Influence of Rapid Glycemic Controlon Lens Opacity in Patients WithDiabetes MellitusSatoshi Kato, MD, Tetsuro Oshika, MD,Jiro Numaga, MD, Hidetoshi Kawashima, MD,Shigehiko Kitano, MD, and Tadayoshi Kaiya, MD

PURPOSE: To report the influence of rapid glycemiccontrol on lens opacity in patients with diabetes mellitus.METHODS: In a prospective study, nine patients with adultonset diabetes mellitus and glycosylated hemoglobin valuesover 9% were divided into two groups, rapid glycemiccontrol and slow glycemic control groups, based on the timecourse of glycosylated hemoglobin values after the initiationof glycemic control. The lens thickness and opacity weremeasured using the anterior eye segment analysis system.RESULTS: One week after onset of treatment, the lens inrapid glycemic control group became significantly thickerthan in pretreatment, but returned to the baseline level atthe subsequent measurement points. The lens opacityindex in the rapid glycemic control group increasedsignificantly (P < .01, paired t test) 4 months after theglycemic control, which persisted throughout the 1-yearstudy period. The lens thickness and opacity in the slowglycemic control group did not change significantly.CONCLUSION: It was suggested that rapid glycemic con-trol can induce an irreversible increase in lens opacifica-tion. (Am J Ophthalmol 2000;130:354–355. © 2000by Elsevier Science Inc. All rights reserved.)

RAPID DECLINE OF SERUM GLUCOSE LEVEL IN PATIENTS

with marked hyperglycemia is known to induce tem-porary lens opacification and swelling as well as transienthyperopia.1,2 The results of long-term follow-up, however,are inconsistent. There have been reports of irreversibleand reversible cataract formations after the rapid reductionof blood glucose in patients with diabetes mellitus.3,4 Thisprospective study was undertaken to evaluate the influenceof rapid glycemic control on lens opacity in patients withdiabetes mellitus.

Nine type II diabetes mellitus patients with correctedvisual acuity of 20/20 or better were recruited (mean age, 42.3years). The patients did not have cataract on slit-lampexamination and their glycosylated hemoglobin values ex-ceeded 9% before glycemic control. These patients weredivided into two groups based on the changes in glycosylatedhemoglobin values by glycemic control; the rapid glycemiccontrol group consisted of 12 eyes of six patients whoseglycosylated hemoglobin value decreased by 3% or moreduring a period of 3 months and glycosylated hemoglobinvalue dropped below 7.5%; the slow glycemic control groupconsisted of six eyes of three patients whose glycosylatedhemoglobin level decreased less than 3% during the 1-yearstudy period. There were no significant differences in back-grounds of diabetes mellitus between the two groups. The lensthickness and opacity were measured under full mydriasisusing the anterior eye segment analysis system (EAS-1000;Nidek, Gamagori, Japan) equipped with area densitometry tomeasure the scattering light intensity, which is equal to theopacification density in the anterior segment of the eye.5

Measurements were conducted before glycemic control, 1week and 1, 2, 3, 4, 6, and 12 months after the initiation oftreatment.

One week after onset of treatment, the lens in therapid glycemic control group became significantlythicker than in pretreatment (P , .01, paired t test), butreturned to the baseline level at the subsequent mea-

Accepted for publication April 26, 2000.From the Department of Ophthalmology, School of Medicine, Uni-

versity of Tokyo (S.Ka., T.O., J.N., H.K.), Tokyo, Japan, Tokyo Women’sMedical University Diabetes Center (S.Ki.), Tokyo, Japan, and Kaiya EyeClinic (T.K.), Hamamatsu, Japan.

Inquiries to Satoshi Kato, MD, Division of Ophthalmology, TokyoUniversity Branch Hospital 3-28-6 Mejirodai Bunkyo-ku, Tokyo 112-8688, Japan; fax: 181-3-3943-5781; e-mail: katou-s@ka2.so-net.ne.jp

TABLE 1. The Index of Lens Thickness and Lens Opacity

Lens thickness

(mm)

Lens opacity

(photon count)

RGC group SGC group RGC group SGC group

Pretreatment 4.62 6 0.16 4.26 6 0.26 9178 6 1103 9897 6 444

Post-treatment

1W 4.89 6 0.13* 4.41 6 0.21 9505 6 1105 9434 6 489

1M 4.47 6 0.12 4.38 6 0.27 9047 6 1080 9899 6 998

2M 4.56 6 0.14 4.23 6 0.22 9195 6 953 9172 6 715

3M 4.62 6 0.16 4.26 6 0.34 9586 6 986 9252 6 780

4M 4.74 6 0.10 4.38 6 0.27 10319 6 1077* 9303 6 1179

6M 4.71 6 0.17 4.47 6 0.23 10713 6 1075* 10442 6 1328

12M 4.59 6 0.15 4.44 6 0.21 10958 6 1066* 9669 6 1040

RGC 5 rapid glycemic control; SGC 5 slow glycemic control.

*Significantly higher than the pretreatment level (P , .01, paired t test). mean 6 SE.

AMERICAN JOURNAL OF OPHTHALMOLOGY354 SEPTEMBER 2000

surement points (Table 1). The lens thickness of theslow glycemic control group did not change significantlyduring the course of this study. The lens opacity indexin the rapid glycemic control group increased signifi-cantly at 4 months after the glycemic control (P , .01,paired t test) and persisted throughout the 1-year studyperiod. The lens opacity index of the slow glycemiccontrol group did not change significantly. In all ninepatients, both eyes behaved similarly.

A transient increase in lens thickness occurred im-mediately after the rapid glycemic control withoutconcurrent, significant opacification of the lens. Irre-versible lens opacification developed after a delay of 3 to4 months. It was assumed that transient lens swellingcaused by changes in osmotic pressure led to subsequentopacification. In this preliminary study, results suggestthat rapid glycemic control can induce an irreversibleincrease in lens opacification.

REFERENCES

1. Saito Y, Ohmi G, Kinoshita S, et al. Transient hyperopia withlens swelling at initial therapy in diabetes. Br J Ophthalmol1993;77:145–148.

2. Saito Y, Ohmi G, Tano Y, Kinoshita S. Lens changes duringrapid tightening of metabolic control in diabetes. Lancet1996;347:1764.

3. White FA, Richert HM. Accelerated bilateral cataract forma-tion in insulin-dependent diabetes mellitus. Diabetes Care1984;7:186–187.

4. Epstein DL. Reversible unilateral lens opacities in a diabeticpatient. Arch Ophthalmol 1976;94:461–463.

5. Sasaki K, Sakamoto Y, Shibata T, Emori Y. The multi-purposecamera; a new anterior eye segment analysis system. Ophthal-mic Res 1990;22:3–8.

Amsler Grid Examination and OpticalCoherence Tomography of a MacularHole Caused by Accidental Nd:YAGLaser InjuryHirokazu Sakaguchi, MD, Masahito Ohji, MD,Akira Kubota, MD, Yasumasa Otori, MD,Atsushi Hayashi, MD, Syunji Kusaka, MD,Yoshihiro Saito, MD, and Yasuo Tano, MD

PURPOSE: To compare a macular hole from accidentalNd:YAG laser injury with idiopathic macular holes.METHODS: Case report. In a 24-year-old man with acciden-tal Nd:YAG laser injury, right eye, Amsler grid testing andoptical coherence tomography were performed.RESULTS: Nd:YAG laser injury was responsible for amacular hole about 700 mm in diameter. The visualacuity was 20/100. Amsler grid testing displayed acentral scotoma with no surrounding distortion. Opticalcoherence tomography showed a defect in all retinallayers at the macula.CONCLUSION: The scotoma caused by Nd:YAG laserinjury is not surrounded by distortion; the hole isproduced by the defect of all retinal layers. In contrast,idiopathic macular holes generally produce a pincushionpattern on Amsler grid testing and have no tissue loss.(Am J Ophthalmol 2000;130:355–356. © 2000 byElsevier Science Inc. All rights reserved.)

AS ND:YAG LASERS BECOME MORE COMMON IN SCI-

ence and industry, they have occasionally causedaccidental eye injuries. 1–3 When the destructive energyof the laser reaches the macula, it destroys tissues andmay create a hole. In this study, we examined results ofAmsler grid testing and optical coherence tomographyof a man with a macular hole caused by occupationalNd:YAG laser injury and compared them with thefindings obtained from patients with idiopathic macularhole.

A 24-year-old physics graduate student suffered anaccidental injury to his right eye with a 1064-nmNd:YAG laser that produced a 3-ns pulse with energy ofabout 10 mJ. Visual acuity testing, optical coherencetomography, scanning laser ophthalmoscopic micrope-rimetry, fundus photography, and Amsler grid testingwere performed.

In the right eye, fundus photography showed a full-thickness macular hole about 700 mm in diameter withhemorrhage within the hole 3 days after injury (Figure1, top). Best-corrected visual acuity was 20/100. Theoptical coherence tomography showed a defect in allretinal layers at the macula, smooth and straight edgesat the border of the macular hole, and no displacementof the retina 3 days after injury (Figure 1, bottom).Scanning laser ophthalmoscopic microperimetry dis-closed an absolute scotoma corresponding to the macu-lar hole 3 days after injury.

One month after the injury, Amsler grid testingdisplayed a central scotoma and no distortion aroundthe scotoma (Figure 2). The best-corrected visual acuitywas 20/100. The hemorrhage within the hole haddiminished.

Johnson and Gass reported that in Amsler grid testingof patients with idiopathic macular hole, the mainsymptom was metamorphopsia.4 Saito and associates

Accepted for publication April 24, 2000.From the Department of Ophthalmology, Osaka University Medical

School, Suita, Japan (H.S., M.O., A.K., Y.O., A.H., S.K., Y.S., Y.T.), andthe Cole Eye Institute, the Cleveland Clinic Foundation, Cleveland,Ohio (H.S.).

Inquiries to Hirokazu Sakaguchi, MD, Cole Eye Institute, the Cleve-land Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195; fax:(216) 445-3670; e-mail: sakaguh@ccf.org

BRIEF REPORTSVOL. 130, NO. 3 355