deposits are reversible after stopping gold therapy but may take 3–12 months, and in some cases many years, to resolve. Visual acuity is unaffected, and deposition of gold in the cornea or lens is not an indication for cessation of therapy. In general, a total of over 1 g of gold deposited is needed before corneal changes are seen. In total dosages of 1.5 g 40–80% of patients will have gold deposition in the cornea. While lens deposits have previously been considered rare, 55% of patients on daily dosages over 1 g for 3 or more years have been reported to develop lens deposits. Corneal deposits may be seen as early as 1 month after starting therapy. It has been suggested that gold deposits in the cornea and lens are secondary to metal from the aqueous fluid or ­perilimbal blood vessels.

The second variant of ocular chrysiasis is much less common. This type presents as an inflammatory response secondary to gold, including corneal ulceration, subepithelial white perilimbal infiltrates, brush-like perilimbal stromal vascularization and interstitial keratitis (Arffa 1991; McCormick et al 1985). Corneal ulceration is more often marginal, crescent shaped and may be 2–3 mm in length. This response is felt to be an idiosyncratic allergic reaction, may be unilateral or bilateral, and is an indication in most patients to stop therapy. Zamir et al (2001) point out in patients presenting with marginal keratitis that this variant of chrysiasis should be considered. Stopping gold therapy along with looking for systemic toxicity is often warranted. Patients must be continuously followed since stromal inflammation may reoccur even after gold is stopped.

References and Further Reading

Arffa RC. Drugs and metals. In: Grayson’s Diseases of the Cornea. 3rd edn, Arffa RC (ed), Mosby, St Louis, pp 617–631, 1991.

Bron A, McLendon B, Camp A. Epithelial deposition of gold in the cornea in patients receiving systemic therapy. Am J Ophthalmol 88: 354–360, 1979.

Dick D, Raman D. The Guillain-Barre syndrome following gold therapy. Scand J Rheumatol 11: 119, 1982.

Evanchick CC, Harrington TM. Transient monocular visual loss after aurothioglucose. J Rheumatol 12: 619, 1985.

Fam AG, Paton TW, Cowan DH. Herpes zoster during gold therapy. Ann Intern Med 94: 712, 1981.

Gottlieb NL, Major JC. Ocular chrysiasis correlated with gold concentrations in the crystalline lens during chrysotherapy. Arthritis Rheum 21: 704–708, 1978.

Kincaid MC, et al: Ocular chrysiasis. Arch Ophthalmol 100: 1791, 1982. Lopez JD, Benitez del Castillo JM, Lopez CD, et al. Confocal microscopy in

ocular chrysiasis. Cornea 22: 573–575, 2003.

McCormick SA, et al. Ocular chrysiasis. Ophthalmology 92: 1432, 1985. Moore AP, et al. Penicillamine-induced myasthenia reactivated by gold. BMJ

288: 192, 1984.

Segawa K. Electron microscopy of the trabecular meshwork in open-angle glaucoma associated with gold therapy. Glaucoma 3: 257, 1981.

Weidle EG. Lenticular chrysiasis in oral chrysotherapy. Am J Ophthalmol 103: 240, 1987.

Zamir E, Read RW, Affeldt JC. Gold induced interstitial keratitis. Br J Ophthalmol 85: 1386–1387, 2001.

Generic names: 1. Celecoxib; 2. etolodac; 3. nimesulide; 4. rofecoxib; 5. valdecoxib.

Proprietary names: 1. Celebrex; 2. Lodine; 3. Ainex; 4. Vioxx; 5. Bextra.

Primary use

These non-steroidal anti-inflammatory drugs are selective ­inhibitors of cyclooxygenase-2 and are used in various forms in the treatment of arthritis, acute pain and dysmenorrhea.

Ocular side effects

Systemic administration

Certain

1. Blurred vision

2. Eyelids and conjunctiva – conjunctivitis

Possible

1. Retinal venous occlusions

2. Eyelids or conjunctiva

a.Stevens-Johnson syndrome

b.Toxic epidermal necrolysis

Conditional/Unclassified

1. Visual field defects

a.Orange spots

b.Central scotomas 2. Temporary blindness 3. Scintillating scotoma 4. Teichopsia

Clinical significance

The above-mentioned side effects are extremely rare. Fraunfelder et al (2006) reported blurred vision and conjunctivitis with multiple cases of positive rechallenge. The onset may occur within a few hours to days and if the drug is discontinued, resolves within 72 hours. Meyer et al (2006) made known a possible association of thrombotic events in selected patients. These findings include central retinal vein or other retinal venous occlusions. Meyer et al (2006) pointed out that the US FDA strongly associate the use of COX-2 inhibitors with Stevens-Johnson syndrome and toxic epidermal necrolysis. Coulter and Clark (2004) reported a case of temporary blindness and another with bilateral jellybean shaped loss of central vision. Lund and Neiman (2001) reported a case of orange spots in both visual fields. All signs and symptoms are fully reversible. The mechanism of action is postulated as inhibition of synthesis of prostaglandins that control blood flow. Also, most of these agents are sulfonamides with known drug-induced transient myopia.

References and Further Reading

Coulter DM, Clark DW. Disturbance of vision by cox-2 inhibitors. Expert Opin Drug Saf 3: 607–614, 2004.

Coulter D, Clark D. Visual disturbances with cox-2 inhibitors. Prescr Update 25: 8–9, 2004.

Coulter DM, Clark DWJ, Savage RL. Celecoxib, rofecoxib, and acute temporary visual impairment. BMJ 327: 1214–1215, 2003.

Cyclooxygenase-2 inhibitors: reports of visual disturbances. WHO Pharmaceuticals Newsletter. 3: 4, 2004.

Fraunfelder FW, Solomon J, Mehelas TJ. Ocular adverse effects associated with cyclooxygenase-2 inhibitors. Arch Ophthalmol 124: 277–278, 2006.

Lund BC, Neiman RF. Visual disturbance associated with celecoxib. Pharmacotherapy 21: 114–115, 2001.

Meyer CH, Mennel S, Schmidt JC, et al: Adverse effects of cyclooxygenase-2 inhibitors on ocular vision. Arch Ophthalmol 124: 1368, 2006.

arthritis treat to used agents and antagonists narcotic Analgesics, • 3 Section