corneal thickness measurements and visual function abnormalities in ocular hypertensive patients

2
REFERENCES 1. Gass JDM. Stereoscopic atlas of macular diseases, 4th ed. St. Louis: Mosby, 1997:316. 2. Dubovy SR, Hairston RJ, Schatz H, et al. Adult-onset foveo- macular pigment epithelial dystrophy. Clinicopathologic cor- relation of three cases. Retina 2000;20:638 –649. 3. Gass JDM. A clinicopathologic study of a peculiar foveomacu- lar dystrophy. Trans Am Ophthalmol Soc 1974;72:139 –156. 4. Patrinely JR, Lewis RA, Font RL. Foveomacular vitelliform dystrophy, adult type. A clinicopathologic study including electron microscopic observations. Ophthalmology 1985;92: 1712–1718. 5. Jaffe GJ, Schatz H. Histopathologic features of adult-onset foveomacular pigment epithelial dystrophy. Arch Ophthalmol 1988;106:958 –960. AUTHOR REPLY WE WELCOME THE OPPORTUNITY TO RESPOND TO THE letter from Dr Ghazi. As we mentioned in our article, “the aim of this study was to analyze the morphology of adult-onset foveomacular vitelliform dystrophy (AFVD) using ocular coherence tomography (OCT), and to com- pare the findings with those of biomicroscopy and fluores- cein angiography (FA).” Clearly, our purpose was not to compare OCT features with histopathologic features. We agree that for discussing on the localization of the material, OCT has to be correlated with the datas of histopathologic studies but this point only represents a part of our discus- sion and could be the topic of an another paper. Doctor Ghazi seems to be hurt by the statement “the exact location of the deposit of material in AFVD, whether below, above, or inside the retinal pigment epithelium, has indeed not yet been determined.” Our purpose in stating that was not to offend the authors of any of the histopathologic studies, which are of great quality but to point out that different conclusions have been drawn from various studies. All of them have to be taken into consideration and not only selected papers. We clearly stated that “it demonstrates, better than biomicros- copy, the location of the yellowish material.” It was not our purpose to compare OCT with histopathology, which can hardly be performed in our patients. Obviously, our OCT analysis does not pretend to provide information better than histopathologic studies. We agree that the definition of the “retinal pigment epithelium band” observed by OCT (with version 1 and 2 of the machine) could not be as precise as the retinal pigment epithelium layer observed by morphologic histopathologic analysis. Nevertheless, OCT allowed safe analysis of a large series of eyes that would have been difficult to obtain for histopathologic purposes and allowed us to distinguish two forms of the disorder. Concerning the question of whether all of the five eyes in the second group had the pigmented spot on fundus, it seemed clear for us and for the reviewers of this Journal that the answer was yes. That could be deduced from the paragraph “Here, in the second group of five eyes. . .degen- eration.” In our article, we analyzed 21 consecutive eyes affected with adult-onset foveomacular vitelliform dystrophy. This study allowed us to distinguish two forms of the dystrophy based on fundus examination, fluorescein angiography, and OCT. As some patients (see Table 1) presented with both forms of the disease, we suggested that these forms corre- sponded to two stages of the disease. We also suggested that group 1 (16 eyes) could correspond to the earlier stager and group 2 to the late stage, and we agree that this remains open to discussion. Doctor Ghazi said that he saw “AFMVD progress in the opposite direction suggested by the authors.” We would appreciate having more informa- tion about the number of eyes, the mean follow-up, and the publication of images of these data. Indeed, only follow-up based on fundus pictures, fluorescein angiogra- phy, and OCT could bring contributive information, avoiding speculation on the evolution of adult-onset fo- veomacular vitelliform dystrophy. NATHANAEL BENHAMOU, MD ERIC H. SOUIED, MD, PHD RICKY ZOLF, MD GABRIEL COSCAS, MD GISE ` LE SOUBRANE, MD FLORENCE COSCAS, MD Creteil, France Corneal Thickness Measurements and Visual Function Abnormalities in Ocular Hypertensive Patients EDITOR: WE READ WITH KEEN INTEREST THE ARTICLE BY MEDEIROS and associates (Am J Ophthalmol 135;131–137, 2003) on corneal thickness measurements and visual function ab- normalities in ocular hypertensive patients. It is, indeed, a beautiful study, and we would like to extend our appreci- ation to all the authors. The corneal thickness has been known to affect mea- surement of the intraocular pressure for a long time. The mean corneal thickness of normal eyes is reported as 544 m, and less than 5% of the normal subjects are expected to show corneal thickness greater than 600 m. 1 The Goldmann applanation tonometer is theoretically only accurate for central corneal thickness at 520 m. 2 A correction factor of 2.5 mm Hg for each 50-m change in the central corneal thickness beyond the normal thickness has been suggested. 1 At this backdrop it is indeed a very useful study. Despite the above facts, most of ophthalmol- ogists do not measure corneal thickness in all glaucoma- tous and suspected glaucoma cases, and the minority of us who sometimes measure the corneal thickness do not know how to correlate it clinically with other factors. Would the AMERICAN JOURNAL OF OPHTHALMOLOGY 964 NOVEMBER 2003

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Page 1: Corneal thickness measurements and visual function abnormalities in ocular hypertensive patients

REFERENCES

1. Gass JDM. Stereoscopic atlas of macular diseases, 4th ed. St.Louis: Mosby, 1997:316.

2. Dubovy SR, Hairston RJ, Schatz H, et al. Adult-onset foveo-macular pigment epithelial dystrophy. Clinicopathologic cor-relation of three cases. Retina 2000;20:638–649.

3. Gass JDM. A clinicopathologic study of a peculiar foveomacu-lar dystrophy. Trans Am Ophthalmol Soc 1974;72:139–156.

4. Patrinely JR, Lewis RA, Font RL. Foveomacular vitelliformdystrophy, adult type. A clinicopathologic study includingelectron microscopic observations. Ophthalmology 1985;92:1712–1718.

5. Jaffe GJ, Schatz H. Histopathologic features of adult-onsetfoveomacular pigment epithelial dystrophy. Arch Ophthalmol1988;106:958–960.

AUTHOR REPLY

WE WELCOME THE OPPORTUNITY TO RESPOND TO THE

letter from Dr Ghazi. As we mentioned in our article, “theaim of this study was to analyze the morphology ofadult-onset foveomacular vitelliform dystrophy (AFVD)using ocular coherence tomography (OCT), and to com-pare the findings with those of biomicroscopy and fluores-cein angiography (FA).” Clearly, our purpose was not tocompare OCT features with histopathologic features. Weagree that for discussing on the localization of the material,OCT has to be correlated with the datas of histopathologicstudies but this point only represents a part of our discus-sion and could be the topic of an another paper.

Doctor Ghazi seems to be hurt by the statement “theexact location of the deposit of material in AFVD,whether below, above, or inside the retinal pigmentepithelium, has indeed not yet been determined.” Ourpurpose in stating that was not to offend the authors of anyof the histopathologic studies, which are of great qualitybut to point out that different conclusions have beendrawn from various studies. All of them have to be takeninto consideration and not only selected papers. Weclearly stated that “it demonstrates, better than biomicros-copy, the location of the yellowish material.” It was not ourpurpose to compare OCT with histopathology, which canhardly be performed in our patients. Obviously, our OCTanalysis does not pretend to provide information betterthan histopathologic studies. We agree that the definitionof the “retinal pigment epithelium band” observed by OCT(with version 1 and 2 of the machine) could not be asprecise as the retinal pigment epithelium layer observed bymorphologic histopathologic analysis. Nevertheless, OCTallowed safe analysis of a large series of eyes that wouldhave been difficult to obtain for histopathologic purposesand allowed us to distinguish two forms of the disorder.

Concerning the question of whether all of the five eyesin the second group had the pigmented spot on fundus, itseemed clear for us and for the reviewers of this Journal thatthe answer was yes. That could be deduced from the

paragraph “Here, in the second group of five eyes. . .degen-eration.”

In our article, we analyzed 21 consecutive eyes affectedwith adult-onset foveomacular vitelliform dystrophy. Thisstudy allowed us to distinguish two forms of the dystrophybased on fundus examination, fluorescein angiography, andOCT. As some patients (see Table 1) presented with bothforms of the disease, we suggested that these forms corre-sponded to two stages of the disease. We also suggestedthat group 1 (16 eyes) could correspond to the earlierstager and group 2 to the late stage, and we agree that thisremains open to discussion. Doctor Ghazi said that he saw“AFMVD progress in the opposite direction suggested bythe authors.” We would appreciate having more informa-tion about the number of eyes, the mean follow-up, andthe publication of images of these data. Indeed, onlyfollow-up based on fundus pictures, fluorescein angiogra-phy, and OCT could bring contributive information,avoiding speculation on the evolution of adult-onset fo-veomacular vitelliform dystrophy.

NATHANAEL BENHAMOU, MD

ERIC H. SOUIED, MD, PHD

RICKY ZOLF, MD

GABRIEL COSCAS, MD

GISELE SOUBRANE, MD

FLORENCE COSCAS, MD

Creteil, France

Corneal Thickness Measurements andVisual Function Abnormalities inOcular Hypertensive Patients

EDITOR:

WE READ WITH KEEN INTEREST THE ARTICLE BY MEDEIROS

and associates (Am J Ophthalmol 135;131–137, 2003) oncorneal thickness measurements and visual function ab-normalities in ocular hypertensive patients. It is, indeed, abeautiful study, and we would like to extend our appreci-ation to all the authors.

The corneal thickness has been known to affect mea-surement of the intraocular pressure for a long time. Themean corneal thickness of normal eyes is reported as 544�m, and less than 5% of the normal subjects are expectedto show corneal thickness greater than 600 �m.1 TheGoldmann applanation tonometer is theoretically onlyaccurate for central corneal thickness at 520 �m.2 Acorrection factor of 2.5 mm Hg for each 50-�m change inthe central corneal thickness beyond the normal thicknesshas been suggested.1 At this backdrop it is indeed a veryuseful study. Despite the above facts, most of ophthalmol-ogists do not measure corneal thickness in all glaucoma-tous and suspected glaucoma cases, and the minority of uswho sometimes measure the corneal thickness do not knowhow to correlate it clinically with other factors. Would the

AMERICAN JOURNAL OF OPHTHALMOLOGY964 NOVEMBER 2003

Page 2: Corneal thickness measurements and visual function abnormalities in ocular hypertensive patients

authors suggest mandatory measurement of central cornealthickness in the patients with ocular hypertension as aroutine procedure along with a correction factor to negateits effect on the intraocular pressure? In previous reports3

and in our experience, normal and less than normalcorneal thickness were more common in angle closureglaucoma and normal tension glaucoma than in ocularhypertensive patients and in those with open-angle glau-coma. It would, indeed, be interesting to know if theauthors also had similar experience with any subset ofpatients and, as such, find any correlation between cornealthickness with respect to the anterior chamber depth.

The authors have also reconfirmed that short wave-length automated perimetry (SWAP) is more sensitivethan standard automated perimetry (SAP) in picking upearliest visual field defects. Would the authors suggestroutine use of SWAP in all patients having one or more ofthe risk factors for developing glaucoma instead of theroutine SAP?

AKASH RAJ, MD, DNB, DRCO, FRCS

London, EnglandRAJNISH SEKHRI, MS, FRCS

Leeds, EnglandINDRANIL CHOUDHURI, MD

Leicester, EnglandSAMREEN UPPAL, MS

London, England

REFERENCES

1. Doughty MJ, Zaman ML. Human corneal thickness and itsimpact on intraocular pressure measurement: A review andmeta-analysis. Surv Ophthalmol 2000;108:1779–1788.

2. Wolfs RCW, Klaver CCW, Vingerline JR, et al. Distributionof central corneal thickness and its association with intraoc-ular pressure: The Rotterdam study. Am J Ophthalmol 1997;123:767–772.

3. Bechmann M, Thiel MJ, Roesen B, Ullrich S, Ulbig MW,Ludwig K. Central corneal thickness determined with opticalcoherence tomography in various types of glaucoma. Br JOphthalmol 2001;85:1394.

AUTHOR REPLY

WE APPRECIATE THE INTEREST OF DR. RAJ AND ASSOCIATES

in our manuscript. Our results indicate that central cornealthickness (CCT) should be evaluated in patients withocular hypertension (OHT).1 In another study, we provideadditional evidence for this by showing that OHT patientswith abnormalities on frequency doubling technology(FDT) perimetry had thinner corneas than OHT patientswith normal FDT results.2 Furthermore, a recent reportfrom the Ocular Hypertension Treatment Study also pro-vided compelling evidence that CCT was a powerfulpredictor for progression to primary open-angle glaucomaamong OHT patients3; CCT appears to be important not

only in the evaluation of patients with ocular hyperten-sion. In a recent study, we showed that CCT was also a riskfactor for development of visual field loss in patientsdiagnosed with preperimetric glaucomatous optic neurop-athy.4 In that study, patients with CCT less than 545 �mhad more than twice the risk of visual field loss thanpatients with CCT greater than or equal to 545 �m. Thisindicates that CCT is important not only in the evaluationof OHT patients but also when establishing target pres-sures for the treatment of patients with glaucomatous opticneuropathy.

Regarding the correction of Goldmann applanationtonometry measurements using algorithms incorporatingCCT, we believe that no standard available nomogram hasyet been fully validated. Furthermore, although the effectof CCT as a risk factor is likely related to its relationshipto intraocular pressure measurement, the hypothesis thatcorneal thickness may be intrinsically related to glauco-matous damage cannot be excluded and needs furtherinvestigation.

Several studies have suggested that patients with normaltension glaucoma have thinner than average corneas, andthis is consistent with our experience. Data on CCTmeasurements in patients with angle closure glaucomashould be forthcoming.

In our study, approximately 20% of OHT patients withnormal standard automated perimetry visual fields hadshort-wavelength automated perimetry (SWAP) abnor-malities. This is in agreement with our own previousreports, as well as that of others, supporting the role ofSWAP for the identification of early visual function loss inglaucoma. However, the routine use of SWAP is stilllimited due to the long test time and presence of cataract.The development of faster strategies incorporating SWAP,like Swedish interactive threshold algorithm (SITA)-SWAP,5 will unquestionably lead to more widespread useof this visual function test.

FELIPE A. MEDEIROS, MD

PAMELA A. SAMPLE, PHD

ROBERT N. WEINREB, MD

La Jolla, California

REFERENCES

1. Medeiros FA, Sample PA, Weinreb RN. Corneal thicknessmeasurements and visual function abnormalities in ocularhypertensive patients. Am J Ophthalmol 2003;135:131–137.

2. Medeiros FA, Sample PA, Weinreb RN. Corneal thicknessmeasurements and frequency doubling technology perimetryabnormalities in ocular hypertensive eyes. Ophthalmology2003;110:1903–1908.

3. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hyper-tension Treatment Study: Baseline factors that predict theonset of primary open-angle glaucoma. Arch Ophthalmol2002;120:714–720.

4. Medeiros FA, Sample PA, Zangwill L, et al. Corneal thicknessas a risk factor for visual field loss in patients with preperi-

CORRESPONDENCEVOL. 136, NO. 5 965