A case of intraocular inflammation after intravitreal brolucizumab injection monitored by laser flare-cell photometer.

Purpose: To report the efficacy of combination therapy using intravitreal injection of brolucizumab (IVbr) and sub-Tenon's injection of triamcinolone acetonide (STTA) and of monitoring with a laser flare-cell photometer (LFP) in a case of polypoidal choroidal vasculopathy (PCV) with intraocular inflammation (IOI). Observations: A 72-year-old Japanese woman with PCV had her treatment switched to IVbr due to being refractory to aflibercept. Two weeks after starting IVbr, her visual acuity (VA) declined to 0.40 from 0.10 logarithm of the minimum angle of resolution (logMAR) VA at baseline. In addition, the LFP flare increased to 51.2 photon count/ms (pc/ms) compared with the baseline of 16.1 pc/ms. We diagnosed her with the onset of IOI and immediately started treatment with sub-Tenon's injection of 20 mg triamcinolone acetonide (STTA). Two weeks after receiving STTA, her VA had recovered to 0.15 logMAR, and the LFP flare had decreased to 17.9 pc/ms with dry macula. Eight weeks after the first IVbr treatment, the logMAR VA had improved to -0.18 with achievement of dry macula and stabilization of the LFP flare at 12.2 pc/ms. We administered combined therapy using IVbr and STTA to our patient, and 12 weeks later, the logMAR VA remained at 0.00 with dry macula and 18.1 pc/ms for LFP flare. We continued combination therapy, and after 8 months, her logMAR VA remained at -0.08, and optical coherence tomography showed dry macula, while the LFP flare had stabilized at 16.6 pc/ms. Conclusions and Importance: Combination therapy of IVbr and STTA stabilized IOI and achieved dry macula. The LFP flare score clearly showed the degree of and changes in inflammation.

N-Methyl-N-Nitrosourea-Induced Photoreceptor Degeneration Is Inhibited by Nicotinamide via the Blockade of Upstream Events before the Phosphorylation of Signalling Proteins.

N-methyl-N-nitrosourea (MNU), a known carcinogen, is generally used in animal models to chemically induce photoreceptor degeneration. It has been reported that nicotinamide (NAM) exerts a protective effect on MNU-induced photoreceptor degeneration. We investigated the molecular mechanisms on MNU-induced photoreceptor degeneration. Intraperitoneal MNU injection (75 mg/kg) in rats induced selective photoreceptor degeneration in 7 days. NAM administration completely inhibited photoreceptor degeneration. Photoreceptor layer abnormality was observed within 6 hours after MNU injection, whereas it was restored in the NAM-treated retina, as detected by optical coherence tomography. One day following MNU administration, phosphorylation of the cell death-associated signalling proteins c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38) increased, while the apoptosis-related proteins, full-length poly(ADP-ribose) polymerase (PARP) and apoptosis-inducing factor (AIF), were depleted. These changes were not observed in the NAM-treated retinas. Cell survival signalling, such as extracellular signal-regulated kinase (ERK), Akt, and cAMP response element binding protein (CREB) phosphorylation, increased in the MNU- but not in the NAM-treated rat retinas. Increased phosphorylated ERK (p-ERK) levels were observed within 6 hours after MNU administration, suggestive of cell survival signalling activation. This did not occur in NAM-treated retinas. These results indicate that NAM regulates upstream cellular events prior to the activation of cell death-related signalling events, such as JNK and p38 phosphorylation.

Macular edema associated with intraocular ointment after cataract surgery.

PURPOSE: To report a case with macular edema associated with uveitis, a decreased corneal endothelial cell density, and vitreous opacity caused by migrated intraocular antibiotic ointment after uneventful cataract surgery. OBSERVATIONS: A 63-year-old man underwent uneventful sutureless superior clear corneal phacoemulsification and implantation of an intraocular lens in his right eye. Eleven months later, he complained of blurred vision when he gazed downward. Three months later, uveitis, vitreous opacity, and retinal hemorrhage were noted. Optical coherence tomography and fluorescein angiography demonstrated macular edema in the right eye. A slit-lamp examination revealed many tiny oily deposits on the iris surface. One month later, a globular oily droplet was detected at the 12 o'clock position of the iridocorneal angle. Because the corneal endothelial cell density appeared to be progressively decreased, the oily droplet was removed, and the anterior chamber was irrigated with a balanced salt solution using an irrigation-aspiration cannula. After surgery, the macular edema, vitreous opacity, and retinal hemorrhage disappeared. CONCLUSIONS AND IMPORTANCE: In this case, ofloxacin ointment had presumably migrated into the anterior chamber through a corneal incision after cataract surgery. The fact that the droplet of ointment was able to be detected more than one year after the cataract surgery suggests that dispersed tiny droplets can slowly coalesce into a globular droplet and wander between the anterior and posterior chambers, thereby causing uveitis, corneal endothelial cell damage, and macular edema. The removal of the intraocular ointment resolved these complications. This is the second report of intraocular ointment causing macular edema.