Clinical Trial: Acute Pseudophakic Cystoid Macular Edema Treatment Trial: Intravitreal Ranibizumab Versus Triamcinolone Acetonide

Study Status: Recruiting
Recruit Status: Recruiting
Study Type: Interventional

Official Title: Acute Pseudophakic Cystoid Macular Edema Treatment Trial: Intravitreal Ranibizumab Versus Triamcinolone Acetonide

Brief Summary:

This is an open-label, Phase I/II study evaluating intravitreal ranibizumab (R) vs. intravitreal Triesence (triamcinolone acetonide) (T) in subjects with acute pseudophakic cystoid macular edema (CME). Twenty consented patients with acute CME after phacoemulsification cataract surgery with posterior chamber intraocular lens implantation (PE/PCIOL) will be randomized 1:1 to treatment with R or T. R patients will receive three monthly R injections, followed by PRN dosing. T patients will receive PRN injections every 3 months. Clinical CME is defined as clinically evident CME, with visual acuity (VA) typically in the 20/40 to 20/200 range. Re-treatment criteria will include clinically evident worsening of CME, combined with any of the following:

• Any increase in spectral domain ocular coherence tomography (OCT) central macular thickness (CMT)
• Any observable fluid on OCT
• Any qualitatively increased perifoveal leakage/pooling on fluorescein angiography (FA).

Patients will be followed monthly through 12 months.

Detailed Summary:

1. BACKGROUND

   1.1 PATHOPHYSIOLOGY

   Despite improved cataract surgery instrumentation and techniques, the incidence of clinical CME remains 1 - 3% following uncomplicated PE/PCIOL. CME remains the most common cause of suboptimal post-operative visual acuity (VA) after uncomplicated PE/PCIOL. 1% clinical CME incidence represents 30,000 new cases annually in the USA. Clinical CME is defined as clinically evident CME, with VA typically 20/40 - 20/200. Diagnostic testing can confirm CME by FA leakage and increased CRT on OCT. If left untreated, chronic photoreceptor degeneration and irreversible VA loss can occur, even if the macular edema was to eventually resolve.

   1.2 TREATMENT OF PSEUDOPHAKIC CYSTOID MACULAR EDEMA Several treatment options for CME have been investigated, including topical, oral, periocular and intravitreal corticosteroids. Corticosteroids inhibit phospholipase A2, inhibiting production of arachidonic acid, precursor of the lipo-oxyenase (LOX) and cyclo-oxygenase (COX) pathways. Because corticosteroids inhibit both the LOX and COX pathways, corticosteroids may be expected to be more effective than non-steroidal anti-inflammatory drugs (NSAIDs) in decreasing inflammation. However, corticosteroids have side effects, including the potential for increased intraocular pressure (IOP) in susceptible patients, and require additional treatment for secondary glaucoma. NSAIDs specifically inhibit COX-2, and therefore avoid potential complications of corticosteroids. NSAIDs may be a good option for CME treatment of patients who are known corticosteroid responders. However, corneal stromal melting is a rare but serious potential side-effect of topical NSAIDs.

   To assess the safety of intravitreal R and T for the treatment of acute pseudophakic cystoid macular edema by evaluating:

   • Incidence and severity of ocular adverse events, as identified by eye examination
   • Incidence and severity of other adverse events, as identified by physical examination, subject reporting, and changes in vital signs