Extraintestinal manifestations are common in patients with inflammatory bowel disease (IBD), and optic neuritis (ON) is a rare but severe one. This study aimed to evaluate possible factors associated with ON in patients with IBD. Adult patients with IBD who were not with concomitant ON on the index date identified from the Taiwan National Health Insurance Research Database (NHIRD) from the years 2000 to 2013 were included. A four-fold matched group was selected using age, sex and year of index date for comparison. All the patients were followed up until the development of ON or the end of the study period. Data of included patients were extracted and analyzed statistically. The mean follow-up time for all patients was 7.13 ± 5.21 years. At the study period conclusion, eight (0.18%) and five (0.003%) patients with and without IBD, respectively, had developed ON (p = 0.001). Adjusted HRs showed that patients with IBD aged between 30 and 39 years, with comorbidities including neuromyelitis optica (NMO), acute disseminated encephalomyelitis (ADEM), systemic lupus erythematosus (SLE) and with a higher Charlson Comorbidity Index, had a significantly higher risk of developing ON (all p < 0.005). Among the eight IBD patients who developed ON, only one patient was diagnosed with Crohn’s disease, the male gender was slightly dominant, and two (25%) patients received antitumor necrosis factor α (anti-TNF α) treatment for IBD. Patients with IBD have a higher risk of developing ON compared to patients without IBD. ON occurs more frequently in IBD patients aged between 30 and 39 years, with comorbidities including NMO, ADEM and SLE. Other factors besides anti-TNF α treatment for IBD are more likely associated with the development of ON.

Background: Ischemic optic neuropathy (ION) is a possible extraintestinal manifestation (EIM) of inflammatory bowel disease (IBD). We investigate the relation between IBD and ION and possible risk factors associated with their incidence.Methods: Medical records were extracted from the National Health Insurance Research Database (NHIRD) from January 1, 2000, to December 31, 2013. The main outcome was ION development. Univariate and multivariate Cox regression analyses were performed.Results: We enrolled 22,540 individuals (4,508 with IBD, 18,032 without). The cumulative risk of developing ION was significantly greater for patients with IBD vs. patients without (Kaplan–Meier survival curve, p = 0.009; log-rank test). Seven (5%) and five (0.03%) patients developed ION in the IBD and control groups, respectively. Patients with IBD were significantly more likely to develop ION than those without IBD [adjusted hazard ratio (HR) = 4.135; 95% confidence interval: 1.312–11.246, p = 0.01]. Possible risk factors of ION development were age 30–39 years, diabetes mellitus (DM), hypertension, ischemic heart disease (IHD), atherosclerosis, and higher Charlson comorbidity index revised (CCI_R) value.Conclusion: Patients with IBD are at increased risk of subsequent ION development. Moreover, for patients with comorbidities, the risk of ION development is significantly higher in those with IBD than in those without.

Background: Diabetic macular edema (DME) is the primary cause of visual impairment in individuals with diabetes. Anti-vascular endothelial growth factor (VEGF) is the current first-line treatment for DME owing to its effectiveness. However, frequent anti-VEGF injections may be inconvenient for patients. Therefore, this study aimed to investigate whether the addition of subthreshold micropulse laser (SML) to anti-VEGF therapy could reduce the requirement for anti-VEGF injections while maintaining the treatment efficacy for DME. Methods: Clinical trials retrieved from the databases of PubMed, EMBASE, and the Cochrane Library were evaluated to determine the effectiveness of combination treatment with SML and anti-VEGF medication compared with that of anti-VEGF treatment alone. The primary outcome measures were the changes in CMT, best-corrected visual acuity (BCVA), and the total number of intravitreal injections (IVIs). Results: The IVI + SML group revealed a substantial increase in the logarithm of the minimum angle of the resolution BCVA and a reduction in CMT at the 12-month follow-up (BCVA: random-effects; mean difference [MD], −0.05; 95% confidence interval [CI]: −0.10 to −0.01; p-value = 0.28, and CMT: random-effects; MD, −18.27; 95% confidence interval, −27.36 to −9.18; p-value = 0.20). The number of required IVIs in the IVI + SML group was lower than that in the IVI only group (random-effects; MD, −2.22; 95% CI: −3.13 to −1.31; p-value < 0.01). Conclusions: Combining SML therapy with anti-VEGF injections may reduce the total number of injections required, improve VA, and reduce CMT at the 12-month follow-up. Although the included studies used different SML regimens and anti-VEGF agents, this review indicates that the application of additional SML therapy results in positive clinical outcomes.

Central serous chorioretinopathy (CSCR) is characterized by central neurosensory retinal detachment from the retinal pigment epithelium. While the association between CSCR and steroid use is widely recognized, it is difficult to distinguish whether the subretinal fluid (SRF) in ocular inflammatory disease results from steroid use or an inflammation-related uveal effusion. We report the case of a 40-year-old man who presented to our department with intermittent redness and dull pain in both eyes that had persisted for three months. He was diagnosed with scleritis with SRF in both eyes and steroid therapy was started. Inflammation improved with steroid use, but SRF increased. This indicated that the fluid was not caused by the posterior scleritis-related uveal effusion but by steroid use. SRF and clinical symptoms subsided after steroids were discontinued completely and immunomodulatory therapy was initiated. Our study highlights that steroid-associated CSCR must be considered in the differential diagnosis of patients with scleritis, and prompt diagnosis with an immediate shift from steroids to immunomodulatory therapy can resolve SRF and clinical symptoms.