Our data suggest that diabetic eyes show retinal microcirculation impairment in the macula even before retinopathy develops. En face OCTA is a useful noninvasive screening tool for detecting early microcirculatory disturbance in patients with diabetes.

In this study, we injected nanospheres containing a fluorescein derivative into the vitreous cavity of pigmented rabbit eyes and evaluated their intraocular kinetics as drug carriers in vivo. Polystyrene nanospheres (2 µm, 200 nm and 50 nm in diameter) containing a fluorescein derivative were used in this study. A suspension of each particle was prepared by diluting with distilled water at a concentration of 10 µg/ml equivalent to sodium fluorescein. The suspension of nanospheres was injected once into the vitreous cavity of unilateral eyes of pigmented rabbits. A sodium fluorescein solution of the same concentration was injected once into the vitreous cavity of the other eye as the control. The intraocular kinetics of nanospheres was evaluated by measuring vitreous fluorescence using a scanning fluorophotometer. To investigate elimination pathways of nanospheres in detail, serial cross-sections of the eyes were examined with a fluorescence microscope. The fluorescence derived from nanospheres was observed in the vitreous cavity for over 1 month (2 µm: t_1/2 = 5.4 ± 0.8 days, 200 nm: t_1/2 = 8.6 ± 0.7 days, 50 nm: t_1/2 = 10.1 ± 1.8 days), whereas that in the control eyes completely disappeared within 3 days (t_1/2 = 7.8 ± 0.7 h). The elimination half-life from the vitreous cavity correlated well with the particle diameter (r = –0.997, p = 0.007). Histological studies using a fluorescence microscope revealed that nanospheres with a diameter of 2 µm were seen in the vitreous cavity and trabecular meshwork, while nanospheres with a diameter of smaller than 200 nm were also observed in the retina as well as these tissues. Our findings indicated that nanospheres may be beneficial as a drug carrier to the retina, vitreous and trabecular meshwork.

All of the associated ocular and systemic anomalies appeared to arise from the maldevelopment of the neural crest cells. Patients with Axenfeld-Rieger syndrome should therefore be examined for the presence of anomalies in the tissues of neural crest origin. Patients with hypoplasia of the iris should be checked for glaucoma.

Aims-To clarify the developmental mechanism and critical period for the uncommon complex of Peters' anomaly and persistent hyperplastic primary vitreous (PHPV). Methods-Two eyes with Peters' anomaly and PHPV were histologically examined by serial section. One eye was enucleated at age 7 months (case 1) and the other at age 4 months (case 2) owing to severe anterior staphyloma. Results-In both eyes, defects in the endothelium, Descemet's membrane, and posterior stroma were observed in the central cornea, and the degenerative lens adhered to the posterior surface of the defective corneal stroma. Also, in both eyes, the anterior chamber space was not formed and the undiVerentiated iris stroma adhered to the posterior surface of the peripheral cornea. Mesenchymal tissue containing melanocytes was observed behind the degenerative lens, and the pigment epithelium was absent at the lower nasal side of the ciliary body in case 1. In case 2, mesenchymal tissue containing scattered melanocytes in the vitreous cavity was seen on the posterior retina. Based on the histological findings, both cases were diagnosed as Peters' anomaly caused by the faulty separation of the lens vesicle, PHPV, maldevelopment of the iris and ciliary body, and goniodysgenesis. Conclusion-Migratory disorders of neural crest cells from 4 to 7 weeks of gestation may be responsible for various ocular anomalies including Peters' anomaly and PHPV, as observed in these cases.

Peters' anomaly accompanying corneolenticular adhesion and/or other ocular anomalies should be evaluated for the presence of systemic anomalies.