Eyelid fistula caused by a scleral buckle.

Complications of scleral buckle procedures for retinal detachments are rather uncommon yet may result in a broad scope of problems. The authors report a case of a chronic eyelid fistula caused by a scleral buckle. The patient was an 81-year-old woman who presented with a nonhealing left upper eyelid wound that was repeatedly misdiagnosed as a chalazion, but diagnostic workup revealed an extruded scleral buckle to be the cause. The patient was treated surgically with removal of the scleral buckle and full-thickness fistula repair and her wound healed well. A scleral buckle can erode through conjunctiva and the full thickness of an eyelid, causing an eyelid fistula and necessitate removal of the buckle.

Unique molecular signatures of microRNAs in ocular fluids and plasma in diabetic retinopathy.

The main objective of this pilot study was to identify circulatory microRNAs in aqueous or plasma that were reflecting changes in vitreous of diabetic retinopathy patients. Aqueous, vitreous and plasma samples were collected from a total of 27 patients undergoing vitreoretinal surgery: 11 controls (macular pucker or macular hole patients) and 16 with diabetes mellitus(DM): DM-Type I with proliferative diabetic retinopathy(PDR) (DMI-PDR), DM Type II with PDR(DMII-PDR) and DM Type II with nonproliferative DR(DMII-NPDR). MicroRNAs were isolated using Qiagen microRNeasy kit, quantified on BioAnalyzer, and profiled on Affymetrix GeneChip miRNA 3.0 microarrays. Data were analyzed using Expression Console, Transcriptome Analysis Console, and Ingenuity Pathway Analysis. The comparison analysis of circulatory microRNAs showed that out of a total of 847 human microRNA probes on the microarrays, common microRNAs present both in aqueous and vitreous were identified, and a large number of unique microRNA, dependent on the DM type and severity of retinopathy. Most of the dysregulated microRNAs in aqueous and vitreous of DM patients were upregulated, while in plasma, they were downregulated. Dysregulation of miRNAs in aqueous did not appear to be a good representative of the miRNA abundance in vitreous, or plasma, although a few potential candidates for common biomarkers stood out: let-7b, miR-320b, miR-762 and miR-4488. Additionally, each of the DR subtypes showed miRNAs that were uniquely dysregulated in each fluid (i.e. aqueous: for DMII-NPDR was miR-455-3p; for DMII-PDR was miR-296, and for DMI-PDR it was miR-3202). Pathway analysis identified TGF-beta and VEGF pathways affected. The comparative profiling of circulatory miRNAs showed that a small number of them displayed differential presence in diabetic retinopathy vs. controls. A pattern is emerging of unique molecular microRNA signatures in bodily fluids of DR subtypes, offering promise for the use of ocular fluids and plasma for diagnostic and therapeutic purposes.

The blepharochalasis syndrome.

Blepharochalasis is a rare eyelid disorder that often presents in childhood or early adolescence. It is characterized by exacerbations and remissions of painless edema of the upper and occasionally lower eyelids. Although the average duration of attack is only two days, multiple attacks eventually lead to atrophic, wrinkled, and discolored periorbital skin. Other clinical manifestations include ptosis, acquired forms of blepharophimosis, lower lid retraction, pseudoepicanthal folds, proptosis, prolapse of orbital fat, and lacrimal tissue. The etiology of blepharochalasis has yet to be fully elucidated, but histpathologic examinations indicate that elastolytic activity, immunoglobulin A (IgA), and other inflammatory processes might play a substantial role in the pathogenesis of the disease. The treatment of blepharchalasis is primarily surgical, and therefore understanding the natural history is essential to avoid overcorrection and recurrences after surgery. In this review we present the clinical characteristics, differential diagnosis, and treatment options of blepharochalsis.

Pharmacological treatments for thyroid eye disease.

Thyroid eye disease (TED), which affects the majority of patients with Grave's disease, is associated with significant ophthalmic morbidity. In patients with mild disease, supportive treatment with lubricating medication can be sufficient. However, in patients with severe TED and disfiguring proptosis or sight-threatening neuropathy, more aggressive medical or surgical interventions are necessary. Corticosteroids remain the preferred pharmacological treatment modality in the majority of patients with an active inflammatory component. Other immunosuppressive drugs in combination with corticosteroids may be helpful in patients with corticosteroid-resistant TED. Newer agents such as somatostatin analogues have not shown to be of significant clinical benefit; however, initial studies on the use of antioxidants and cytokine antagonists are encouraging.

Comparison of In Vivo Gene Expression Profiling of RPE/Choroid following Intravitreal Injection of Dexamethasone and Triamcinolone Acetonide.

Purpose. To identify retinal pigment epithelium (RPE)/choroid genes and their relevant expression pathways affected by intravitreal injections of dexamethasone and triamcinolone acetonide in mice at clinically relevant time points for patient care. Methods. Differential gene expression of over 34,000 well-characterized mouse genes in the RPE/choroid of 6-week-old C57BL/6J mice was analyzed after intravitreal steroid injections at 1 week and 1 month postinjection, using Affymetrix Mouse Genome 430 2.0 microarrays. The data were analyzed using GeneSpring GX 12.5 and Ingenuity Pathway Analysis (IPA) microarray analysis software for biologically relevant changes. Results. Both triamcinolone and dexamethasone caused differential activation of genes involved in "Circadian Rhythm Signaling" pathway at both time points tested. Triamcinolone (TAA) uniquely induced significant changes in gene expression in "Calcium Signaling" (1 week) and "Glutamate Receptor Signaling" pathways (1 month). In contrast, dexamethasone (Dex) affected the "GABA Receptor Signaling" (1 week) and "Serotonin Receptor Signaling" (1 month) pathways. Understanding how intraocular steroids affect the gene expression of RPE/choroid is clinically relevant. Conclusions. This in vivo study has elucidated several genes and pathways that are potentially altering the circadian rhythms and several other neurotransmitter pathways in RPE/choroid during intravitreal steroid injections, which likely has consequences in the dysregulation of RPE function and neurodegeneration of the retina.

Improving visual outcomes by preserving outer retina morphology in eyes with resolved pseudophakic cystoid macular edema.

PURPOSE: To use ultra-high-resolution optical coherence tomography (OCT) subclinical anatomic alterations to explain suboptimum vision despite pseudophakic cystoid macula edema (CME) resolution. SETTING: University of California-Davis, Sacramento, California, USA. DESIGN: Case study. METHODS: This study comprised patients who had cataract phacoemulsification surgery. Cases of resolved postoperative CME (diagnosed postoperatively by 1 month and resolved by 1 year) were included. Exclusion criteria included any other cause for decreased vision or compounding factors. Patients with a history of resolved pseudophakic CME were imaged using a purpose-built ultra-high-resolution OCT system with 4.5 µm axial resolution and an acquisition speed of 9 frames/sec (1000 A-scans/frame). The corrected distance visual acuity (CDVA) was determined by Early Treatment Diabetic Retinopathy Study standards. Statistical analysis was by the unpaired t test. A P value less than 0.05 was considered significant. RESULTS: The review identified 56 patients with a pseudophakic CME diagnosis at least 1 month postoperatively. Fifteen eyes (26.8%) had less than 20/20 CDVA despite resolution of CME; 7 participated. Four patients with 20/20 CDVA after resolution of pseudophakic CME participated. Eyes with reduced CDVA after macula edema showed ultra-high-resolution OCT evidence of blurring of outer segments of photoreceptors, while controls showed normal outer retina morphology (P<.05). CONCLUSIONS: Persistent anatomic alteration of photoreceptors visualized by ultra-high-resolution OCT correlated with reduced CDVA in patients with pseudophakic CME compared with patients who had 20/20 CDVA after macula edema. This anatomic alteration in outer photoreceptor morphology is a plausible explanation for the reduced CDVA in this disease. FINANCIAL DISCLOSURE: No author has a financial or proprietary interest in any material or method mentioned.

In vivo gene expression profiling of retina postintravitreal injections of dexamethasone and triamcinolone at clinically relevant time points for patient care.

PURPOSE: To identify retinal genes and their relevant expression pathways affected by intravitreal injections of dexamethasone (Dex) and triamcinolone acetonide (TAA) in mice at clinically relevant time points for patient care. METHODS: Differential gene expressions of over 34,000 well-characterized mouse genes, in the retinas of 6-week-old C57BL/6J mice, were analyzed after intravitreal steroid injections at 1 week and 1 month time points, using mouse genome microarrays. The data were analyzed using commercial microarray analysis software for biologically relevant changes in gene expression pathways. RESULTS: A common gene pathway, with differentially activated genes for both steroids and time points, was "Semaphorin Signaling in Neurons," a member of the "Axonal Guidance Signaling System." At 1 week postinjection a common theme was activation of genes expressed in retinal glial cells, tumor necrosis factor-α, and transforming growth factor-ß signaling pathways and upregulation of stress response proteins (Serpina3n, Cebpd), as well as neuropeptide signaling somatostatin receptor (Sstr2). Unique for Dex was the upregulation of acute phase proteins (Gfap, Cp, Edn2) as well as Plexna2, a semaphorin signaling receptor, whereas EphrinB receptor ephexin 1 (Argef15) was downregulated. Folate signaling appears to be unique for TAA at 1 week (Folh1, Cubn), whereas aryl-hydrocarbon receptor signaling might be important for both steroids at 1 month postinjection. CONCLUSIONS: Understanding the molecular and genetic effects of intraocular steroid treatments is of clinical relevance. This in vivo study has elucidated several genes and pathways that are potentially altering the neuroprotective/neurodegenerative balance between glial and retinal ganglion cells during intravitreal steroid treatment.

Lipids and age-related macular degeneration.

Given the considerable public health burden imposed by age-related macular degeneration (AMD), much effort has been directed towards elucidating principles of pathogenesis in order to identify risk factors and develop preventive measures and treatments. Together with epidemiological evidence linking cardiovascular risk factors with AMD risk and basic science work examining the role of lipid metabolism in AMD, numerous human studies have assayed a potential relationship between dietary lipids and the development of AMD. We examine the evidence for a role for lipid metabolism in AMD, highlighting key basic biochemical principles, work in animal models, and relevant human studies. The topics of lipoprotein modulation and omega-3 fatty acid intake receive special attention from both a basic science and clinical study standpoint. The evidence suggests that consumption of omega-3 fatty acids, perhaps in concert with antioxidants, may constitute a rational preventative strategy against AMD development, though, absent an appropriately developed double-blind, randomized control trial, insufficient data exist to recommend implementation in the clinical setting at this time.

Neuroretinitis associated with serologies positive for bartonella henselae and borrelia burgdorferi.

PURPOSE: To describe a patient with neuroretinitis with features of both cat-scratch disease and Lyme disease who had serologies positive for both Bartonella henselae and Borrelia burgdorferi. METHODS: Case report of a single individual undergoing diagnostic testing and treatment for neuroretinitis. RESULTS: A 47-year-old woman developed acute painless loss of vision and was found to have neuroretinitis. Diagnostic workup yielded serologies positive for both B. henselae and B. burgdorferi. The patient was treated with oral antibiotics for coverage of both etiologies, and her condition improved. CONCLUSION: Serologies positive for both B. henselae and B. burgdorferi can be obtained in the workup of neuroretinitis. Clinicians should be aware and use clinical judgment in guiding their diagnosis and treatment of neuroretinitis.

Gender: a possible determinant in dosing of dermatologic drugs--an overview.

The role of gender in pharmacokinetics could play a significant role in tailoring HIV and other drug regimens. Here we investigate sex as a factor in saquinavir pharmacokinetics. The HIV-positive women who use saquinavir in combination with other protease inhibitors frequently demonstrate higher saquinavir concentrations than their male counterparts. The majority of the data indicates that the root of women's higher saquinavir concentrations is not inherent to their gender. Rather, extenuating factors associated with HIV play a prominent role in the observed difference between men and women's pharmacokinetic parameters. The source of observed differences in saquinavir pharmacokinetics could not be definitively traced to CYP3A, the enzyme responsible for saquinavir's metabolism or drug transporters. Hormonal changes associated with HIV infection together with concurrent use of other protease inhibitors could help explain development of sex differences. These findings can be used to further investigate when and why gender-based differences in saquinavir pharmacokinetics exist and possible future dosage and therapy considerations. Our knowledge of gender-related pharmacokinetics should be extended for other systemic drugs in dermatology.