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1 dict future development of radiation-induced retinal toxicity.
2 creased ERG response, which is indicative of retinal toxicity.
3      There is no intraocular inflammation or retinal toxicity.
4  choroidal and retinal NV, and did not cause retinal toxicity.
5 ight exposure exacerbates vigabatrin-induced retinal toxicity.
6 uroprotective agent against rotenone-induced retinal toxicity.
7  aminoglycosides is associated with cases of retinal toxicity.
8 l optic disc edema, and cyclosporine-related retinal toxicity.
9 (ONL) thinning in HCQ users without apparent retinal toxicity.
10  DR in in vivo studies due to cumate-induced retinal toxicity.
11 evelopment was terminated due to nonclinical retinal toxicity.
12 0-2 visual field signs of hydroxychloroquine retinal toxicity.
13 but their use has been limited mainly due to retinal toxicity.
14 rve as an early diagnostic indicator for HCQ retinal toxicity.
15 king HCQ, even in the absence of of manifest retinal toxicity.
16 take and ONL damage in eyes without manifest retinal toxicity.
17 retinal detachment, vitreous hemorrhage, and retinal toxicity.
18 ] vs 0), retinal injury (5 [0.2%] vs 0), and retinal toxicity (3 [0.1%] vs 0) were proportionately mo
19 quantitative SD-OCT biomarkers to detect HCQ retinal toxicity and predict progression to toxicity in
20 imal studies need to be performed to examine retinal toxicity and sustained delivery mechanisms.
21 those affected by hydroxychloroquine-induced retinal toxicity and those unaffected.
22                                              Retinal toxicity as determined by characteristic visual
23 tinoid byproducts of this pathway can induce retinal toxicity, as occurs in Stargardt disease type 1
24  necroses were observed, suggesting isolated retinal toxicity at this concentration of moxifloxacin.
25 g exposure of at least 6 months, 2 developed retinal toxicity (at 11 and 17 months of exposure).
26 stages and could be a novel method to detect retinal toxicity before irreversible damage is manifest.
27  based largely on short-term users or severe retinal toxicity (bull's eye maculopathy).
28 gression, preserving vision while minimizing retinal toxicity complications.
29                                Dose- related retinal toxicity could occur in pre-treated eyes even wh
30 are no prior reports of erlotinib-associated retinal toxicity despite over a decade of use in oncolog
31 in angiography, and there was no evidence of retinal toxicity due to BDNF treatment.
32 omplete release within 2 weeks and localized retinal toxicity due to high daunorubicin concentration.
33                 Both drugs however can cause retinal toxicity eventually leading to irreversible macu
34 etime imaging ophthalmoscopy seems to detect retinal toxicity from HCQ at very early stages and could
35  The highest AAV-RP2 dose group demonstrated retinal toxicity, highlighting the importance of careful
36 on, it is well-established that it can cause retinal toxicity i.e. HCQ maculopathy.
37 ry has previously documented formate-induced retinal toxicity in a rodent model of methanol intoxicat
38                The incidence of definite HCQ retinal toxicity in patients treated with HCQ at <6.5 mg
39              Two patients experienced severe retinal toxicity, including 1 with severe vision loss.
40           Additionally, a high prevalence of retinal toxicities is becoming more and more an issue of
41 wever, IVT cumate injections led to apparent retinal toxicity, manifesting as retinal layer abnormali
42 ile effective in rheumatology, pose risks of retinal toxicity, necessitating regular screening to pre
43 logic examination were used to determine the retinal toxicity of dasatinib.
44                                              Retinal toxicity of ISIS 2922 and ISIS 4015, phosphoroth
45 d to suggest immediate or delayed widespread retinal toxicity of IVTK.
46 nflammatory response, and 1 microM caused no retinal toxicity or inflammation.
47  modulator and a drug previously linked with retinal toxicity, paradoxically provided potent neuropro
48 us autoimmune diseases but carries a risk of retinal toxicity, particularly with prolonged use.
49 ption of 4.0 to 5.0 mg/kg, the prevalence of retinal toxicity remained less than 2% within the first
50                                  In rabbits, retinal toxicity resulted when intravitreal injections o
51                           Guidelines for HCQ retinal toxicity screening include factors like body wei
52 n administered after IAC; however, melphalan retinal toxicity still poses a challenge.
53 topathological evaluation showed no signs of retinal toxicity to anecortave acetate delivery alone or
54 ide (AIP) was used in a rat in vivo model of retinal toxicity to compare the effects of on NMDA-induc
55 , we demonstrated a substantial reduction in retinal toxicity upon injection in bovine vitreoretinal
56 hange chromatography and found that in vitro retinal toxicity was also associated with phosphatidylch
57                                    Manganese retinal toxicity was assessed by comparing full-field, w
58                               In this study, retinal toxicity was determined after intravitreal injec
59                                              Retinal toxicity was observed at high vector doses, high
60 idence of corneal, lenticular, choroidal, or retinal toxicity was observed by histopathologic evaluat
61                     No toxic AC reactions or retinal toxicity was observed in the study group confirm
62 reous seeding at higher doses, but permanent retinal toxicity was observed.
63  and previously linked to a low incidence of retinal toxicity, was unexpectedly found to exert marked
64              Clinical features indicative of retinal toxicity were scored for the 2 groups and were d
65 cal posterior subcapsular cataract and local retinal toxicity with high doses.
66 ychloroquine can initiate the development of retinal toxicity within 1-2 years.