Diffuse lamellar keratitis after laser in situ keratomileusis with femtosecond laser flap creation.

PURPOSE: To identify possible associations with the development of diffuse lamellar keratitis (DLK) after laser in situ keratomileusis (LASIK) with femtosecond laser flap creation. SETTING: University-based academic practice, Ann Arbor, Michigan, USA. DESIGN: Case-control study. METHODS: Myopic LASIK was performed between October 2006 and December 2010 using an Intralase 60 kHz femtosecond laser for flap creation. Preoperative clinical characteristics, treatment parameters, and intraoperative and postoperative complications were recorded. Statistical comparisons were made using t, chi-square, and Fisher exact tests and repeated-measures logistic regression to adjust for inter-eye dependency. RESULTS: The study enrolled 801 eyes (419 patients). Ninety-nine eyes (12.4%) of 70 patients developed DLK; most cases comprised mild flap interface inflammation and were treated with a routine postoperative antiinflammatory regimen. Twenty-two eyes (2.7%) required more than 1 week of antiinflammatory treatment. There was a statistically significant increase in the incidence of DLK with larger flap diameter (P=.0171), higher side-cut energy (P=.0037), and higher raster energy (P=.0033). Patients with DLK were less likely to achieve corrected distance visual acuity of 20/20 or better 1 day postoperatively (P=.0453). The difference in acuity was no longer present at 1 week. There were no significant associations between the incidence of DLK and preoperative refractive error, flap thickness, ablation depth, or other treatment parameters. CONCLUSIONS: Diffuse lamellar keratitis after LASIK with femtosecond laser flap creation tended to be mild with little effect on visual acuity. Higher energy level for flap creation and larger flap diameter were associated with an increased risk for DLK.

Fabry disease in mice is associated with age-dependent susceptibility to vascular thrombosis.

Fabry disease is an X-linked lysosomal storage disorder due to deficiency of alpha-galactosidase A (GLA) activity that results in the widespread accumulation of neutral glycosphingolipids. Renal failure, neuropathy, premature myocardial infarction, and stroke occur in patients with this condition primarily due to deposition of glycosphingolipids in vascular endothelial cells. The clinical consequences of Fabry disease suggest that vascular thrombosis may play a prominent role in the pathogenesis of this disease; however, the vasculopathy associated with Fabry disease has not been extensively studied. To determine if mice genetically deficient in Gla are susceptible to vascular thrombosis, a photochemical carotid injury model was used to induce occlusive thrombosis. In this model, Gla-/0 mice displayed a progressive age-dependent shortening of the time to occlusive thrombosis after vascular injury that correlated with progressive accumulation of globotriasylceramide (Gb3) in the arterial wall. Bone marrow transplantation from Gla-/0 to Gla+/0 mice and from Gla+/0 to Gla-/0 mice did not change the thrombotic phenotype of the host. These studies reveal a potent vascular prothrombotic phenotype in Gla-deficient mice and suggest that antithrombotic therapies as well as therapies designed to reduce the vascular accumulation of Gb3 may have beneficial effects on thrombotic complications in patients with Fabry disease.