Use of recombinant tissue plasminogen activator for treatment of recalcitrant anterior uveitis: A case series

Abstract

Management of inflammation after surgery for recalcitrant anterior uveitis is challenging. Herein, we report successful treatment using intracameral injection of recombinant tissue plasminogen activator (rtPA) in two patients with recalcitrant anterior uveitis, due to infective uveitis and Vogt–Koyanagi–Harada disease, respectively. A 40-year-old woman presented with bilateral redness and vision reduction that had persisted 2 weeks. She also had bilateral anterior uveitis, vasculitis, retinitis, and optic disc swelling. Serology was positive for Bartonella henselae and Toxoplasma gondii . She was treated using long-term systemic corticosteroids and appropriate antibiotics. Our second case; a healthy 30-year-old man with bilateral eye redness and reduced vision without pain, and associated with headache and tinnitus for 1 weeks. He showed bilateral granulomatous inflammation with vitritis, choroiditis, retinitis, and hyperemic optic disc. The patient was diagnosed with Vogt-Koyanagi-Harada disease and treated with systemic corticosteroids. Both patients developed secondary cataracts and glaucoma that necessitated surgical intervention. Persistent chronic inflammation led to the formation of a thick fibrin membrane anterior to the intraocular lens (IOL) after phacoemulsification surgery with IOL implantation. This membrane was removed surgically, and intracameral injection of rtPA (25 μg) was carried out. The persistent inflammation had resolved and visual acuity had significantly improved within 1 week of intracameral rtPA injection. There were no reported ocular or systemic side effects. Intracameral rtPA is beneficial in patients with recalcitrant anterior uveitis who have undergone intraocular surgery. In most cases, surgical intervention improves the patients' vision. Intracameral rtPA should be considered in cases of persistent inflammation of varying etiology.

Intracameral tenecteplase during phacoemulsification in rabbits: clinical assessment of the anterior segment and biochemical analysis of the aqueous humor

“…The aqueous flare is due to the presence of plasma proteins and cell components derived from postoperative uveitis and BAB disruption (8) . In the TG, starting at TP 15 , a larger number of eyes did not exhibit aqueous flare, which might be a reflection of BAB stabilization and lower degrees of uveal inflammation (14,24) . Additional studies are needed to more accurately establish whether TNK may influence BAB and intraocular inflammation.…”

“…TPAs are trans operatively used in cases of congenital cataracts among humans (14) due to the high rates of fibrin formation in the AC. TNK is a third-generation TPA with high specificity for fibrin and high resistance to the action of the plasminogen activator inhibitor (PAI-1) enzyme secreted by platelets, thus more effectively decreasing the formation of fibrin clots however (23) , this effect was not found in the animals from TG in the present study.…”

“…It is activated when TPA converts plasminogen into plasmin, triggering fibrin degradation (25) . The studies investigated the use of intracameral TPA in the immediate postoperative period after PHACO in humans and found dissolution of the fibrin clots (11,14) . On these grounds, the expected outcome was a decreased presence of fibrin in the TG as a function of the fibrinolytic action of TPA.…”

“…In addition, TNK might cause superficial bleeding at the site of application due to the lysis of the fibrin in the clot during the first hours following application of the drug. However, several studies have shown that use of TPA for treatment of eye problems was associated with low rates of hemorrhagic complications (11,12,13,14,19,24) .…”

“…Tenecteplase (TNK) is a third-generation TPA, has a 6-fold prolonged plasma half-life, 15-fold higher fibrin specificity, and 80-fold reduced binding affinity to physiological plasminogen activator inhibitor (PAI-1) (14,15) . In addition, the TNK vehicle contains lesser L-arginine (below one-third of the tPA) probably the cause of toxicity in the posterior segment (13,15,16) .…”