## 4 Discussion  
This study showed that subjects with DME who received an intravitreal dexamethasone injection did not show changes in CVI, TA, LA, and SA from baseline to the 2- and 4-month post-injection follow-ups. However, among the responsive patients, there was a notable decrease in CVI, with the most significant change occurring at 4 months post-injection. Considering that the objective of intravitreal dexamethasone injection is to decrease intra- and subretinal edema, and consequently reduce CMT, we considered this result to be the most significant in interpreting our data. Previous studies explored the impact of diabetes on the choroid, revealing that the CVI is altered in affected patients [17; 22; 23; 25]. This is reported to be due to microscopic and macroscopic changes caused by diabetes at cellular and vascular levels, such as vessel narrowing with focal dilation of vessels, vascular permeability increase, pro-inflammatory cytokine production, and polymorphonuclear stromal cells, with gradual alteration of choroidal tissue [26; 27]. These alterations impact the CVI, causing structural changes in both the choroidal vessel lumen and the choroidal stroma. [PERSON] et al. showed TA, SA, and LA increases, which were statistically significant, in diabetic patients with central-involving DME versus patients with DR in the absence of DME, while observing no difference in the CVI [25]. The authors suggested that these changes could be responsible for the onset of DME. They suggested that the increase in choroidal tissue volume, resulting from vasodilation, production of humoral factors, and accumulation of advanced glycation end products in the choroidal stroma, induced an increase in choroidal pressure [25; 28]. This increased pressure, in turn, could cause mechanical stress on the RPE cells, leading to altered RPE cell polarity and secretion of factors into the sensory retina [25]. The intravitreal injection of dexamethasone is known to be beneficial for DME by reducing intraretinal edema and resolving neuroepithelial detachment. This treatment is particularly effective in cases where inflammatory factors are prominent, as indicated by biomarkers such as hyper-reflective dots, subfoveal serous retinal detachment, and alterations in the external limiting membrane and ellipsoid zone integrity [29]. Corticosteroids have several effects that help reduce inflammation in the eye. They limit the recruitment of pro-inflammatory cells, suppress the production of inflammatory cytokines such as VEGF, inhibit the action of nitric oxide synthase, and prevent the release of histamine and prostaglandin. Additionally, they improve the function of the BRB by acting on the tight junctions of endothelial cells. These effects impact the vascular and tissue levels in both the retina and choroid [17]. \begin{table}
\begin{tabular}{l c c c} \hline \hline  & **Baseline** & **2 Months Post-IVD** & **4 Months Post-IVD** \\  & **(_n = 29_)** & **(_n = 29_)** & **(_n = 29_)** \\ \hline SRF \(n\) (\%) & 2 (3.3) & 0 (0) & 2 (3.3) \\ \hline DRIL \(n\) (\%) & 14 (23) & 14 (23) & 14 (23) \\ \hline Disruption of EZ (\(\mu\)m) & 360.58 \(\pm\) 241.45 & 359.13 \(\pm\) 232.51 & 358.92 \(\pm\) 231.57 \\ \hline HRF & 2.07 \(\pm\) 2.01 & 2.06 \(\pm\) 1.86 & 2.05 \(\pm\) 1.56 \\ \hline SRF: subretinal fluid; DRIL: disorganization of the retinal inner layers; EZ: ellipsoid zone; HRF: hyperreflective foci; IVD: intravitreal dexamethasone. & \\ \hline \hline \end{tabular}
\end{table} 
Table 4: Descriptive features of retinal morphological parameters at baseline, 2 months, and 4 months after intravitreal dexamethasone (IVD) injection. In the literature, there are limited studies in which the effect of an intravitreal dexamethasone injection on the CVI for DME in diabetic patients is explored. [PERSON] et al., in a study on DME patients managed with intravitreal dexamethasone, both naive and previously treated with anti-VEGF injections, found no differences in choroidal thickness and CVI at 10 weeks post-injection [30]. [PERSON] et al.