development of a mixed cataract (odds ratio, 2.48), but not of a pure posterior subcapsular, cortical, or nuclear cataract in the Final Polychotomous Logistic Regression Model (Table 5 in the article). We assume that the gout medication in question is allopurinol because the authors cited five studies on cataracts and allopurinol therapy, but omitted our findings published in 1988.2
We examined 53
patients who attended the gout clinic
at
Charing Cross Hospital, London, England. All the patients, except three, had been receiving regular allopurinol therapy for at least 18 months, in the usual dose of 300 mg daily. Twenty-five of these patients had been receiving treatment
for more than 6 years. We found an unusual morphologic thinning of the anterior clear zone of the lens in 25% of our patients. There was some evidence of a relationship between the cumulative dose and this thinning. It is known that there is an association between the development of anterior subcapsular cataract and thin¬ ning of the anterior clear zone,2 and indeed, we found a high prevalence of such opacities (11.7%) in our series. Although it is generally more common for posterior subcapsular changes to precede anterior subcapsular changes, this was not the case with patients receiving allopurinol therapy. In eight (66%) of 12 eyes with an anterior subcapsular opacity, a posterior subcapsular opacity was absent. Leske et al1 suggested a need for periodic lens evaluations for subjects with diabetes and those using oral steroids or gout medications, which could lead to early identification of lens changes and appropriate patient treatment. We agree that periodic ocular examination is good practice; however, visually significant cataract is symptomatic, and cessation of gout therapy probably will not result in resolution of cataract. Nevertheless, although the serum uric acid rapidly returns to pretreatment levels when allopurinol treatment is discontin¬ ued, attacks of gout may not return for many years,3 and the drug could, therefore, be withdrawn if symptomatic cataract occurs.
Christopher S. Liu, FCOphth Timothy J. Leonard, FRCS
London, England Nicholas A. Brown, FRCS Oxford, England
1. Leske MC, Chylack LT Jr, Wu S-Y, The Lens Opacities Case-Control Study Group. The Lens Opacities Case-Control Study: risk factors for cataract. Arch Ophthalmol. 1991;109:244-251. 2. Liu CSC, Brown NAP, Leonard TJK, Bull PW, Scott JT. The prevalence and morphology of cataract in patients on allopurinol treatment. Eye.
1988;2:600-606.
3. Loebel WY, Scott JT. Withdrawal of Ann Rheum Dis. 1974;33:304-307.
allopurinol
in
patients with gout.
Myopia and Cataract To the Editor. \p=m-\Whilecontroversy swirled over the association between exposure to the short-wavelength region of sunlight (UVB, 290 to 320 nm) and increased risk of cataract, I smugly assumed that my lifelong use of eyeglasses for correction of myopia protected my lenses from this damaging radiation. This assumption was based on the fact that glass absorbs UVB radiation. Now Leske et al1 suggest that myopia, as indicated by eyeglass use before age 20 years, is associated with increased risk of mixed cataract. They specified the composition of their mixed group in terms of the four permutations of posterior subcapsular, cortical, and nuclear cataracts. Each subgroup contained 91 or more subjects, and I wonder if individual risk assessments were performed. Small subgroup size may obscure the assessment of risk. On the other hand, if risk were concentrated in one or two subgroups,
association with eyeglass use may be significant. Since UVB exposure appears associated with increased risk of posterior subcapsular and cortical cataracts but not nuclear cataracts,2 risk assessments of mixed subgroups may provide useful information. Dermatologists employ the criterion of development of symptoms after exposure to sunlight through window glass as an indication that a photosensitive patient is sensitive to UVA radiation (320 to 400 nm). However, the optical glass in eye¬ glasses allows considerable transmission of UVB.3 Since the cornea and aqueous humor transmit wavelengths above 300 nm,4 the ocular lenses of eyeglass wearers are exposed to high levels of UVB and UVA. Future studies of eyeglass use and risk of cataract must control for other variables; ie, use of plastic and coated eyeglass lenses. These modifications offer much more protection against UV radiation than does optical glass.3 Other confounding factors are use of tinted lenses, which vary widely in their absorption spectra,5 contact lenses, and sunglasses. John A. Johnson, PhD Omaha, Neb 1. Leske MC, Chylack LT Jr, Wu S-Y, The Lens Opacities Case-Control Study Group. The lens opacities case-control study: risk factors for cataract. Arch Ophthalmol. 1991;109:244-251. 2. West SK. Who develops cataracts? Arch Ophthalmol. 1991;109:196-198. 3. McDonagh AF, Nguyen ML. Spectacles, ultraviolet radiation and formation of cataracts. N Engl J Med. 1989;321:1478-1479. 4. Lerman S. Ocular phototoxicity. N Engl J Med. 1988;319:1475-1477. 5. Borgwardt B, Fishman GA, Vander Meulen D. Spectral transmission characteristics of tinted lenses. Arch Ophthalmol. 1981;99:293-297.
In Reply. \p=m-\Weappreciate the interest raised by our article. Liu et al cite our findings of an association between gout medications and mixed cataract, and summarize their previously reported findings among 53 patients using allopurinol. In our study, the use of any type of gout medication was investigated. Such use was found to be related to mixed cataract, our largest case group, but our results do not exclude associations of gout medications with individual cataract types.
Dr Johnson comments on possible mechanisms to explain finding of an association between use of eyeglasses before age 20 years and mixed cataract. Although our study obtained data on use of sunglasses, as suggested by Dr Johnson, no significant relationships with cataract were found. We agree with him that analyses exploring associations of risk factors with mixed cataract subgroups are of interest. Such analyses are ongoing and will be included in a future publication. M. Cristina Leske, MD, MPH Roger Grimson, PhD Leslie Hyman, PhD Suh-Yuh Wu, MA Stony Brook, NY our
Large Rectus Muscle Recessions for the Treatment of Congenital Nystagmus To the Editor.\p=m-\We read the article
by
von
Noorden and
Sprunger1 in the February 1991 issue of the ARCHIVES with
great interest. The authors present an approach to the operative treatment of manifest congenital nystagmus that might,
in principle, be applied to many patients with this unfortunate condition. Although not a new condition, this is the first description of the operative intervention in the American literature, for which we are grateful to the authors. Because of its potential profound implications for therapy, we wish to raise questions that the careful clinician may want answered
Downloaded From: http://archopht.jamanetwork.com/ by a Western University User on 06/08/2015
before applying the formidable muscle procedure to patients with congenital nystagmus. How often do the authors see patients with manifest congenital nystagmus of various origins to whom they offer this operative intervention? Since the report describes only three patients, it is important to know what percentage of patients with these diagnoses are candidates, in the authors' opinion. Since "modest improvement of visual acuity" is presented as a potential benefit, what steps were taken to insure that this was, in fact, real, and not simply a training effect from repeat¬ ed exposure to acuity targets? This is particularly critical in our opinion, in documenting changes in this patient group, since the underlying sensory defect cannot be changed with the operative procedure. This is also not a trivial point since, if the improvement in visual acuity is real, would it not be better to perform the procedure earlier, during visual development, to obtain maximum improvement? This makes it all the more critical to carefully control the documentation of visual acuity to prevent bias. The authors present nystagmographic evidence of im¬ provement in the amplitude and frequency of the nystagmus after surgery. What precautions were taken to control accom¬ modation and convergence in the preoperative and postopera¬ tive recordings, to prevent the well-known artifactual damp¬ ing of the nystagmus due to convergence being confused with a real improvement in either frequency or amplitude of the
nystagmus? Although no immediate deleterious effects of the surgery were seen on alignment and/or gaze movements, these largescale recessions and their effect on ocular alignment on the above remain an open question. We have doubts about the proffered benefits of such sur¬ gery—improvement in visual acuity and dampening of the nystagmus—as well as its cost to the patient in terms of possible strabismus and restriction of gaze movements in the long term. These patients are difficult to treat and have been told by many clinicians (including us) that nothing could be done for them. By advocating eye muscle surgery for these conditions, the authors have opened a new, potentially valu¬ able addition to the therapeutic armamentarium for them. We therefore feel all the more constrained to raise these ques¬ tions in this letter and await their answer before any wide¬ spread treatment of such patients is undertaken by the oph¬
thalmologic community.
1. Von Noorden
John T. Flynn, MD William E. Scott, MD Burton J. Kushner, MD Marshall M. Parks, MD Creig S. Hoyt, MD Henry S. Metz, MD David S. Friendly, MD John D. Baker, MD Arthur Jampolsky, MD Iowa City, Iowa
GK, Sprunger DT. Large rectus muscle recessions for the nystagmus. Arch Ophthalmol. 1991;109:221-224.
treatment of congenital
surprising that the possibility of improving nystagmus, a condition thought by most to be incurable, In Reply.\p=m-\It is not
raises doubts and concerns. Such reactions are common every time a new and unconventional therapy is advocated. We remember the indignant outcries when phacoemulsification and intraocular lenses were first introduced. Dr Flynn and those he enlisted to sign this letter need not feel "constrained" in asking their questions, but some of these were explicitly and, we believe, adequately addressed in our article. We reiterate that our results must be considered preliminary
since no follow-up beyond 19 months is available. However, do not share the concern about the possible long-term effects on "gaze movements," or the late development of strabismus. There is no mechanism known to us by which the minimal postoperative limitation of ductions would increase with time. There is also no reason to suspect the late development of strabismus, because the balance of forces between antagonistic horizontal recti, recessed by the same amount, remains essentially undisturbed by the surgery. Indeed, one may ask why the writers of this letter did not raise their voices when "hang-loose" sutures or 12-mm recessions of the superi¬ or rectus muscle for dissociated vertical deviation, now prac¬ ticed by many strabismologists apparently without ill effects, were first advocated? We also stated in our article that visual acuity gains after this procedure were modest, and pointed out possible sources of error in measuring visual acuity in nystagmic patients. In spite of this caveat, Flynn and coauthors raise this issue, and suggest that acuity gains may have been caused by a training effect. We believe that this possibility can be discounted since the brief exposures to a visual acuity chart, with months between the preoperative and postoperative examinations, were insufficient to have improved letter recognition by we
training.
We reiterate that the subjective improvement of vision, especially during reading, experienced by the patients includ¬ ed in our study and by those subsequently operated on by the senior author, was conspicuous and is noteworthy. We do not know the reason for this improvement, but suspect that pro¬ longed foveation time after decreasing the nystagmus may improve recognition. Such improvement is not always mea¬ surable in Snellen acuity, and we are currently recording reading time before and after surgery to gain further insight
into this mechanism. There is no argument with Flynn et al that the visual acuity deficit in a sensory nystagmus cannot be improved by de¬ creasing its amplitude, and nowhere in our writings have we made this claim. However, our response to this comment is to point out that the nystagmus in the patients described was, at least in part, motor in character since visual acuities were considerably better at near fixation than at distance fixation. We are asked what precautions were taken to control ac¬ commodation and convergence in the preoperative and post¬ operative recordings, implying that postoperative improve¬ ment may have been caused by convergence damping during near vision. Flynn et al choose to ignore the fact that our article clearly stated that preoperative and postoperative recordings were obtained under the same conditions, namely at 100-cm fixation distance from the patient whose head was fixed in a head rest. Damping by additional convergence (nystagmus blockage) did not occur and would have been noted clinically and on electronystagmography. To date, we have performed this operation in six patients and have scheduled it for an additional three of an estimated 250 patients with congenital nystagmus who presented at our clinic since January 1987, when we operated on the first patient. We limit this type of surgery to patients with congen¬ ital nystagmus who wish to improve their appearance and to those with predominantly motor nystagmus, that is, with a significant improvement of visual acuity during near fixation. Such patients are more likely to benefit in visual function than those with a predominantly sensory nystagmus. We restrict the operation to patients who can cooperate reliably with preoperative and postoperative evaluations, which must in¬ clude electronystagmography and electrooculographic re¬ cordings of eye movements during reading, and who can make a decision on their own in favor of surgery for a cosmetically disturbing eye condition. It follows that at the current state of
Downloaded From: http://archopht.jamanetwork.com/ by a Western University User on 06/08/2015
We examined 53
patients who attended the gout clinic
at
Charing Cross Hospital, London, England. All the patients, except three, had been receiving regular allopurinol therapy for at least 18 months, in the usual dose of 300 mg daily. Twenty-five of these patients had been receiving treatment
for more than 6 years. We found an unusual morphologic thinning of the anterior clear zone of the lens in 25% of our patients. There was some evidence of a relationship between the cumulative dose and this thinning. It is known that there is an association between the development of anterior subcapsular cataract and thin¬ ning of the anterior clear zone,2 and indeed, we found a high prevalence of such opacities (11.7%) in our series. Although it is generally more common for posterior subcapsular changes to precede anterior subcapsular changes, this was not the case with patients receiving allopurinol therapy. In eight (66%) of 12 eyes with an anterior subcapsular opacity, a posterior subcapsular opacity was absent. Leske et al1 suggested a need for periodic lens evaluations for subjects with diabetes and those using oral steroids or gout medications, which could lead to early identification of lens changes and appropriate patient treatment. We agree that periodic ocular examination is good practice; however, visually significant cataract is symptomatic, and cessation of gout therapy probably will not result in resolution of cataract. Nevertheless, although the serum uric acid rapidly returns to pretreatment levels when allopurinol treatment is discontin¬ ued, attacks of gout may not return for many years,3 and the drug could, therefore, be withdrawn if symptomatic cataract occurs.
Christopher S. Liu, FCOphth Timothy J. Leonard, FRCS
London, England Nicholas A. Brown, FRCS Oxford, England
1. Leske MC, Chylack LT Jr, Wu S-Y, The Lens Opacities Case-Control Study Group. The Lens Opacities Case-Control Study: risk factors for cataract. Arch Ophthalmol. 1991;109:244-251. 2. Liu CSC, Brown NAP, Leonard TJK, Bull PW, Scott JT. The prevalence and morphology of cataract in patients on allopurinol treatment. Eye.
1988;2:600-606.
3. Loebel WY, Scott JT. Withdrawal of Ann Rheum Dis. 1974;33:304-307.
allopurinol
in
patients with gout.
Myopia and Cataract To the Editor. \p=m-\Whilecontroversy swirled over the association between exposure to the short-wavelength region of sunlight (UVB, 290 to 320 nm) and increased risk of cataract, I smugly assumed that my lifelong use of eyeglasses for correction of myopia protected my lenses from this damaging radiation. This assumption was based on the fact that glass absorbs UVB radiation. Now Leske et al1 suggest that myopia, as indicated by eyeglass use before age 20 years, is associated with increased risk of mixed cataract. They specified the composition of their mixed group in terms of the four permutations of posterior subcapsular, cortical, and nuclear cataracts. Each subgroup contained 91 or more subjects, and I wonder if individual risk assessments were performed. Small subgroup size may obscure the assessment of risk. On the other hand, if risk were concentrated in one or two subgroups,
association with eyeglass use may be significant. Since UVB exposure appears associated with increased risk of posterior subcapsular and cortical cataracts but not nuclear cataracts,2 risk assessments of mixed subgroups may provide useful information. Dermatologists employ the criterion of development of symptoms after exposure to sunlight through window glass as an indication that a photosensitive patient is sensitive to UVA radiation (320 to 400 nm). However, the optical glass in eye¬ glasses allows considerable transmission of UVB.3 Since the cornea and aqueous humor transmit wavelengths above 300 nm,4 the ocular lenses of eyeglass wearers are exposed to high levels of UVB and UVA. Future studies of eyeglass use and risk of cataract must control for other variables; ie, use of plastic and coated eyeglass lenses. These modifications offer much more protection against UV radiation than does optical glass.3 Other confounding factors are use of tinted lenses, which vary widely in their absorption spectra,5 contact lenses, and sunglasses. John A. Johnson, PhD Omaha, Neb 1. Leske MC, Chylack LT Jr, Wu S-Y, The Lens Opacities Case-Control Study Group. The lens opacities case-control study: risk factors for cataract. Arch Ophthalmol. 1991;109:244-251. 2. West SK. Who develops cataracts? Arch Ophthalmol. 1991;109:196-198. 3. McDonagh AF, Nguyen ML. Spectacles, ultraviolet radiation and formation of cataracts. N Engl J Med. 1989;321:1478-1479. 4. Lerman S. Ocular phototoxicity. N Engl J Med. 1988;319:1475-1477. 5. Borgwardt B, Fishman GA, Vander Meulen D. Spectral transmission characteristics of tinted lenses. Arch Ophthalmol. 1981;99:293-297.
In Reply. \p=m-\Weappreciate the interest raised by our article. Liu et al cite our findings of an association between gout medications and mixed cataract, and summarize their previously reported findings among 53 patients using allopurinol. In our study, the use of any type of gout medication was investigated. Such use was found to be related to mixed cataract, our largest case group, but our results do not exclude associations of gout medications with individual cataract types.
Dr Johnson comments on possible mechanisms to explain finding of an association between use of eyeglasses before age 20 years and mixed cataract. Although our study obtained data on use of sunglasses, as suggested by Dr Johnson, no significant relationships with cataract were found. We agree with him that analyses exploring associations of risk factors with mixed cataract subgroups are of interest. Such analyses are ongoing and will be included in a future publication. M. Cristina Leske, MD, MPH Roger Grimson, PhD Leslie Hyman, PhD Suh-Yuh Wu, MA Stony Brook, NY our
Large Rectus Muscle Recessions for the Treatment of Congenital Nystagmus To the Editor.\p=m-\We read the article
by
von
Noorden and
Sprunger1 in the February 1991 issue of the ARCHIVES with
great interest. The authors present an approach to the operative treatment of manifest congenital nystagmus that might,
in principle, be applied to many patients with this unfortunate condition. Although not a new condition, this is the first description of the operative intervention in the American literature, for which we are grateful to the authors. Because of its potential profound implications for therapy, we wish to raise questions that the careful clinician may want answered
Downloaded From: http://archopht.jamanetwork.com/ by a Western University User on 06/08/2015
before applying the formidable muscle procedure to patients with congenital nystagmus. How often do the authors see patients with manifest congenital nystagmus of various origins to whom they offer this operative intervention? Since the report describes only three patients, it is important to know what percentage of patients with these diagnoses are candidates, in the authors' opinion. Since "modest improvement of visual acuity" is presented as a potential benefit, what steps were taken to insure that this was, in fact, real, and not simply a training effect from repeat¬ ed exposure to acuity targets? This is particularly critical in our opinion, in documenting changes in this patient group, since the underlying sensory defect cannot be changed with the operative procedure. This is also not a trivial point since, if the improvement in visual acuity is real, would it not be better to perform the procedure earlier, during visual development, to obtain maximum improvement? This makes it all the more critical to carefully control the documentation of visual acuity to prevent bias. The authors present nystagmographic evidence of im¬ provement in the amplitude and frequency of the nystagmus after surgery. What precautions were taken to control accom¬ modation and convergence in the preoperative and postopera¬ tive recordings, to prevent the well-known artifactual damp¬ ing of the nystagmus due to convergence being confused with a real improvement in either frequency or amplitude of the
nystagmus? Although no immediate deleterious effects of the surgery were seen on alignment and/or gaze movements, these largescale recessions and their effect on ocular alignment on the above remain an open question. We have doubts about the proffered benefits of such sur¬ gery—improvement in visual acuity and dampening of the nystagmus—as well as its cost to the patient in terms of possible strabismus and restriction of gaze movements in the long term. These patients are difficult to treat and have been told by many clinicians (including us) that nothing could be done for them. By advocating eye muscle surgery for these conditions, the authors have opened a new, potentially valu¬ able addition to the therapeutic armamentarium for them. We therefore feel all the more constrained to raise these ques¬ tions in this letter and await their answer before any wide¬ spread treatment of such patients is undertaken by the oph¬
thalmologic community.
1. Von Noorden
John T. Flynn, MD William E. Scott, MD Burton J. Kushner, MD Marshall M. Parks, MD Creig S. Hoyt, MD Henry S. Metz, MD David S. Friendly, MD John D. Baker, MD Arthur Jampolsky, MD Iowa City, Iowa
GK, Sprunger DT. Large rectus muscle recessions for the nystagmus. Arch Ophthalmol. 1991;109:221-224.
treatment of congenital
surprising that the possibility of improving nystagmus, a condition thought by most to be incurable, In Reply.\p=m-\It is not
raises doubts and concerns. Such reactions are common every time a new and unconventional therapy is advocated. We remember the indignant outcries when phacoemulsification and intraocular lenses were first introduced. Dr Flynn and those he enlisted to sign this letter need not feel "constrained" in asking their questions, but some of these were explicitly and, we believe, adequately addressed in our article. We reiterate that our results must be considered preliminary
since no follow-up beyond 19 months is available. However, do not share the concern about the possible long-term effects on "gaze movements," or the late development of strabismus. There is no mechanism known to us by which the minimal postoperative limitation of ductions would increase with time. There is also no reason to suspect the late development of strabismus, because the balance of forces between antagonistic horizontal recti, recessed by the same amount, remains essentially undisturbed by the surgery. Indeed, one may ask why the writers of this letter did not raise their voices when "hang-loose" sutures or 12-mm recessions of the superi¬ or rectus muscle for dissociated vertical deviation, now prac¬ ticed by many strabismologists apparently without ill effects, were first advocated? We also stated in our article that visual acuity gains after this procedure were modest, and pointed out possible sources of error in measuring visual acuity in nystagmic patients. In spite of this caveat, Flynn and coauthors raise this issue, and suggest that acuity gains may have been caused by a training effect. We believe that this possibility can be discounted since the brief exposures to a visual acuity chart, with months between the preoperative and postoperative examinations, were insufficient to have improved letter recognition by we
training.
We reiterate that the subjective improvement of vision, especially during reading, experienced by the patients includ¬ ed in our study and by those subsequently operated on by the senior author, was conspicuous and is noteworthy. We do not know the reason for this improvement, but suspect that pro¬ longed foveation time after decreasing the nystagmus may improve recognition. Such improvement is not always mea¬ surable in Snellen acuity, and we are currently recording reading time before and after surgery to gain further insight
into this mechanism. There is no argument with Flynn et al that the visual acuity deficit in a sensory nystagmus cannot be improved by de¬ creasing its amplitude, and nowhere in our writings have we made this claim. However, our response to this comment is to point out that the nystagmus in the patients described was, at least in part, motor in character since visual acuities were considerably better at near fixation than at distance fixation. We are asked what precautions were taken to control ac¬ commodation and convergence in the preoperative and post¬ operative recordings, implying that postoperative improve¬ ment may have been caused by convergence damping during near vision. Flynn et al choose to ignore the fact that our article clearly stated that preoperative and postoperative recordings were obtained under the same conditions, namely at 100-cm fixation distance from the patient whose head was fixed in a head rest. Damping by additional convergence (nystagmus blockage) did not occur and would have been noted clinically and on electronystagmography. To date, we have performed this operation in six patients and have scheduled it for an additional three of an estimated 250 patients with congenital nystagmus who presented at our clinic since January 1987, when we operated on the first patient. We limit this type of surgery to patients with congen¬ ital nystagmus who wish to improve their appearance and to those with predominantly motor nystagmus, that is, with a significant improvement of visual acuity during near fixation. Such patients are more likely to benefit in visual function than those with a predominantly sensory nystagmus. We restrict the operation to patients who can cooperate reliably with preoperative and postoperative evaluations, which must in¬ clude electronystagmography and electrooculographic re¬ cordings of eye movements during reading, and who can make a decision on their own in favor of surgery for a cosmetically disturbing eye condition. It follows that at the current state of
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