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Inflammatory bowel disease (IBD) is a complex, multisystemic disease and is associated with ocular pathology in 4–12% of patients. In general, ocular disease affects Crohn's patients more frequently than those with ulcerative colitis. Episcleritis and uveitis are the most common presentations, with episcleritis often correlating with IBD flares, whereas uveitis presents independently of IBD activity and, in some cases, may even alert clinicians to a new diagnosis of IBD. Corneal EIMs encompass a range of pathologies, such as the common and benign keratoconjunctivitis sicca (dry eye disease), which nevertheless causes significant patient discomfort, and the rarer condition of peripheral ulcerative keratitis, which warrants urgent review due to the risk of corneal perforation. Alongside EIMs, clinicians should also be aware of the iatrogenic consequences to the eye following treatment of IBD. Corticosteroids may cause cataracts, glaucoma, and—indirectly via hyperglycaemia—diabetic retinopathy. Methotrexate is irritating to ocular tissues and may cause conjunctivitis and blepharitis. Biologic medications, such as anti-TNFα agents, overlap in their use as treatment of both IBD and uveitis, and yet in some patients may also increase the risk of acute uveitis flares, as well as opportunistic, sight-threatening infections. With integrated care between gastroenterology and ophthalmology, patient outcomes can be improved by facilitating earlier detection and management of ocular disease. This narrative review summarises the ocular extraintestinal manifestations of IBD, including pathophysiology, epidemiology, and current treatment strategies. [ABSTRACT FROM AUTHOR]

Many inhalation exposures induce pulmonary inflammation contributing to disease progression. Inflammatory processes are actively regulated via mediators including bioactive lipids. Bioactive lipids are potent signaling molecules involved in both pro-inflammatory and resolution processes through receptor interactions. The formation and clearance of lipid signaling mediators are controlled by multiple metabolic enzymes. An imbalance of these lipids can result in exacerbated and sustained inflammatory processes which may result in pulmonary damage and disease. Dysregulation of pulmonary bioactive lipids contribute to inflammation and pulmonary toxicity following exposures. For example, inhalation of cigarette smoke induces activation of pro-inflammatory bioactive lipids such as sphingolipids, and ceramides contributing to chronic obstructive pulmonary disease. Additionally, exposure to silver nanoparticles causes dysregulation of inflammatory resolution lipids. As inflammation is a common consequence resulting from inhaled exposures and a component of numerous diseases it represents a broadly applicable target for therapeutic intervention. With new appreciation for bioactive lipids, technological advances to reliably identify and quantify lipids have occurred. In this review, we will summarize, integrate, and discuss findings from recent studies investigating the impact of inhaled exposures on pro-inflammatory and resolution lipids within the lung and their contribution to disease. Throughout the review current knowledge gaps in our understanding of bioactive lipids and their contribution to pulmonary effects of inhaled exposures will be presented. New methods being employed to detect and quantify disruption of pulmonary lipid levels following inhalation exposures will be highlighted. Lastly, we will describe how lipid dysregulation could potentially be addressed by therapeutic strategies to address inflammation. [ABSTRACT FROM AUTHOR]

Air pollution accounts for more than 7 million premature deaths worldwide. Using ultrafine carbon black (CB) and ozone (O3) as a model for an environmental co-exposure scenario, the dose response relationships in acute pulmonary injury and inflammation were determined by generating, characterizing, and comparing stable concentrations of CB aerosols (2.5, 5.0, 10.0 mg/m3), O3 (0.5, 1.0, 2.0 ppm) with mixture CB + O3 (2.5 + 0.5, 5.0 + 1.0, 10.0 + 2.0). C57BL6 male mice were exposed for 3 h by whole body inhalation and acute toxicity determined after 24 h. CB itself did not cause any alteration, however, a dose response in pulmonary injury/inflammation was observed with O3 and CB + O3. This increase in response with mixtures was not dependent on the uptake but was due to enhanced reactivity of the particles. Benchmark dose modeling showed several-fold increase in potency with CB + O3 compared with CB or O3 alone. Principal component analysis provided insight into response relationships between various doses and treatments. There was a significant correlation in lung responses with charge-based size distribution, total/alveolar deposition, oxidant generation, and antioxidant depletion potential. Lung tissue gene/protein response demonstrated distinct patterns that are better predicted by either particle dose/aerosol responses (interleukin-1β, keratinocyte chemoattractant, transforming growth factor beta) or particle reactivity (thymic stromal lymphopoietin, interleukin-13, interleukin-6). Hierarchical clustering showed a distinct signature with high dose and a similarity in mRNA expression pattern of low and medium doses of CB + O3. In conclusion, we demonstrate that the biological outcomes from CB + O3 co-exposure are significantly greater than individual exposures over a range of aerosol concentrations and aerosol characteristics can predict biological outcome. [ABSTRACT FROM AUTHOR]

A 77-year-old female patient who had been treated for glaucoma for many years was referred to an outpatient clinic to extend the diagnostic work-up because of rapidly deteriorating vision despite anti-glaucoma treatment. During the visit, in addition to characteristic ophthalmic symptoms, behavioral and orientation disturbances were found, which raised a suspicion of Foster Kennedy syndrome and prompted the examining physician to refer the patient for an urgent brain scan. A computed tomography examination revealed the presence of focal lesions. Rapid diagnosis enabled immediate transfer of the patient to a neurosurgical center for further treatment [ABSTRACT FROM AUTHOR]

This study reports three cases of toxoplasmosis retinochoroiditis following coronavirus disease 2019 (COVID-19) infection or vaccination from the national Canadian COVID-19 Eye Registry between December 2020 and September 2021. A 56-year-old male presented 15 days after a positive COVID-19 test with toxoplasmosis retinochoroiditis. He later relapsed 8 days following a first Pfizer-BioNTech vaccine dose. Two patients presented with toxoplasmosis retinochoroiditis following COVID-19 vaccination: A 58-year-old female presenting 4 days following a first Pfizer-BioNTech vaccine dose with anterior uveitis and a posterior pole lesion discovered 3 months later and a 39-year-old female presenting 17 days after a first Moderna vaccine dose. Resolution was achieved with oral clindamycin, oral trimethoprim/sulfamethoxazole, and topical prednisolone acetate 1%. Patients were offered prophylactic trimethoprim/sulfamethoxazole for subsequent doses without relapse. Following COVID-19 infection or vaccination, patients may be at risk for toxoplasmosis retinochoroiditis. Prophylactic antibiotics for future doses may be offered to patients with known ocular toxoplasmosis to prevent recurrence. [ABSTRACT FROM AUTHOR]

Background: Cases of Toxoplasma reactivation or more severe primary infection have been reported in patients receiving immunosuppressive (IS) treatment for autoimmune diseases (AID). The purpose of this study was to describe features of toxoplasmosis occurring in patients with AID treated by IS therapy, excluded HIV-positive and transplant patients. Methods: A multicenter descriptive study was conducted using data from the French National Reference Center for Toxoplasmosis (NRCT) that received DNA extracts or strains isolated from patients, associated with clinical data. Other cases were retrieved through a questionnaire sent to all French parasitology and internal medicine departments. Furthermore, a systematic literature review was conducted. Results: 61 cases were collected: 25 retrieved by the NRCT and by a call for observations and 36 from a literature review. Half of the cases were attributed to reactivation (50.9%), and most of cases (49.2%) were cerebral toxoplasmosis. The most common associated AID were rheumatoid arthritis (28%) and most frequent treatments were antimetabolites (44.3%). Corticosteroids were involved in 60.7% of cases. Patients had a favorable outcome (50.8%) but nine did not survive. For 12 cases, a successful Toxoplasma strain characterization suggested the possible role of this parasitic factor in ocular cases. Conclusion: Although this remains a rare condition, clinicians should be aware for the management of patients and for the choice of IS treatment. Author summary: Severe forms of toxoplasmosis are well described in HIV-infected or transplant patients. However, they have been described in a less studied category of patients: those with autoimmune diseases and treated with immunosuppressive agents, corticosteroid and biotherapies. We report, conjointly with the French National Reference Center for Toxoplasmosis, the largest collection of cases of toxoplasmosis occurring in these patients to clarify the risk factors and epidemiology associated with these serious forms of toxoplasmosis. In our series, as well as in the literature, rheumatoid arthritis and systemic lupus erythematosus are the most common autoimmune diseases associated with toxoplasmosis, and antimetabolites, anti-TNF-α and corticosteroids were involved in most cases. The originality of this work lies in the molecular characterization of Toxoplasma to study the possible role of the strain factor in diverse clinical forms. Atypical strains, as those observed in South America, were more often observed in ocular toxoplasmosis cases. The significant proportion of cerebral toxoplasmosis (49,2%) and a 14.8% mortality risk highlight the necessity to inform clinicians of this opportunistic infectious complication and encourages them to evoke toxoplasmosis quickly even in case of occurrence of non-specific symptoms. [ABSTRACT FROM AUTHOR]