THE PRESSURE STILL ON!

CURRENT & EMERGING

THERAPIES FOR MANAGING
GLAUCOMA
Pembimbing : dr. Novanita Satolom, Sp.M
Moderator : dr. Felly A. Toad, Sp.M
Penyaji : dr. Herdy Veristian
Penyebab
Utama
Kebutaan
Permanen Terapi
di Dunia &
Faktor resiko
baru
 Definisi : (POAG) sebagai “... neuropati optik progresif
kronis pada orang dewasa dengan karakteristik :
GLAUKOMA Atrofi saraf optik dan hilangnya sel-sel ganglion retina
dan akson. Kondisi ini dikaitkan dengan sudut bilik
mata depan terbuka dengan gonioskopi. ”2
(September 2015 Preferred Practice Patter updates, the American Academy of Ophthalmology)
FAKTOR
RISIKO
The American Academy of
Ophthalmology Glaucoma
Preferred Practice Pattern
guidelines recognize several
risk factors that have been
identified in carefully
conducted population-
based studies.
1 Umur 2 Ras
Afrika-Amerika & Latin resiko > Orang kulit Putih
31% POAG di Amerika
usia 70-79 th
3
Riwayat Keluarga
Prevalensi 1,1% keturunan (9.2 x terkena glaukoma) &
0,4% saudara kandung.
4 Ketebalan Kornea
Ketebalan sentral kornea <555 lebih berisiko terjadi
Glaukoma dibanding ≥588.
5 Tekanan Intra Okular (IOP)
6 Tekanan Perfusi Okular rendah (OPP)
7 Tekanan Cairan Serebro Spinal rendah (CSF-P)
Tekanan Cairan Serebro Spinal (CSF-P)

Studi Retrospektif &

Prospektif menunjukkan
secara nyata rendahnya CSF-P
pada penderita Glaukoma (
P< 0.001 ).8,9
Tekanan Perfusi Okular rendah (OPP)

1 Estimated number of people with POAG and
angle-closure glaucoma worldwide is
Insidensi
expected to increase to approximately 80
2 Glaukoma
million by 2020.1
& disease begins to be detectable by visual field testing.
Approximately 8.4 million patients with
Progesivitas
glaucoma have bilateral blindness, and this
number is expected to rise to 11.1 million
Penyakit
by 2020.1
The progression from asymptomatic disease to blindness is a
multistep process that takes years to manifest. Weinreb and
colleagues describe a “glaucoma continuum” that illustrates
the ocular deterioration that occurs throughout the course of
disease (Figure 1).
Years of apoptotic retinal ganglion cell death have already
taken place before any retinal damage can be detected.21
Factors that can cause retinal nerve damage and death include
increased IOP levels, inflammatory signals, ischemia, and
autoimmunity.
It is only after the retinal nerve fiber layer deteriorates that
Visual impairment from retinal nerve fiber damage is
irreversible, so although treatment is typically recommended
upon detectable damage,21 patients with elevated IOP, thin
central corneal thicknesses, and enlarged cup/disc ratios might
benefit from preventative treatment.23 Preventative
treatment with IOP-reducing medication has been shown to
reduce the risk of developing glaucoma, particularly in patients
with > 13% estimated 5-year risk of developing POAG.24
Recently, intake of nitrates from leafy green vegetables
(240 mg/d) has been shown to reduce the relative risk of
developing POAG with paracentral vision loss by 44%;
moreover, nitrate intake reduces the relative risk of developing
PATHOPHYSIOLOG
Y
OF GLAUCOMA
  Goal Terapi POAG ( ! TIO & menjaga sesuai target )
THERAPEUTIC  Mencegah kerusakan nervus optikus & RNFL
TARGETS FOR  Progresifitas glaukoma dapat diturunkan dengan menurunkan TIO
GLAUCOMA lebih dari sama dengan 25mmHg
 Direkomendasikan penurunan TIO dimulai dari 20-30% pada terapi
TREATMENT awal
 Terapi baru sedang dalam perkembangan
Kerja obat meningkatkan aliran keluar langsung pada Trabekula Meshwork

NO-donating agents (PGAs and CAIs)

&
Rho kinase/norepinephrine transporter inhibitors.
 Meningkatkan aliran keluar
Menurunkan resistensi TM uveosklera

LBN (Nutrisi Oxide) Prostaglandin

Netrasudil
Alpha-reseptor adrenergic
agonis

LBN (Prostaglandin analogue)

Terapi
Glaukoma
&
Area target
Menekan produksi Aqueous

Beta Booker
Menurunkan tekanan vena
Carbonic Anhydrase Inhibitors
episklera
Alpha-reseptor adrenergic
agonist
Netrasudil
Netrasudil
CURRENT TREATMENTS (INTRAOCULAR
PRESSURE–LOWERING MEDICATIONS)
71% of patients receiving bimatoprost SR did not require rescue
or retreatment

Conjunctival hyperemia with an onset later than 2 days after the

injection procedure occurred more often with topical
bimatoprost (17.3%) than with the SR implant (6.7%)

Alternative delivery methods such as this can help increase

the poor adherence to POAG medication Bimatoprost

Bimatoprost Bimatoprost Bimatoprost

+ Konjungtiva
Timolol Forniks – 6 Bulan
TIO ! 3.2-6.4
Implant – 16 Tetes – 16 Mgg mmHg
Mgg TIO ! 8.4 mmHg
TIO ! 7.2, 7.4, 8.1, Konjungtiva
& 9.5mmHg Forniks – 6 Bulan
TIO ! 4.2-6.4
mmHg
EMERGING DRUG DELIVERY METHODS
 Faktor Risiko baru ( OPP & CSF-P )

Regimen Terapi sedang Target Pengobatan – Kontrol Tekanan Intra Okular

dalam perkembangan :
-Mekanisme kerja obat
- Kerja obat pada Trabekular
meshwork dan tekanan vena episklera POAG – Penyakit Kompleks dan multifaktor
- Sediaan obat berupa implan dan cini-
cin konjungtiva lepas lambat