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HIV+ (AIDS) CD4 usually <100/mm3 Cytomegalovirus See Table 14, page 146  
HIV+ (AIDS) CD4 usually <100/mm3 Cytomegalovirus See Table 14, page 146  
Occurs in 5–10% of AIDS patients  
Occurs in 5–10% of AIDS patients  
Most common cause of blindness in AIDS patients with <50/mm3 CD4 counts. 19/30 pts (63%) with inactive CMV retinitis who re-sponded to HAART (Ĺ of ≥60 CD4 cells/mL) developed immune recovery vitreitis (vision Ļ & floaters with posterior segment inflammation —vitreitis, papillitis & macular changes) an average of 43 wks after rx started (JID 179: 697, 1999). Corticosteroid rx Ļ inflammatory reaction of immune recovery vitreitis without reactivation of CMV retinitis, either periocular corticosteroids or short course of systemic steroid.
Most common cause of blindness in AIDS patients with <50/mm3 CD4 counts. 19/30 pts (63%) with inactive CMV retinitis who responded to HAART (increase of ≥60 CD4 cells/mL) developed immune recovery vitreitis (vision decreases and floaters with posterior segment inflammation vitreitis, papillitis & macular changes) an average of 43 wks after teatment  started. Corticosteroid treatment decreases inflammatory reaction of immune recovery vitreitis without reactivation of CMV retinitis, either periocular corticosteroids or short course of systemic steroid.
For immediate sight-threatening lesions: Ganciclovir intraocular implant & valganciclovir 900 mg po q24h. For peripheral lesions: Valganciclovir 900 mg po q12h x 14–21d, then 900 mg po q24h for maintenance therapy Ganciclovir 5 mg/kg IV q12h x 14–21d, then valganciclovir900 mg po q24h OR Foscarnet 60 mg/kg IV q8h or 90 mg/kg IV q12h x 14–21d, then 90–120 mg/kg IV q24h ORCidofovir 5 mg/kg IV x 2wks, then 5 mg/kg every other wk; each dose should be administered with IV saline hydration & oral probenecid OR Repeated intravitreal injections with fomivirsen (for relapses only, not as initial therapy) Differential diagnosis: HIV retinopathy, herpes simplex retinitis, varicella-zoster retinitis (rare, hard to diagnose). Valganciclovir po equal to GCV IV in induction of remission: (NEJM 346:1119, 2002). Cannot use ganciclovir ocular implant alone as approx. 50% risk of CMV retinitis other eye at 6 mos. & 31% risk visceral disease. Risk Ļ with systemic rx but when contralateral retinitis does occur, ganciclovir-resistant mutation often present (JID 189:611, 2004). Concurrent systemic rx recom-mended! Because of unique mode of action, fomivirsen may have a role if isolates become resistant to other therapies. Retinal detachments 50–60% within 1yr of dx of retinitis. (Ophthal 111:2232, 2004). Equal efficacy of IV GCV & FOS. GCV avoids nephrotoxicity of FOS; FOS avoids bone marrow suppression of GCV. Although bone marrow toxicity may be similar to ganciclovir. Oral valganciclovir should replace both.
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::::* '''Preferred regimen (1) for immediate sight-threatening lesions''': [[Ganciclovir]] intraocular implant {{and}} [[Valganciclovir]] 900 mg PO q24h.  
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  Patients who discontinue suppression therapy should undergo regular eye examination for early detection of relapses.Post treatment suppression (Prophylactic) if CD4 count <100/mm3: Valganciclovir 900 mg po q24h. Discontinue if CD4 >100/mm3 x 6 mos on  
::::* '''Preferred regimen (2) for peripheral lesions''': [[Valganciclovir]] 900 mg PO q12h for 14–21 days, then 900 mg PO q24h for maintenance therapy
::::* Alternative regimen: [[Ganciclovir]] 5 mg/kg IV q12h for 14–21 days, then [[Valganciclovir]] 900 mg PO q24h {{or}} Foscarnet 60 mg/kg IV q8h or 90 mg/kg IV q12h for 14–21d, then 90–120 mg/kg IV q24h {{or}} Cidofovir 5 mg/kg IV x 2wks, then 5 mg/kg every other wk; each dose should be administered with IV saline hydration {{and}} oral probenecid {{or}} Repeated intravitreal injections with fomivirsen (for relapses only, not as initial therapy) Differential diagnosis: HIV retinopathy, herpes simplex retinitis, varicella-zoster retinitis (rare, hard to diagnose). [[Valganciclovir]] PO equal to [[Ganciclovir]] IV in induction of remission:  Cannot use [[Ganciclovir]] ocular implant alone as approx. 50% risk of CMV retinitis other eye at 6 months.and 31% risk visceral disease. Risk decreases with systemic treatment but when contralateral retinitis does occur, [[Ganciclovir]]-resistant mutation often present. Concurrent systemic treatment recommended. Because of unique mode of action, fomivirsen may have a role if isolates become resistant to other therapies. Retinal detachments 50–60% within 1 year of diagnosis of retinitis. Equal efficacy of IV [[Ganciclovir]] {{and}} [[Foscarnet]]. [[Ganciclovir]] avoids nephrotoxicity of [[Foscarnet]]; [[Foscarnet]] avoids bone marrow suppression of [[Ganciclovir]]. Although bone marrow toxicity may be similar to [[Ganciclovir]]. Oral [[Valganciclovir]] should replace both.
 
  Patients who discontinue suppression therapy should undergo regular eye examination for early detection of relapses.Post treatment suppression (prophylactic) if CD4 count <100/mm3: [[Valganciclovir]] 900 mg PO q24h. Discontinue if CD4 >100/mm3 for 6 months on ART.





Revision as of 13:04, 8 July 2015

Retinitis HIV+ (AIDS) CD4 usually <100/mm3 Cytomegalovirus See Table 14, page 146 Occurs in 5–10% of AIDS patients Most common cause of blindness in AIDS patients with <50/mm3 CD4 counts. 19/30 pts (63%) with inactive CMV retinitis who responded to HAART (increase of ≥60 CD4 cells/mL) developed immune recovery vitreitis (vision decreases and floaters with posterior segment inflammation vitreitis, papillitis & macular changes) an average of 43 wks after teatment started. Corticosteroid treatment decreases inflammatory reaction of immune recovery vitreitis without reactivation of CMV retinitis, either periocular corticosteroids or short course of systemic steroid.

  • Preferred regimen (1) for immediate sight-threatening lesions: Ganciclovir intraocular implant AND Valganciclovir 900 mg PO q24h.
  • Preferred regimen (2) for peripheral lesions: Valganciclovir 900 mg PO q12h for 14–21 days, then 900 mg PO q24h for maintenance therapy
  • Alternative regimen: Ganciclovir 5 mg/kg IV q12h for 14–21 days, then Valganciclovir 900 mg PO q24h OR Foscarnet 60 mg/kg IV q8h or 90 mg/kg IV q12h for 14–21d, then 90–120 mg/kg IV q24h OR Cidofovir 5 mg/kg IV x 2wks, then 5 mg/kg every other wk; each dose should be administered with IV saline hydration AND oral probenecid OR Repeated intravitreal injections with fomivirsen (for relapses only, not as initial therapy) Differential diagnosis: HIV retinopathy, herpes simplex retinitis, varicella-zoster retinitis (rare, hard to diagnose). Valganciclovir PO equal to Ganciclovir IV in induction of remission: Cannot use Ganciclovir ocular implant alone as approx. 50% risk of CMV retinitis other eye at 6 months.and 31% risk visceral disease. Risk decreases with systemic treatment but when contralateral retinitis does occur, Ganciclovir-resistant mutation often present. Concurrent systemic treatment recommended. Because of unique mode of action, fomivirsen may have a role if isolates become resistant to other therapies. Retinal detachments 50–60% within 1 year of diagnosis of retinitis. Equal efficacy of IV Ganciclovir AND Foscarnet. Ganciclovir avoids nephrotoxicity of Foscarnet; Foscarnet avoids bone marrow suppression of Ganciclovir. Although bone marrow toxicity may be similar to Ganciclovir. Oral Valganciclovir should replace both.
Patients who discontinue suppression therapy should undergo regular eye examination for early detection of relapses.Post treatment suppression (prophylactic) if CD4 count <100/mm3: Valganciclovir 900 mg PO q24h. Discontinue if CD4 >100/mm3 for 6 months on ART.



Herpesvirus Infections Cytomegalovirus (CMV)

Marked decrease in HIV associated CMV infections & death with Highly Active Antiretroviral Therapy. Initial treatment should optimize HAART.
Primary prophylaxis not generally recommended. Preemptive therapy in patients with increased in  CMV DNA titers in plasma & CD4 <100/mm3. Recommended by some: valganciclovir 900 mg po q24h. Authors rec. primary prophylaxis be dc if response to HAART with incerase in CD4 >100 for 6 months. 
Risk for developing CMV disease correlates with quantity of CMV DNA in plasma: each log10Ĺ associated with 3.1-fold increase in disease.