John pigment effects. testing plasmosis, ‘Assistant infections University occlusions neuropathy, Department toxoplasmosis, Scope lovirus microvascular show simplex of Kaposi’s tions, have 0.25 mosis people Columbia the likely approximately Cytomegalovirus microvasculopathy acquired deficiency Ophthalmologic Medications Over Although the agents A. percent Acquired significant to Burns anterior and involvement or of placed clinical 70% without Rifabutin-associated (CMV), cause , epithelial of herpetic of immunodeficiency Hawaii sarcoma, 90% can in School Surgery available are candida, syndrome Hawaii cranial the of 1996.’ professor of segment possible. 6 be used abnormalites, visual Hawaii of pneumocystis, patients 2,300 the of herpes infectious toxicities. findings seen. patients and (CMV) . Medicine problem atrophy The with population virus to dry of and to nerve is loss microsporidiosis. treat Ocular the slow to (AIDS) of at a Hawaii simplex, eyes, with endogenous Loss “HTV retinitis relatively (HIV) the and 3,200 19th in have Ganciclovi, palsies, the have the individuals syndrome eye nerve iritis 8 AIDS of must herpes are HIV progression among cryptococcus, or retinopathy” ocular Department live is visual been individuals is include: herpes one the fairly the fiber orbital be and patient small can in bacterial Immunodeficiency zoster reported. 9 disease of most the differentiated the function opportunistic foscarnet, (AIDS) Didanosine The with develop has layer common. every varicella-zoster, molluscum state, 50 islands. 2 lymphoma, can of of frequent retina the ophthalmicus, (retinal infected been states mycobacteria, CMVretinitis, at Health infarcts), Manifestations retinitis. 4’5 result 400 of on autopsy. 3 the acquired HAWAII ocular and 16.7 and psychophysical A studied. 7 This persons. and related annual from hemorrhages, infection manifestation. contagiosum, in estimates noninfectious Byron with cidofovir MEDICAL per and ocular cytomega manifesta District represents Vascular toxoplas Diseases syphilis, immuno 100,000 but orbital retinal human herpes rate histo Optic JOURNAL, most side M.W. they that can are of of 285 Treatment as VOL use. drugs refractile active Successfully retinal have istration Active, resolve may likened associated each CMV foci of retina, discovered may patient visual CMV CD4+ CMV leukemia, artery sion, is HIV distinguished Wong HIV tomatic do nerve changes Ganciclovir Medications The The The an The nonspecific, a 56, not This resemble focal been be of eye OCTOBER infection, implant collagen are diagnosis retinopathy fiber granular retinitis differential retinitis disease, T-cell represent most pigment most or field retinitis expanding in to may asymptomatic retinal and at nucleoside MD* of separately. virostatic particles, an shown that necrotizing time. radiation, hemorrhage. this layer on HIV common common defect, individual present will treated counts 1997 into was a from of against vascular of a may anemia, which cotton-wool-spot, and retinal time they epithelium. of Untreated whitening an screening infarcts), to a retinopathy. resolve CMV diagnosis developed the CMV borders cheese opportunistic effective and includes: be an or are analogue or retinitis have are pancreatitis, with ophthalmoscopic ocular can CMV retinitis vitreous because whitening infectious the white disease, may high blurred usually must ganciclovir, retinitis The spontaneously. retinitis pizza hemorrhages, no symptoms affect leave CMV presenting ophthalmoscopic with of of approved not altitude in shows first, infection prognostic be HIV red plaques The is Syndrome There cotton-wool-spots slowing they cavity. below (Figure retinal vision. behind available taken be is infection. retinitis up areas lesion. (Figures but and and and retinopathy, cotton-wool-spots based paying the chorioretinal are to retinopathy, foscarnet, a are of 0.05 opportunistic systemic by white therefore can indefinitely. The nerve and vascular 30% finding the atrophic of small The 1). and , value on multiple, the For spreads intravenously, They 2, A confluence x progression sometimes attention cause Hawaii the microvascular patients Federal fiber examination. retinitis 1091L.” appearance small a 3). and and is clinical patient diabetes, infections. it occlusions, and retina are Fibroglial the flashing dysproteinemias, like and scarring has for layer in granular, need area AIDS usually infection. cidofovir. to the microvascular Drug Occasionally, with visual had may (representing hemorrhages a and with occur. appearance the of often infarct brush of peripheral only orally, hyperten has the retinitis. Clinical Admin lights, with mottled retinitis AIDS.’° Lesions changes sight also asymp carotid tissue, known loss white most been to with The fire. will The All no or be be in is a Research Program (HACRP) with participating local ophthalmolo CMV opticneuritisinthe lefteyeofa39-year- Fig.1.—Active retinitisand gists was involved in two of the clinical trials involving oral old manwithAIDS.White,necrotizingretinitiswithassociated hemor 1CM1774). and rhage.Notethe granularityat the borders. ganciclovir (Syntex 1CM1653and The intravenous oral form should be taken daily for maximal efficacy. Bone marrow suppression is a major side effect. The intravitreal implant involves an operation to suture a sustained-release device into the vitreous cavity. The drug diffuses through a polyvinyl alcohol coating and is effective for five to eight months. Systemic toxicity is avoided, but there is no treatment outside the eye or prophylaxis for the fellow eye. Foscarnet is administered intravenously also on a daily basis. Infusion times are more lengthy than ganciclovir to avoid the side effects of renal toxicity and metabolic shifts. Cidofoviris the most recently available agent. It has the advantage of having a maintenance schedule of an intravenous infusion once every two weeks. Probenecid is used to help decrease the nephrotox icity. Ocular hypotony is possible. Relapse of CMV retinitis after initial response to an anti-CMV medication is common and drug testing is measured by median time to progression (50 days for intravenous ganciclovir’ 93 days for 120 days for cidofovir’ 226 days for the ganciclovir Fig.2.—InactiveCMVretinitiswithatrophicretinaand pigmentepithelial 2 three monthsfollowingtreatment.Sameeyeas figure1.Visionremains implant’ Reinduction with4 the same drug or switching to another 20/20,butthereisa persistentinferotemporalvisualfielddefectintheleft 5).agent may again slow the retinitis. Combination, treatment may be eye. , is an in drug toxicities. Addi effective, but the trade-off increase tional drugs are under investigation. Physicians in this state through the HACRP were involved with MSL 109 which is a monoclonal antibody against CMV. This study was terminated in 1997 due to preliminary data showing lack of efficacy and possibly increased mortality. is a serious complication of CMV retinitis. In one study, 24% of patients with CMV retinitis for one year devel oped a retinal detachment.’ Active retinitis and larger lesions are associated with6a higher risk for detachment. The patient notices an abrupt shadow and loss of sight. With extensive areas of atrophic retina, a standard scleral buckling operation is usually not success ful. Surgical treatment with the techniques of vitrectomy and silicone oil injection are needed to help reposition the retina and preserve sight. Other important causes of retinitis Fig.3.—InactiveCMVretinitiswithatrophicretinaand pigmentepithelial Toxoplasmosis causes a focal necrotizing retinitis in immuno mottlinginthe inferiorperipheryofthe lefteyeofa 34-year-oldmanwith competent individuals and can also present in the patient with HIV AIDS.Yellowobjectto the rightis a partialviewofa ganciclovirimplant infection. Clinically, toxoplasmosis has more inflammation in the inthe viteouscavity. vitreous and less hemorrhage than CMV retinitis. In the immunocompromised patient, the infection may be more fulminant making differentiation from CMV more difficult. The distinction is important because of the different treatment options which include pyrimethamine, sulfadiazine, clindamycin, folinic acid, and pred nisone. Acute retinal necrosis is a severe, rapidly spreading, necrotizing retinitis with vitritis, occlusive vasculitis, and caused by herpes zoster or simplex developing in an otherwise healthy individual. In the patient with AIDS, it may present with no vascular occlusion and minimal intraocular inflammation. This has been given the name progressive outer retinal necrosis (PORN).’ The rapid progression helps distinguish this infection from7 CMV retini tis. Prompt treatment with intravenous acyclovir is recommended,

HAWAIIMEDICALJOURNAL, VOL 56. OCTOBER 1997 286 but sight can still be abruptly and permanently lost. There is a high Summary rate of retinal detachment. Ocular manifestations of AIDS are not uncommon in Hawaii. Most of the conditions mentioned above have been seen in Hono Screening lulu. The goal of the ophthalmologist is to maintain useful sight in Studies have shown that the risk of CMV is inversely related tothe an illness which has a high mortality. With early diagnosis of ocular CD4+ T-cell counts. Some experts have used those counts to diseases, this has been the case. Improved systemic treatment establish the frequency ophthalmologic examinations as follows: including new combinations of anti-HTV medications have pro yearly for CD4+ T-cell counts greater than 0.10 x 9IL,1O every 6 longed the lives of many patients with AIDS. The challenge to months for CD4+ T-cell counts between 0.1 and 0.05 x 910/L, and preserve sight and decrease the ocular morbidity of AIDS continues every 4 months for CD4+ T-cell counts less than 0.05 x 91101L. to evolve with novel presentations of known diseases, new condi ° tions, and advances in treatment modalities.

References 1. CentersforDiseaseControl.AIDSrates.MMWRMorbMortWklyRep. 1997;46:333. 2. HawaiiDepartmentof Health.RecentHawaiiAIDStrends.AIDS SurveillanceQuarterlyReport.February1997Supplement;S1-S4. 3. Pepose JS. Ophthalmicmanifestationsof HIVinfection.CurrTop AIDS.1989;2:191-206. 4. Jabs DA,GreenWR,FoxR,PolkBF,BartlettJG.Ocularmanifesta tionsofthe acquiredimmunedeficiencysyndrome.Ophthalmology. 1989;96:1092-1099. 5. WhitcupSM.OcularmanifestationsofAIDS.JAMA.1996;275:142- 144. 6. FdedmanSM,MargoCE.Bilateralcentralretinalveinocclusionsina patientwithacquiredinirnunodeficiencysyndrome.ArchOphthalmol. 1995;113:1184-1188. 7. PlummerDJ,SamplePA,ArevaloJF, et al.VisualfieldlossinHIV positivepatientswithoutinfectiousretinopathy.AmJ Ophthalmol. 1996;122:542-549. 8. JacobsDS,PilieroPJ,KuperwaserMG,etal.Acuteuveifisassociated withtifabutinuse in patientswithhuman immunodeficiencyvirus infection.AmJ Ophthalmol.1994;118:716-722. 9. WhilcupSM,DastgheibK,Nussenblatt,RB,WaltonRC,PizzoPA, ChanCC.Aclinicopathologicreportofretinallesionsassociatedwith didanosine.ArchOphthalmoL1994;112:1594-1598. 10. Jabs DA,GreenWR,FoxR,PolkBF,BartlettJG. Ocularmanifesta tionsofacquiredimmunedeficiencysyndrome.Ophthalmology.1989; 96:1092-1099. 11. KuppermannBD,PeltyJG, RichmanDD,et al. Correlationbetween CD4+countsandprevalenceofcytomegalovirusretinitisandhuman immunodeficiencyvirus-relatednoninfectiousretinalvasculopathyin patientswittracquiredimmunodehciencysyndrome.AmJOphthalmot 1993;115:575:582. 12. RocheLaboratones.Cytovene(ganciclovir).PhysiciansDeskRefer ence5lstedihon1997.Montvale,N.J.:MedicalEconomics;1997:2270- 2277. TheywouldifyouwerestoyinatfxecutiveCentreHotel,thesmarttraveler’s 13, AstraUSA.Foscavir(foscamet).PhysiciansDeskReference51st edition1997.PhysiciansDeskReference5lstedition1997.Montvale, choiceatthecenteroftheHonolulubusinessdistrict.JoinfxecutivePassfor N.J.:MedicalEconomics;1997:541-545. 14. GileadSciences.Vistide(cidofovir).PhysiciansDeskReference5lst preferredsuite,officeandmeetingroomrates,andextraaddedbenefits, edition1997.PhysiciansDeskReference5lstedition1997.Monfvale, includn: N.J.:MedicalEconomics;1997:1057-1060. 15. MartinDF,ParksDJ,MellowSD,etal.Treatmenfofcytomegalovirus retinitiswitfranintraocularsustained-releaseganciclovirimplanf.Arch • freeContinentalBreakfast • freeLocal800andAccess(ails OphfhalmoL1994;112:1531-1539. 16. Freeman,WR,FriedbergDN,BerryC,etal.Riskfactorsfordevelop. mentofrhegmatogenousretinaldetachmentinpatientswithcytome • freeIn-SuiteCoffee • freeLocalNewspaper galovirusretinitis.AmJOphfhalmol.1993;116:713-720. 17. EngstromRE,HollandGN,MargolisTP,et al.Theprogressiveouter retinalnecrosissyndrome.Avatiantofnecrotizingherpeticretinopa thyinpatientswithAIDS.Ophthalmology.1994;101:1488-1502. per from nihf 18. Jabs DA,Acquiredimmunodeficiencysyndromeand the eye.Arch Ophthalmol.1997;115:292-293. (allourCorporateSalesManagerkehauAmorinformembershipinformation

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