Herpes simplex dendritic keratitis after treatment with latanoprost for primary open angle glaucoma

Ekatomatis, Pantelis

doi:10.1136/bjo.85.8.1007a

Cited by 40 publications

(21 citation statements)

References 5 publications

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“…[12][13][14][15] Subsequently, Kaufman et al 16 substantiated these findings in a study in rabbits in which topical latanoprost treatment was associated with increased disease severity and increased incidence of spontaneous recurrence of herpetic keratitis.…”

Section: Introductionmentioning

confidence: 85%

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Inhibition of Cyclooxygenase 2 Synthesis SuppressesHerpes simplexVirus Type 1 Reactivation

Gebhardt

Varnell

Kaufman

2005

Journal of Ocular Pharmacology and Therapeutics

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Recurrent herpes virus infection, in which the virus reactivates from the nervous system and causes painful lesions in peripheral tissues, is a significant clinical problem. Our recent studies showing that the amount of cyclooxygenase 2 (COX-2) in the trigeminal ganglia of heat-stressed untreated mice is higher than the amount in heat-stressed mice treated with the COX-2 inhibitor, celecoxib, have indicated that the prostaglandin synthesis pathway--and in particular COX-2--may be an intermediate in the pathway to herpes viral reactivation. To further study this process, we infected the corneas of mice using topical application to a lightly scratched epithelium and waited 30 days for Herpes simplex virus type 1 (HSV-1) latency to be established in the trigeminal ganglia. Prior to the induction of viral reactivation, the mice were treated orally with celecoxib. Treated and untreated mice were induced to undergo reactivation by immersion in 43 degrees C water for 10 min. The shedding of virus at the ocular surface was determined by culturing ocular swabs with indicator cells. The presence of infectious virus in the trigeminal ganglion was evaluated by incubating ganglion homogenates with indicator cells and observing for cytopathic effect. Celecoxib treatment significantly suppressed viral reactivation when given prophylactically by the gastrointestinal route. The numbers of corneas and ganglia containing infectious virus were significantly lower in the celecoxib-treated animals, compared to the placebo-treated mice. These experiments demonstrate that a selective COX-2 inhibitor can suppress hyperthermic stress-induced herpes viral reactivation in the nervous system. It may be possible to use COX-2 inhibitors to prevent viral reactivation in high-risk patients by drug prophylaxis.

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Section: Introductionmentioning

confidence: 85%

“…[6][7][8][9][10][11] Both experimental and clinical studies have implicated a role for prostaglandins in HSV-1 replication and reactivation. [12][13][14][15][16] The aim of this study was to test the ability of a cyclooxygenase-2 (COX-2) inhibitor to prevent HSV-1 reactivation in mice.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Cyclooxygenase 2 Synthesis SuppressesHerpes simplexVirus Type 1 Reactivation

Gebhardt

Varnell

Kaufman

2005

Journal of Ocular Pharmacology and Therapeutics

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“…Topical carbonic anhydrase inhibitors should be avoided in patients who have increased risk of graft rejection [109,110]. Prostaglandin analogs increase uveoscleral outflow and are frequently avoided in patients with active inflammation or a history of herpes simplex keratitis, because they can induce recurrent inflammation [159][160][161] and herpetic re-activation [162][163][164][165][166][167][168]. Furthermore, the preservative (benzalkonium chloride) used in many topical glaucoma medications can cause toxic effect to the corneal epithelium [169][170][171][172].…”

Section: Medical Treatments For Post-keratoplasty Glaucomamentioning

confidence: 99%

Graft failure: III. Glaucoma escalation after penetrating keratoplasty

Greenlee

Kwon

2008

Int Ophthalmol

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Glaucoma after penetrating keratoplasty is a frequently observed post-operative complication and is a risk factor for graft failure. Penetrating keratoplasty performed for aphakic and pseudophakic bullous keratopathy and inflammatory conditions are more likely to cause postoperative glaucoma compared with keratoconus and Fuchs' endothelial dystrophy. The intraocular pressure elevation may occur immediately after surgery or in the early to late postoperative period. Early postoperative causes of glaucoma include pre-existing glaucoma, retained viscoelastic, hyphema, inflammation, pupillary block, aqueous misdirection, or suprachoroidal hemorrhage. Late causes include pre-existing glaucoma, angle-closure glaucoma, ghost cell glaucoma, suprachoroidal hemorrhage, and steroid-induced glaucoma. Determining the cause of IOP elevation can help guide therapeutic intervention. Treatments for refractory glaucoma include topical anti-glaucoma medications such as beta-adrenergic blockers. Topical carbonic anhydrase inhibitors, miotic agents, adrenergic agonists, and prostaglandin analogs should be used with caution in the post-keratoplasty patient, because of the possibility of corneal decompensation, cystoid macular edema, or persistent inflammation. Various glaucoma surgical treatments have reported success in post-keratoplasty glaucoma. Trabeculectomy with mitomycin C can be successful in controlling IOP without the corneal toxicity noted with 5-fluorouracil. Glaucoma drainage devices have successfully controlled intraocular pressure in postkeratoplasty glaucoma; this is, however, associated with increased risk of graft failure. Placement of the tube through the pars plana may improve graft success compared with implantation within the anterior chamber. In addition, cyclophotocoagulation remains a useful procedure for eyes that have refractory glaucoma despite multiple surgical interventions.

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“…17,18 Latanoprost kullanan pek çok hasta olduğu dikkate alınırsa, glokom polikliniklerinde herpes enfeksiyonları ile çok daha sık karşılaşılması gerekirdi. Pratikte bu kadar sık izlenmemesi prostaglandin analogları ile herpes enfeksiyonu rekürrensinin direkt ilişkilendirmenin doğru olmayacağını göstermektedir.…”

Section: Discussionunclassified

Herpetik Keratit Skarı Nedeniyle Penetran Keratoplasti Yapılan Olguda Latanoprost Kullanımı Sonrası Görülen Allograft Reaksiyonu

...

2012

Tjo

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ÖzetYirmi yedi yaşında erkek hastanın sağ gözüne herpetik keratite ikincil kornea skarı nedeniyle penetran keratoplasti (PK) uygulandı. Takip sürecinin 14.ayında tedaviye dirençli göz içi basıncı yüksekliği nedeniyle latanoprost başlandı. Tedavinin 15. gününde allograft reaksiyonu (AR) gelişti. Yoğun immunsüpresif tedaviye rağmen, yeterli cevabın alınamaması, steroid tedavisine ikincil herpetik keratoüveiti düşündürdü. Oral antiviral tedavi ile keratik presipitatların dramatik azalması, bu düşünceyi doğruladı. AR tedavisi sonrası 3. ayda greft saydamlığı devam etmektedir. PK yapılan gözlerde inflamasyon, ön kamaranın immun ayrıcalığını bozarak greft başarısını tehlikeye atabilmektedir. Prostaglandin analoglarının kan-aköz bariyeri üzerine etkileri göz önüne alındığında, bu olguda latanoprost kullanımının AR ile ilişkili olabileceği akla gelmektedir. Olguda dikkat çeken bir diğer özellik ise AR tedavisine ikincil olarak herpes simpleks virüs (HSV) reaktivasyonunun izlenmesidir. Bu nedenle, HSV hikayesi olan olgularda AR tedavisi ile beraber oral antiviral profilaksinin verilmesi greft başarısını arttıracaktır. (Turk J Oph thal mol 2012; 42: 150-3) Anah tar Ke li me ler: Allograft reaksiyonu, herpes simpleks virüs, latanoprost, oral asiklovir profilaksisi, penetran keratoplasti Sum maryA 27-year-old male patient with a corneal scar secondary to herpetic keratitis in the right eye underwent penetrating keratoplasty (PK). At the 14 th month of follow-up, latanoprost was started to treat high intraocular pressure which was refractory to treatment. On the 15 th day of latanoprost use, allograft reaction (AR) developed. Insufficient clinical response despite intensive immunosuppressive therapy made us consider the possibility of recurrent herpetic keratouveitis secondary to steroid treatment. The dramatic reduction in the number of keratic precipitates with oral valacyclovir treatment confirmed this diagnosis. The graft remained clear 3 months after the AR treatment. Inflammation in eyes that had undergone PK jeopardizes the graft success by disrupting the immune privilege of anterior chamber. Considering the effects of prostaglandin analogues on blood-aqueous barrier, latanoprost use might have been related to allograft reaction in this case. Another remarkable characteristics of this case was the herpes simplex virus (HSV) reactivation secondary to AR therapy. For this reason, oral acyclovir prophylaxis together with AR therapy would improve graft success in cases with HSV history. (Turk J Oph thal mol 2012; 42: 150-3)

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Herpes simplex dendritic keratitis after treatment with latanoprost for primary open angle glaucoma

Cited by 40 publications

References 5 publications

Inhibition of Cyclooxygenase 2 Synthesis SuppressesHerpes simplexVirus Type 1 Reactivation

Inhibition of Cyclooxygenase 2 Synthesis SuppressesHerpes simplexVirus Type 1 Reactivation

Graft failure: III. Glaucoma escalation after penetrating keratoplasty

Herpetik Keratit Skarı Nedeniyle Penetran Keratoplasti Yapılan Olguda Latanoprost Kullanımı Sonrası Görülen Allograft Reaksiyonu

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