Long-term follow-up results of ilm peeling during vitrectomy surgery for premacular fibrosis.

PURPOSE: To evaluate the outcomes of surgical removal of premacular fibrosis (PMF) with peeling of the internal limiting membrane (ILM). Determination of factors associated with favorable outcomes (visual acuity between 20/20 and 20/40). METHODS: Retrospective chart review, evaluating visual outcomes in 38 patients who underwent pars plana vitrectomy (PPV) and triamcinolone-assisted ILM peeling by a single surgeon between December 2003 and December 2004. Data collected included visual acuity before and 3 months after surgery, and at final follow-up, as well as complications (cataract formation, endophthalmitis, retinal detachment, vitreous hemorrhage, retinal or subretinal hemorrhage, macular hole formation, cystoid macular edema [CME], and PMF recurrence). RESULTS: Pretreatment visual acuity averaged at 20/90. Vision improved or was unchanged in 89.5% of operated eyes with ILM peeling. Average follow-up was 20.2 months. The average improvement in visual acuity was 2.2 lines. The most common complication was cataract formation. There were no other complications until patients underwent cataract extraction. Two patients developed CME within 4 weeks of cataract surgery. Biomicroscopic recurrence of PMF was an asymptomatic and rare event with an incidence of 2.6% (n = 1 of 38 patients). No adverse outcomes were noted in patients with higher levels of visual acuity and these were in fact the patients with best final visual acuity. CONCLUSION: ILM peeling may not have the harmful consequences previously attributed to it. Stripping of the ILM may reduce reformation rates of PMF. Surgical removal of PMF with ILM peeling was not associated with unfavorable outcomes in our group of patients.

Intravitreal bevacizumab for choroidal neovascularization in ocular histoplasmosis.

PURPOSE: To define the role of intravitreal bevacizumab in individuals with choroidal neovascularization (CNV) resulting from Ocular Histoplasmosis syndrome (OHS). DESIGN: Retrospective chart review of a surgical therapy. METHODS: We reviewed the course of 28 eyes of 28 patients who underwent intravitreal injection of bevacizumab for treatment of CNV secondary to OHS. Outcome was measured by pretreatment and posttreatment visual acuity (VA). RESULTS: The average pretreatment logarithm of the minimum angle of resolution (logMAR) VA was 0.65 (Snellen equivalent of 20/88). Mean follow-up was 22.43 weeks with an average of 1.8 intravitreal injections. Average final logMAR VA was 0.43 (Snellen equivalent of 20/54). Twenty eyes (71%) experienced an increase in central VA, whereas four eyes (14%) were unchanged and four eyes (14%) experienced a decrease in vision. CONCLUSIONS: Intravitreal bevacizumab may improve or stabilize VA in a significant majority of patients with neovascular complications of OHS (24 eyes [85.7%] in our study population).

Optical coherence tomography findings in autosomal dominant macular dystrophy.

The authors report a case of autosomal dominant cystoid macular dystrophy in which optical coherence tomography outlined the pathology and assisted in determining the etiology of the patient's macular edema.

Topiramate for the treatment of chronic corneal pain.

PURPOSE: To explore the option of using anticonvulsant drugs to modulate pain from corneal erosions. METHODS: N.M. is a 28-year-old woman with posttraumatic recurrent corneal erosions treated with bandage contact lenses, Muro-128, topical ketorolac, doxycycline, stromal micropuncture, and laser epithelial keratomileusis over the course of 4 years. Because of persistent episodes of corneal pain, she was prescribed topiramate. RESULTS: Before starting topiramate therapy, N.M. had experienced 3-4 awakenings at night because of pain and 5-6 episodes of spontaneous tearing and pain during the day. She started topiramate at 25 mg orally 4 times a day without significant change in her symptoms. After 1 week, the dose was escalated to 50 mg orally 4 times a day, and within 1 day, she experienced 0-1 awakenings at night. She had approximately 2-3 episodes of pain and tearing during the day. The dose was escalated to 100 mg orally 4 times a day. At that dose, the patient continued to have pain relief but complained of nausea. The patient's topiramate was weaned off to determine whether her symptom relief was caused by the medication or improvement in her condition. Once off the topiramate, N.M.'s nausea resolved but her corneal symptoms returned at the same frequency as before the initiation of topiramate. Therefore, she was restarted on topiramate 50 mg orally 4 times a day with rapid onset of improvement in her symptoms. CONCLUSIONS: Anticonvulsants such as topiramate may be effective in the management of pain caused by recurrent corneal erosions.

Intravitreal pharmacotherapy: applications in retinal disease.

Intravitreal pharmacotherapies have been used with increasing frequency in the treatment of retinal disease. Indications for their use include choroidal neovascular membranes, diabetic macular edema, ischemic neovascularization, inflammatory and infectious processes, and neoplasia. Complications of intravitreal therapies include cataract formation, glaucoma, and endophthalmitis. Recent developments of pharmacologic agents administered intravitreally and the new applications of systemic medications in retinal disease present the practitioner with expanded treatment options. Current and emerging data will help guide therapy in order to maximize the benefits and limit the systemic and ocular complications of these new treatment options.

Atrial natriuretic peptide enhances cortisol secretion from guinea-pig adrenal gland: evidence for an indirect paracrine mechanism probably involving the local release of medullary catecholamines.

Atrial natriuretic peptide (ANP) is a regulatory hormone widely expressed, along with its receptors, in organs and body tissues. ANP is well known to inhibit aldosterone secretion from mammalian adrenals, but its effect on glucocorticoid-hormone production is controversial. In vivo experiments showed that prolonged ANP administration raised the plasma concentration of cortisol in both normal and dexamethasone/captopril-treated guinea pigs (i.e. in animals with pharmacologically interrupted hypothalamic-pituitary-adrenal axis and renin-angiotensin system). ANP did not affect cortisol secretion from dispersed guinea pig zona fasciculata-reticularis cells, but enhanced catecholamine release from adrenomedullary cells. ANP stimulated cortisol output from guinea pig adrenal slices containing medullary chromaffin tissue, and the beta-adrenoceptor antagonist l-alprenolol blocked this effect. The conclusion is drawn that ANP, when the structural integrity of the adrenal gland is preserved, is able to enhance glucocorticoid secretion in guinea pigs, through an indirect mechanism involving the rise in the catecholamine release, which in turn, acting in a paracrine manner, stimulate secretion of inner adrenocortical cells.

Modulation of serum cortisol by substance P in albino rats: evidence of a direct effect on adrenal gland.

Effect of prolonged administration of substance P on the plasma cortisol level in the albino rats has been investigated. An inhibitory impact on intact individuals and a stimulatory effect in pharmacologically annulled rats has been observed. It is concluded that in normal conditions substance P presumably acts as a preventive agent for any excess secretion of cortisol while during stress or disturbed HPA or RAS conditions, it stimulates the secretion of cortisol. An intraglandular modulatory role of substance P has been suggested.

Presumed ocular histoplasmosis syndrome.

PURPOSE OF REVIEW: Presumed ocular histoplasmosis syndrome remains a significant cause of visual morbidity. We review recent literature on the pathogenesis and particularly on the treatment of complications of presumed ocular histoplasmosis syndrome. RECENT FINDINGS: The pathogenesis of presumed ocular histoplasmosis syndrome remains mysterious; although some recent molecular evidence suggests a direct link between Histoplasma capsulatum and presumed ocular histoplasmosis syndrome, other reports document nearly identical disease occurring in the absence of H. capsulatum seropositivity. Treatment options have advanced rapidly in the past few years. Small case series and clinical trials suggest excellent efficacy for photodynamic therapy in the treatment of subretinal neovascularization associated with presumed ocular histoplasmosis syndrome. Preliminary studies also suggest efficacy of intravitreal corticosteroids. A large randomized controlled clinical trial failed to show efficacy for subretinal surgery in the management of presumed ocular histoplasmosis syndrome, however. SUMMARY: Despite continued debate on the etiology of presumed ocular histoplasmosis syndrome, there have been significant advances in treatment of the blinding complications of presumed ocular histoplasmosis syndrome.

Intact {alpha}-1,2-endomannosidase is a typical type II membrane protein.

Rat endomannosidase is a glycosidic enzyme that catalyzes the cleavage of di-, tri-, or tetrasaccharides (Glc(1-3)Man), from N-glycosylation intermediates with terminal glucose residues. To date it is the only characterized member of this class of endomannosidic enzymes. Although this protein has been demonstrated to localize to the Golgi lumenal membrane, the mechanism by which this occurs has not yet been determined. Using the rat endomannosidase sequence, we identified three homologs, one each in the human, mouse, and rat genomes. Alignment of the four encoded protein sequences demonstrated that the newly identified sequences are highly conserved but differed significantly at the N-terminus from the previously reported protein. In this study we have cloned two novel endomannosidase sequences from rat and human cDNA libraries, but were unable to amplify the open reading frame of the previously reported rat sequence. Analysis of the rat genome confirmed that the 59- and 39-termini of the previously reported sequence were in fact located on different chromosomes. This, in combination with our inability to amplify the previously reported sequence, indicated that the N-terminus of the rat endomannosidase sequence previously published was likely in error (a cloning artifact), and that the sequences reported in the current study encode the intact proteins. Furthermore, unlike the previous sequence, the three ORFs identified in this study encode proteins containing a single N-terminal transmembrane domain. Here we demonstrate that this region is responsible for Golgi localization and in doing so confirm that endomannosidase is a type II membrane protein, like the majority of other secretory pathway glycosylation enzymes.

Environmental estrogens alter early development in Xenopus laevis.

A growing number of environmental toxicants found in pesticides, herbicides, and industrial solvents are believed to have deleterious effects on development by disrupting hormone-sensitive processes. We exposed Xenopus laevis embryos at early gastrula to the commonly encountered environmental estrogens nonylphenol, octylphenol, and methoxychlor, the antiandrogen, p,p-DDE, or the synthetic androgen, 17 alpha-methyltestosterone at concentrations ranging from 10 nM to 10 microM and examined them at tailbud stages (approximately 48 hr of treatment). Exposure to the three environmental estrogens, as well as to the natural estrogen 17 beta-estradiol, increased mortality, induced morphologic deformations, increased apoptosis, and altered the deposition and differentiation of neural crest-derived melanocytes in tailbud stage embryos. Although neural crest-derived melanocytes were markedly altered in embryos treated with estrogenic toxicants, expression of the early neural crest maker Xslug, a factor that regulates both the induction and subsequent migration of neural crest cells, was not affected, suggesting that the disruption induced by these compounds with respect to melanocyte development may occur at later stages of their differentiation. Co-incubation of embryos with the pure antiestrogen ICI 182,780 blocked the ability of nonylphenol to induce abnormalities in body shape and in melanocyte differentiation but did not block the effects of methoxychlor. Our data indicate not only that acute exposure to these environmental estrogens induces deleterious effects on early vertebrate development but also that different environmental estrogens may alter the fate of a specific cell type via different mechanisms. Finally, our data suggest that the differentiation of neural crest-derived melanocytes may be particularly sensitive to the disruptive actions of these ubiquitous chemical contaminants.