HIV/AIDS PADA KULIT

Oleh : dr. Richard hutapea

Spkk ( K)
Pendahuluan
Human Immunodeficiency Virus (HIV) adalah
virus penyebab Acquired immune deficiency
syndrome( AIDS), yang merupakan suatu
kumpulan gejala akibat menurunnya kekebalan
tubuh seseorang .

HIV menyerang motor dari kekebalan tubuh

yaitu Limfosit T reseptor CD4( Th), juga
menyerang monosit makrofag (memiliki ko-
reseptor CCR5) meningkatkan kerentanan
terhadap berbagai infeksi parasit dan infeksi
intraseluler lainnya yang pada kondisi normal
dilindungi oleh sistem kekebalan yang
 Sifat HIV dalam sel Limfosit Th ( CD4 ) memakai
sel tsb untuk memperbanyak diri dan mematikan
sel tersebut Sehingga sel Th ( CD4 ) semakin lama
semakin menurun ( normal 600-1200 ) akibat
replikasi virus terutama bila disertai (ko-faktor)
infeksi Virus Epstein Barr , virus Sitomegalo , virus
hepatitis B, virus herpes simplex , atau bakteri
seperti mikoplasma .

Kelainan sel B dapat terjadi akibat tidak adanya

pengaturan dan induksi sel T terhadap fungsi sel
B.
 Akibat penurunan sel tersebut mengakibatkan
jamur/bakteri/ parasit opurtunistik baik dalam
organ sistemik maupun dikulit akan bermanifestasi
menjadi penyakit, begitu juga bila terpapar dengan
agent penyakit dari lingkungan karena imunitas
sudah lumpuh.

Dengan semakin menurunnya kekebalan tubuh

bisa sekaligus timbul berbagai penyakit di kulit
atau bentuk penyakit yang tidak spesifik atau
penyakit resisten terhadap standar pengobatan .
 Diantara penyakit non neoplasma yang paling
sering dijumpai pada penderita HIV adalah
dermatitis seboroika, folikulitis
dan infeksi oportunistik .

Maka perlu untuk mengetahui kelainan kulit

secara dini pada
pasien HIV sehingga dapat mengetahui stage
klinis dan
penatalaksanaan sedini mungkin pasien HIV .
Epidemiology
38.6 million people
now living with the
diseases world wide.
As of january 2006,the
joint United Nations
Programme On HIV/
AIDS (NAIDS) and
WHOAIDS has killed
more than 25 million
people.
In 2005AIDS claimed
an estimated 2,4-3,3
million lives,of which
more than 570.000
were children.
JUMLAH PASIEN BARU YANG KONSELING DAN TESTING
DIKLINIK VCT PUSYANSUS RSUP. H. ADAM MALIK
2005 (JULI-DESEMBER) S/D 2010 (JANUARI-MEI)

TAHUN
2005 2010
NO INDIKATOR 2008 2009 (Jan- JLH
(Juli-
2006 2007 (Januari Mei)
Desem
-Maret)
ber)
Kunjungan ke
1 170 2577 751 436 1219 506 4908
VCT
4908
2 Pre Test 147 2541 746 436 1219 506

4908
3 Testing 53 2348 728 436 1219 506

436 4908
4 Ambil Hasil 51 2315 728 1219 506

4908
5 Post Test 51 2307 728 436 1219 506

6 HIV (+) 33 247 260 175 528 227 1572

Struktur Genomik HIV
 Patofisiologis infeksi HIV
Pada percobaan binatang, memperlihatkan sel-
sel langerhans
target utama dari pada virus, yang memfasilitasi
fusi virus ke
limfosit CD4 dan membawa ke jaringan kulit yang
lebih dalam.

Pada percobaan pada manusia,envelop virus,

glycoprotein 120 berikatan dengan CD4 ,supaya
dapat berikatan diperlukan ko-reseptor ,yaitu
reseptor permukaan kimokin ( CCR5).
 Patofisiologi

Setelah inokulasi virus cepat terjadi viremia dalam plasma

dan
menyebar secara diseminata.
Viremia terjadi 4-11 hari setelah virus masuk ke mukosa.
Replikasi virus menurun dengan adanya respon imun yang
diperantarai limfosit sitotoksik , merupakan spesial target
untuk membunuh virus. Ada beberapa Sitokin yang dilepas
dari limfosit sitotoksik dapat menurunkan jumlah virus.
Setelah kejadian ini maka akan masuk ke episode viral set
point.
Staging klinis menurut WHO pada pasien HIV

Ada 4 :
Stadium I: Asimtomatis
Stadium II: Simtomatis ringan
Stadium III: Simtomatis lanjut
Stadium IV: Simtomatis berat
Manisfestasi kutaneous pada infeksi HIV
Kriteria untuk mengenal infeksi HIV dari gambaran
klinis yang terjadi di mukokutaneous, pada anak
(usia < 15 tahun)
Kriteria untuk mengenal infeksi HIV dari gambaran
klinis yang terjadi di mukokutaneous, pada orang
dewasa dan remaja (usia > 15 tahun)
Klinikal staging ini digunakan :
untuk mengenal secara dini penderita HIV
untuk monitoring semakin buruknya imunitas
tubuh
berat ringannya penyakit
prognosis .
Diantara penyakit non neoplasma yang paling
sering dijumpai pada penderita HIV adalah
dermatitis seboroika,
folikulitis dan infeksi oportunistik .
 Lesi makula dan papula..
Makula eritem dan papula pada infeksi HIV akut
 Dermatitis seboroika( Sd)

Sd occur in 3% of the general

population and in up to 50% of
patient with HIV infection.
Sd increases in prevalence and
severity as the CD 4+T cell
count
decline.
More severe,persistent and
recalcitrant condition,
especially those with
advanced stage of HIV
disease.
. InHIV-infected pateint,Sd may
be
aggravated by concomitant
infection with pityrosporum
Patients treated with with anti-
retroviral therapy enjoyed
regression of the condition.
Topical ketokonazole cream ,
and oral ketokonazol,200mg
perday for 4 weeks,itraconazole
200mg,fluconazole .
 Bacterial infection
Folliculitis
The most prevalent
dermatologic disorder in
patient with HIV infection and
is seen in 20 % of patient.
It is more common in patien
with CD 4+ Tcell Count< 200
cell/l.
One form of folliculitis,
eosinophilic pustular
folliculitis, is a rare
dermatologic condition that is
seen with increased frequency
in patient with HIV infection .
Chronic pruritic, edematous
papule distributed over the
face,neck,and upper trunk.
Respon poorly to
antibacterials.
Respons to combination of
ultraviolet-B light
therapy,high-potency topical
steroid,and non sedating
antihistamines.
 Staphylococcal infection
can occur as abscesse
Staphylococus aureus is
the most
skin and systemic bacterial
pathogen in HIV-infected
patients.
Around 50%chronic
staphylococcus nasal
carriage.
 Staphylococcal infection can occur as
ulcers
 Numerous ecthymatous lesion due to
S.aureus
 Staphyloccocal infection can occur as
folliculitis.
 Staphylococcal infection can occur as
cellulitis.
 Bacillary angiomatosis(BA)
Characteristic exophytic angiomatousnodules of BA with and
Bartonella henselae and
without surrounding cellulitic.
B.quintana
As solitary or multiple vascular
lesion that clinically resemble
Kaposis sarcoma.
Involvement of the liver, spleen,
lymph nodes, bone, lung and
central nervous system.
BA HIV-infected patients
withCD4 > 100 cells/l.
Typical :dermal vascular
proliferastion, with plump
endothelial cell lining the vessels.
Erythromycin,500po qid 8
weeks.
Mycobacterial infections
Skin mycobacterial infection
in HIV patient are caused
primarily by Mycobacterium
tuberculosis.
Skin manifestation : papulo-
necrotic lesion, papulo
pustular lesion, nodules,
plaque, abscesses, ecthyma
and ulcer.
Scrofuloderma is also not
uncommon.

papulo-pustular lesions of
disseminated tuberculosis.
 Parasite
Norwegian scabies with hyperkeratotic psoriasiform
lesion
Increased incidence of atypical
manifestations of scabies,
including face and scalp
involvement, nodular lesion, and
hyperkeratotic ( crusted or
norwegian
,CD4<150cells/mm3)scabies.
The teatment of choice is topical
scabicide, such permethrin 5%
cream.
Single-dose oral
ivermectin,200g/kg.
 Auto imun diseases
Prurigo nodularis
Pruritus is common symptom in
patients with HIV infection and
can lead to prurigo nodularis.
More frequently seen in patients
with CD4+ cell counts below 50/l

numerous papule smaller than

those
typically seen in prurigo
nodularis.
 Psoriasis
Although they are not reported to be
increased in frequency,may be par-
ticularly severe when they occur in
patient with HIV infection.
Individual infected with HIV do have
increased prevalence of arthritis
associated with psoriasis.
can have unusual presentation
((inverse psoriasis )
 Inverse psoriasis of the feet. Inverse psoriasis of
the under
arm
 Pompholyx Eczema as
manifestation
of HIV infection

Viral infection
Varicella-zoster
Scattered facial verrucous lesion
of ACV-resistant VZV.
In HIV, Vzv can be the cause of
varicella, even in adults,and can
cause manifestation more severe.
Chronic verrucous or
vegetative nodules can
develop.
Herpes zoster in young, sexually
active adults is one of the common
presenting feature of HIV .
Multi-dermatomal herpes zoster
is often seen ( widespread
dissemination).
Post-herpetic neuralgia is more
common.
Dermatomal vesiculo-pustular
lesion, preceded by localized
itching, tenderness,or burning
painthe hallmark.
 Chronic vegetative nodules of
varicella lesions.
 Reactivation herpes zooster
(shingles)
10-20 % of patients with HIV
infection.
This reactivation syndrome of
varicella- zoster virus indicates a
modes decline in immune function
and may be the first indication of
clinical immunodeficiency .
AIDS was more likely to develop if
the outbreak of zoster was
associated with severe pain, e
xtensive skin involvement ,or
involvement of cranial or cervical
dermatomes.
 Herpes simplex virus
With advanced HIV diseases, HSV
can manifest itself as very painful,
persistent, progresive,clean-based
ulcers.
Sometimes HSV can also present
with atypical deep ulcers,
verrucous or vegetative erosion, or
folliculitis.
Extensive lesions are usually seen
when the CD4<50 cells/mm3
Disseminated HSV from
hematognous spread of the virus
rarely occurs.
Widespread HSV ,knows as eczema
herpeticum.
 Chronic, progressive, clean based ulcer of
HSV infection.
 Molluscum
contangiosum(MC)
Diffuse skin eruption due to MC may
be seen in patient with advanced
HIV infection.
Lesions tend to be more numerous
and
may be nodular ( so-called giant
molluscum if 1 cm or more ) and
disfiguring .
Treatment option :cryoterapy,
electro dessicasi, gentle
curettage,topical trtinoin,and
superficial chemical peeling.
Respon well to effective
antiretroviral therapy .
 CD4+ cell count < 100/l
 Giant Molluscum contangiosum.
CD4 cell < 50 cells/mm3
Human Papilloma virus (HPV)
To be infected with more HPV types.
HPV infection has also been shown to
facilitate HIV gene expression.
Frequently manifestations of HPV
infection :multiple common warts on
hands, facial warts, intra-oral warts, and
anogenital warts (conyloma acumoinata
)
IEN can develop more frequently in HIV.
Extensive diseases can often be seen
when the CD4 cell count< 500
cells/mm3.
Treatment:cryoterapy,CO2,laser
surgery, ED,podophylin,and 5%
imiquimod Cr .
HPV infection refractory to conventional
Topical treatment and recurrence can
usually be anticipated.
 Mosaic warts
 Drug eruption
Drug reaction producing full-body
erythema.CD 4+ cell counts< 50l.
Skin of patient with HIV
infection is often a target organ
for drug reaction.
Patient may have particularly
severe cutaneous reaction,
including erythoderma and
stevens-johnson syndrome.
 Toxic epidermal necrolysis due to trimethoprim
sulfamethoxazole.
 Photosensitive

Patient with HIV infection are

Photodermatitis of the face andvee
of the neck often quite photosensitive and
burn easily following exposure to
sunlight or as a side effect of
radiation therapy .
HIV infection itself is
photosensitizing, and patient
with low CD4 +cell count may
receiving photo sensitizing drugs
Such as
trimethoprim/sulfamethoxa
zole.
 Photodermatitis of the arm and hand.
 Perioral dermatitis

Sifilis
Generalized rashed can develop
in patiens with secondary
syphilis, including the macular
and papular variants.
Papular > maccular form.
Incidence of the Jarisch
Herxheimer reaction is 95 %
in patient with seropositive
primary syphilis or secondary .
Papular lesions are typically
on the face, flexural fold ,and
trunk.
Annular lesion > seen on the
faces of black ,can resembles
sarcoidosis
or tinea.
Fungal infection
Manifestation can be very
extensive and have unusual
morphologies.
In advanced HIVCentral
clearing
may be absent and patients
can have widespread
dermatophytosis.
Fungal nail infection most
commonly presents as distal
subungual onychomycosis.
Trichophyton rubrum is the
most frequently encountered
fungal pathogen.
Systemic antifungal :
itraconazole,
terbinafine,use of antifungal
shampoo.
Deep or systemic fungal infections
Penicilliosis, histoplasmosis, and
Crytococcosis are common systemic
fungal
Infection in HIV infected patient .
70% of patient with
penicillinosisskin lesion.
10-20 % of histoplasmosis and
crytococcosisskin lesion.
The most common skin lesion is the
molluscum-like lesion .
Treatment : Systemic antifungal agent
( amphotericin,itraconazole,fluconazol
e).

Crytococcus neoformans
 Generalized dermatophytosis with
onychomycosis.
 Kaposis sarcoma( KS)
KS on the face of a homosexually
active man with AIDS

The lesion typically violaceous

papule and nodule that can be
single, few, or multiple and widely
scattered.
No symtom, the lesions
progressively
extend into the subcutaneous and
lympahatic tissue, chronic
lymphedema may form .