From the Department of Ophthalmology, Hofstra North Shore-Long Island Jewish Medical Center (KMC, RML), Great Neck; and Mt. Sinai University Medical Center (RML), New York, New York.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Khurram M. Chaudhary, MD, Hofstra North Shore-Long Island Jewish Medical Center, Department of Ophthalmology, 600 Northern Blvd., Ste. 107, Great Neck, NY 11021. E-mail: email@example.com
Immune reconstitution uveitis (IRU) is defined as an increase in both anterior and posterior inflammation, seen in patients with quiescent intraocular infection, usually cytomegalovirus retinitis (CMVR), who have experienced immune recovery (defined as an increase of at least 50 cells/mL to more than 100 cells/mL) for at least 6 months. This process is observed in patients who have experienced immune recovery after an active intraocular infection. IRU may manifest symptomatically with decreased vision and/or floaters and may be complicated by cataract, cystoid macular edema, epiretinal membrane, neovascularization, and papillitis.1
The reported incidence of immune recovery uveitis has varied from 0.109 to 0.8 per person-year, with a prevalence of 9.6% in patients with an immunologic response to highly active antiretroviral therapy (HAART).1,2 Risk factors for reported IRU include: CD4 T-cell count that had risen more than 50 cell/μL above nadir to at least 100 cell/μL (definition of immune recovery), larger retinitis lesions (because of higher antigen load), presence of HLA-B18, and use of intravitreal cidofovir.3–5
A 43-year-old HIV-positive man presented with a 2-week history of decreased vision in the right eye. Best-corrected visual acuity (BCVA) was 20/30 and 20/20 in the right and left eyes, respectively. Anterior segment examination revealed fine keratic precipitates in the right eye with rare cell noted. The intraocular pressure was 12 mm Hg bilaterally. Dilated fundus examination of the right eye was remarkable for areas of active CMVR in the superior and temporal quadrants, extending into the posterior pole (Fig. 1). The posterior hyaloid was attached; in addition, the patient was not myopic and had no previous ophthalmic history. The left eye did not show any abnormalities on retinal examination.
Figure 1. Active cytomegalovirus retinitis in the superior and superior temporal quadrants with minimal vitritis in the right eye.
Discussion with the primary medical physician and patient revealed that the patient was intermittently compliant with his medications, and had a CD4+ T-cell count of 43 cells/μL and HIV viral load of 292,366 copies/mL. The patient was given valganciclovir 900 mg twice daily (induction dosing) in addition to intravitreal injections of foscarnet (2,400 μg/0.01 mL). Both the patient and primary medical physician agreed to halt HAART until the CMVR was quiescent to decrease potential development of IRU. The CMVR responded well to treatment and the patient subsequently received maintenance therapy. HAART was restarted. His CD4+ T-cell count was found to be 147 cells/μL with an undetectable viral load on subsequent visits. The patient was observed for the next several months, with a slow resolution of the anterior uveitis. BCVA varied from 20/30 to 20/20 during this period. The retinal examinations did not show any active posterior or peripheral retinal disease (Fig. 2).
Figure 2. Healed cytomegalovirus retinitis involving (A) posterior pole and (B) superior retina. There was no involvement of any other quadrant.
Thirteen months later, the patient complained of floaters. Examination disclosed a BCVA of 20/30 in the right eye, with rare fine keratic precipitates and 1+ flare in the anterior chamber, and 2+ vitreous cells noted as well. Intraocular pressure was 12 mm Hg. Dilated examination revealed inactive CMVR, with 1+ vitreous cell overlying the macula area and a partial posterior vitreous detachment. CD4+ count was 279 cells/μL with an undetectable viral load and a diagnosis of IRU was made. In addition, a large retinal tear was noted in the inferior retina. This was associated with vitreoretinal traction and was not within an area of previously infected retina. Laser retinopexy was performed (Fig. 3), and IRU responded to topical steroids. The patient’s condition has remained stable for more than 2 years.
Figure 3. Retinal tear after laser retinopexy. Note the area of viteroretinal fibrosis and traction.
IRU has been found to occur between 2 and 26 weeks after HAART initiation.5 Our patient had demonstrated durable immune reconstitution, with maintenance of CD4 count greater than 100 cells/μL for more than a year associated with an undetectable viral load. This, in addition to inactive retinitis associated with both anterior and posterior inflammation, allows for the diagnosis of IRU. He developed IRU at week 56, in the setting of concurrent HAART and anti-CMVR medications with resolution of a large retinal area affected by CMVR.
Several late complications secondary to IRU have been described, including macular edema, epiretinal membrane formation, vitreoretinal traction, neovascular membranes, and cataract. We believe this is the first report of development of a retinal tear in association with vitreoretinal traction. Although the area of active retinitis was large, and this may have predisposed the patient toward the development of IRU, the retinal tear developed in an area unaffected by the CMVR. During the time of active retinitis, the patient was noted to have an attached posterior hyaloid. We postulate that when the patient developed inflammation (IRU), this resulted in a partial vitreous detachment and the subsequent vitreoretinal traction, leading to his retinal tear. Both the retinal tear and IRU were appropriately treated and the patient has continued to maintain good vision.
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