Acta Ophthalmologica Scandinavica 2007
(Mensah et al. 1998). Retinal pigment epithelial changes seen following illumination are a sign of destruction, even if most changes do not result in symptomatic change (Zamir et al. 1999). This is analogous to injuries that occur elsewhere in the body and which do not cause loss in function. Luckily, as seen in previously published cases, symptoms tend to resolve and most return to normal, with little if any residual effect. However, threshold retinal burns in rhesus monkeys can be achieved at levels as low as 1.0–4.4 mW for 1 second (Ham et al. 1970). Those suggestions that laser pointers are ‘safe’ have either relied on theoretical discussion based on the physics of the eye and the laser, or on subjective measurements of visual function. Clinicopathological studies have shown inconclusive retinal changes from red (870 nm) laser pointer exposure, whereas green (532 nm) laser pointer exposure of 60 seconds duration revealed clinically and pathologically distinguishable damage similar to that caused by solar burns (Robertson et al. 2005). Others have demonstrated fundoscopic proof of insult to the retinal pigment epithelium (Luttrull & Hallisey 1999). In our patient, the two hypofluorescent spots (Fig. 2) match the two episodes of exposure. Some may feel that our patient suffered from idiopathic central serous choroidopathy (ICSC) and that the laser injury was coincidental. We feel the sudden nature of symptoms in addition to the paracentral scotoma suffered by our patient makes ICSC unlikely. However, we do agree the fluorescein angiogram and OCT are characteristic of ICSC and we feel the effects of the laser pointer incident followed a pathological process similar to that of ICSC. This case illustrates the seriousness of retinal exposure to laser pointers. We urge others to use their laser pointers with care.
References Ham WT Jr, Geeraets WJ, Mueller HA et al. (1970): Retinal burn thresholds for the helium-neon laser in the rhesus monkey. Arch Ophthalmol 84: 797–809. Luttrull JK & Hallisey J (1999): Laser pointer-induced macular injury. Am J Ophthalmol 127: 95–96.
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Mensah E, Vafidis G & Marshall J (1998): Laser pointers: the facts, media hype and hysteria. Lancet 351: 1291. Robertson DM, McLaren JW, Salomao DR & Link TP (2005): Retinopathy from a green laser pointer: a clinicopathologic study. Arch Ophthalmol 123: 629–634. Zamir E, Kaiserman I & Chowers I (1999): Laser pointer maculopathy. Am J Ophthalmol 127: 728–729.
Correspondence: Roger Wong MRCOphth Ophthalmology Department Frimley Park Hospital NHS Trust Portsmouth Road Guildford Surrey GU16 7UJ UK Tel ⁄ Fax: + 44 1276 604604 Email:
[email protected]
Anosmia as an adverse effect of dorzolamid Burak Turgut, Peykan Tu¨rkc¸u¨og˘lu, Mete Gu¨ler, Nuray Akyol, U¨lku¨ C¸eliker and Tamer Demir Fırat University School of Medicine, Department of Ophthalmology, Elazıg˘, Turkey doi: 10.1111/j.1600-0420.2006.00857.x
Editor,
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combination of timolol 0.5% with dorzolamide 2% is available as a timolol-dorzolamide fixed combination (Cosopt, Merck, Inc., West Point, Pennsylvania, USA). According to Cosopt’s approved label, non-ocular adverse events reported were skin rash, itching, palpitations, headache, depression, bitter taste feeling, nausea and so on. In our patient, we demonstrated anosmia as an adverse effect of Cosopt. A 49-year-old male patient was treated with 0.5% timolol two times daily because of primary open-angle glaucoma previously. We added dorzolamid as adjunctive therapy to timolol (substituted Cosopt for Timoptic 0.5%) in July 2005 when the intraocular pressure (IOP) was around 23–24 mmHg. He returned to our clinic 6 months later with loss of smell
(anosmia). The patient reported that distortion of smell (dysosmia) began approximately 1 month after the initiation of Cosopt; at the second month of Cosopt treatment he could not smell anything. After the substitution of latanoprost for Cosopt, patient’s smell sensation returned to normal in 20 days. After his account of the event, we performed some trials with his written informed consent. His medication was switched to a new bottle of Cosopt, and dysosmia reoccurred. His medication was then switched to another bottle of Cosopt, but timolol + dorzolamide was replaced with latanoprost in a patient-blind way. Dysosmia did not occur during treatment for 2 months thereafter. Dorzolamide was given again in a Xalatan bottle, and dysosmia recurred. Latanoprost was then prescribed and dysosmia did not occur during the following 2 months. During the follow-up period IOP was recorded as high as 23–24 mmHg and so latanoprost-timolol fixed combination (Xalacom) was substituted for latanoprost. Dysosmia did not occur with Xalacom. Intraocular pressure was 18 mmHg at 1400 hr on two visits. However, when latanoprost-timolol was replaced with dorzolamide in a Xalacom bottle in a patient-blind way, dysosmia recurred. Another bottle of Cosopt was given, but timololdorzolamide was replaced with normal saline in a patient-blind way, and he did not complain of dysosmia. Oral acetazolamide trial was refused by the patient. Carbonic anhydrase (CA), a zinc metalloenzyme that catalyses the reversible hydration of carbon dioxide, plays different roles in various tissues. In the nasal mucosa the balanced ion concentration that is maintained by CA enzyme is necessary for depolarization of the olfactory receptor neurons during olfactory transduction (Cavaliere et al. 1996; Paysan & Breer 2001). Olfactory dysfunction after an influenza-like illness may be the result of CA decrement in nasal mucus (Doherty et al. 1997). In humans, carbonic anhydrase exists as a number of isoenzymes. Abundance of the CA isoenzyme transcripts in human nasal mucosa is as follows: CA XII > CA II > CA VB > CA IV > CA IX > CA III > CA XIV > CA I > CA VI > CA VII (Tarun et al. 2003). Dorzolamide hydrochloride is an inhibitor of CA
Acta Ophthalmologica Scandinavica 2007
II; however, no such adverse reaction is reported. Individual variability in the expression of CA isoenzymes (Tarun et al. 2003) may be the reason for anosmia in our patient.
References Cavaliere F, Masieri S, Nori S & Magalini SI (1996): Carbonic anhydrase in human nasal epithelium: localization and effect of the inhibition by dichlorphenamide. Am J Rhinol 10: 113–117. Doherty AE, Martin BM, Dai WL & Henkin RI (1997): Carbonic anhydrase (CA) activity in nasal mucus appears to be a marker for loss of smell (hyposmia) in humans. J Invest Med 45: 237A. Paysan J & Breer H (2001): Molecular physiology of odor detection: current views. Pflugers Arch 441: 579–586. Tarun AS, Bryant B, Zhai W, Solomon C & Shusterman D (2003): Gene expression for carbonic anhydrase isoenzymes in human nasal mucosa. Chem Senses 28: 621–629.
Correspondence: Peykan Tu¨rkc¸u¨og˘lu Assistant Professor of Ophthalmology Fırat University School of Medicine Department of Ophthalmology Elazıg˘ Turkey Tel: + 90 42 4247 9334 Fax: + 90 42 4233 3555 Email:
[email protected]
Acute angle-closure glaucoma following sildenafil citrate-aided sexual intercourse Balasubramanian Ramasamy,1 Fiona Rowe,1,2 Harish Nayak,1 Clive Peckar1 and Carmel Noonan1 1
Department of Ophthalmology, North Cheshire Hospitals NHS Trust, Warrington, UK 2 Division of Orthoptics, University of Liverpool, Liverpool, UK doi: 10.1111/j.1600-0420.2006.00803.x
Editor, ildenafil citrate (Viagra) is now commonly prescribed for male
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erectile dysfunction. The ocular effects of the drug are well documented but no significant changes in the anterior segment or intraocular pressure (IOP) induced by the drug have been noted (Marmor & Kessler 1999) We present a case of acute angle-closure glaucoma with onset following sexual intercourse aided by sildenafil citrate. A 71-year-old man presented with painful loss of vision in the left eye. He had taken 50 mg Viagra at about 21.00 hours the previous night, after which he had sexual intercourse. The ocular symptoms started about midnight. He had no significant past ophthalmic history. Visual acuity on presentation was 20 ⁄ 20 in the right eye and hand movements in the left. The anterior chamber in the right eye was shallow with a grade 2 angle (Shaffer 1960). The left eye showed circumferential corneal injection with diffuse corneal oedema and a very shallow anterior chamber. Intraocular pressure was 14 mmHg and 60 mmHg in the right and left eyes, respectively. A presumed diagnosis of angle-closure glaucoma was made. The subject was treated with systemic and ocular hypotensive medications. The corneal oedema cleared and narrow angles in both eyes were confirmed by gonioscopy. He subsequently underwent bilateral YAG laser peripheral iridotomies, followed by combined cataract extraction and glaucoma surgery (phacoemulsification with viscocanalostomy) in the left eye. On his last visit 4.5 years after the initial angle-closure attack, the subject’s aided vision was 20 ⁄ 20 and 20 ⁄ 40 in the right and left eyes, respectively; IOP was 15 mmHg and 12 mmHg in the right and left eyes, respectively. The visual field in the right eye was normal, whereas the left eye showed a double arcuate scotoma. Sildenafil citrate is a selective inhibitor of the enzyme phospho-diesterase type 5 and also a weak inhibitor of phospho-diesterase type 6, which is found predominantly in the retina. Inhibition of phospho-diesterase types 5 and 6 results in increased levels of cyclic guanosine monophosphate (cGMP). Because cGMP participates in photo transduction in rod and cone cells, visual function may be affected
by sildenafil in the form of transient blurred vision, difficulty in discriminating blue)green colours and increased light sensitivity (Vobig et al. 1999). Previous studies have not shown sildenafil to have any significant effects on IOP in normal subjects or in patients with chronic open-angle glaucoma (Yajima et al. 2000). Increased ocular and choroidal blood flow has been demonstrated in animals and humans with sildenafil (Paris et al. 2001). In an eye with a narrow angle, it is possible to speculate on the possibility of further crowding of the angle due to increased choroidal blood flow, leading to acute angle closure. It is known that sympathetic stimulation occurring during sexual activity (for which sildenafil is taken!) can cause pupillary dilation and in a susceptible eye may precipitate angle-closure glaucoma. Our patient had a narrow angle in the fellow eye, suggesting a predisposition towards developing angle-closure glaucoma. A combination of factors including increased choroidal blood flow, pupillary dilatation during sexual activity and a relatively thicker crystalline lens may have been responsible for precipitating angle closure. In view of the absence of any other identifiable precipitating factors, we feel that this case of acute angleclosure glaucoma was precipitated by sexual intercourse combined with the intake of sildenafil citrate. To our knowledge this is the first case of acute angle-closure glaucoma following aided sexual intercourse to be reported.
References Marmor MF & Kessler R (1999): Sildenafil (Viagra) and ophthalmology. Surv Ophthalmol 44: 153–162. Paris G, Sponsel WE, Sandoval SS, Elliott WR, Trigo Y, Sanford DK & Harrison JM (2001): Sildenafil increases ocular perfusion. Int Ophthalmol 23: 355–358. Shaffer RN (1960): Gonioscopy, ophthalmoscopy and perimetry. Trans Am Acad Ophthalmol Otolaryngol 64: 112–127. Vobig MA, Klotz T, Staak M, Bartz-Schmidt KU, Engelmann U & Walter P (1999): Retinal side-effects of sildenafil. [Letter.] Lancet 353: 375. Yajima T, Yajima Y, Koppiker N, Grunwald J & Laties A (2000): No clinically important effects on intraocular pressure after
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