ABSTRACT
PurposeTo investigate the recovery of photoreceptors following the treatment in Vogt-Koyanagi-Harada (VKH) disease.Patients and methodsThis was a retrospective study. We enrolled 28 patients with VKH (56 eyes). The clinical and optical coherence tomography (OCT) findings were recorded for 12 months after treatment. The patterns of photoreceptor recovery on OCT were defined: pattern F group=Foveal photoreceptor recovery visible first; pattern E group=Extrafoveal photoreceptor recovery visible first; and pattern S group=Simultaneous foveal and extrafoveal photoreceptor recovery.ResultsPhotoreceptor recovery varied in different parts of the fundus among patients. Among the 56 eyes, the ellipsoid zone (EZ) recovery of 10 eyes and the interdigitation zone (IZ) recovery of 17 eyes belonged to pattern F group. In most eyes (46 eyes for EZ and 26 eyes for IZ), the recovery of these structures were pattern S. Only in 10 eyes, the recovery of IZ was pattern E. The different patterns of recovery correlated with how promptly the patients had been treated and with the anatomical and visual outcomes at 12 months. Patients in pattern F group were characterized by delayed treatment, delayed recovery of EZ or IZ, and a less favourable prognosis at 12 months relative to other patients, while those in pattern E group had the most prompt treatment and recovery as well as a more favourable outcome at 12 months.ConclusionsIn VKH patients with delayed treatment, foveal photoreceptors tended to recover more rapidly than photoreceptors in other regions.
Subject(s)
Anti-Inflammatory Agents/therapeutic use , Photoreceptor Cells, Vertebrate/pathology , Prednisolone/therapeutic use , Uveomeningoencephalitic Syndrome/drug therapy , Uveomeningoencephalitic Syndrome/pathology , Adult , Aged , Female , Fluorescein Angiography , Fovea Centralis/pathology , Humans , Macula Lutea/pathology , Male , Middle Aged , Retinal Detachment/pathology , Retinal Pigment Epithelium/pathology , Retrospective Studies , Tomography, Optical CoherenceABSTRACT
The purpose of the present study was to investigate the potential neuroprotective effect of neuroserpin (NSP) on acute retinal ischemic/reperfusion-induced (IR) injury. An IR injury model was established by elevating intraocular pressure (IOP) for 60 minutes in wild type and tPA-deficient (tPA-/-) mice. Prior to IR injury, 1 µL of 20 µmol/L NSP or an equal volume of bovine serum albumin (BSA) was intravitreally administered. Retinal function was evaluated by electroretinograph (ERG) and the number of apoptotic neurons was determined via TUNEL labeling. Caspase-3, -8, -9,poly (ADP-ribose) polymerase (PARP)and their cleaved forms were subsequently analyzed. It was found that IR injury significantly damaged retinal function, inducing apoptosis in the retina, while NSP attenuated the loss of retinal function and significantly reduced the number of apoptotic neurons in both wild type and tPA-/- mice. The levels of cleaved caspase-3, cleaved PARP (the substrate of caspase-3) and caspase-9 (the modulator of the caspase-3), which had increased following IR injury, were significantly inhibited by NSP in both wild type and tPA-/- mice. NSP increased ischemic tolerance in the retina at least partially by inhibiting the intrinsic cell death signaling pathway of caspase-3. It was therefore concluded that the protective effect of neuroserpin maybe independent from its canonical interaction with a tissue-type plasminogen activator.
