CHANGES IN SUBFOVEAL CHOROIDAL THICKNESS AFTER INTRAVITREAL DEXAMETHASONE IMPLANT THERAPY FOR DIABETIC MACULAR EDEMA.

PURPOSE: To investigate changes in subfoveal choroidal thickness (SFCT) and their relationship with best-corrected visual acuity and optical coherence tomography parameters after intravitreal dexamethasone implant injection for diabetic macular edema. METHODS: Eighty-one eyes treated with dexamethasone implant injection for diabetic macular edema were evaluated for best-corrected visual acuity, central macular thickness, SFCT, and optical coherence tomography parameters at baseline and Weeks 7 and 14. RESULTS: The mean baseline SFCT significantly decreased at Weeks 7 (P < 0.001) and 14 (P < 0.001). At Week 7, each 1-µm reduction in central macular thickness and five Early Treatment Diabetic Retinopathy Study letters (-0.1 logarithm of the minimal angle of resolution) improvement were associated with SFCT reductions of 0.09 (P = 0.002) and 3.91 (P = 0.044) µm, respectively. At Week 14, each 1-µm reduction in central macular thickness was associated with a 0.14-µm reduction in SFCT (P < 0.001). Eyes with good functional and anatomical responses exhibited significantly greater SFCT reductions. Subretinal fluid resulted in greater SFCT changes (P = 0.039) and better best-corrected visual acuity (P = 0.033) at Week 7. A continuous ellipsoid zone/interdigitation zone layer was associated with a smaller mean SFCT at Week 7 (P = 0.002) and better best-corrected visual acuity at Weeks 7 and 14 (both, P < 0.001). CONCLUSION: Changes in SFCT after dexamethasone implant injection therapy for diabetic macular edema may predict anatomical and functional outcomes and correlate with optical coherence tomography features that are known as predictors of treatment response.

SUBFOVEAL CHOROIDAL THICKNESS AND VASCULAR DIAMETER IN ACTIVE AND RESOLVED CENTRAL SEROUS CHORIORETINOPATHY.

PURPOSE: To determine the subfoveal choroidal thickness and analyze Haller's layer, Sattler's layer, and large choroidal vessel diameter in eyes with active central serous chorioretinopathy (CSC) and after resolution of CSC. METHODS: Ocular and clinical features of 32 eyes with CSC were analyzed retrospectively from October 2014 to September 2015. Subfoveal choroidal thickness and thicknesses of Haller's layer and Sattler's layer were measured in the active and resolved states. The diameter of the subfoveal choroidal hyporeflective lumen (i.e., the large choroidal vessel in Haller's layer) was also measured. RESULTS: The mean subfoveal choroidal thickness, mean thickness of Haller's layer, and mean choroidal vessel diameter were significantly less after the resolution of CSC (P < 0.001). However, the thickness of Sattler's layer did not change after the resolution of CSC (P = 0.731). There were no significant differences among the different treatment modalities. CONCLUSION: After the resolution of CSC, the subfoveal choroidal thickness and thickness of Haller's layer declined, but the reduced diameter of subfoveal choroidal vessels accounted for only about half of the total thickness changes in the choroid. These results suggest that nonvascular smooth muscle cells might play a role in the thickening of the choroid during CSC and possibly in the pathogenesis and progression of CSC.

Association of statin use and hypertriglyceridemia with diabetic macular edema in patients with type 2 diabetes and diabetic retinopathy.

BACKGROUND: To investigate the effects of dyslipidemia and statin therapy on progression of diabetic retinopathy and diabetic macular edema in patients with type 2 diabetes. METHODS: The medical records of 110 patients with type 2 diabetes (70 statin users and 40 non-users) were retrospectively reviewed. The two outcome measures were progression of diabetic retinopathy by two or more steps on the early treatment diabetic retinopathy study scale and diabetic macular edema based on optical coherence tomography. Serum lipid profiles were analyzed from 6 months prior to diagnosis of diabetic macular edema. RESULTS: Diabetic retinopathy progressed in 23% of statin users and 18% of non-users (p = 0.506), but diabetic macular edema was present in 23% of statin users and 48% of non-users (p = 0.008). Statins reduced low-density lipoprotein cholesterol levels in patients with and without diabetic macular edema (p = 0.043 and p = 0.031, respectively). Among statin users, patients with diabetic macular edema had higher levels of triglycerides (p = 0.004) and lower levels of high-density lipoprotein cholesterol (p = 0.033) than those without diabetic macular edema. Logistic regression analysis showed that statin use significantly lowered the risk of diabetic macular edema [odds ratio (OR): 0.33, 95% confidence interval (CI) 0.12-0.91, p = 0.032]. Hypertriglyceridemia at 6 months prior to development of macular edema was significantly associated with central retinal thickness (OR: 1.52; 95% CI 1.14-2.02, p = 0.005). CONCLUSIONS: Lipid lowering therapy with statins protected against the development of diabetic macular edema and progression of diabetic retinopathy in patients with type 2 diabetes. Hypertriglyceridemia could be used as a surrogate marker for diabetic macular edema.

A survey of fish viruses isolated from wild marine fishes from the coastal waters of southern Korea.

A survey was conducted to investigate viral infection in 253 wild marine fishes harvested in the southern coastal area of Korea from 2010 to 2012. The fish that were captured by local anglers were randomly bought and sampled for virus examination. The samples were tested for presence of virus by virus isolation with FHM, FSP, and BF-2 cells and molecular methods (polymerase chain reaction and sequencing). Of the 253 fish sampled, 9 fish were infected with virus. Aquabirnaviruses (ABVs), Viral hemorrhagic septicemia virus (VHSV), and Red seabream iridovirus (RSIV) were detected in 7, 1, and 1 fish, respectively. Molecular phylogenies demonstrated the detected viruses (ABV, VHSV, and RSIV) were more closely related to viruses reported of the same type from Korea and Japan than from other countries, suggesting these viruses may be indigenous to Korean and Japanese coastal waters.