The effect of different potency glucocorticosteroids treatments on tear inflammatory factors and corneal optical density after femtosecond-assisted laser in situ keratomileusis.

To assess the impact of glucocorticosteroids with varying potencies on inflammatory mediators in tears and corneal optical density after femtosecond-assisted laser in situ keratomileusis (FS-LASIK). In a prospective study, 110 patients (220 eyes) who underwent FS-LASIK were divided into 2 groups: 55 patients (110 eyes) received dexamethasone, and another 55 patients (110 eyes) received fluorometholone. Visual acuity, intraocular pressure, and corneal optical density were measured before, 1 week, and 1 month after surgery. Tear fluid samples were also collected to assess expression levels of TNF-α, IL-1α, IL-6, and TGF-ß1. One week after the procedure, the dexamethasone group exhibited elevated intraocular pressure (IOP) levels (P > .05) and a decreased expression of TNF-α in tears (P < .001) compared to the fluorometholone group. Within the 0 to 2 mm range from the corneal apex, the anterior corneal layer's optical density in the fluorometholone group surpassed that of the dexamethasone group (P < .05). At 1 month post-surgery, the IOP in the fluorometholone group was higher than that in the dexamethasone group (P < .05). In both the 0 to 2 mm and 2 to 6 mm intervals from the corneal apex, the optical density of the anterior corneal layer was significantly higher in the fluorometholone group compared to the dexamethasone group (P < .05). There was no statistically significant difference in visual acuity between the 2 groups at any postoperative time point. Short-term use of potent corticosteroids after FS-LASIK can swiftly address ocular surface inflammation, enhance corneal wound healing, reduce corneal edema, and accelerate the restoration of corneal transparency, in contrast to prolonged use of milder corticosteroids post-surgery.

Acquired Ocular Toxoplasmosis: a Case Report and Review of the Literature.

BACKGROUND: Toxoplasmosis is a zoonotic illness caused by Toxoplasma gondii. Ocular infection frequently manifests as acute necrotizing retinal chorioretinitis. In this paper, we describe a case of retinal chorioretinitis caused by Toxoplasma gondii infection, as well as the most recent diagnostic and treatment techniques. METHODS: Serum and vitreous fluid were collected and analyzed, and PCR for Toxoplasma gondii DNA, ELISA for Toxoplasma gondii IgG and Goldmann-Witmer coefficient, fundus fluorescein angiography (FFA), indocyanine green angiography (ICGA), and fundus autofluorescence were done (FAF). RESULTS: Toxoplasma gondii DNA (-), serum and vitreous IgG from Toxoplasma gondii (+) cells, and the Goldmann-Witmer coefficient of Toxoplasma gondii were all considerably enhanced, indicating Toxoplasma gondii infection. Antiparasitic infection in combination with an anti-inflammatory glucocorticoid were given, laser treatment of the fundus was provided, and the patient's condition has been stable with no indication of recurrence to date following conclusion of therapy. CONCLUSIONS: Toxoplasma gondii can infect the whole retina, causing variable degrees of visual impairment; thus, rapid diagnosis and tailored therapy are necessary to enhance prognosis and reduce disease recurrence.