CURRICULUM VITAE

NAMA : dr. Rudy Hidayat, SpPD-KR, FINASIM

TTL : Malang, 3 Mei 1975
PEKERJAAN : Staf Divisi Reumatologi
Departemen Ilmu Penyakit Dalam FKUI/
RSUPN Ciptomangunkusumo Jakarta
PENDIDIKAN :
Pendidikan Dokter Umum 1992-1999 FKUB
Pendidikan Spesialis Penyakit Dalam 2004-2008 FKUI
Pendidikan Subspesialis Reumatologi 2009-2012 FKUI
ORGANISASI :
Ikatan Dokter Indonesia (IDI)
Perhimpunan Dokter Spesialis Penyakit Indonesia (PAPDI)
Perhimpunan Reumatologi Indonesia (IRA)
Perhimpunan Osteoporosis Indonesia (PEROSI)
Perhimpunan SLE Indonesia (PESLI)
Asia Pacific League of Associations for Rheumatology (APLAR)
 Rudy Hidayat
Division of Rheumatology
Departement of Internal Medicine
Faculty of Medicine, Universitas Indonesia
Cipto Mangunkusumo National Hospital
KASUS
Seorang laki-laki berusia 32 tahun datang
ke poliklinik dengan keluhan nyeri sendi
lutut kanan sejak dua hari yang lalu,
merah, bengkak, sulit berjalan.
Keluhan nyeri dirasakan mendadak saat
bangun tidur pagi hari. Tersentuh selimut
juga sakit
KASUS
Keluhan serupa pernah dialami dua kali di
sendi yang berbeda, setahun yang lalu
(cepat hilang dengan obat dalam 3-4 hari).
Pasien tidak pernah mendapatkan terapi
asam urat sebelumnya
Pemeriksaan fisik : IMT =29 kg/m2, artritis
regio genu dekstra
Kadar asam urat serum : 8,7 mg/dL
Analisa cairan sendi : kristal MSU (+)
 8 score
Sn 92%
Sp 89%
The ACR/EULAR gout classification criteria (2015)
DISCRIPTION CATEGORIES SCORE
CLINICAL
Pattern of joint/bursa involvement during Ankle or midfoot (without 1
symptomatic episode(s) ever involvement of 1ST MTP joint)
Involvement of the 1ST MTP 2
Characteristics :
- Erythema overlying affected joint One characteristic 1
- Cant bear touch or pressure Two characteristics 2
- Great difficulty with walking or inability to Three characteristics 3
use
Time course ( 2 ) :
- Time to maximal pain < 24 hours One typical episode 1
- Resolution of symptoms in 14 days Recurrent typical episodes 2
- Complete resolution
Clinical evidence of tophus Present 4
The ACR/EULAR gout classification criteria (2015)
DISCRIPTION CATEGORIES SCORE
LABORATORY
Serum urate : Ideally < 4 mg/dl -4
not receiving urate-lowering treatment and 6 8 mg/dl 2
during intercritical period 8 < 10 mg/dl 3
10 mg/dl 4
Synovial fluid analysis MSU negative -2
IMAGING
Imaging of urate deposition :
- US : double-contour sign Present 4
- DECT urate deposition
Imaging evidence of gout-related joint
damage : Present 4
- at least 1 erosion in conventional
radiography
Diagnosis : acute gouty arthritis
NEXT QUESTION :
1. Drug of choice for acute gout attack ?
Role of colchicine?

2. Drug for prophylactic of gout attack?

Role of colchicine?
ACUTE GOUT ATTACK
TREATMENT
EVIDENCE :
GOUT PROPHYLAXIS
TREATMENT
EVIDENCE :

The 3 trials enrolled a total of 4101 patients with gout

CONCLUSION OF STUDY
Flare prophylaxis (colchicine or naproxen) for
up to 6 months during the initiation of ULT
appeared to provide greater benet than are
prophylaxis for 8 weeks, with no increase in
AEs
EVIDENCE :

75 patients w/o prophylaxis, 103 patients with etoricoxib, and

129 patients with colchicine
weeks
 PHARMACOLOGY OF
COLCHICINE
It is a very old drug
first isolated in 1820 by the two French
chemists P.S. Pelletier and J. Caventon
 Pharmacokinetic-dynamic :
COLCHICINE
Readily bioavailable after oral administration
Almost completely absorbed via jejunum and ileum

Systemic circulation

Enterohepatic recirculation predominantly eliminated

by biliary and fecal excretion

Renal excretion (<<)

Reaching a peak plasma level in 30 min - 2 hours

Terkeltaub R. In : Horcberg MC, et al, Rheumatology. 2015.p.1575-80

 OVERVIEW OF COLCHICINE METABOLISM

Terkeltaub R. In : Horcberg MC, et al,

Rheumatology. 2015.p.1575-80
 Pharmacokinetic-dynamic :
COLCHICINE
Drug enrichment in bile with ABCB1 (P-
glycoprotein multidrug resistance transporter) and
cytochrome P450 3E4 (CYP3A4)
Increased risk of colchicine toxicity :
Hepatobiliary dysfunction
Aging (decreased ABCB1 expression)
Interaction with clarithromycin, erythromycin and
cyclosporine
Interaction with statins synergistically potentiate
myopathy (including rhabdomyolysis)

Terkeltaub R. In : Horcberg MC, et al, Rheumatology. 2015.p.1575-80

 MECHANISM OF ACTION
Colchicine binds tightly to unpolymerized
tubulin microtubule cytoskeleton
function
Effect :
cell proliferation
signal transduction
gene expression
chemotaxis
neutrophil secretion of granule contents
Terkeltaub R. In : Horcberg MC, et al, Rheumatology. 2015.p.1575-80
 MECHANISM OF ACTION
Acts on highly proliferating cells (e.g., bone
marrow, GI tract lining)
Also concentrates in neutrophils
related to low ABCB1 expression
low daily prophylactic doses of colchicine
suppresses E-selectin redistribution in the
endothelial cell plasma membrane suppressing
neutrophil adhesion

Terkeltaub R. In : Horcberg MC, et al, Rheumatology. 2015.p.1575-80

 SIDE EFFECT
Related with narrow margin of safety
Not recommended for intravenous use
Not recommended for high dose oral
colchicine
Weakly dialyzable
Severe cases of colchicine intoxication
supportive care

Terkeltaub R. In : Horcberg MC, et al, Rheumatology. 2015.p.1575-80

 SIDE EFFECT
GI toxicity (>>>) :
diarrhea (sometimes severe)
nausea
vomiting
Bone marrow depression
Cardiac toxicity arrhythmia
Hepatotoxic
Alopecia
Myopathy (proximal > distal muscles + elevated CK)
Neuropathy

Terkeltaub R. In : Horcberg MC, et al, Rheumatology. 2015.p.1575-80

 TAKE HOME MESSAGE
Colchicine is an old drug for GOUT
The efficacy of low dose oral colchicine has
been proved for acute gout attack treatment
and also for prophylactic treatment
Colchicine has a narrow drug safety window
Use in caution, especially in some high risk
population