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Pytriasis Vesicolor

Yunifa Oktaviani Paputungan

Rachmi Maharani
Pembimbing : dr. Syahriani Syahrir, Sp.KK
DEFINITION
A mild, chronic infection of the skin caused
by Malassezia yeasts, and characterized by
discrete or confl uent, scaly, discoloured or
depigmented areas, mainly on the upper
trunk.
EPIDEMIOLOGY
The prevalence of tinea versicolor in the United
States is estimated to be 2%8% of the
population. The infection occurs more frequently in
regions with higher temperatures and relative
humidity. Tinea versicolor has a worldwide
prevalence of up to 50% in the hot and humid
environments and as low as 1.1% in colder
climates. Incidence of tinea versicolor is the same
in all races, but the eruption is often more
apparent in darkerskinned individuals due to
resulting alteration in skin pigmentation. No sex
predominance is apparent. Tinea versicolor is most
common among adolescents and young adults.
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TOTAL OF CULTURE POSITIVE CASES 88

M. furfur 53(60.23%)

M. globosa 25(28.41%)

M. restricta 6(6.82%)

M. sympodialis 4(4,55%)

Demonstrating the prevalence of four malassezia

species among 88 culture positive isolates. M.
furfur isolates are highest (60.23%) in number
followed by M.globosa (28.41%), M. restricta
(6.82%), M. Sympodialis (4,55%).
 Etiology and Pathogenesis.
Malassezia produce various metabolites that can cause
discoloration of the lesion. Hypopigmentation caused by: (1)
pitiriasitrin and pitirialakton which can absorb UV rays; (2)
azaleat acid, dekarboksilat acid which lowers the production of
melanocytes by inhibiting the tyrosinase enzyme; (3) that
induces apoptosis malassezin melanocytes; (4) malassezindole
A, inhibits the action of tyrosinase activity and interfere with
the synthesis of tyrosinase; (5) keto-malassezin as a tyrosinase
inhibitor to inhibit the reaction of DOPA (3,4-di
hidroksifenilalanin) melanocytes; (6) other metabolites such as
Indirubin, ICZ, pitiriarubin, and triptanthrin. Hyperpigmented
lesions may be related to variations Amasi inl response to
infection. Seemed to increase the size of melanosomes
(makromelanosom) and thickening of the stratum corneum.
Although in vitro proved that L-3,4-dihydroxyphenylalanine (L-
DOPA) on Malassezia able to induce the synthesis of melanin,
but in vivo has not been proven.
CLINICAL FINDINGS
The typical presentation of tinea versicolor is
scaly oval to round macules scattered over
characteristic areas of the body, including the
upper trunk, neck, and upper arms.
The macules often coalesce forming irregular
shaped patches of pigmentary alteration.
The color of patches varies from almost white to
pink to reddish brown or fawn colored.
Pruritus is usually mild or absent.
The diagnosis made on clinical grounds is
supported by Woods light (365 nm) examination
which may show yelloworange fluorescence.
Diagnostic
1. History
Patients usually complain of mild itching, which
is the reason for treatment, patients generally
only complain about their spots / macula white
(hypopigmentation) or brown
(hyperpigmentation) with itching that will arise
when sweating.
2. Physical examination
Skin disorders were found to body seen as
patches of colorful, shape is irregular to regular,
clear limits to diffuse. Are common lesions or
greater follikuler shape, or form numular
widespread form plaque. Sometimes found mixed
form, ie with numular follicular, follicular with a
a) KOH examination
The clinical appearance of tinea versicolor is
usually characteristic, and KOH examination is
confirmatory.
The finding on direct examination of
coarse mycelium, fragmented to short fi
laments 25 m wide and up to 25 m
long, together with spherical, thick-walled
yeasts 28 m in diameter confi rms the
presence of the condition.
However, it is the mycelium that is the
diagnostic feature, and sometimes this
predominates to the extent that there are
few yeast forms. The characteristic
appearance on microscopy has been
likened to spaghetti and meatballs or
bananas and grapes.
b) A Woods lamp examination
May show orangeyellowish fluorescence
of involved skin, suspected to be a due to
pteridine. In some cases, however, the
eruption may appear darker, rather than
more fluorescent, than unaffected skin under
theWoods light.
 Treatment
Although many treatments will temporarily clear the yeast
fungus, we do not have a permanent cure. Although the infection is
gone, the return to normal skin color can take several months. Tinea
Versicolor being caused by a normal skin inhabitant tends to recur.
When tinea versicolor recurs, repeat the treatment youve found to
succeed. We may prescribe a number of different treatments, since
more than one approach may be necessary. Any of the following
treatments will clear more than 80 percent of cases of tinea
versicolor.
 Topical Treatment
1. Selenium sulfide suspension, 2.5 %, applied to
the affected area before showering. Massage in
well and allow to remain on the skin for 10
minutes before rinsing off. Repeat once daily
for 7-10 days. Selenium sulfide may also be
used as a single treatment; apply it at bed
time, leave it on overnight, and shower it off
the next day. Repeat once a month until clear.
2. Ketoconazole shampoo 2%, apply to damp
skin, lather and rinse after 5 minutes. This
should be done once daily for 1-3 days in a
row.
3. Certain prescription antifungal creams, applied
 Sistemic Treatment
1. Ketoconzole - 400 mg taken once as a single
dose, or once weekly for 2 weeks (2 doses total).
This treatment is most effective if the medication
is taken with orange juice or a carbonated
beverage and followed by a sweat-inducing
workout one hour later. It is best if the medicated
sweat is not washed off for at least 4 hours.
2. Itraconazol 800-1000mg
Differential Diagnosis
Vitiligo Tinea Corporis Pytriasis Rosea
Prognosis
The prognosis is good in terms of healing.
when pengobataan done thoroughly, diligently
and consistently. Treatment should be
forwarded two weeks after the negative
fluorescence with Wood's lamp examination
and negative direct preparation.
 References
1. Ahmed AM, Madkan VK, Mendeza N, Tyning Sk, Lowy DR.
Viral disease: General consideration. Wolff K, Goldsmith
LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, eds.
Fitzpatrick dermatology in general medicine. 7 th ed. USA:
Mc graw hill; 2008.p.1911-3
2. Wolff K, Johnson RA, Fitzpatrick color atlas & synopsis of
clinical dermatology. 6th ed. USA: Mcg raw hill;2009.p.810
- 814
3. Sterling JC. Virus infection. Burns T, Breathnach S, Cox N,
Griffiths C, eds. Roks textbook of dermatology. 8 th ed.
USA: Wiley Blackwell; 2010.p.33.11-12, 33.42-3
4. Ben Tallon. Pityriasis versicolor pathology.
Dermatologist/Dermatopathologist, Tauranga, New
Zealand. 2016.
http://www.dermnetnz.org/topics/pityriasis-versicolor-pat
hology
 Thank You
For Your Attention