Low-grade Intraocular Inflammation Research Articles

High irisin and low BDNF levels in aqueous humor of high myopia.

The pathogenesis of myopia remains unclear. Both genetic and environmental factors play a role in the disease progression. Reasons including reduced physical activity (PA) and low-grade intraocular inflammation may be involved in the development of myopia. To analyze the levels of irisin, brain-derived neurotrophic factor (BDNF) and other intraocular cytokines in aqueous humor of high myopia patients, and to evaluate the roles of PA and inflammation in developing myopia. We collected aqueous humor samples from patients with axial length (AL) over 26 mm (n = 35) or shorter than 25 mm (n = 38) during cataract extraction surgery. Samples were assayed using the enzyme-linked immunosorbent assay (ELISA) kit for irisin and a multiplex immunoassay kit for BDNF, interleukin (IL)-6, IL-8 and IL-10, and tumor necrosis factor alpha (TNF-α). Irisin levels in the aqueous samples of the highly myopic eyes were significantly higher than in the control group (p = 0.027). The BDNF levels of the highly myopic group were significantly lower than in the control group (p = 0.043). Median level of leukemia inhibitory factor (LIF) for highly myopic group (2.035 pg/mL) was statistically significantly higher than in the control group (0.750 pg/mL) (U = 210.5, Z = -4.495, p < 0.001). Interleukin 1 receptor antagonist (IL-1ra) level in the aqueous samples of the highly myopic group was significantly lower than in the shorter AL group (p = 0.049). Interleukin 6, IL-8 and IL-10 levels were not significantly different between the 2 groups (p = 0.501, p = 0.059 and p = 0.192, respectively). Tumor necrosis factor α levels could only be detected in 30 samples and median levels in the 2 groups were not statistically significantly different (U = 99, Z = -0.482, p = 0.650). No correlation was found between IL-6, IL-8, IL-10 and TNF-α, and the AL (p > 0.05). Irisin was positively correlated with AL (p = 0.028, r = 0.287). The BDNF was negatively correlated with AL (p = 0.040, r = -0.246). Interleukin 1ra was negatively correlated with AL (p = 0.038, r = -0.276). There was also a correlation between LIF and AL (p < 0.001, r = 0.486). Higher irisin level in high myopia group opens a new direction to discover the relationship between PA and myopia. The decreased BDNF in high myopia group probably demonstrates the connection between myopia and neurodegenerative disease.

Inflammatory cytokines in highly myopic eyes

Currently, myopic retinopathy is the most common irreversible blinding disease but its pathophysiology is not completely clear. A cross-sectional, observational study was conducted in a single center to analyze aqueous samples from highly myopic eyes (axial length >25 mm, n = 92) and ametropic or mild myopic eyes (n = 88) for inflammatory cytokines. Vascular endothelial growth factor (VEGF), Interleukin 6 (IL-6), and matrix metalloproteinase-2 (MMP-2) were measured using an enzyme-linked immunosorbent assay. IL-6 and MMP-2 were significantly higher in the highly myopic eyes than in the non-high myopic eyes (IL-6: 11.90 vs. 4.38 pg/mL, p < 0.0001; MMP-2: 13.10 vs. 8.82 ng/mL, p = 0.0003) while adjusting for age, gender, and intraocular pressure. There was a significant positive association between levels of IL-6 and MMP-2 in aqueous humor and the axial lengths of the eye globes (IL-6, β = 0.065, p < 0.0001, n = 134; MMP-2, β = 0.097, p < 0.0001, n = 131). Conversely, VEGF in aqueous humor was significantly lower in the highly myopic eyes than in the non-high myopic eyes (45.56 vs. 96.90 pg/mL, p < 0.0001, n = 153) while age, gender, and intraocular pressure were adjusted. The results suggest that low-grade intraocular inflammation may play an important role in the development and progression of high myopia and myopic retinopathy.

Inflammatory Eye Disease in Children with Chronic Arthritis

Uveitis is the most common extra-articular manifestation of juvenile idiopathic arthritis ( JIA). Chronic iridocyclitis with an indolent course is the most common type of intraocular inflammation and is observed predominantly in antinuclear antibody (ANA)-positive girls with oligoarticular JIA. Because of the insidious nature of the disease, several complications, including posterior synechia, cataract, band keratopathy, glaucoma, and macular edema, may be present even at first presentation. The presence of complications at the time of diagnosis and the long period of chronic inflammation are considered the most important risk factors for the development of further complications. JIA-associated uveitis has a blinding potential which is often underappreciated. The disease and its complications are not confined to childhood only, with patients continuing to suffer even in adult hood. Therefore, an aggressive treatment as soon as the diagnosis has been made should be started in order to improve the visual prognosis. An earlier institution of immunosuppressive therapy with less tolerance for even a low-grade intraocular inflammation is the best approach in JIA patients. Despite the use of new therapeutic agents and advances in surgical treatment of ocular complications, JIA-associated uveitis still has a severe course and blinding potential in some patients. Besides a prompt and aggressive treatment, routine ophthalmologic examinations, awareness of worse prognostic factors, early referral to uveitis subspecialists before permanent ocular damage develops, and collaboration between rheumatologists and ophthalmologists are all crucial in improving the visual prognosis.

Chronic postoperative endophthalmitis caused by Actinomyces neuii

Uneventful phacoemulsification with implantation of a foldable, acrylic posterior chamber intraocular lens was performed in the right eye of a 73-year-old white man. Postoperatively, the patient developed a chronic, low-grade intraocular inflammation. Cultures from the aqueous specimen grew Actinomyces neuii, an unusual gram-positive bacillus. The low-grade intraocular inflammation persisted with intensive topical steroid-antibiotic medication and systemic antibiotics. A diagnostic, 3-port, pars plana vitrectomy was performed, and aqueous aspirate specimens were sent for culture and sensitivity and to look for abnormal cells. Intracameral antibiotics were not injected. The specimens were sterile to culture, and chronic inflammatory cells were reported on the vitreous specimen. On examination 6 months later, inflammation had not recurred and the best corrected visual acuity was 6/18.

Ophthalmologic Aspects of Headache

Pain around the eye can be caused by local ophthalmic disorders or by disease of other structures sharing trigeminal nerve sensory innervation. In general, most ocular causes for pain also cause the eye to be red, thus alerting the examiner to the focality of the problem. However, conditions like eyestrain, intermittent angleclosure glaucoma or neovascular glaucoma, and low-grade intraocular inflammation can be painful and not be associated with obvious redness. Ocular signs and symptoms also occur with numerous other causes of headache. Double vision in association with periocular pain can result from orbital lesions, isolated cranial neuropathies, and cavernous sinus lesions. Pupillary abnormalities like Horner's syndrome may result from a variety of painful conditions, including cluster headache, parasellar neoplasms or aneurysms, internal carotid dissection or occlusion, and Tolosa-Hunt syndrome. Pain with a dilated and unreactive pupil may reflect a benign condition like Adie's syndrome or ophthalmoplegic migraine, or it may herald the presence of a life-threatening posterior communicating artery aneurysm. Headache and transient visual loss can be manifestations of classic migraine, or be symptoms of ocular hypoperfusion from ipsilateral internal carotid occlusion or increased intracranial pressure from pseudotumor cerebri. In a young patient, head pain with a fixed visual deficit may result from optic neuritis, in an older adult, temporal arteritis may be the culprit. Ophthalmologic aspects of headache thus encompass problems that range from simple and benign to complex and formidable.

Corneal Endothelial Cell Loss, Cystoid Macular Edema, and Iris-supported intraocular Lenses

Endothelial cell loss, persistent cystoid macular edema and a chronic low-grade uveitis may complicate intracapsular cataract extraction combined with iris supported intraocular lenses. Clinical examination of 19 eyes of 17 patients, at 1.1 to 5 years after cataract surgery, and correlation with wide field specular microscopy and fluorescein angiography, documents this problem. The mean central corneal endothelial cell count was 497 cells/mm2 (standard deviation, 119). In ten cases, focal edema was localized to the corneal periphery. Cystoid macular edema was present in all but one case. Intermittent cornea/ implant touch or low-grade intraocular inflammation, possibly from iris/implant contact, may explain the natural history of the endothelial cell loss and cystoid macular edema. Monitoring endothelial cell counts and macular function in patients with iris-supported implants may afford the early recognition of this problem. In such cases, early implant removal may alter the natural history and preserve corneal and macular function.