SPIO accumulates in aortic plaques of atherosclerotic rabbits, producing a characteristic MRI finding. As SPIO accumulates in plaques with increased endothelial permeability and a high macrophage content, two established features of plaque inflammation, it may have a potential for noninvasive assessment of inflammatory atherosclerotic plaques.

Careful and ongoing observation of IOP, especially in the first year after PK, is recommended for patients after penetrating keratoplasty and prompt treatment of IOP elevation when indicated. Early filtering surgery with a better outcome than other surgery procedures should be preferred if medical treatment is not sufficient. Despite anti-glaucoma therapy, good visual outcome can remain beyond expectations despite a clear graft. While there is a potential option for graft exchange, damage to the optic nerve from end-stage glaucoma leads immutably to visual loss.

Posner-Schlossman-Syndrome (PSS) is clinically characterized by acute, recurrent, mild, unilateral uveitis anterior accompanied by elevated intraocular pressure (IOP). Fuchs´ Uveitis (FU) is a chronic, low-grade-inflammatory disorder, involving anterior uvea and vitreous. The clinical findings show remarkable similarities as well as differences. In our study, we determine the composition of immune mediators in aqueous humor of patients with PSS and FU and evaluate if immune mediators play a crucial role in specific viral intraocular inflammation and IOP rises. Aqueous humor samples from 81 uveitis patients (= eyes) presenting with either PSS or FU were collected at one time point. Local intraocular antibody synthesis to rubella virus was confirmed in 65 patients, whereas 16 were tested positively for human cytomegalovirus. Thirteen patients with PSS and 10 patients with FU were treated with glaucoma medications. Additionally, 11 cataract patients acted as control group. Immune mediator concentrations were measured by Bio-Plex Pro assay. We observed in both PSS (IFN-γ: 174.9 pg/mL; TNF-α: 25.1 pg/mL) and FU (IFN-γ: 25.4 pg/mL; TNF-α: 27.2 pg/mL) groups a significantly increased level of T-helper 1 immune mediators compared to controls (IFN-γ, TNF-α: 0 pg/mL) [median]. Notably, PSS patients (IL-1RA: 73.4 pg/mL; IL-8: 199.4 pg/mL; IL-10: 33.4 pg/mL; IP-10: 126350 pg/mL) showed a stronger and more active ocular inflammatory response, than FU patients (IL-1RA: 4.3 pg/mL; IL-8: 72.4 pg/mL; IL-10: 1.6 pg/mL; IP-10: 57400 pg/mL). Furthermore, a negative correlation between mediators and IOP was seen in the PSS group, potentially caused by acetazolamide-treatment. Our findings show that immune mediators play a crucial role in specific viral intraocular inflammation and influence IOP levels. Remarkable similarities but also significant differences of immune mediator concentrations are apparent in PSS compared to FU. High concentrations of IL-1RA, IL-8, IL-10, and IP-10 correlate with active inflammation in PSS, while FU may trigger chronic inflammation. Our data also substantiated a very similar composition of cytokines in those patients from the PSS group suffering from ocular hypertension and thus offers a potential explanation model for a negative correlation between mediators and IOP.

IVB leads to faster regression of active ROP in infants with posterior ROP compared with laser photocoagulation. Spherical equivalent after 12 months was comparable in those treated with IVB and laser photocoagulation, but it was significantly lower in posterior ROP than in peripheral zone II.

The animal model showed that direct MR imaging of the thrombus improved 24 hours after USPIO administration with a T1-weighted sequence. No improvement was seen with the T2*-weighted sequence.

The repeated longer-term administration of DEX inserts in noninfectious uveitis patients, either alone or in combination with other therapies, led to improved CRT, BCVA, and VH. Underlying diseases and concomitant systemic therapy seem to have an impact on overall treatment benefit. Ocular complications were reversible and were managed by local treatment, with exception of cataract formation.

Purpose: Intraocular pressure (IOP) elevation occurs regularly after Descemet membrane endothelial keratoplasty (DMEK). This study evaluated the long-term incidence of IOP elevation and post-DMEK glaucoma after DMEK. Methods: A total of 463 consecutive DMEKs in 352 patients performed between September 2011 and September 2014 at the Universitätsmedizin-Charité Berlin were reviewed. Data of the second treated eye of each patient and of re-DMEKs during the follow-up were excluded. The 12- and 36-month incidence of IOP elevation and post-DMEK glaucoma was analyzed using the Kaplan–Meier survival analysis. IOP elevation was defined as IOP ≥22 mm Hg or ≥10 mm Hg from preoperative baseline. COX regression analysis was used to evaluate the risk factors for IOP elevation and the development of a post-DMEK glaucoma. Results: The 12-month incidence of IOP elevation was 15.9% [95 confidence interval (CI), 12.0%–19.8%] and that of post-DMEK glaucoma was 3.9% (95 CI, 1.7%–6.1%); the 36-month incidence was 18.8% (95 CI, 14.5%–23.1%) and that of post-DMEK glaucoma was 6.6% (95 CI, 3.7%–9.5%). The most frequent cause was steroid-induced IOP elevation with a 12-month incidence of 11.7% (95 CI, 8.2%–15.2%) and a 36-month incidence of 12.9% (95 CI, 9.2%–16.6%), respectively. The incidence of postoperative pupillary block IOP elevation was 7.5% (95 CI, 4.8%–10.2%). A preexisting glaucoma increased the risk of IOP elevation [P < 0.001, hazard ratio (HR) 3.331; 95% CI, 1.919–5.782] and the development of a post-DMEK glaucoma (P < 0.001, HR 6.633; 95% CI, 2.556–17.215). The preoperative diagnosis also influenced the risk of IOP elevation [Fuchs corneal dystrophy (FED) vs. bullous keratopathy; P = 0.012, HR 2.354; 95% CI, 1.203–4.608] and post-DMEK glaucoma (FED vs. graft failure; P = 0.01, HR 4.412; 95% CI, 1.419–13.723, FED vs. bullous keratopathy; P = 0.09, HR 2.679; 95% CI, 0.858–8.358). Conclusions: Incidence of IOP elevation is high in the first 12 months after DMEK, especially steroid-induced IOP elevation. Steroid-induced IOP elevation could be treated effectively by tapering down the steroid medication or changing the steroid drug. A preexisting glaucoma and the preoperative diagnosis increase the risk for an IOP elevation and a post-DMEK glaucoma.

OCTA adds new insights in a multimodal imaging approach of retinal vascular layer visualization in BSRC and may contribute to existing methods for diagnosing severity and potentially progression of the disease.