Diabetische Makulopathie und Retinopathie: Funktionelle und sozialmedizinische Bedeutung

Zusammenfassung: Hintergrund: Die diabetische Makulopathie ist in den entwickelten Ländern führende Ursache für eine Erblindung vor dem Erreichen des Rentenalters. Die weltweit zunehmende Zahl von Diabetikern lässt vermuten, dass die Bedeutung der diabetischen Retinopathie und Makulopathie als Ursache einer schweren Sehbehinderung eher noch zunimmt. Methode: Zu den Stichworten in der Kapitelüberschrift zu Epidemiologie, Bedeutung und Ursachen der Sehstörung bei diabetischer Makulopathie wurde eine Literatursuche durchgeführt, um Übersichtsartikel sowie kontrollierte Studien der letzten Jahre zusammenzustellen. Ziel war eine Übersicht über funktionelle und sozioökonomische Konsequenzen der diabetischen retinalen Mikroangiopathie und über neue therapeutische Strategien. Ergebnisse: Erste Veränderungen in Richtung einer diabetischen Mikroangiopathie sind bereits früh nach Auftreten der Hyperglykämie nachweisbar. Langfristig verursacht sie schwere Organschäden. Für deren Behandlung werden wesentlich mehr Ressourcen benötigt als für die Behandlung der Hyperglykämie. Die diabetischen Mikroangiopathie verursacht darüber hinaus einen bemerkenswerten sozialmedizinischen Schaden. Der Früherkennung der vermehrten Gefäßpermeabilität bei Diabetikern kommt ein erheblicher Stellenwert für die Steuerung der Therapie zu. Für ein Hinauszögern der mikrovaskulären Komplikationen steht immer noch die Kontrolle der metabolischen Risikofaktoren Hyperglykämie und Hyperlipidämie sowie der Hypertonie im Vordergrund. Schlussfolgerungen: Moderne therapeutische Möglichkeiten erlauben heute eine medikamentöse Frühintervention mit dem Ziel, das Auftreten irreversibler mikrovaskulärer Schäden, namentlich der diabetischen Retinopathie und Makulopathie, hinauszuzögern. Das ophthalmologische Screening darf nicht mehr bei der Erkennung von Spätschäden diabetischer mikrovaskulärer Komplikationen am Auge beginnen. Eine enge interdisziplinäre Zusammenarbeit mit früher Implementation der neueren Therapieansätze bilden dabei die Grundlage für den therapeutischen Erfolg, bevor sich eine Sehbeeinträchtigung entwickel

Varicella-Zoster-Virus und atypische nekrotisierende Retinopathien bei HIV- und AIDS-Patienten [Varicella zoster virus and atypical necrotizing retinopathies in HIV and AIDS patients]

BACKGROUND: Necrotizing retinopathies of suspected viral origin, but which do not meet the criteria for either CMV-retinitis or acute retinal necrosis syndrome, have been grouped together under the term atypical necrotizing retinopathies. Nothing is known about their etiology. PATIENTS AND METHODS: Aqueous humor samples were drawn from two HIV-positive and eight patients with AIDS presenting with an atypical necrotizing retinopathy, additionally from six patients with acute retinal necrosis syndrome and 28 patients with active CMV-retinitis at the time of diagnosis as well as from thirty healthy controls at surgery. All samples underwent DNA extraction and amplification for viral DNA of HSV-1, VZV and CMV. RESULTS: VZV-DNA was detected in seven of nine aqueous humor samples derived from patients with atypical necrotizing retinopathies and in four of six samples from patients with acute retinal necrosis syndrome, but not in any one from the 28 patients with CMV retinitis. In the latter group, CMV DNA was detectable in 23 samples, in two of these additionally HSV-1 DNA. No viral DNA was amplified from any of the samples from healthy controls. CONCLUSIONS: Varicella zoster virus ist the leading cause of atypical necrotizing retinopathies. This should be considered in the antiviral chemotherapy. Moreover, we were able to establish the diagnosis using DNA amplification for the viruses of the herpes family irrespective of the etiology in 80% of necrotizing retinopathies

Brolucizumab in Neovascular Age-Related Macular Degeneration and Diabetic Macular Edema: Ophthalmology and Diabetology Treatment Aspects.

Anti-vascular endothelial growth factor (anti-VEGF) therapies have become the standard of care in the treatment of neovascular age-related macular degeneration (nAMD) and diabetic macular edema (DME), resulting in a remarkable decrease in disease-related vision loss. However, the need for regular injections places a significant burden on patients, caregivers, and the healthcare system and improvements in vision may not be maintained long term. As a result of its drying potency and duration of action, brolucizumab, an intravitreal anti-VEGF therapy approved for the treatment of nAMD and DME, could decrease injection frequency for patients and provide an efficacious treatment; however, balancing its benefits and risks can be challenging. There have been reports of intraocular inflammation (IOI) in patients treated with brolucizumab, which, if left untreated, may result in severe vision loss. Recent evidence, however, indicates that early recognition of IOI and prompt and aggressive systemic corticosteroid treatment in response to posterior segment involvement can lead to favorable outcomes in these relatively rare but severe cases. A series of consensus meetings were conducted in 2022 between Swiss medical retina experts and diabetologists, discussing the current data for brolucizumab and exploring various challenges to its use, including the associated risk of IOI. The outcome is a collation of practical insights and guidance for ophthalmologists on the use of brolucizumab in patients with nAMD and DME, including patient selection and assessment, treatment regimen and monitoring, and the recognition and management of adverse events

Intravitreal Dexamethasone as a Rescue for Anti-Vascular Endothelial Growth Factor Therapy in Neovascular Age-Related Macular Degeneration with Persistent Disease Activity and High Treatment Demand.

Purpose: To assess the impact of switching to, or adding, an intravitreal dexamethasone implant (Dex; Ozurdex <sup>®</sup> ) in anti-vascular endothelial growth factor (VEGF) therapy on disease stability and treatment intervals in eyes with neovascular age-related macular degeneration (nAMD) and persistent disease activity and high treatment demand. Methods: This retrospective noncomparative multicenter longitudinal case series included pseudophakic eyes with nAMD and persistent retinal fluid despite regular anti-VEGF therapy (ranibizumab or aflibercept) that received at least 1 intravitreal Dex implant. Visual acuity, central retinal thickness (CRT), and intraocular pressure were recorded before, and after, the addition of Dex to anti-VEGF therapy. Results: Sixteen eyes of 16 patients met the inclusion criteria of persistent fluid despite anti-VEGF therapy, under treatment intervals of ≤7 weeks in 14 instances. Patients were 80.9 ± 7.4 years old and had received 25.5 ± 17.4 anti-VEGF injections before Dex over a period of 36.4 ± 21.9 months before switching. The treatment interval increased from 5.5 ± 3.2 weeks between the last anti-VEGF and first Dex injection to 11.7 ± 7.3 weeks thereafter (P = 0.022). CRT remained stable (385.3 ± 152.1, 383.9 ± 129.7, and 458.3 ± 155.2 μm before switching as well as 12 and 24 months after switching; P = 0.78 and P = 0.36, respectively). An insignificant mean short-term early increase in visual acuity was not sustained over time. Conclusions: The addition of Dex resulted in a relevant and sustained increase in treatment intervals, whereas CRT and visual acuity remained stable in these difficult-to-treat eyes. It may be discussed whether inflammation or other steroid-responsive factors play a significant role in cases of nAMD with nonsatisfactory responses to anti-VEGF

Long-term Efficacy of TNF-alpha Inhibitors on Persistent Uveitic Macular Edema: A Swiss Multicenter Cohort Study.

To assess the efficacy of tumor necrosis factor-alpha inhibitors (TNFi) on uveitic macular edema (ME) unresponsive to conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs). This multicenter retrospective study included patients with uveitic ME persisting despite csDMARDs. The effect of an additional TNFi on central retinal thickness (CRT), best corrected visual acuity (BCVA) and corticosteroid need was evaluated. Thirty-five eyes (26 patients, mean age 42.9 ± 15.2 years) were included. CRT decreased from 425 ± 137 µm to 294 ± 66 µm (p < .001) and 280 ± 48 µm (p < .001) at 1 and 4 years of follow-up, respectively. BCVA improved from 0.28 ± 0.22 to 0.21 ± 0.48 (1 year, p = .013) and 0.08 ± 0.13 logMAR (4 years, p = .002). The proportion of patients requiring systemic corticosteroids decreased from 88.5% to 34.8% (1 year) and 15.4% (4 years). The addition of a TNFi resulted in an improvement of CRT and BCVA for up to 4 years in uveitic ME but rescue treatments were needed for some patients