CMV Retinitis

GENERAL PRINCIPLES

CMV retinitis accounts for 85% of CMV disease in patients with AIDS. It commonly develops in a setting of profound CD4 depletions (CD4 cell count lt;50 cells#8725;#956;L).

DIAGNOSIS

• CMV viremia can be detected by PCR and is usually present in end-organ disease but can also be seen in the absence of end-organ disease.

• The diagnosis of CMV retinitis is made based on characteristic findings during ophthalmoscopic examination. Patients may report floaters, scotomata, or peripheral visual field defects.

TREATMENT

• Treatment of CMV retinitis can be local or systemic and is administered in two phases, induction and maintenance.

• Ganciclovir is given at an induction dosage of 5 mg/kg IV bid for 14-21 days and a maintenance dosage of 5 mg/kg IV daily indefinitely (unless immune reconstitution occurs). The most common side effect of ganciclovir is myelotoxicity, resulting in neutropenia. The neutropenia may respond to granulocyte colony-stimulating factor therapy. An intraocular ganciclovir implant is effective but does not provide systemic CMV therapy.

• Valganciclovir, a ganciclovir prodrug, has drug levels equivalent to those of IV ganciclovir. For induction, 900 mg PO bid for 14-21 days is given, followed by 900 mg once a day. Treatment is indefinite unless immunologic recovery occurs. Adverse effects are similar to those of ganciclovir.

• Alternatives include IV foscarnet and IV cidofovir. These drugs carry a significant risk of nephrotoxicity; therefore, adequate hydration and electrolyte monitoring (including calcium) are required.

• For other invasive CMV diseases, the optimal therapy is with IV ganciclovir, PO valganciclovir, IV foscarnet, or a combination of two drugs (in persons with prior anti-CMV therapy), for at least 3-6 weeks. Foscarnet has the best CSF penetration and is the drug of choice for CMV encephalitis and myelopathy. Long-term maintenance therapy is indicated.