas have a number of sebaceous glands, sweat glands pilosebasea and more. Although the results of percutaneous absorption of large but not found in plasma ketoconazole.

A study in the United States about the effect of ketoconazole shampoo 2% with a frequency of 40-10 times per week for 6 months in 40 patients with DS and dandruff does not increase toxicity. From 2 studies can be dismpulkan that both ketoconazole cream or shampoo is not absorbed by percutaneous. By means of autoradiographic to note that once diapplikasikan ketoconazole in the skin, then it will survive antifungal preparations in the outer layer of the epidermis, the fungus Malassezia grows. Both ketoconazole cream or shampoo form has no significant side effects, so that long-term use can diteleransi well.

Oral ketoconazole absorbed in the small intestine is brought rapidly within 1 hour through sweat and passive diffusion through blood vessels to the skin and settle in the stratum corneum for 10 - 12 days. Malalui a slower path to reach the stratum basalis and sabum after 3-4 weeks.

A single dose of 200 mg oral ketoconazole produces peak plasma concentrations 3 to 4.5 μmg / ml in 1-2 hours. This value will meninggkat when ketoconazole drunk at meals.Ketoconazole is lipophilic, so therefore biovailabilitas higher when taken at or before eating. Provision of ketoconazole together with lower semitidinakan absorbs, especially when keasamaan stomach is reduced by giving bicarbonate. Gastric acid is an important role pasa ketoconazole absorption, so that required gastric acid secretion enough to destroy the drug and the subsequent process absorbs.

Ketoconazole is metabolized in the liver and metabolites excreted in the gall bladder.The drug is widely distributed throughout the body and can be detected in urine, saliva, sebum, ekrin gland, wax, cerebrospinal fluid, joint fluid and various tissues.

SOME THINGS THAT NEED TO BE CONSIDERED IN GRANTING ketoconazole

Some things to consider in the provision of ketoconazole are:

• Liver - the liver when administered to patients with a history of abdominal discomfort, because ketoconazole can menyababkan nausea and vomiting.

• Giving oral ketoconazole is contraindicated in pregnant women, because the drug was included in the category "C" which proved teratogenic in animal experiments.

• There were increases of serum transaminases in 50-10% of patients who received ketoconazole therapy. We recommend that liver function tests performed on patients who will receive long-term ketoconazole treatment or administration of drugs together degna other drugs that are hepatotoxic.

• ketoconazole with conventional doses can sometimes inhibit the synthesis of testosterone and adrenal response. Increasing the dose to 800 mg - 1200 mg / day can decrease the concentration of testosterone. When given in the long term can lead to oligospermia or azoospermia, decreased libido, impotence, and alopecia genikomasti.

• In patients with tuberculosis, histoplasmosis, paracoccidioidomycosis or AIDS is advisable given the circumstances hipoadrenal daapt burdensome disease.

Ketoconazole ROLE IN TREATMENT AND DUNDRUFF seborrheic dermatitis: EFFECT OF ANTI-AINFLAMASI ketoconazole

Topical corticosteroids as anti-aflamasi quickly to reduce the severity of this disease, but will quickly lead to relapse soon after the drug was stopped.

In addition to the antifungal, ketoconazole also has anti-inflammatory effect. Both these functions have beneficial effects for the treatment of DS. As an antifungal no significant side effects although given repeatedly, and therefore anti-fungal anti-inflammatory potential premises can provide multiple benefits for the treatment of DS. Azole class that has anti-inflammatory effect is bifonazole, itrakonazole and ketoconazole, and econazole oxiconazole while having less effect. Experiments on animals guinea-pigs showed that ketoconazole has anti-inflammatory effect equivalent to weak corticosteroid (hydrocortisone 1%).

How it works ketoconazole as anti-inflammatory is premises inhibit thromboxane synthase, an enzyme in the synthetic route of thromboxane A2, which works as a potent pulmonary vasoconstrictor and aggregator of platelets and neutrophils. Antifungal also inhibit 5-lypoxygenase, an enzyme needed to produce and menyababkan leucotrienes leucotrine B4 production decline.

SUMMARY

Dandruff is always discussed with the DS because of its clinical gamabaran skuama fine form on the scalp and the relationship between the two sparked controversy since the first. Some researchers refer to the DS as severe dandruff while others refer to as exfoliation pasa dandruff scalp dandruff is whatever the cause or the clinical picture of Ringa DS because clinically the two diseases is indeed a unity, even a few other researchers as a condition called dandruff is not beradang DS. From the data that there is much to conclude that the DS and the dandruff is a disease that has different clinical manifestation of the same disease.

DS included in the group papulosquamos chronic dermatosis that can be easily identified. Can be found at the age of infants and adults, often associated degna increased production of sebum (seborrehea) on the scalp and sebaceous filokel pasda face and body.

In infants the disease is commonly called the DS infatil. The disease is predominant in the first 1 month, at most at 3 months pertamadan will disappear spontaneously at the age of 8 to 12 months even without treatment. DS infatil mainly on the scalp and oily areas skuama intertrigenosa premises and crusting. In adults the disease is often found in the fourth to seventh decade of age and have the levels vary from mild to severe, including lesions that resemble psoriasis or pitiriasi patterns and erythroderma.

DS prevalence in immunocompetent adults of 1-3% and is found more in men than in women, whereas dandruff about 5-10% of the population. The incidence of DS in patients imunokompromais (HIV / AIDS) was found higher at around 30-85%. DS is one of the manifestations of skin disease most commonly found in patients infected with HIV and AIDS.

Some factors suggested as contributor to the emergence of the DS, including impaired immune system conditions such as HIV / AIDS infection. Factor - factor causing the DS include seborrhea, microbial effect, kerentana individuals, certain drugs, neurotransmitter abnormalities, physical factors, nutritional deficiencies, emotional stress, and hormonal imbalances.

Many studies mendukungperana sebgai Malassezia fungus causes DS. Evident from several antifungal drugs both topical and systemic can provide relief to many sufferers.

Successful treatment of DS with some particular class of azole antifungal preparations such as ketoconazole can open new horizons DS treatment had previously only known keratolik and kortikostroid. Especially after investigation that ketoconazole has anti-inflammatory effect that can be used as the DS treatment of chronic and recurrent nature.

 

REFERENCES

1. Degree H, Jacobs PH, Rosenberg EW, Shuster S. ketoconazole in Seberrhosic Dermatitis and Dandruff A Review. Manchester: AIDS Press International Limited, 1989

2. Gupta AK, Kogan N. Seberrohoeic dermatitis: current treatment practiceas, Expert Opin om Pharmacop 2004; 5:1755-65

3. Gupta AK, Brata R, Bluhm R, Boekhout T, Dawson TL, Skin diseases associated with Malassezia spscies. J Am Acad Dermatol 2004; 51:785-98

4. Plewig G, JnasenT, Seberrheic dermatitis, in: Wolff K, Goldsmith LA, KAzt SI, Gilchrest BA, Paller AS, Leffel DJ, editors 7th ed. Fitzpatrick's dermatology in General Medicine. New York: Mc Graw Hill; 2008.p.219-24

5. Jawas FA, Agusni I. Pasda seborrheic dermatitis sufferers of HIV / AIDS. BIPKK 2006; 18:150-5

Edting By: EnongXp