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Abstract Macular edema is a known side effect of taxane-based anticancer drugs. We retrospectively investigated data from 11 centers between January 2016 and December 2021. Among 14,260 patients, 30 (0.21%) developed macular edema; from these, the number of cases associated with nab-paclitaxel was 16 (0.43%), significantly higher than the number of cases associated with paclitaxel or docetaxel (P

Introduction: Post-vitrectomy cystoid macular edema (CME) can lead to failure of macular hole (MH) closure. We report 2 cases of failure of MH closure due to post-vitrectomy CME, which were successfully treated using sub-Tenon triamcinolone acetonide (STTA) injection. Case Presentations: Case 1 involved a 72-year-old male patient with a Gass Stage 3 MH in the right eye. He underwent pars plana vitrectomy (PPV), internal limiting membrane translocation, and sulfur hexafluoride (SF6) gas injection with cataract surgery in his right eye. The MH did not close postoperatively; further, CME developed at the edge of the MH. Accordingly, the patient underwent an STTA injection. Approximately 2 weeks after the STTA injection, the CME disappeared and the MH closed, which has remained closed 1 year after PPV. Case 2 involved a 78-year-old female patient with Gass Stage 3 MH in the left eye. The patient underwent the same surgical procedure as that performed in case 1. Further, she presented with failure of MH closure caused by CME; therefore, an STTA injection was performed. Approximately 6 weeks after STTA injection, the CME disappeared and the MH closed; further, there was maintained improvement of best-corrected visual acuity for 6 months. Conclusions: STTA injection could be considered before reoperation in cases involving failure of MH closure due to postoperative CME.

Introduction: Hypoxia-inducible factor-prolyl hydroxylase (HIF-PH) inhibitors, used in the treatment of renal anemia, hold the potential to increase the production of vascular endothelial growth factors. Therefore, HIF-PH inhibitors may exacerbate retinal hemorrhage in diseases such as diabetic retinopathy. Here, we present a case involving the administration of an HIF-PH inhibitor, resulting in the exacerbation of retinal hemorrhage in a patient with diabetic retinopathy. Case Presentation: A 32-year-old man with diabetes mellitus and renal anemia caused by diabetic nephropathy was referred to our department for ophthalmic examination, revealing diabetic retinopathy with scattered retinal hemorrhages, exudates, and diabetic maculopathy in both eyes. Darbepoetin alfa was initially administered and switched to the HIF-PH inhibitor roxadustat on day 74. By day 88, fresh retinal hemorrhage was observed in the right eye. On day 132, the retinal hemorrhage had further worsened, with new preretinal hemorrhage in both eyes. Roxadustat was discontinued, replaced with darbepoetin alfa, resulting in retinal hemorrhage improvement by day 181 (49 days post-roxadustat cessation). On day 201, fundus hemorrhage further improved, optical coherence tomography showed no macular edema or subretinal fluid, and the retina was thinning. Fluorescein angiography showed neovascular vessels, active fluorescein leakage, and extensive avascular areas in both eyes, prompting pan-retinal photocoagulation. Visual acuity remained stable throughout treatment. Conclusion: Patients with advanced diabetic retinopathy taking HIF-PH inhibitors should be aware of retinal hemorrhage exacerbations. If observed, the treatment plan, including discontinuation of the HIF-PH inhibitor or switching to another agent, should be discussed with a diabetologist, nephrologist, and ophthalmologist.

Abstract Anti-vascular endothelial growth factor (VEGF) therapy is the first-line treatment for diabetic macular edema (DME), but is less effective in some patients. We conducted a prospective study to determine whether laser combination therapy with anti-VEGF was more effective than Ranibizumab monotherapy in anti-VEGF-resistant DME patients. There was no significant difference in the improvement of the best-corrected visual acuity (BCVA) between the laser combination therapy and Ranibizumab monotherapy groups (3.2 letters and -7.5 letters, p = 0.165). BCVA did not significantly change between visits 1 and 7 (the laser combination group, 64.3 letters 70.3 letters, respectively, p = 0.537; the Ranibizumab monotherapy group, 72.3 letters and 64.8 letters, respectively, p = 0.554), with no significant improvements in central foveal retinal thickness (the laser combination therapy group, 9.3%: the Ranibizumab monotherapy groups, − 7.3%; p = 0.926). There was no significant difference in the number of Ranibizumab intravitreal therapy (IVT) sessions between the groups (laser combination therapy, 5.2; ranibizumab monotherapy, 6.0; p = 0.237). This study did not show that laser combination therapy was significantly more effective for anti-VEGF-resistant DME than anti-VEGF monotherapy alone. Therefore, for anti-VEGF-resistant DME, alternative therapeutic approaches beyond combined laser therapy may be considered.

AIM: To investigate the efficacy of ripasudil, a Rho kinase inhibitor, in reducing intraocular pressure (IOP) and medication scores of anti-glaucoma drugs in patients with ocular hypertension with inflammation and corticosteroid. METHODS: The study included 11 patients diagnosed with ocular hypertension with inflammation and corticosteroid, all of whom were prescribed ripasudil eye drops and followed up for at least 2y after the initiation of treatment. IOP was measured using a non-contact tonometer before enrollment and at each follow-up visit. The medication score of glaucoma eye drops was calculated for each patient. RESULTS: The mean IOP (26.4±2.9 mm Hg before treatment) significantly decreased after ripasudil therapy (13.7±3.3 mm Hg at 3mo) and remained stable in the low-teens during the 2-year follow-up period (P

Uveitis and scleritis are eye diseases associated with immunoglobulin A (IgA) nephropathy, but reports on retinal pigment epithelial detachment (PED) in relation to IgA nephropathy are scarce. We have experienced a case of PED associated with IgA nephropathy that was improved by pulse steroid treatment. A 68-year-old woman underwent examination for visual loss in the right eye. Her corrected visual acuity was 20/20 on both sides, and serous PED was observed in both eyes. One month later, the PED improved in both eyes but recurred 3 months later. Results of blood examination raised suspicion of IgA nephropathy, and she was referred to a nephrologist. Two weeks later, the PED in both eyes worsened, and a retinal pigment epithelium (RPE) tear appeared in the right eye. A sub-Tenon’s injection of triamcinolone acetonide was performed to address the PED, but it was not effective; thus, pulse steroid therapy was performed twice. The PED disappeared from both eyes, and the visual acuity in her left eye was maintained at 20/20, but it decreased to 20/200 in her right eye due to macular atrophy after the RPE tear. The PED had not recurred despite having no improvement in renal function. In conclusion, in IgA nephropathy, deposition of immune complexes on the RPE causes its inflammation, which may lead to PED. In cases of unexplained PED, the possibility of a systemic disease as the cause should be considered.

Abstract We evaluated the early effects of pars plana vitrectomy (PPV) on corneal biomechanics by comparing corneal hysteresis (CH) after cataract surgery (phacoemulsification and aspiration with intraocular lens implantation; PEA + IOL) alone and PPV combined with cataract surgery. This study included 20 eyes (18 patients), who underwent cataract surgery alone (PEA + IOL group), and 28 eyes (27 patients) who underwent PPV combined with cataract surgery (PPV triple group). The CH was 11.1 ± 1.1, 10.4 ± 1.1, and 11.0 ± 1.0 mmHg in the PEA + IOL group and 11.0 ± 1.4, 9.8 ± 1.4, and 10.6 ± 1.6 mmHg in the PPV triple group, preoperatively, at 2 weeks, and 3 months after surgery, respectively. The CH was not significantly different after surgery in the PEA + IOL group, but decreased significantly in the PPV triple group 2 weeks following surgery (p

Age-related macular degeneration (AMD) is one of the leading causes of blindness in the elderly, affecting the macula of the retina and resulting in vision loss. There are two types of AMD, wet and dry, both of which cause visual impairment. Wet AMD is called neovascular AMD (nAMD) and is characterized by the formation of choroidal neovascular vessels (CNVs) in the macula. nAMD can be treated with intravitreal injections of vascular endothelial growth factor (VEGF) inhibitors, which help improve vision. However, approximately half the patients do not achieve satisfactory results. Subretinal fibrosis often develops late in nAMD, leading to irreversible photoreceptor degeneration and contributing to visual loss. Currently, no treatment exists for subretinal fibrosis, and the molecular mechanisms of fibrous tissue formation following neovascular lesions remain unclear. In this review, we describe the clinical features and molecular mechanisms of macular fibrosis secondary to nAMD. Myofibroblasts play an essential role in the development of fibrosis. This review summarizes the latest findings on the clinical features and cellular and molecular mechanisms of the pathogenesis of subretinal fibrosis in nAMD and discusses the potential therapeutic strategies to control subretinal fibrosis in the future.

Diabetic macular edema (DME) is the main cause of visual loss in patients with diabetic retinopathy. DME has been treated using intravitreal anti-vascular endothelial growth factor (VEGF) drugs, steroids, laser photocoagulation, vitreoretinal surgery, and their combinations. These modalities are generally effective in preserving vision, but they sometimes produce only limited responses in patients with persistent or refractory DME. The levels of various inflammatory factors, including cytokines, chemokines, and extracellular matrices, as well as VEGF in the vitreous fluid, are increased in patients with DME. Excessive fibrinogen/fibrin levels in the vitreous fluid or fibrin deposition in the retina also contribute to DME pathogenesis. Tissue plasminogen activator (t-PA) promotes the degradation of fibrinogen or fibrin. Intravitreal t-PA injection is a commonly used treatment for subretinal hemorrhage secondary to age-related macular degeneration. Intravitreal t-PA injections have previously been used to restore vision by inducing posterior vitreous detachment in patients with DME. Herein, we describe the visual outcomes of intravitreal t-PA injection in a 78-year-old woman with treatment-resistant DME in her vitrectomized eye after several previous treatments. Before the injection, her best-corrected visual acuity (BCVA) was 0.7 logMAR and central foveal retinal thickness (CRT) was 735 μm. At 1 month after the injection, her BCVA was 0.8 logMAR and CRT was 558 μm, and 3 months later, her BCVA was 0.8 logMAR and CRT was 207 μm. Her BCVA was sustained, and CRT showed gradual improvements. These findings suggested the effectiveness of intravitreal t-PA injections for DME in the vitrectomized eye.

Abstract Benzalkonium chloride (BAC) is used as a preservative in eyedrops but induces subconjunctival fibrosis that can result in failure of glaucoma surgery. Tenon’s capsule fibroblasts in subconjunctival tissue interact with the corneal epithelium through tear fluid. With the use of a coculture system, we have now investigated the effect of human corneal epithelial (HCE) cells on myofibroblastic transdifferentiation of human Tenon fibroblasts (HTFs) induced by BAC (5 × 10−6%). Immunofluorescence and immunoblot analyses revealed that the BAC-induced expression of α smooth muscle actin (αSMA) in HTFs was suppressed by coculture of these cells with HCE cells (p

Abstract Epithelial–mesenchymal transition (EMT) in retinal pigment epithelial (RPE) cells plays a key role in proliferative retinal diseases such as age-related macular degeneration by contributing to subretinal fibrosis. To investigate the potential role of retinoic acid receptor-α (RAR-α) signaling in this process, we have now examined the effects of the RAR-α agonist Am580 on EMT induced by transforming growth factor-β2 (TGF-β2) in primary mouse RPE cells cultured in a three-dimensional type I collagen gel as well as on subretinal fibrosis in a mouse model. We found that Am580 inhibited TGF-β2-induced collagen gel contraction mediated by RPE cells. It also attenuated the TGF-β2-induced expression of the mesenchymal markers α-smooth muscle actin, fibronectin, and collagen type I; production of pro-matrix metalloproteinase 2 and interleukin-6; expression of the focal adhesion protein paxillin; and phosphorylation of SMAD2 in the cultured RPE cells. Finally, immunofluorescence analysis showed that Am580 suppressed both the TGF-β2-induced translocation of myocardin-related transcription factor-A (MRTF-A) from the cytoplasm to the nucleus of cultured RPE cells as well as subretinal fibrosis triggered by laser-induced photocoagulation in a mouse model. Our observations thus suggest that RAR-α signaling inhibits EMT in RPE cells and might attenuate the development of fibrosis associated with proliferative retinal diseases.

Purpose: We present a case of a gastrointestinal stromal tumor (GIST) metastasis of the rectal primary resisting chemotherapy to the right orbit 15 years after excision of the primary lesion. Observations: A 79-year-old man was diagnosed with rectal GIST at the age of 65 years and underwent rectal amputation. He underwent hepatectomy for GIST liver metastases at the age of 69 years and pericardiectomy for GIST pericardial metastases at 72 years of age. At the age of 79 years, positron emission tomography-computed tomography revealed the possibility of liver metastasis and metastasis to the right orbit of 10 mm in size. Magnetic resonance imaging revealed a well-circumscribed mass of 10 mm × 12 mm in the deep medial rectus muscle of the right orbit, which was referred to our department for ophthalmic examination. The latter revealed only mild abduction disorder in the right eye. Although chemotherapy was initiated, the tumor gradually increased, causing exophthalmos in the right eye, visual field impairment due to optic nerve exclusion, and decreased visual acuity. Due to repeated multiple metastases, the patient underwent right orbital exenteration and free flap reconstruction at the age of 83 years for radical cure. Pathological examination revealed c-Kit positive, CD34 positive, S100 protein minority positive, MIB-1 positive rate of 10% or more, and α-SMA negative, and the diagnosis was intraorbital metastasis of GIST. Conclusions and importance: Orbital metastases in GISTs are extremely rare, and there is no established standard treatment. Therefore, a comprehensive decision must be made based on the final treatment goal and the patient's background when selecting treatment.

Administration of intravitreal anti-vascular endothelial growth factor (anti-VEGF) therapy is the first-line therapy for diabetic macular oedema (DME). However, some patients show no or insufficient response to repeated anti-VEGF injections. Therefore, it is necessary to identify factors that can predict this resistance against anti-VEGF treatment. Presence of microaneurysms (MAs) is a predictor of the development and progression of DME, but its relationship with the treatment response to the anti-VEGF agents is not well known. Therefore, we aimed to elucidate the relationship between the distribution of MAs and the response to anti-VEGF therapy in patients with DME. The number of MAs was measured before anti-VEGF therapy in each region using fluorescein angiography, indocyanine green angiography (IA), and optical coherence tomography angiography. Patients with DME were divided into the responder and non-responder groups after three loading phases. Differences in the distribution of MAs between the groups were investigated. Pre-treatment IA revealed more MAs in the nasal area in the non-responder group than in the responder group (10.7 ± 10.7 and 5.7 ± 5.7, respectively, in the nasal macula) (1.4 ± 2.1 and 0.4 ± 0.7, respectively, in the nasal fovea). Whereas, pre-treatment FA and OCTA could not reveal significantly difference between the groups. Detection of MAs in the nasal macula using pre-treatment IA may indicate resistance to anti-VEGF therapy. We recommend the clinicians confirm the presence of MAs in the nasal macula, as shown by IA, as a predictor of therapeutic response to anti-VEGF therapy in patients with treatment naive DME.

Abstract Purpose  Diabetic complications are associated with abnormality of the basement membranes. We have developed a light-scattering detection system (LSDS) specifically for measurement of light scattering at the corneal epithelial basement membrane, and have determined the reproducibility and clinical significance of the results obtained by the LSDS in diabetic patients. Methods  Thirty nondiabetic controls and 40 diabetic subjects participated in the study. Light scattering at the corneal epithelial basement membrane was measured with the LSDS. Results  The measurement of light scattering at the corneal basement membrane was found to be reproducible. The LSDS index (mean SD) was 28.1 4.8 in controls, 35.7 6.3 in mild diabetic retinopathy subjects, and 42.7 8.6 in severe diabetic retinopathy subjects. This demonstrated that the LSDS index at the corneal basement membrane is proportional to the extent of diabetic retinopathy. Conclusions  Measurement of light scattering at the corneal epithelial basement membrane is possible with the LSDS, is relatively easy to perform, and is reproducible. The LSDS may prove suitable for the early detection of diabetic ocular complications. Jpn J Ophthalmol 2007;51:185–190 Japanese Ophthalmological Society 2007 [ABSTRACT FROM AUTHOR]