Explore the vast range of titles available.

Dry eye disease (DED) is a broad term that includes a diverse group of clinical disorders. Aqueous-deficient dry eye (ADDE), a subtype of DED, is characterized by decreased tear production by the lacrimal gland. It can be seen in up to one-third of individuals with DED and can be comorbid with a systemic autoimmune process or occur secondary to an environmental insult. Since ADDE can be a source of long-term suffering and severe visual impairment, early identification and adequate treatment are imperative. Multiple etiologies can underlie ADDE, and it is critical to identify the underlying cause to not only improve the ocular health but also to improve the overall quality of life and well-being of affected individuals. This review discusses the various etiologies of ADDE, highlights a pathophysiology-based approach for evaluating underlying contributors, outlines various diagnostic tests, and reviews treatment options. We present the current standards and discuss ongoing research in this field. Through this review, we propose a treatment algorithm that would be useful for an ophthalmologist in diagnosing and managing individuals with ADDE.

Air pollution has broad effects on human health involving many organ systems. The ocular surface is an excellent model with which to study the effects of air pollution on human health as it is in constant contact with the environment, and it is directly accessible, facilitating disease monitoring. Effects of air pollutants on the ocular surface typically manifest as dry eye (DE) symptoms and signs. In this review, we break down air pollution into particulate matter (organic and inorganic) and gaseous compounds and summarize the literature regarding effects of various exposures on DE. Additionally, we examine the effects of weather (relative humidity, temperature) on DE symptoms and signs. To do so, we conducted a PubMed search using key terms to summarize the existing literature on the effects of air pollution and weather on DE. While we tried to focus on the effect of specific exposures on specific aspects of DE, environmental conditions are often studied concomitantly, and thus, there are unavoidable interactions between our variables of interest. Overall, we found that air pollution and weather conditions have differential adverse effects on DE symptoms and signs. We discuss these findings and potential mitigation strategies, such as air purifiers, air humidifiers, and plants, that may be instituted as treatments at an individual level to address environmental contributors to DE.

Dry eye (DE) is a chronic ocular condition with high prevalence and morbidity. It has a complex pathophysiology and is multifactorial in nature. Chronic ocular surface inflammation has emerged as a key component of DE that is capable of perpetuating ocular surface damage and leading to symptoms of ocular pain, discomfort, and visual phenomena. It begins with stress to the ocular surface leading to the production of proinflammatory mediators that induce maturation of resident antigen-presenting cells which then migrate to the lymph nodes to activate CD4 T cells. The specific antigen(s) targeted by these pathogenic CD4 T cells remains unknown. Two emerging theories include self-antigens by autoreactive CD4 T cells or harmless exogenous antigens in the setting of mucosal immunotolerance loss. These CD4 T cells migrate to the ocular surface causing additional inflammation and damage. Lifitegrast is the second topical anti-inflammatory agent to be approved by the US Food and Drug Administration for the treatment of DE and the first to show improvement in DE symptoms. Lifitegrast works by blocking the interaction between intercellular adhesion molecule-1 and lymphocyte functional associated antigen-1, which has been shown to be critical for the migration of antigen-presenting cells to the lymph nodes as well as CD4 T cell activation and migration to the ocular surface. In four large multicenter, randomized controlled trials, lifitegrast has proven to be effective in controlling both the signs and symptoms of DE with minimal side effects. Further research should include comparative and combination studies with other anti-inflammatory therapies used for DE.

BackgroundChalazia are common inflammatory eyelid lesions, but their epidemiology remains understudied. This retrospective case–control study examined the prevalence, risk factors and geographic distribution of chalazia in a large veteran population.MethodsData on all individuals seen at a Veterans Affairs (VA) clinic between October 2010 and October 2015 were extracted from the VA health database. Subjects were grouped based on International Classification of Diseases, Ninth Revision (ICD-9) code for chalazion. Univariable logistic regression modelling was used to identify clinical and demographic factors associated with chalazion presence, followed by multivariable modelling to examine which factors predicted risk concomitantly. All cases were mapped across the continental US using geographic information systems modelling to examine how prevalence rates varied geographically.ResultsOverall, 208 720 of 3 453 944 (6.04%) subjects were diagnosed with chalazion during the study period. Prevalence was highest in coastal regions. The mean age of the population was 69.32±13.9 years and most patients were male (93.47%), white (77.13%) and non-Hispanic (93.72%). Factors associated with chalazion risk included smoking (OR=1.12, p<0.0005), conditions of the tear film (blepharitis (OR=4.84, p<0.0005), conjunctivitis (OR=2.78, p<0.0005), dry eye (OR=3.0, p<0.0005)), conditions affecting periocular skin (eyelid dermatitis (OR=2.95, p<0.0005), rosacea (OR=2.50, p<0.0005)), allergic conditions (history of allergies (OR=1.56, p<0.0005)) and systemic disorders (gastritis (OR=1.54, p<0.0005), irritable bowel syndrome (OR=1.45, p<0.0005), depression (OR=1.35, p<0.0005), anxiety (OR=1.31, p<0.0005)). These factors remained associated with chalazion risk when examined concomitantly.ConclusionPeriocular skin, eyelid margin and tear film abnormalities were most strongly associated with risk for chalazion. The impact of environmental conditions on risk for chalazion represents an area in need of further study.

BackgroundPhotophobia is a potentially debilitating symptom often found in dry eye disease (DE), migraine and traumatic brain injury (TBI).MethodsWe conducted a review of the literature via a PubMed search of English language articles with a focus on how photophobia may relate to a shared pathophysiology across DE, migraine and TBI.ResultsDE, migraine and TBI are common conditions in the general population, are often comorbid, and share photophobia as a symptom. Across the three conditions, neural dysregulation of peripheral and central nervous system components is implicated in photophobia in various animal models and in humans. Enhanced activity of the neuropeptide calcitonin gene-related peptide (CGRP) is closely linked to photophobia. Current therapies for photophobia include glasses which shield the eyes from specific wavelengths, botulinum toxin, and inhibition of CGRP and its receptor. Many individuals have persistent photophobia despite the use of these therapies, and thus, development of new therapies is needed.ConclusionsThe presence of photophobia in DE, migraine and TBI suggests shared trigeminothalamic pathophysiologic mechanisms, as explained by central neuroplasticity and hypersensitivity mediated by neuropeptide CGRP. Treatment strategies which target neural pathways (ie, oral neuromodulators, transcutaneous nerve stimulation) should be considered in patients with persistent photophobia, specifically in individuals with DE whose symptoms are not controlled with traditional therapies.

Infrared (IR) thermographic assessment of ocular surface temperature (OST) is gaining interest as an adjuvant method to evaluate the ocular surface. It is a quick, non-invasive test that causes minimal, if any, discomfort to patients. The purpose of this article was to summarize research on how OST relates to tear film parameters and dry eye disease (DED). PubMed, Google Scholar, and Scopus searches for specific terms were carried out and eligible articles reviewed. OST of the central cornea is ~34-35°C when measured as a single time-point (typically right after a blink). Dynamically, OST values decrease over time at a rate of ~ -0.01 °C/s in healthy eyes. Single time-point OST values are impacted by temperature, with positive correlations noted with both ambient (1°C↓ results in ~0.16°C↓ in OST) and body (1°C↑ results in ~0.98°C↑ in OST) temperature. Single time-point OST values are also impacted by tear parameters, with negative correlations noted with tear break-up time (TBUT; r=-0.61) and positive correlations with lipid layer thickness (~r=0.50). Dynamically, the rate of OST cooling over the interblink period correlates with various tear parameters including Schirmer's test scores (r=-0.39), tear meniscus height (r=-0.52) and the rate of tear film break-up (r=-0.74). These data imply that OST decreases more rapidly in individuals with greater tear production, larger tear volumes, and shorter tear break-up times (faster rates of tear film break-up). There are discrepancies in relationships between OST and DED across studies, which is not surprising given that DED encompasses a number of different phenotypic presentations. However, most studies found that OST decreases at a more rapid rate in DED vs. control groups. As such, cooling rate may have utility as a screening tool in DED in combination with established point-of-care tests.

Background Autoimmune diseases have been associated with changes in the gut microbiome. In this study, the gut microbiome was evaluated in individuals with dry eye and bacterial compositions were correlated to dry eye (DE) measures. We prospectively included 13 individuals with who met full criteria for Sjögren’s (SDE) and 8 individuals with features of Sjögren’s but who did not meet full criteria (NDE) for a total of 21 cases as compared to 21 healthy controls. Stool was analyzed by 16S pyrosequencing, and associations between bacterial classes and DE symptoms and signs were examined. Results Results showed that Firmicutes was the dominant phylum in the gut, comprising 40–60% of all phyla. On a phyla level, subjects with DE (SDE and NDE) had depletion of Firmicutes (1.1-fold) and an expansion of Proteobacteria (3.0-fold), Actinobacteria (1.7-fold), and Bacteroidetes (1.3-fold) compared to controls. Shannon’s diversity index showed no differences between groups with respect to the numbers of different operational taxonomic units (OTUs) encountered (diversity) and the instances these unique OTUs were sampled (evenness). On the other hand, Faith’s phylogenetic diversity showed increased diversity in cases vs controls, which reached significance when comparing SDE and controls (13.57 ± 0.89 and 10.96 ± 0.76, p = 0.02). Using Principle Co-ordinate Analysis, qualitative differences in microbial composition were noted with differential clustering of cases and controls. Dimensionality reduction and clustering of complex microbial data further showed differences between the three groups, with regard to microbial composition, association and clustering. Finally, differences in certain classes of bacteria were associated with DE symptoms and signs. Conclusions In conclusion, individuals with DE had gut microbiome alterations as compared to healthy controls. Certain classes of bacteria were associated with DE measures.

Laser in-situ keratomileusis (LASIK) is a commonly performed surgical procedure used to correct refractive error. LASIK surgery involves cutting a corneal flap and ablating the stroma underneath, with known damage to corneal nerves. Despite this, the epidemiology of persistent pain and other long-term outcomes after LASIK surgery are not well understood. Available data suggest that approximately 20–55% of patients report persistent eye symptoms (generally regarded as at least 6 months post-operation) after LASIK surgery. While it was initially believed that these symptoms were caused by ocular surface dryness, and referred to as “dry eye,” it is now increasingly understood that corneal nerve damage produced by LASIK surgery resembles the pathologic neuroplasticity associated with other forms of persistent post-operative pain. In susceptible patients, these neuropathological changes, including peripheral sensitization, central sensitization, and altered descending modulation, may underlie certain persistent dry eye symptoms after LASIK surgery. This review will focus on the known epidemiology of symptoms after LASIK and discuss mechanisms of persistent post-op pain due to nerve injury that may be relevant to these patients. Potential preventative and treatment options based on approaches used for other forms of persistent post-op pain and their application to LASIK patients are also discussed. Finally, the concept of genetic susceptibility to post-LASIK ocular surface pain is presented.