[Unilateral Ranibizumab Treatment and Reduction of Macular Edema in the Contralateral Eye. Medication Effect or Natural Course?]. / Rückgang von Makulaödemen unter Ranibizumab-Therapie des Partnerauges - Kollateraleffekte oder natürlicher Verlauf?

BACKGROUND: During unilateral treatment with ranibizumab, a reduction in the retinal thickness in the non-treated eye is occasionally observed. This may be due to the natural progression of the condition. It could also be the consequence of systemic absorption of intravitreal injections, leading to effects in the contralateral eye. PATIENTS: We describe 40 patients with either exsudative age-related macular degeneration (AMD) or diabetic macular oedema (DME). During treatment with ranibizumab, a reduction in retinal thickness in the contralateral eye was observed in this group (observation group). Another 40 AMD or diabetes patients under treatment with ranibizumab were selected as control group. These patients showed retinal swelling in the contralateral eye, which remained stable or increased. RESULTS: In the observation group, 58 % of the patients had a DME and 42 % had an AMD; in the control group, 25 % of the patients had a DME and 75 % of the patients had an AMD (p = 0.003). Retinal thickness before injection was 519 ± 126 µm in the observation group and 432 ± 87 µm in the control group (p = 0.003). Retinal thickness in the contralateral eye was then 511 ± 162 µm in the observation group and 436 ± 149 µm in the control group (p = 0.036). The reduction in retinal thickness in the injected eye was 214 ± 144 µm in the observation group and 150 ± 89 µm in the control group (p = 0.06). CONCLUSION: In the group of patients that showed reduction in retinal thickness under ranibizumab in the contralateral eye, there were more diabetes patients than in the comparable control group. Even before injection, these patients showed higher retinal thickness in both eyes than did those in the control group. Further prospective studies would be required to confirm a possible causal connection between ranibizumab injection and reduction in DME in the contralateral eye.

[Intravitreal bevacizumab for recurring choroidal neovascularisation]. / Intravitreales Bevacizumab bei rezidivierender idiopathischer chorioidaler Neovaskularisation.

We administered bevacizumab intravitreally to treat a recurrence of CNV after confocal laser coagulation and photodynamic therapy in a 32-year-old female patient with a single functional eye. Before and after treatment the vision in the affected eye was stable at 1.0. Before administration of the VEGF antibody leakage was distinctly seen on fluorescein angiography, which did not appear on examination after the treatment. Despite the entailed measure of risk we decided in favour of intravitreal application because it seemed promising in view of earlier positive clinical experience with it in exsudative AMD and macular oedema following central retinal vein occlusion. Intravitreal bevacizumab is an alternative that should also be considered for the treatment of idiopathic CNV. Careful clinical studies will follow.

[Eye globe reconstruction after severe injury of the posterior segment]. / Bulbusrekonstruktion bei ausgedehnten Verletzungen des Hinterabschnittes.

Severe injuries of the posterior eye segment mostly occur during perforation or rupture of the globe. The first treatment includes primary surgical repair of the ocular wound and prophylactic scleral buckling in case of involvement of the posterior segment. Thereafter, a vitrectomy should be performed to remove vitreous hemorrhage and intraocular foreign bodies and to achieve a stable attachment of the retina. Therefore, temporary perfluorocarbon and permanent silicone oil tamponade are used. A predictor of poor visual outcome is the presence of retinal and choroidal injury. In our patients, the most important prognostic factor was the initial visual acuity after the injury. Vitrectomy can significantly reduce the incidence of enucleation. Currently, better visual outcome is achieved by advances in surgical techniques.

[Management of submacular hemorrhage by tissue plasminogen activator and SF(6) gas injection]. / Submakuläre Blutungen.Therapie mit Gewebe-Plasminogen-Aktivator und SF(6)-Gas.

UNLABELLED: The formation of platelet-fibrin clots causes degeneration of foveolar photoreceptors by subretinal hemorrhage. PATIENTS: Twenty-two patients with submacular hemorrhages were treated by intravitreal injection of 50 microg tpa and 0.5 ml SF(6) gas within 1 h. Biomicroscopy, fundus photography and fluorescein angiography were performed pre- and postoperatively. Further multifocal electroretinograms were recorded. RESULTS: The subfoveolar hemorrhages were dissoluted and displaced out of the macular region. The visual acuity increased in 18 cases and ranged from hand movement and 0.3 to values between 1/10 and 0.5. CONCLUSIONS: Toxic and hypoxic damage of foveolar photoreceptors by subretinal hemorrhage can be prevented by early and minimal invasive fibrinolytic therapy. After localization of choroidal neovascularizations, treatment by focal laser coagulation is possible in some cases.

The role of glutathione and protein thiols in CBrCl3-induced cytotoxicity in isolated rat hepatocytes.

The role of glutathione (GSH) and protein thiols in the pathobiochemical process of CBrCl3 cytotoxicity was investigated in isolated hepatocytes. Administration of 0.5, 1.0 and 1.5 mmol/l CBrCl3 affected cellular viability as assessed by trypan blue exclusion, release of lactate dehydrogenase and loss of intracellular potassium in a dose-dependent manner. Intracellular glutathione and the capacity to reduce 3-(4,5-dimethylthiazolyl-2-)-2,5-diphenyltetrazolium bromide (MTT, thiazolyl blue) decreased almost independently of the CBrCl3 concentration. Protein thiols were not markedly oxidized in the presence of CBrCl3. However, compromising cellular defence mechanisms by either inhibition of glutathione regeneration or depletion of glutathione enhanced the cytotoxicity of CBrCl3 and induced a loss of protein thiols in the late phase of cellular injury. Under these conditions the thiol-dependent Na+,K+ATPase revealed high sensitivity towards CBrCl3. Thus, glutathione proved to exert effective cytoprotection, and sulfhydryl groups of particular proteins were supposed to be an important target of radical attack.

Trichlorobromomethane-induced changes of purine nucleotides in hepatocytes.

The changes in nucleotide content during CBrCl3 treatment were investigated. In the first 5-10 minutes a significant ATP decrease was detected. The GTP loss leading to 57% of the initial level after 10 min surpasses the ATP loss which leads to 70% of the initial value after 10 min. The increase in uric acid is not only the result of CBrCl3 induced reaction, because of no significant changes in adenine and hypoxanthine values. The uric acid pool reflected different influx and efflux processes. These changes were compared with nucleotide degradation and accumulation of nucleotide degradation products during anoxia.