reumatoid arthritisfdh2013.ppt
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8/9/2019 Reumatoid ArthritisFDH2013.ppt
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Artritis Reumatoid :
Tersebar luas, semua kelompok, ras, etnik di dunia
Penyakit inflamasi sistemik autoimun
Inflamasi yg kronik pd sendi
Suatu poli artritis progresif Sendi dan organ tubuh lain
Gejala penyakit kronis yang hilang timbul
kerusakan sendi deformitasdisabilitas
Etiologi pasti ????
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Autoimmune Diseases Autoimmune Diseases
Autoimmune diseases occur Autoimmune diseases occur
when the immune systemwhen the immune system
mistake self tissue for non-mistake self tissue for non-
self and mounths anself and mounths an
inappropriate attackinappropriate attack
Most autoimmune disordersMost autoimmune disorders
affect women moreaffect women more
frequentlyfrequently
RA-3: 1RA-3: 1
Autoimmune disorders may Autoimmune disorders mayresult from multipleresult from multiple
interactions of genes andinteractions of genes and
environmental factorsenvironmental factors
Autoimmune diseases can affectdifferent systems within the ody
!ervous system
Multiple sclerosis
"lood
Autoimmune
haemolyticanaemia
#kin
$soriasis
%ndocrine system
&ype 1 diaetes
Multiple organs
#ystemic lupus%rythematosus
"ones and 'oints
Arthritis
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Penyakit autoimun :Penyakit autoimun :
Sistem imun teraktivasiSistem imun teraktivasi
Menyerang 'aringan yg sehatMenyerang 'aringan yg sehat
(nflamasi dan kerusakan 'aringan ) organ(nflamasi dan kerusakan 'aringan ) organ
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$roses autoimun meliatkan :$roses autoimun meliatkan :
Sel limfosit T & sel Messenger molecules
Antiodi *R+,
Anti cyclyc citrullinated -peptic antiody *anti-$-a, er!a"ai sitokin
- (nterleukin-1β *(.-1β,
- &umor necrosis factor α *&!+- α,
- /emokin dan Reseptornya
#ignalling and co stimulatory molecules
#el mast
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#inoviosit#inoviosit
%ctopic lymphoid neogenesis%ctopic lymphoid neogenesis
Angiogenesis Angiogenesis
0.A-class ((0.A-class ((
!on-M0 risk genes!on-M0 risk genes
Arthritogenic antigen Arthritogenic antigen MacrofagMacrofag
#el dendrit#el dendrit
"lys *"-lymphocytes stimulator,"lys *"-lymphocytes stimulator,
A$R(. *a proliferating inducing legand, A$R(. *a proliferating inducing legand,
MerokokMerokok
enderender
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"anyak sekali faktor yg terliat"anyak sekali faktor yg terliat
Ada interaksi diantara faktor-faktor ts Ada interaksi diantara faktor-faktor ts
# !reak$o%n of self tolerane# !reak$o%n of self tolerane
# inflamasi y" merusak 'arin"an# inflamasi y" merusak 'arin"an
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%pidemiology%pidemiology
ommon disease: affects 21 of the populationommon disease: affects 21 of the population
$redominantly affects women$redominantly affects women
4nset of disease is usually etween 56 and 764nset of disease is usually etween 56 and 76
years of age8 ut can start at any ageyears of age8 ut can start at any age
4ccurs in all races and ethnic groups8 ut is rare in4ccurs in all races and ethnic groups8 ut is rare in
less developed and more rural parts of the worldless developed and more rural parts of the world
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Aetiology)pathogenesis Aetiology)pathogenesis
Rheumatoid arthritis *RA, is a chronic8 inflammatory8Rheumatoid arthritis *RA, is a chronic8 inflammatory8
systemic8 autoimmune diseasesystemic8 autoimmune disease
Mainly a polyarticular diseaseMainly a polyarticular disease
hronic inflammation in the synovial memrane ofhronic inflammation in the synovial memrane of
affected 'ointsaffected 'oints
&he specific cause of RA is unknown8 ut the immune&he specific cause of RA is unknown8 ut the immune
response is well characterisedresponse is well characterised
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PATOGENESIS ETIOLOGIK
Perubahan berupa :
Kerusakan mikrovaskuler, oedem jarinan sinovial, proli!erasi
linin sel pada sinovial"
Terdapa# sel leukosi# polimor!onuklear pada permukaan
sinovial"
Terjadi obli#erasi pada pembuluh darah ke$il akiba# adan%ain!lamasi dan #rombi %an #eroranisir"
&airan sinovial menandun ban%ak sel mononuklear leukosi#
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PATOLOGI SEL'LE(
Tampak adan%a :
Oedema sinovial
)iperplasia dan hiper#ropi sel linin sinovial %an dapa#
menebal oleh karena peninka#an sel A *re#i$uloendo#helial
like+ dan sel #ipe
Lisosom merusak
Obs#ruksi kapiler
in!il#rasi sel neu#ro!il pada dindin ar#eri
-aerah #rombosis
Perdarahan perivaskuler
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%tiopathogenese RA%tiopathogenese RA
/ominasi eragai faktor genetik/ominasi eragai faktor genetik
Respon imun atau inflamasi akiat infeksiRespon imun atau inflamasi akiat infeksi
Autoimunitas terhadap eragai komponen sendi8 Autoimunitas terhadap eragai komponen sendi8
seperti sinovium dan rawan sendi8 akiat auto antiodiseperti sinovium dan rawan sendi8 akiat auto antiodipatogen atau sel & yg mengalami auto reaksipatogen atau sel & yg mengalami auto reaksi
/elainan pengaturan produksi eragai sitokin yg/elainan pengaturan produksi eragai sitokin yg
erfungsi seagai sitokin proinflamasi atau dlmerfungsi seagai sitokin proinflamasi atau dlm
kerusakan sendikerusakan sendi
&ransformasi komponen seluler sinovium men'adi&ransformasi komponen seluler sinovium men'adi
autonom8 mementuk sel-sel yg dpt menginvasi 'aringanautonom8 mementuk sel-sel yg dpt menginvasi 'aringan
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#itokin $roinflamasi :#itokin $roinflamasi :
T()#T()#
* I+#,* I+#,
** M-#+8 M-#+ dan (.-9M-#+8 M-#+ dan (.-9
#itokin anti inflamasi :#itokin anti inflamasi :
(.-168 (.-118 &+-(.-168 (.-118 &+-ββ Antagonis reseptor (.-18 reseptor &!+ terlarut Antagonis reseptor (.-18 reseptor &!+ terlarut
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PATO-E(ESAPATO-E(ESA
Rantai .eristi%a imunolo"is
Antigen dalam memran sinovial diproses A$ *sinoviosit
A8 sel dendritik8 makrofag,
0.A DR
Ag dikenali8 diproses8 diikat oleh D5
kompleks trimolekular; Dengan antuan (.-1
menyeakan aktivasi D5
Ag kompleks trimolekular mengekspresikan (.-< pada
permukaan D5
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+agositosis kompleks imun disertai pementukan+agositosis kompleks imun disertai pementukandan pemeasan radikal eas8 leukotrin 8 $8dan pemeasan radikal eas8 leukotrin 8 $8
protease neutralprotease neutral erosi rawan sendi dan tulangerosi rawan sendi dan tulang
Ra$ikal !e!asRa$ikal !e!as depolimerasi hialuronatdepolimerasi hialuronat viskositas cairan sendiviskositas cairan sendi ;;
Ra$ikal !e!asRa$ikal !e!as 'uga merusak kolagen dan 'uga merusak kolagen danproteoglikan rawan sendiproteoglikan rawan sendi
Masuknya sel radang ke memran sinovialMasuknya sel radang ke memran sinovial .annus.annus *'ar; ranulasi yang terdiri dari firolas8*'ar; ranulasi yang terdiri dari firolas8mikrovaskular dan eragai 'enis sel radang,mikrovaskular dan eragai 'enis sel radang,
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P(OSES PENG('SAKAN
- Kerusakan ra.an / Kerusakan liamen#
/ Kerusakan #endon / Kerusakan #ulan
Penipisan pro#eolikan : / Tidak normal
/ Tidak menkila#
/ Tidak ken%al
/ Kuran kua#
Proli!erasi membran sinovial
Pannus : jarinan ranulasi vaskuler #erdiri dari
!ibroblas %an berproli!erasi
pembuluh darah ke$il
sel in!lamasi
→
menimbulkan kerusakan
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Primer penyakit synovial,
Sekunder perobahan pada sinovial, fluid,cartilage, paraarticuler, tendon dan komponen
vascular.
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$athogenesis$athogenesis
A$ = antigen presenting cell
Maini; Rheumatology
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$otential Roles of " ells in the$otential Roles of " ells in the
(mmunopathogenesis of RA(mmunopathogenesis of RA
(Dörner & Burmester, 2003; Edwards et al, 1999; Gause & Berek,
2001; Shaw et al, 2003; Takemura et al, 2001; Zhan & Br!des,19"#$
#ecretion of proinflammatory#ecretion of proinflammatory
cytokinescytokines
Antigen presentation Antigen presentation
&-cell activation&-cell activation
Autoantiody production Autoantiody production
and self-perpetuationand self-perpetuation
Cartilage lossCartilage loss
IL-6
B cell
T cell
Macrophage
Dendriticcell
IL-10TNF-α
TNF-αIL-10
RF
Fix complementFix complement
InamedInamed
s!no"ias!no"ia
Inammator!Inammator!
damagedamage
TNF-α
B cell
IL-6
B cell
#lasmacell
RFRF
RF
RF
IL-1
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ompromised integrity ofompromised integrity of
the 'oint structure leading to disailitythe 'oint structure leading to disaility
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linical patternlinical pattern
%!sk' (199"$; )l*e(199#$
$rogressive onset *from$rogressive onset *fromweeks to months,weeks to months,
$ain and stiffness$ain and stiffness*synovitis,*synovitis,
#wollen 'oints#wollen 'oints
#ymmetric articular pattern#ymmetric articular pattern
+lu-like symptoms+lu-like symptoms Morning stiffnessMorning stiffness
+atigue+atigue
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linical pattern *cont?d,linical pattern *cont?d,
At onset8 RA usually affects hands8 wrists At onset8 RA usually affects hands8 wrists
and feetand feet
4ften a chronic cyclical course4ften a chronic cyclical course
During flare-ups8 new 'oints are affectedDuring flare-ups8 new 'oints are affected
and e@isting lesions are worsenedand e@isting lesions are worsened
oints ecome deformed8 leading tooints ecome deformed8 leading toadditional disailityadditional disaility
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TANGAN
• en#uk jari spindle/ shape !usi!orm ok pembenkakan PIP
• S.an ne$k de!ormi#is * hipere0#ensi PIP !le0i -IP +
• ou#onniere de!ormi#as * 1le0i PIP e0#ensi -IP+
• Ibu jari :
/ hipere0#ensi sendi in#erphalan dan !le0si 2&P
→ da%a jepi# jempol menhilan
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.ateral deviation of the M$ 'oints.ateral deviation of the M$ 'oints
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Slide 9
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/ Sime#ris
Pen#in un#uk (A
edakan denan ar#hri#is %an lain
-IP #ak kena
→
mornin s#i!!ness dapa# dipakai sebaai ukuran bera#n%a
pen%aki#
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PE(GELANGAN TANGAN
*Sana# serin #erkena A"("+
3 o% s%novium
3 Pembenkakan ulnar
3 -orso!le0i perelanan #anan #eranu
3 Sindrome &arpal/#unnel * N"2edianus #er#ekan+
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SIK'
3 !leksi kon#rak#ur
3 Pembenkakan
3 -es#ruksi para/olekranon
3 -islokasi sendi
A)'
3 Sendi lenohumeralis
3 A$romio$lavi$ularis
3 Thora$os$apularis
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PANGG'LPANGG'L*jaran #erkena A"(+*jaran #erkena A"(+
3 Lankah abnormal
3 Gerak sendi #erba#as
3 (asa #ak enak pd lipa#an
paha
L'T'TL'T'T
*serin #erkena A"(+*serin #erkena A"(+
3 )%per#ro!i sinovium
3 E!usi sendi
3 A#ro!i o#o# 4uadri$ep
3 Terben#uk kis#a aker
*bila pe$ah keluhan mirip
#hromboplebi#is+
3 Ins#abili#as sendi
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KAKI -AN PE(GELANGAN KAKI
• Gerakan !leksi dan eks#ensi #erba#as
• Saki# pada daerah #umi# a#au bursa diba.ah
#endon A$hiles dan #elapak kaki bila berjalan
• )allu0 valus *deviasi la#eral ibu jari
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&E(5I&AL&E(5I&AL
3 N%eri dan kaku leher
3 Erosi proressi!
3 Sub lu0a#io A#lan#o a0ial"
6 $ompressi 2ed" Spinalis
ejala neurolois
6 perpu#aran dan penekanan ar#eri ver#ebralis
*dp# menimbulkan sinkope se.ak#u menundukan kepala+
3 N%eri lokal
3 Spasme o#o# erak memu#ar #erba#as
3 Saki# kepala daerah o$$ipu#
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%@tra-articular pattern%@tra-articular pattern
(n some cases8 RA has an e@tra-articular pattern(n some cases8 RA has an e@tra-articular pattern
*involvement of other organ systems,*involvement of other organ systems,
Bsually occurs in rheumatoid factor *R+,-positiveBsually occurs in rheumatoid factor *R+,-positivepatients with more severe articular diseasepatients with more severe articular disease
More common in menMore common in men
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5askuli#isKelainan Paru *Pleuri#is, Pneumoni#is+
Perikardi#is
Nodul (euma#ik : / bursa olekranon
/ eks#ernal lenan a#as
/ #endo A$hilles
/ #elina
Neuropa#i
Lesi kornea dan konjun$#iva
Skleri#is
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Pembesaran kelenjar e#ah benin
Pembesaran lim!a
)iperpimen#asi
'lkus di kuli#
Lim! adenopa#i
Anemia
Thrombosi#openia
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LAO(ATO(I'2LAO(ATO(I'2
3 S( menini
3 Anemia rinan
3 (heuma !a$#or :
(ose .aaler lebih spesi!i$ 7 la#e0 lebih sensi#i!"
3 1ak#or AP1 ama# spesi!ik
3 -arah ru#in, urine ru#in, !aal injal, !aal hepar
3 &airan sinovial berupa e0uda#
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Dia"nosisDia"nosis
linical patternlinical pattern
"iology"iology
(magery(magery
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"iology"iology %levation of common non-specific serum markers of%levation of common non-specific serum markers of
inflammation contriutes to the assessment of diseaseinflammation contriutes to the assessment of diseaseactivity levelactivity level
%rythrocyte sedimentation rate *%#R,%rythrocyte sedimentation rate *%#R,-reactive protein *R$,-reactive protein *R$,
Rheumatoid factors *R+,Rheumatoid factors *R+,Bsually appear in the first year of the diseaseBsually appear in the first year of the disease 296 of RA patients are R+ *(gM the main isotype,296 of RA patients are R+ *(gM the main isotype, Associated with more rapidly evolving the more erosive Associated with more rapidly evolving the more erosive
disease and a higher incidence of e@tra-articulardisease and a higher incidence of e@tra-articularmanifestationsmanifestations
R+ can e detected in healthy patients during infections *5R+ can e detected in healthy patients during infections *5in aucasians,in aucasians,
R+ also associated with other chronic diseases *1,R+ also associated with other chronic diseases *1,
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(magery C conventional -ray(magery C conventional -ray
$erformed at disease onset and on a regular asis$erformed at disease onset and on a regular asis
Bsually hands and feetE other 'oints monitoredBsually hands and feetE other 'oints monitored
according to the disease patternaccording to the disease pattern "one erosions and 'oint space narrowing patterns"one erosions and 'oint space narrowing patterns
notednoted
Appro@imately 36 of patients already have ony Appro@imately 36 of patients already have ony
erosion at disease onset *>F6 at < years,erosion at disease onset *>F6 at < years,
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Bltrasounds and MR(Bltrasounds and MR(
#ynovitis detection is mainly assessed#ynovitis detection is mainly assessed
clinicallyclinically
(n difficult cases8 ultrasound may e useful(n difficult cases8 ultrasound may e useful
to detect synovitis and tenosynovitisto detect synovitis and tenosynovitis
MR( is not used in routine practiceMR( is not used in routine practice
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Artritis Reumatoid ( ACR, 1987 ) :1. Kaku pagi minimal 1 jam untuk jangka waktu minimal 6 minggu
2. Bengkak 3 sendi atau lebih untuk jangka waktu minimal 6 minggu
3. Bengkak sendi pergelangan tangan,
metacapofalangeal atau proksimal interfalang selama 6 minggu atau lebih
4. Bengkak sendi yang simetrik
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5. Perubahan radilogik tangan yang tipikal untuk artritis reumatoid yang harusmeliputi erosi dan dekalsifikasi tulang
unequivocal.
6. Nodul reumatoid
7. Faktor reumatoid positif (dengan metode dimana orang normal positif kurang dari 5 %)
Diagnosa artritis reumatoid ditegakkan biladitemukan 4 kriteria atau lebih.
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-IAGNOSA AN-ING-IAGNOSA AN-ING
(heuma#i$ 1ever : / respons denan salis%la#e
/ $ardi#is, $horea, skin rash
/ ASTO menini
SLE : / u##er!l% rash
/ (enal disease
/ L"E posi#i!
Os#eoar#hrosis :: / #anda in!lamasi minimal
/ Pain sore
Gou#% Ar#hri#is: / a$u#e onse#$ / r%s#al ura#e
/ #ophi
P%oeni$ Ar#hri#is : demam, mi$r" oranism didapa#
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&herapeutic goals&herapeutic goals
$rimary goals in the treatment of RA$rimary goals in the treatment of RA$revention or control of structural damage to$revention or control of structural damage to
'oints 'oints
$revention or reversal of disaility$revention or reversal of disaility$ain relief $ain relief &o improve quality of life&o improve quality of life
&he ultimate goal is to achieve disease&he ultimate goal is to achieve diseaseremissionremission
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urrent treatment strategy in RAurrent treatment strategy in RA
The "oal is to ahieve lo% $isease ativity
or remission
Early an$ intensive treatment intervention
0ontrol effiay !y monitorin" $isease ativity
Ra.i$ s%ithin" %ith lak of im.rovement
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Treatment strate"y a..roahesTreatment strate"y a..roahes
Dramatically changed over the last decadeDramatically changed over the last decade
Moved towards anMoved towards an early .harmaolo"ialearly .harmaolo"ial
treatment interventiontreatment intervention
To in$ue remission
To slo% /.revent1 ra$iolo"ial
.ro"ression an$ .revent $isa!ility
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AR B(D%.(!%# (! RA &R%A&M%!&AR B(D%.(!%# (! RA &R%A&M%!&
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ESTA+ISHESTA+ISH
RA DIA-(OSISRA DIA-(OSIS EvaluateEvaluateH Disease ativity5e6tent of synovitisDisease ativity5e6tent of synovitisH Strutural $ama"eStrutural $ama"eH )untional5.syhosoial status)untional5.syhosoial status
Initiate TreatmentInitiate TreatmentH Patient e$uationPatient e$uationH Physial an$ ou.ational thera.y* et7Physial an$ ou.ational thera.y* et7
H (SAIDs(SAIDsH Possi!le loal or oral steroi$s /Possi!le loal or oral steroi$s /
≤
,4 m"7 Pre$nisone1,4 m"7 Pre$nisone1
Assess Disease AtivityAssess Disease Ativity
AR B(D%.(!%# (! RA &R%A&M%!& AR B(D%.(!%# (! RA &R%A&M%!&
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AR B(D%.(!%# (! RA &R%A&M%!&AR B(D%.(!%# (! RA &R%A&M%!&
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AR B(D%.(!%# (! RA &R%A&M%!& AR B(D%.(!%# (! RA &R%A&M%!&
Refratory Rheumatoi$ ArthritisRefratory Rheumatoi$ Arthritis
0onsult Rheumatolo"ist0onsult Rheumatolo"istH Most effetive (SAIDMost effetive (SAIDH Most effetive DMARDMost effetive DMARDH Possi!le loal or oral steroi$sPossi!le loal or oral steroi$sH Reha!ilitationReha!ilitation
$ersistent
Active
Disease
Monitor Disease AtivityMonitor Disease Ativity
Perio$iallyPerio$ially
Mechanical oint #ymptoms
Remission or #atisfactory ontrol
Reactivation of Disease
Sur"ial InterventionSur"ial Intervention
Mechanical oint #ymptoms
Revise Treatment PlanRevise Treatment PlanH 0onsult Rheumatolo"ist0onsult Rheumatolo"istH 0han"e (SAIDs0han"e (SAIDsH 0han"e5a$$ DMARDs0han"e5a$$ DMARDsH +oal or oral steroi$s+oal or oral steroi$sH Reha!ilitationReha!ilitation
EU+AR D fi iti f I t i RAEU+AR D fi iti f I t i RA
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EU+AR Definition of Im.rovement in RAEU+AR Definition of Im.rovement in RA %B.AR response criteria are ased on DA#<9%B.AR response criteria are ased on DA#<9 DA# is divided into 3 categories:DA# is divided into 3 categories:
.ow disease activity *.ow disease activity *≤≤<;5,<;5,
Moderate disease activity *><;5 andModerate disease activity *><;5 and ≤≤3;I,3;I, 0igh disease activity *>3;I,0igh disease activity *>3;I,
(mprovement in the DA# is compared with a patient?s aseline DA#(mprovement in the DA# is compared with a patient?s aseline DA# ood response is defined as a >1;< improvement in the DA# compared withood response is defined as a >1;< improvement in the DA# compared with
aseline and a DA# attained during follow-up ofaseline and a DA# attained during follow-up of ≤≤<;5<;5
*van estel 1JJF,
*(mprovement in DA# from aseline,
≤<;5
><;5 and ≤3;I
>3;I
*DA# attained
during follow-up,
>1;< ≤1;< and >6;F ≤6;F
ood response
Moderate response
!o response
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Tabel ;" eberapa jenis anale#ik dan NSAI- %an umum diunakan
dalam #erapi pen%aki# reuma#ik
(ama -enerik -olon"an Pre.arat
$arasetamol $anadol 766 mg
Mefenamic acid $onstant <768 766 mg
&ramadol !ovalges 76 mg
MetamiGole !ovalgin 766 mg
!eoralgin 766 mgMethampyron
Melo@icam
!imesulide
Melo@in tas I87 mg8 17 mg
!ico@ tas 166 mg
Morphin sulfate M#& continus 168178368F68166 mg
%todolac lonene 1668 366 mg+enufen yufe 366 mg
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(ama -enerik -olon"an Pre.arat
!a;Diclofenac
(ndomethasin
Diflunisal
&iaprofenic acid (uprofen
/etoprofen
!apro@en
$irprofen
arprofen
eleco@i
Acetic Acid
Acetic Acid
aronic Acid
$ropionic Acid$ropionic Acid
$ropionic Acid
$ropionic Acid
$ropionic Acid
$ropionic Acid
Koltaren tas <78768#RI7 mg
(ndocid caps <7 mg
Diflonid tas <768766 mg
#urgam tas <66 mgMotrin tas <668566 mg
$rofenid %768 %1668 <66 mg L supp
!a@en tas <768766 mg
Rengasil tas <66 mg
(madil tas 176 mg
o@ < inhiitor elere@ 1768 366 mg
$iro@icam&eno@icam
4@icam4@icam
+eldene caps 168<6 mg
&ilcotil tas <6 mg
O A O A
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• ekerja lamba# menunu kadar di darah $ukup
Khasia# baru mulai =/;< bulan
• Side e!!e$# dan #oksisi#as #ini
• -iharapkan dapa# menhen#ikan proresi!i#as7
menjadi remisi"
6 des#ruksi sendi pada masa dini *B (A erosi < #hn per#ama"
6 )asil penoba#an %an buruk munkin karena #erlamba#
memulai -2A(-
OAT/OAT (E2ITI1OAT/OAT (E2ITI1
-2A-(S-2A-(S
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• -ianosa pas#i : -2A(- seera diberi
• Tersanka (A, respons NSAI- minimal → mulai -2A(-
• Se#elah pakai =/9 bulan #ak memuaskan
→ Gan#i -2A(- lain
→ Kombinasi denan %an lain
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/lasifikasi oat-oat anti rematik *%dmon et al, :
1; #ymptom-modifying anti-rheumatic drugs *#MARDs,
(ni akan memperaiki simptom dan ge'ala klinis
!#A(Ds
/ortikosteroid
4at-oat ker'a lamat : antimalaria8 #A#$8 garam emas8
D$8 oat sitotoksik
<; Disease controlling anti rheumatic therapy
4at ini meruah per'alanan penyakit RA8 dengan cara:
Memperaiki dan mempertahankan fungsi sehuungan
dengan erkurangnya peradangan sinovial
Mencegah dan mengurangi progresifitas kerusakan struktur
sendi
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DMARD yang laGim digunakan dalampengoatan AR
1; /lorokuin atau hidroksiklorokuinm1; /lorokuin atau hidroksiklorokuinm
<; #ulfasalaGine<; #ulfasalaGine
3; D-penisilamin3; D-penisilamin
5; aram emas5; aram emas
7; M&7; M&
F; #iklosporin -AF; #iklosporin -A
I; .eflunomideI; .eflunomide ene therapyene therapy "iological agent"iological agent
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0H+ORO8UI( PHOSPHAT : 94 # 44 M- 5 HARI
H;DRO<;0H+ORO8UI( : 944 # 244 M- 5 HARI
Tera.i AR se'ak tahun ,34#an
Di In$onesia .alin" !anyak
Men"an$un" 2#amino=uinoline7 >[email protected] ethyl* hi$roksiklorokuin ?@
hy$ro6yethyl