DOCSLIB.ORG

Increased Homocysteine Levels in Tear Fluid of Patients with Primary Open-Angle Glaucoma

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Increased Homocysteine Levels in Tear Fluid of Patients with Primary Open-Angle Glaucoma Original Paper Ophthalmic Res 2008;40:249–256 Received: September 20, 2006 DOI: 10.1159/000127832 Accepted after revision: July 6, 2007 Published online: April 25, 2008 Increased Homocysteine Levels in Tear Fluid of Patients with Primary Open-Angle Glaucoma a b a c b J.B. Roedl S. Bleich U. Schlötzer-Schrehardt N. von Ahsen J. Kornhuber a a a G.O.H. Naumann F.E. Kruse A.G.M. Jünemann a b Department of Ophthalmology, University Eye Hospital, and Department of Psychiatry and Psychotherapy, c Friedrich-Alexander University, Erlangen-Nuremberg , and Department of Clinical Chemistry, Georg-August University, Goettingen , Germany Key Words Introduction Glaucoma ؒ Homocysteine ؒ Tears ؒ Vitamins The pathogenesis of primary open-angle glaucoma (POAG) is still not fully understood. There is accumulat- Abstract ing evidence that vascular [1] , extracellular matrix [2] , Aims: We assessed homocysteine (Hcy) levels in tear fluid and neurotoxic [3] changes contribute to the develop- and plasma of patients with primary open-angle glaucoma ment of POAG besides increased intraocular pressure (POAG). We determined the association between Hcy levels, (IOP). Extracellular matrix and proinflammatory chang- dry eye syndrome and B vitamin status. Methods: This pro- es are also involved in ocular surface disorders seen in spective case-control study included 36 patients with POAG POAG including fibrosis of the filtering bleb after tra- and 36 controls. Hcy concentrations were measured by high- beculectomy [4, 5] and dry eye syndrome [6, 7] . performance liquid chromatography. Results: Patients with Homocysteine (Hcy) is a highly reactive amino acid POAG had significantly higher mean Hcy levels both in tear that can induce typical pathological changes found in fluid (205 8 84 nmol/l; p ! 0.001, t test) and in plasma (13.43 POAG including apoptotic death of retinal ganglion cells 8 3.53 ␮ mol/l; p = 0.001, t test) than control subjects (130 8 [3] , vascular [8–10] , extracellular matrix [8, 11, 12] , and 53 nmol/l and 10.50 8 3.33 ␮ mol/l, respectively). Hcy in tear proinflammatory alterations [13] . In POAG and pseudo- fluid was significantly correlated with plasma Hcy in POAG exfoliation glaucoma (PEXG), elevated plasma Hcy levels patients (r = 0.459; p = 0.005, Pearson’s correlation), but not were observed in previous studies of our group [14–17] . in controls (r = 0.068; p = 0.695). POAG patients with dry eye Moreover, increased Hcy values in aqueous humor were disease had significantly higher Hcy levels both in tear fluid found both in POAG [17] and in PEXG [16] . Accordingly, and plasma than POAG patients without dry eye disease. we detected a significantly higher prevalence of the most There was no association between Hcy levels and B vitamin common genetic cause for hyperhomocysteinemia in status in subjects with POAG. Conclusions: The study sug- POAG [18] . Several following studies confirmed our re- gests increased Hcy levels in tear fluid and plasma of pa- sults of increased Hcy levels in PEXG [19, 20] . Hyperho- tients with POAG. Elevated Hcy levels might be a risk factor mocysteinemia was also shown to be a risk factor for var- for POAG and dry eye syndrome in subjects with glaucoma. ious other ocular diseases [21–23] . However, there are in- Copyright © 2008 S. Karger AG, Basel © 2008 S. Karger AG, Basel Johannes B. Roedl, MD, Department of Ophthalmology 0030–3747/08/0405–0249$24.50/0 Friedrich-Alexander University of Erlangen-Nuremberg Fax +41 61 306 12 34 Schwabachanlage 6, DE–91054 Erlangen (Germany) E-Mail [email protected] Accessible online at: Tel. +49 9131 853 4519, Fax +49 9131 853 6401 www.karger.com www.karger.com/ore E-Mail [email protected] Table 1. Characteristics of POAG patients and controls Nongenetic determinants of Hcy Controls POAG p value (n = 36) (n = 36) (differences) Age (mean 8 SD), years 68.589.8 67.388.2 0.59a Male sex 17 (48) 15 (42) 0.81b Caffeinated beverages (>3 per day) 13 (36) 12 (33) 1.0b Alcoholic drinks (>1 per day) 5 (14) 7 (20) 0.54b Smoking 6 (17) 8 (22) 0.77b Systemic hypertension 12 (33) 14 (39) 0.81b Diabetes mellitus 4 (11) 5 (14) 1.0b Hyperlipidemia 6 (17) 4 (11) 0.74b Atherosclerotic vascular disease 4 (11) 3 (8) 1.0b Figures in parentheses are percentages. a t test; b Fisher’s exact test. consistent results in the literature regarding plasma Hcy mm Hg), and normal eye examination, including open angles, levels of POAG patients [14, 17, 24–27] , possibly due to normal appearance of the optic disks and normal visual fields. Each patient was evaluated for dry eye syndrome based on three different assessments of critical determinants of Hcy, criteria which had been used in previous studies [28, 29] : (1) his- such as nutritional and B vitamin status of enrolled sub- tory of, treatment of, or symptoms of dry eye syndrome defined jects. In order to illuminate the role of Hcy in glaucoma- according to the Ocular Surface Disease Index [30] questionnaire; tous neuropathy and its possible implication in ocular (2) tear dynamics which were assessed by the Schirmer 1 test and surface disorders associated with POAG, we evaluated as- tear breakup time; if one of those two tests was positive (Schirm- er 1 test ! 10 mm, or breakup time ! 10 s), the tear dynamics were sociations between Hcy in plasma, Hcy in tear fluid, and considered abnormal; (3) ocular surface abnormalities which blood B vitamins. were identified by positive vital staining with fluorescein. Pa- tients with positive results in all three criteria were considered to have definite dry eye, whereas patients with abnormalities in only two of the three criteria were defined to have probable dry eye Materials and Methods disease [28] . Exclusion criteria for controls and POAG patients were: medical history of disorders associated with increased Hcy Patients and Design levels such as thromboembolic, renal, hepatic, gastrointestinal or In this investigation, 36 consecutive Caucasian German pa- neurologic disease, as well as prior ocular surgery, a history of tients with POAG and 36 healthy controls without glaucoma, but ocular inflammation, age-related macular degeneration, diabetic concurrent diagnosis of cataract were enrolled. All subjects un- retinopathy, myopia, retinal occlusive disease, rubeosis iridis and derwent glaucoma or cataract surgery at the Department of Oph- glaucoma other than POAG. Patients taking hormone substitu- thalmology at the University of Erlangen-Nuremberg, Germany. tion and medications known to affect Hcy measurements were Patients of the present clinical trial were not enrolled in any of our excluded. previous studies [14–17] . Informed consent was obtained from all Matching of controls and POAG patients was performed by participants after detailed explanation of the purpose and meth- demographic, common clinical, and lifestyle factors known to ods of the trial. The University of Erlangen-Nuremberg Human cause increased Hcy levels ( table 1 ) [31] . Subjects Committee approved all protocols of this prospective Nutritional and lifestyle status was assessed using the Sub- case-control study, and the methods described adhered to the te- jective Global Nutritional Assessment test [32] . Since all pa- nets of the Declaration of Helsinki. All controls and patients were tients and controls were classified as well nourished, we used 11.7 thoroughly examined by slit lamp inspection, applanation to- ␮ mol/l as the primary cutoff value to define hyperhomocystein- nometry, fundoscopy, gonioscopy, pupillometry, and perimetry emia as in previous investigations [14, 16] . Additionally, we per- (Octopus 101, program G1). All POAG patients had open angles formed statistical analysis with 15.0 ␮ mol/l as the threshold. on gonioscopy, characteristic glaucomatous optic disk damage Twenty-nine of the 36 patients in the POAG group were on topical (excavation, presence of neuroretinal rim thinning, notching, or antiglaucomatous therapy: 53% (19/36) of the POAG patients were retinal nerve fiber layer defects), and pathological cumulative on beta-blocker, 47% (17/36) on prostaglandin analog, 36% (13/36) perimetric defect curves, that is, local as well as diffuse visual field on carbonic anhydrase inhibitor, 19% (7/36) on alpha-agonist, 3% loss in white-on-white perimetry. In POAG patients, the mean (1/36) on cholinergic, and 3% (1/36) on adrenergic topical medica- duration of disease was 11.2 8 5.2 years, the mean IOP was 18.3 tion. In order to avoid the possible influence of eyedrops on Hcy 8 2.7 mm Hg, and the global indices mean defect was 11.7 8 2.5 measurements, topical therapy was stopped in all patients at least dB. Control subjects had no history of ocular disease (except re- 12 h prior to sampling of reflex tears. fractive error, strabismus, or cataracts), normal IOP values (! 21 250 Ophthalmic Res 2008;40:249–256 Roedl et al. L a b o r a t o r y A n a l y s e s All patients underwent blood and tear fluid collection at the 500 25 day of ocular surgery, ensuring that the patients were fasting. Se- cretion of reflex tears was incited by the yawn reflex and by stim- 400 20 ulation of the trigeminal nerve with a nasal alcohol stimulus. A disposable glass capillary was placed near the cul-de-sac of the eye and 100 ␮ l of tear fluid were collected according to Choy et al. 300 15 [33] . Reflex tear collection with the capillary tube was shown to be the method of choice in the study by Choy et al. [33] . They com- pared basal tears with reflex tears as sources of tear fluid, and 200 10 Schirmer strips with capillary tubes as collection methods. The Plasma Hcy (µmol/l) Schirmer strips have the disadvantage that they are associated Lacrimal fluid Hcy (nmol/l) 100 5 with direct conjunctival contact and therefore risk of vascular transudation and cell damage with leakage of plasma and intra- cellular constituents [34, 35] .
Load more

Recommended publications
  • 12 Retina Gabriele K
    299 12 Retina Gabriele K. Lang and Gerhard K. Lang 12.1 Basic Knowledge The retina is the innermost of three successive layers of the globe. It comprises two parts: ❖ A photoreceptive part (pars optica retinae), comprising the first nine of the 10 layers listed below. ❖ A nonreceptive part (pars caeca retinae) forming the epithelium of the cil- iary body and iris. The pars optica retinae merges with the pars ceca retinae at the ora serrata. Embryology: The retina develops from a diverticulum of the forebrain (proen- cephalon). Optic vesicles develop which then invaginate to form a double- walled bowl, the optic cup. The outer wall becomes the pigment epithelium, and the inner wall later differentiates into the nine layers of the retina. The retina remains linked to the forebrain throughout life through a structure known as the retinohypothalamic tract. Thickness of the retina (Fig. 12.1) Layers of the retina: Moving inward along the path of incident light, the individual layers of the retina are as follows (Fig. 12.2): 1. Inner limiting membrane (glial cell fibers separating the retina from the vitreous body). 2. Layer of optic nerve fibers (axons of the third neuron). 3. Layer of ganglion cells (cell nuclei of the multipolar ganglion cells of the third neuron; “data acquisition system”). 4. Inner plexiform layer (synapses between the axons of the second neuron and dendrites of the third neuron). 5. Inner nuclear layer (cell nuclei of the bipolar nerve cells of the second neuron, horizontal cells, and amacrine cells). 6. Outer plexiform layer (synapses between the axons of the first neuron and dendrites of the second neuron).
    [Show full text]
  • RETINAL DISORDERS Eye63 (1)
    RETINAL DISORDERS Eye63 (1) Retinal Disorders Last updated: May 9, 2019 CENTRAL RETINAL ARTERY OCCLUSION (CRAO) ............................................................................... 1 Pathophysiology & Ophthalmoscopy ............................................................................................... 1 Etiology ............................................................................................................................................ 2 Clinical Features ............................................................................................................................... 2 Diagnosis .......................................................................................................................................... 2 Treatment ......................................................................................................................................... 2 BRANCH RETINAL ARTERY OCCLUSION ................................................................................................ 3 CENTRAL RETINAL VEIN OCCLUSION (CRVO) ..................................................................................... 3 Pathophysiology & Etiology ............................................................................................................ 3 Clinical Features ............................................................................................................................... 3 Diagnosis .........................................................................................................................................
    [Show full text]
  • Neovascular Glaucoma: Etiology, Diagnosis and Prognosis
    Seminars in Ophthalmology, 24, 113–121, 2009 Copyright C Informa Healthcare USA, Inc. ISSN: 0882-0538 print / 1744-5205 online DOI: 10.1080/08820530902800801 Neovascular Glaucoma: Etiology, Diagnosis and Prognosis Tarek A. Shazly Mark A. Latina Department of Ophthalmology, Department of Ophthalmology, Massachusetts Eye and Ear Massachusetts Eye and Ear Infirmary, Boston, MA, USA, and Infirmary, Boston, MA, USA and Department of Ophthalmology, Department of Ophthalmology, Tufts Assiut University Hospital, Assiut, University School of Medicine, Egypt Boston, MA, USA ABSTRACT Neovascular glaucoma (NVG) is a severe form of glaucoma with devastating visual outcome at- tributed to new blood vessels obstructing aqueous humor outflow, usually secondary to widespread posterior segment ischemia. Invasion of the anterior chamber by a fibrovascular membrane ini- tially obstructs aqueous outflow in an open-angle fashion and later contracts to produce secondary synechial angle-closure glaucoma. The full blown picture of NVG is characteristized by iris neovas- cularization, a closed anterior chamber angle, and extremely high intraocular pressure (IOP) with severe ocular pain and usually poor vision. Keywords: neovascular glaucoma; rubeotic glaucoma; neovascularization; retinal ischemia; vascular endothe- lial growth factor (VEGF); proliferative diabetic retinopathy; central retinal vein occlusion For personal use only. INTRODUCTION tive means of reversing well established NVG and pre- venting visual loss in the majority of cases; instead bet- The written
    [Show full text]
  • Genes in Eyecare Geneseyedoc 3 W.M
    Genes in Eyecare geneseyedoc 3 W.M. Lyle and T.D. Williams 15 Mar 04 This information has been gathered from several sources; however, the principal source is V. A. McKusick’s Mendelian Inheritance in Man on CD-ROM. Baltimore, Johns Hopkins University Press, 1998. Other sources include McKusick’s, Mendelian Inheritance in Man. Catalogs of Human Genes and Genetic Disorders. Baltimore. Johns Hopkins University Press 1998 (12th edition). http://www.ncbi.nlm.nih.gov/Omim See also S.P.Daiger, L.S. Sullivan, and B.J.F. Rossiter Ret Net http://www.sph.uth.tmc.edu/Retnet disease.htm/. Also E.I. Traboulsi’s, Genetic Diseases of the Eye, New York, Oxford University Press, 1998. And Genetics in Primary Eyecare and Clinical Medicine by M.R. Seashore and R.S.Wappner, Appleton and Lange 1996. M. Ridley’s book Genome published in 2000 by Perennial provides additional information. Ridley estimates that we have 60,000 to 80,000 genes. See also R.M. Henig’s book The Monk in the Garden: The Lost and Found Genius of Gregor Mendel, published by Houghton Mifflin in 2001 which tells about the Father of Genetics. The 3rd edition of F. H. Roy’s book Ocular Syndromes and Systemic Diseases published by Lippincott Williams & Wilkins in 2002 facilitates differential diagnosis. Additional information is provided in D. Pavan-Langston’s Manual of Ocular Diagnosis and Therapy (5th edition) published by Lippincott Williams & Wilkins in 2002. M.A. Foote wrote Basic Human Genetics for Medical Writers in the AMWA Journal 2002;17:7-17. A compilation such as this might suggest that one gene = one disease.
    [Show full text]
  • Anterior Segment Ischemia with Rubeosis Iridis After A
    ANTERIOR SEGMENT ISCHEMIA WITH RUBEOSIS IRIDIS AFTER A CIRCULAR BUCKLING OPERATION TREATED SUCCESSFULLY WITH AN INTRAVITREAL BEVACIZUMAB INJECTION: A CASE REPORT AND REVIEW OF THE LITERATURE JANSSENS K, ZEYEN T, VAN CALSTER J ABSTRACT ly detection of rubeosis iridis. This report demon- strates the rapid resolution of rubeosis iridis on iris Purpose: To report a case of anterior segment ischemia fluorescein angiography after a second intravitreal in- (ASI) with rubeosis iridis after circular buckling sur- jection of bevacizumab. How long this regression will gery in a highly-myopic patient which was success- persist is unknown and repeated injections of fully treated with a second intravitreal bevacizumab bevacizumab may be necessary if rubeosis re- injection. appears. Methods: Case report and review of the literature. KEYWORDS Discussion: ASI is a rare but potentially serious com- plication of posterior segment surgery. Finally it leads Anterior segment ischemia (ASI); rubeosis iridis; to neovascular glaucoma as a result of rubeosis iri- neovascular glaucoma (NVG); circular buckling dis. An encircling band can compromise anterior seg- surgery; intravitreal bevacizumab (IVB); iris ment circulation in different ways: by manipulation fluorescein angiography. or disinsertion of the recti muscles, by occlusion of the vortex veins through compression or by changes in the blood supply of iris and ciliary body. This pa- tient developed rubeosis iridis secondary to ASI. There was a remarkable regression of rubeosis iridis one month after a second intravitreal bevacizumab in- jection. Other case reports of bevacizumab use in neovascular glaucoma have shown clinical improve- ments of these patients, with intraocular pressure control and reduction of the neovascularization process.
    [Show full text]
  • Redalyc.Uveitis in Dogs Infected with Ehrlichia Canis
    Ciência Rural ISSN: 0103-8478 [email protected] Universidade Federal de Santa Maria Brasil Pontes Oriá, Arianne; Mendes Pereira, Patrícia; Laus, José Luiz Uveitis in dogs infected with Ehrlichia canis Ciência Rural, vol. 34, núm. 4, julho-agosto, 2004, pp. 1289-1295 Universidade Federal de Santa Maria Santa Maria, Brasil Disponível em: http://www.redalyc.org/articulo.oa?id=33134455 Como citar este artigo Número completo Sistema de Informação Científica Mais artigos Rede de Revistas Científicas da América Latina, Caribe , Espanha e Portugal Home da revista no Redalyc Projeto acadêmico sem fins lucrativos desenvolvido no âmbito da iniciativa Acesso Aberto Ciência Rural, Santa Maria, v.34, n.4, p.1289-1295,Uveitis jul-ago, in dogs 2004 infected with Ehrlichia canis. 1289 ISSN 0103-8478 Uveitis in dogs infected with Ehrlichia canis Uveíte em cães infectados com Ehrlichia canis Arianne Pontes Oriá1 Patrícia Mendes Pereira1 José Luiz Laus2 - REVISÃO BIBLIOGRÁFICA - RESUMO ANATOMY AND PHYSIOLOGY OF THE UVEAL TRACT As uveítes, que se constituem em oftalmopatias comuns entre os cães, decorrem de inúmeras causas. Em nosso meio, destaca-se a erliquiose. Este artigo discute as várias causas Uveitis refers to the inflammation of the da enfermidade ocular, bem como aspectos importantes da uveal tract, which is the vascular and pigmented coat enfermidade parasitária, incluindo os sinais, o diagnóstico e o of the eye (HAKANSON & FORRESTER, 1990). The tratamento. uveal tract or uvea is deeply located on the sclera, Palavras-chave: canino, corioretinite, hifema, uveíte, Ehrlichia where it attaches itself. It consists of three zones: canis. choroid, ciliary body and iris (HAKANSON & FORRESTER, 1990).
    [Show full text]
  • Canine Red Eye Elizabeth Barfield Laminack, DVM; Kathern Myrna, DVM, MS; and Phillip Anthony Moore, DVM, Diplomate ACVO
    PEER REVIEWED Clinical Approach to the CANINE RED EYE Elizabeth Barfield Laminack, DVM; Kathern Myrna, DVM, MS; and Phillip Anthony Moore, DVM, Diplomate ACVO he acute red eye is a common clinical challenge for tion of the deep episcleral vessels, and is characterized general practitioners. Redness is the hallmark of by straight and immobile episcleral vessels, which run Tocular inflammation; it is a nonspecific sign related 90° to the limbus. Episcleral injection is an external to a number of underlying diseases and degree of redness sign of intraocular disease, such as anterior uveitis and may not reflect the severity of the ocular problem. glaucoma (Figures 3 and 4). Occasionally, episcleral Proper evaluation of the red eye depends on effective injection may occur in diseases of the sclera, such as and efficient diagnosis of the underlying ocular disease in episcleritis or scleritis.1 order to save the eye’s vision and the eye itself.1,2 • Corneal Neovascularization » Superficial: Long, branching corneal vessels; may be SOURCE OF REDNESS seen with superficial ulcerative (Figure 5) or nonul- The conjunctiva has small, fine, tortuous and movable vessels cerative keratitis (Figure 6) that help distinguish conjunctival inflammation from deeper » Focal deep: Straight, nonbranching corneal vessels; inflammation (see Ocular Redness algorithm, page 16). indicates a deep corneal keratitis • Conjunctival hyperemia presents with redness and » 360° deep: Corneal vessels in a 360° pattern around congestion of the conjunctival blood vessels, making the limbus; should arouse concern that glaucoma or them appear more prominent, and is associated with uveitis (Figure 4) is present1,2 extraocular disease, such as conjunctivitis (Figure 1).
    [Show full text]
  • Vascular Changes in the Iris in Chronic Anterior Uveitis LEILA LAATIKAINEN from the Department of Ophthalmology, University of Helsinki, Finland
    Br J Ophthalmol: first published as 10.1136/bjo.63.3.145 on 1 March 1979. Downloaded from British Journal of Ophthalmology, 1979, 63, 145-149 Vascular changes in the iris in chronic anterior uveitis LEILA LAATIKAINEN From the Department of Ophthalmology, University of Helsinki, Finland SUMMARY Vascular changes of the iris were studied in 6 patients with chronic anterior uveitis of varying aetiology by means of fluorescein angiography. In 1 case the angiographic findings of the second eye were compared with the histopathological changes in the fellow eye enucleated earlier because of absolute glaucoma. In the milder cases abnormal superficial vessels were seen mainly in relation to the minor arterial circle of the iris, while in advanced cases a coarse vascular network covered the whole surface of the iris. Both mild and severe changes were found to differ from the arborising type of neovascularisation usually seen in vascular eye diseases. Instead, a resemblance in the vascular pattern was found between some of these cases and eyes with chronic capsular glaucoma. In 1 patient clinical rubeosis seemed to be partly due to dilatation of the pre-existing capillaries rather than true neovascularisation. Rubeosis iridis is one of the late complications of with bilateral chronic uveitis, and 1 case with many vascular, neoplastic, and inflammatory eye phakogenic iridocyclitis due to traumatic cataract diseases (Schulze, 1967; Hoskins, 1974). It has and subluxation of the lens. Further details of the therefore been considered to be a nonspecific patients are presented in Table 1. reaction of the iris vasculature to a variety of The technique used in fluorescein angiography of noxious stimuli.
    [Show full text]
  • Clinical Practice Guidelines: Care of the Patient with Anterior Uveitis
    OPTOMETRY: OPTOMETRIC CLINICAL THE PRIMARY EYE CARE PROFESSION PRACTICE GUIDELINE Doctors of optometry are independent primary health care providers who examine, diagnose, treat, and manage diseases and disorders of the visual system, the eye, and associated structures as well as diagnose related systemic conditions. Optometrists provide more than two-thirds of the primary eye care services in the United States. They are more widely distributed geographically than other eye care providers and are readily accessible for the delivery of eye and vision care services. There are approximately 32,000 full-time equivalent doctors of optometry currently in practice in the United States. Optometrists practice in more than 7,000 communities across the United States, serving as the sole primary eye care provider in more than 4,300 communities. Care of the Patient with The mission of the profession of optometry is to fulfill the vision and eye Anterior Uveitis care needs of the public through clinical care, research, and education, all of which enhance the quality of life. OPTOMETRIC CLINICAL PRACTICE GUIDELINE CARE OF THE PATIENT WITH ANTERIOR UVEITIS Reference Guide for Clinicians Prepared by the American Optometric Association Consensus Panel on Care of the Patient with Anterior Uveitis: Kevin L. Alexander, O.D., Ph.D., Principal Author Mitchell W. Dul, O.D., M.S. Peter A. Lalle, O.D. David E. Magnus, O.D. Bruce Onofrey, O.D. Reviewed by the AOA Clinical Guidelines Coordinating Committee: John F. Amos, O.D., M.S., Chair Kerry L. Beebe, O.D. Jerry Cavallerano, O.D., Ph.D. John Lahr, O.D.
    [Show full text]
  • Intravitreal Angiogenesis Inhibitors
    Intravitreal Angiogenesis Inhibitors Number: OTH903.020, OTH903.027 Effective Date: 02-15-2019 Coverage: *CAREFULLY CHECK STATE REGULATIONS AND/OR THE MEMBER CONTRACT* Medical policies are a set of written guidelines that support current standards of practice. They are based on current peer-reviewed scientific literature. A requested therapy must be proven effective for the relevant diagnosis or procedure. For drug therapy, the proposed dose, frequency and duration of therapy must be consistent with recommendations in at least one authoritative source. This medical policy is supported by FDA- approved labeling and nationally recognized authoritative references. These references include, but are not limited to: MCG care guidelines, DrugDex (IIb strength of recommendation or higher), NCCN Guidelines (IIb level of evidence or higher), NCCN Compendia (IIb level of evidence or higher), professional society guidelines, and CMS coverage policy. Intravitreal injection of anti-VEGF therapies, i.e., pegaptanib (Macugen®), ranibizumab (Lucentis™), bevacizumab (Avastin™), or aflibercept (Eylea™), may be considered medically necessary for the treatment of neovascular (wet) age-related macular degeneration (AMD). Intravitreal injection of anti-VEGF therapies may be considered medically necessary for the treatment of choroidal neovascularization (CNV; includes myopic CNV or mCNV) due to: • Angioid streaks, • Central serous chorioretinopathy, • Choroidal retinal neovascularization, secondary to pathologic myopia, • Choroidal retinal neovascularization,
    [Show full text]
  • Rubeosis Iridis After Vitrectomy for Diabetic Retinopathy
    Graefe's Arch Clin Exp Ophthalmol (1998) 236:730±733 Springer-Verlag 1998 CLINICAL INVESTIGATION Horst Helbig Rubeosis iridis after vitrectomy Ulrich Kellner Norbert Bornfeld for diabetic retinopathy Michael H. Foerster Received: 3 December 1997 Abstract l Background: Iris rubeo- erative retinal detachment. Six Revised version received: 18 February 1998 sis and neovascular glaucoma (NVG) months after surgery, regression of Accepted: 27 February 1998 are serious complications of vitrec- preexisting iris rubeosis was observed tomy for proliferative diabetic reti- in 57% of the eyes. In eyes without nopathy. The present study analyzes preoperative iris rubeosis, progres- Presented at the annual meeting of the incidence and risk factors of these sion was found in 13% of cases 6 Deutsche Ophthalmologische Gesellschaft, 20.±23. September 1997, Berlin complications. l Methods: Preoper- months postoperatively. l Conclu- ative and postoperative iris rubeosis sion: With current surgical tech- H. Helbig ´ U. Kellner ´ N. Bornfeld were compared in 389 diabetic eyes niques iris rubeosis is more com- M.H. Foerster after vitrectomy. Minimum follow-up monly regressive than progressive Augenklinik, was 6 months (median 26 months). after vitreous surgery in diabetic Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Berlin, Germany Risk factors were studied using mul- eyes. tivariate logistic regression analysis. H. Helbig ()) l Results: Following vitrectomy, in Klinik für Augenkrankheiten, Kantonsspital St. Gallen, 8.5% of the eyes stromal iris rubeosis CH-9007 St. Gallen, Switzerland developed de novo; NVG occurred in Tel. +41-71-4941754; fax +41-71-4942881 5%. Significant risk factors for post- N. Bornfeld operative rubeosis were preexisting Augenklinik, Universität Essen, Essen iris neovascularizations and postop- Introduction Methods Rubeosis of the iris and neovascular glaucoma (NVG) are Between 1990 and 1994, a total of 337 patients (420 eyes) were op- serious complications of diabetic eye disease.
    [Show full text]
  • Ophthalmologic Policy: Vascular Endothelial Growth Factor (VEGF) Inhibitors
    UnitedHealthcare® Value & Balance Exchange Medical Benefit Drug Policy Ophthalmologic Policy: Vascular Endothelial Growth Factor (VEGF) Inhibitors Policy Number: IEXD0042.02 Effective Date: June 1, 2021 Instructions for Use Table of Contents Page Related Policies Applicable States ........................................................................... 1 • Macular Degeneration Treatment Procedures Coverage Rationale ....................................................................... 1 • Maximum Dosage and Frequency Definitions ...................................................................................... 2 • Oncology Medication Clinical Coverage Applicable Codes .......................................................................... 3 Background.................................................................................. 24 Benefit Considerations ................................................................ 24 Clinical Evidence ......................................................................... 24 U.S. Food and Drug Administration ........................................... 35 References ................................................................................... 36 Policy History/Revision Information ........................................... 40 Instructions for Use ..................................................................... 40 Applicable States This Medical Benefit Drug Policy only applies to the states of Arizona, Maryland, North Carolina, Oklahoma, Tennessee, Virginia, and Washington.
    [Show full text]