الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 104 |  |  |
| | | from | 104 | | |
Abstract
Among patients treated for uveitis in academic ophthalmology clinics and referral centers, 20% to 70% experience major vision loss. Up to 50% of patients will experience reduced visual function, and 10% to 15% will become blind. Studies have shown a strong correlation between delayed treatment and the likelihood of poor visual outcomes. Vision loss associated with uveitis has a negative impact on quality of life and activities of daily living. Non-infectious uveitis (NIU) encompasses a wide range of ocular inflammatory disorders, accounting for up to 20% of cases of severe vision impairment in adult population. There is great variability of clinical presentations, all associated with intraocular inflammation which results in cumulative damage to ocular tissues ultimately resulting in visual loss. The main objective of treatment strategies, which are currently non-specific, is to control active inflammation and try to prevent recurrences. Collaboration among health providers, specifically, ophthalmologists and rheumatologists, is needed to improve management of patients with NIU and help identify previously undiagnosed conditions associated with uveitis. Helicobacter pylori is a spiral, gram-negative bacteria that was isolated for the first time in 1983. In contrast to other gram-negative bacteria that colonize the gut, H. pylori is present exclusively in the stomach. Only a small percent of H. pylori infected persons develop symptoms of gastrointestinal disease, probably as a consequence of different virulence of H. pylori strains, as well as differences in host immune responses. A considerable amount of evidence links H. pylori infection with extra gastric diseases, and in many of these diseases there is a clear beneficial effect of eradication therapy. The proposed mechanism, which establishes the relationship between this infection and autoimmune diseases, alludes to an inflammatory response perpetuated by chronic H. pylori infection. The chronic release of inflammatory mediators caused by H. pylori or cross-mimicry mechanisms between bacterial and self-antigens could affect extra digestive organs. Infection by itself is not capable of perpetuating extra intestinal inflammation, so a genetic predisposition is proposed to be involved. These same mechanisms could be related to NIU. This study was conducted to elucidate the relationship between H. pylori infection and NIU. Data from 100 patients with active NIU was included in this study, where H. pylori was detected in 38% of patients with NIU, with the majority had bilateral (64%) anterior uveitis. Our work confirmed that the prevalence of H. pylori infection is significantly higher in patients with idiopathic NIU, suggesting a causal relationship between H. pylori infection and NIU. Our results also highlight the slightly elevated IOP among NIU patients testing positive for H. pylori antigens in their stools. Treatment of H. pylori infection should be considered in patients with idiopathic NIU, however, this recommendation merits further investigation. Additional clinical trials are required to clearly discern the role of H. pylori eradication in the prognosis of patients with idiopathic NIU. If, this relationship is confirmed, a new therapeutic protocol for idiopathic NIU could be introduced in the future. Conclusions : •H. Pylori infection might be a significant factor in the etiology of NIU. •H. pylori may have a role in NIU patients presented with high IOP, as a secondary contributing factor. Further studies are needed to provide evidence to support Effectiveness of H. pylori eradication in halting the progression of NIU.