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Figure 1.
The increase in corneal thicknessafter 1 month was significantly higher in the diabetic group than in the nondiabeticgroup (P = .03).

The increase in corneal thicknessafter 1 month was significantly higher in the diabetic group than in the nondiabeticgroup (P = .03).

Figure 2.
The endothelial cell losses occurring1 day and 1 week after surgery were significantly higher in the diabetic groupthan in the nondiabetic group (after 1 day, P = .03; and after1 week, P = .04).

The endothelial cell losses occurring1 day and 1 week after surgery were significantly higher in the diabetic groupthan in the nondiabetic group (after 1 day, P = .03; and after1 week, P = .04).

Figure 3.
The coefficients of variation1 day, 1 week, and 1 month after operation were not different in the diabeticand nondiabetic groups.

The coefficients of variation1 day, 1 week, and 1 month after operation were not different in the diabeticand nondiabetic groups.

Figure 4.
The percentages of hexagonal cells1 day, 1 week, and 1 month after operation were not different in the diabeticand nondiabetic groups.

The percentages of hexagonal cells1 day, 1 week, and 1 month after operation were not different in the diabeticand nondiabetic groups.

Preoperative Data*
Preoperative Data*
1.
Foulks  GNThoft  RAPerry  HDTolentino  FI Factors related to corneal epithelial complications after closed vitrectomyin diabetics. Arch Ophthalmol. 1979;971076- 1078
PubMedArticle
2.
Brightbill  FSMyers  FLBresnick  GH Postvitrectomy keratopathy. Am J Ophthalmol. 1978;85651- 655
PubMed
3.
Perry  HDFoulks  GNThoft  RATolentino  FI Corneal complications after closed vitrectomy through the pars plana. Arch Ophthalmol. 1978;961401- 1403
PubMedArticle
4.
Schultz  ROMatsuda  MYee  RWEdelhauser  HFSchultz  KJ Corneal endothelial changes in type I and type II diabetes mellitus. Am J Ophthalmol. 1984;98401- 410
PubMedArticle
5.
Yee  RWMatsuda  MKern  TSEngerman  RLEdelhauser  HF Corneal endothelial changes in diabetic dogs. Curr Eye Res. 1985;4759- 766
PubMedArticle
6.
Itoi  MNakamura  TMizobe  KKodama  YNakagawa  NItoi  M Specular microscopic studies of the corneal endothelia of Japanesediabetics. Cornea. 1989;82- 6
PubMedArticle
7.
Matsuda  MOhguro  NIshimoto  IFukuda  M Relationship of corneal endothelial morphology to diabetic retinopathy,duration of diabetes and glycemic control. Jpn J Ophthalmol. 1990;3453- 56
PubMed
8.
Keoleian  GMPach  JMHodge  DOTrocme  SDBourne  WM Structural and functional studies of the corneal endothelium in diabetes. Am J Ophthalmol. 1992;11364- 70
PubMed
9.
Larsson  LIBourne  WMPach  JMBrubaker  RF Structure and function of the corneal endothelium in diabetes mellitustype I and type II. Arch Ophthalmol. 1996;1149- 14
PubMedArticle
10.
Roszkowska  AMTringali  CGColosi  PSqueri  CAFerreri  G Corneal endothelium evaluation in type I and type II diabetes mellitus. Ophthalmologica. 1999;213258- 261
PubMedArticle
11.
Inoue  KKato  SInoue  YAmano  SOshika  T The corneal endothelium and thickness in type II diabetes mellitus. Jpn J Ophthalmol. 2002;4665- 69
PubMedArticle
12.
Goebbels  MSpitznas  M Endothelial barrier function after phacoemulsification: a comparisonbetween diabetic and non-diabetic patients. Graefes Arch Clin Exp Ophthalmol. 1991;229254- 257
PubMedArticle
13.
Herse  PHooker  B Corneal edema recovery dynamics in diabetes: is the alloxan induceddiabetic rabbit a useful model? Invest Ophthalmol Vis Sci. 1994;35310- 313
PubMed
14.
Saini  JSMittal  S In vivo assessment of corneal endothelial function in diabetes mellitus. Arch Ophthalmol. 1996;114649- 653
PubMedArticle
15.
Weston  BCBourne  WMPolse  KAHodge  DO Corneal hydration control in diabetes mellitus. Invest Ophthalmol Vis Sci. 1995;36586- 595
PubMed
16.
Diaz-Valle  DBenitez del Castillo Sanchez  JMCastillo  ASayagues  OMoriche  M Endothelial damage with cataract surgery techniques. J Cataract Refract Surg. 1998;24951- 955
PubMedArticle
17.
Walkow  TAnders  NKlebe  S Endothelial cell loss after phacoemulsification: relation to preoperativeand intraoperative parameters. J Cataract Refract Surg. 2000;26727- 732
PubMedArticle
18.
Dick  HBKohnen  TJacobi  FKJacobi  KW Long-term endothelial cell loss following phacoemulsification througha temporal clear corneal incision. J Cataract Refract Surg. 1996;2263- 71
PubMedArticle
19.
Matsuda  MSawa  MEdelhauser  HFBartels  SPNeufeld  AHKenyon  KR Cellular migration and morphology in corneal endothelial wound repair. Invest Ophthalmol Vis Sci. 1985;26443- 449
PubMed
20.
Furuse  NHayasaka  SYamamoto  YSetogawa  T Corneal endothelial changes after posterior chamber intraocular lensimplantation in patients with or without diabetes mellitus. Br J Ophthalmol. 1990;74258- 260
PubMedArticle
21.
Cogan  DGKinoshita  JHKador  PF  et al.  NIH conference: aldose reductase and complications of diabetes. Ann Intern Med. 1984;10182- 91
PubMedArticle
22.
Kinoshita  JH Mechanisms initiating cataract formation: Proctor Lecture. Invest Ophthalmol. 1974;13713- 724
PubMed
23.
Kador  PF The role of aldose reductase in the development of diabetic complication. Med Res Rev. 1988;8325- 352
PubMedArticle
24.
Kinoshita  JHNishimura  C The involvement of aldose reductase in diabetic complication. Diabetes Metab Rev. 1988;4323- 337
PubMedArticle
25.
Akagi  YYajima  YKador  PFKuwabara  TKinoshita  JH Localization of aldose reductase in the human eye. Diabetes. 1984;33562- 566
PubMedArticle
26.
Kern  TSEngerman  RL Distribution of aldose reductase in ocular tissues. Exp Eye Res. 1981;33175- 182
PubMedArticle
27.
Ohguro  NMatsuda  MOhashi  YFukuda  M Topical aldose reductase inhibitor for correcting corneal endothelialchanges in diabetic patients. Br J Ophthalmol. 1995;791064- 1065
PubMedArticle
28.
Matsuda  MAwata  TOhashi  YInaba  MFukuda  MManabe  R The effects of aldose reductase inhibitor on the corneal endothelialmorphology in diabetic rats. Curr Eye Res. 1987;6391- 397
PubMedArticle
Clinical Sciences
July 2004

Corneal Changes After Small-Incision Cataract Surgery in Patients WithDiabetes Mellitus

Author Affiliations

From the Division of Ophthalmology, School of Medicine, Fukui University,Fukui, Japan. The authors have no relevant financial interest in this article.

Arch Ophthalmol. 2004;122(7):966-969. doi:10.1001/archopht.122.7.966
Abstract

Objective  To evaluate functional impairment in the corneal endothelium of eyesin patients with diabetes mellitus, after small-incision cataract surgery.

Methods  Evaluation was performed in 93 eyes in patients with type 2 diabetesmellitus (diabetic group) and 93 eyes in patients without diabetic mellitus(nondiabetic group) who underwent cataract surgery. Using a topography system,the corneal thickness in the central area was measured before surgery and1 day, 1 week, and 1 month after surgery. Corneal endothelial cells were countedusing a noncontact specular microscope.

Results  No significant differences in any preoperative measures were observedbetween the diabetic and nondiabetic groups. The increase in corneal thickness1 month after surgery was significantly higher in the diabetic group thanin the nondiabetic group (P = .03). The corneal endothelialcell losses 1 day and 1 week after surgery were significantly higher in thediabetic group than in the nondiabetic group (after 1 day, P = .03; and after 1 week, P = .04).

Conclusion  Compared with nondiabetic eyes, eyes of patients with diabetes mellitusshowed more damage in corneal endothelial cells due to cataract surgery anda delay in the postoperative recovery of corneal edema.

In recent years, advances have been made in cataract surgery becauseof improvement in surgical equipment, viscoelastic agents, and techniques,expanding the indications for this surgery. After the development of phacoemulsification,corneal endothelial damage was not an absolute contraindication for cataractsurgery. However, bullous keratopathy induced by mechanical injury in thecorneal endothelium is intractable; therefore, preoperative evaluation ofendothelial tissue is important.

Corneal damage is often encountered after intraocular surgery in patientswith diabetes mellitus. Based on this finding, fragility of the cornea inpatients with diabetes mellitus has been suggested.13 Ingeneral, the cornea of patients with type 1 diabetes mellitus shows morphologicalabnormalities of endothelial cells (polymegethism and pleomorphism),411 butnormal barrier function as represented by fluorescein permeability.8,9,12 In addition, althoughcorneal edema induced by contact lens wear is similar in diabetic and nondiabeticgroups, corneal edema recovery is slower in patients with diabetes mellitusthan in control subjects.13,14 Thissuggests that the cornea in patients with diabetes mellitus is weaker thanthe normal cornea against physical stress. In contrast, Weston et al15 reported that induced swelling was less in patientswith diabetes mellitus than in controls, and the corneal deswelling rate wasnot different between diabetic and control subjects. Therefore, in the presentstudy, we evaluated functional impairment in the corneal endothelium of eyesof patients with diabetes mellitus after small-incision cataract surgery.

METHODS

Evaluation was performed in 93 eyes in patients with type 2 diabetesmellitus (diabetic group) and 93 eyes in patients without diabetes mellitus(nondiabetic group) who underwent cataract surgery (phacoemulsification andintraocular lens implantation) at our division between March 15, 2000, andJune 20, 2002. The nondiabetic group was selected randomly, and both groupswere age-matched. Written informed consent was obtained from all patientsbefore surgery and examinations, and the study was approved by an ethics committee.The mean ± SD age was 68.8 ± 8.9 years in the nondiabetic groupand 68.6 ± 8.8 years in the diabetic group (Table 1). Because the cornea was evaluated, patients with cornealdisorder or history of ocular operation, contact lens wear, and ocular injurywere excluded. Surgery was performed by 4 experienced surgeons, who had performedcataract surgery in more than 500 cases. There were no differences betweenthe 2 study groups in phacoemulsification time and intraocular infusion volume.

Cataract surgery was performed under Tenon anesthesia. A nonsuture sclerocornealincision (3.5 mm from the 12-o'clock position) was made, and continuous curvilinearcapsulorrhexis was performed, using Healon (Pharmacia, Uppsala, Sweden) asa viscoelastic agent. The nucleus was divided by the phaco-chop method, andphacoemulsification and aspiration were performed. For cataract surgery, Accurus(Alcon Laboratories, Inc, Fort Worth, Tex) equipment was used, and BSS PLUS(Alcon Laboratories, Inc) was the perfusion fluid used. After cortical aspiration,an acryl-foldable intraocular lens (Acrysof MA60BM; Alcon Laboratories, Inc)was inserted.

The corneal thickness in the central area was measured using the ORBSCANtopography system (ORBTEK; Bausch & Lomb, Rochester, NY) before surgeryand 1 day, 1 week, and 1 month after surgery. Corneal endothelial cells werecounted using a noncontact specular microscope, NONCON ROBO (Konan Medical,Inc, Hyogo, Japan). These examinations were performed in a masked manner byone technician (S.M.).

The items evaluated in this study were central corneal thickness (inmicrometers), endothelial cell density (cells per square millimeter), percentageof hexagonal cells, and the coefficient of variation before and after operation.Changes in each item after operation were compared between the diabetic andnondiabetic groups by t test.

RESULTS

Before cataract operation, the age-matched nondiabetic group had a mean± SD central corneal thickness of 541.9 ± 33.3 µm, cornealendothelial cell density of 2721.6 ± 348.1 cells/mm2, coefficientof variation of 0.306 ± 0.066, and 58.8% ± 10.4% hexagonal cells.The diabetic group had a mean ± SD central corneal thickness of 544.0± 37.2 µm, corneal endothelial cell density of 2727.9 ±404.0 cells/mm2, coefficient of variation of 0.314 ± 0.072,and 57.7% ± 13.2% hexagonal cells. No significant difference was observedin any preoperative item measured between the diabetic and nondiabetic groups.In addition, in the diabetic group, central corneal thickness, endothelialcell density, coefficient of variation, and percentage of hexagonal cellswere not significantly associated with the severity of diabetic retinopathy(Table 1).

Serial changes in the increase in central corneal thickness after operationare shown in Figure 1. Comparedwith the preoperative thickness, increases observed 1 day, 1 week, and 1 monthafter operation were 4.2%, 0.9%, and 0.04%, respectively, in the nondiabeticgroup and 3.9%, 1.6%, and 1.6%, respectively, in the diabetic group. The increaseafter 1 month was significantly higher in the diabetic group than in the nondiabeticgroup (P = .03).

Serial changes in endothelial cell loss after operation are shown in Figure 2. The endothelial cell losses occurring1 day, 1 week, and 1 month after operation were 2.1%, 3.6%, and 3.2%, respectively,in the nondiabetic group and 7.0%, 7.9%, and 7.2%, respectively, in the diabeticgroup. Endothelial cell losses occurring after 1 day and 1 week were significantlyhigher in the diabetic group than in the nondiabetic group (after 1 day, P = .03; and after 1 week, P =.04).

The coefficients of variation 1 day, 1 week, and 1 month after operationwere 0.334, 0.316, and 0.308, respectively, in the nondiabetic group and 0.331,0.314, and 0.312, respectively, in the diabetic group, without significantdifferences between the 2 groups (Figure 3).

The percentages of hexagonal cells 1 day, 1 week, and 1 month afteroperation were 56.7%, 57.7%, and 57.2%, respectively, in the nondiabetic groupand 53.3%, 55.6%, and 55.7%, respectively, in the diabetic group, withoutsignificant differences between the 2 groups (Figure 4).

COMMENT

Corneal endothelial abnormalities in diabetic patients have been reported.411 However,these are morphological abnormalities, such as polymegethism and pleomorphism,and do not include abnormal permeability. Studies4,5,79 havefound no significant differences in the endothelial cell density between eyesof patients with and without diabetes mellitus. The cornea has been reportedto be thicker in eyes of diabetic patients than in eyes of nondiabetic subjectsby some authors9,10 but shownto be similar by others.6,9 Roszkowskaet al10 demonstrated that the cornea in diabeticpatients is significantly thicker than the cornea in nondiabetic subjects,speculating that the pump function of the corneal endothelium is decreased,resulting in edema against osmotic pressure in eyes of diabetic patients.On the other hand, no association between corneal thickness and retinopathyor diabetic control has been reported.7,11 Inthis study, the mean thickness of the central cornea before operation wasslightly thicker in the diabetic group (544.0 µm) than in the nondiabeticgroup (541.9 µm), but the endothelial cell density, coefficient of variation,and percentage of hexagonal cells did not significantly differ between the2 groups. However, because cataract surgery was indicated in both groups inthis study, the results cannot be directly compared with those of other studiesthat assessed diabetic and nondiabetic groups irrespective of surgical indications.

Concerning postoperative changes, the increase in central corneal thicknesswas highest 1 day after operation among the 3 time points measured in thediabetic and nondiabetic groups, but recovered thereafter. However, the recoveryrate was slow in the diabetic group compared with the nondiabetic group. Theincrease in central corneal thickness 1 month after operation was 0.04% inthe nondiabetic group and 1.6% in the diabetic group, showing significantlypoor recovery in the latter. Therefore, recovery of corneal edema after cataractsurgery may be delayed in the cornea of diabetic patients, as the cornealthickness will not have returned to the preoperative level 1 month after surgery.

Previous studies1618 haveshown that endothelial cell density decreases 6% to 10% after phacoemulsificationfor cataract. In this study, the decrease in endothelial cells was maximal1 week after operation among the 3 time points measured in the diabetic andnondiabetic groups. The endothelial cell losses 1 day and 1 week after operationwere significantly greater in the diabetic group (7.0% and 7.9%, respectively)than in the nondiabetic group (2.1% and 3.6%, respectively). Based on theseresults, we speculated that the corneal endothelium in diabetic patients isunder metabolic stress, and weaker against mechanical loads, such as cataractsurgery, than that in nondiabetic subjects.

The percentage of hexagonal cells decreased after 1 day and was slightlylower in the diabetic group than in the nondiabetic group at each measurementpoint. The coefficient of variation slightly increased 1 day after operation,but did not significantly differ between the 2 groups. The corneal endothelium,once decreased, does not proliferate, and the defects are covered by stretching,extension, and transfer of the residual corneal endothelium.19 Althoughwe considered that the coefficient of variation and percentage of hexagonalcells can be indexes of the repair mechanism, no marked difference was observedin either variable between the diabetic and nondiabetic groups in this study.

Goebbels and Spitznas12 performed fluorophotometryof the corneal endothelium before and 4 days, 3 weeks, and 6 weeks after phacoemulsificationand intraocular lens implantation, and endothelial permeability was evaluatedin the presence or absence of diabetes mellitus. Endothelial permeabilitydid not differ between the diabetic and nondiabetic groups before operation,markedly increased in both groups 4 days after operation, and recovered 3weeks after operation in the nondiabetic group but 6 weeks after operationin the diabetic group. This result was consistent with the delayed recoveryof endothelial function in the cornea of diabetic patients after cataractsurgery observed in our study. On the other hand, Furuse et al20 comparedthe endothelial cell density, coefficient of variation, and endothelial cellloss 3, 6, and 12 months after extracapsular cataract extraction and intraocularlens implantation between patients with and without diabetic mellitus andobserved endothelial cell density decreases of 10% to 20% in both groups,without noticeable differences. This variation in findings between their studyand ours may be because extracapsular cataract extraction is more invasiveto the cornea than phacoemulsification and masks diabetes mellitus–associateddifferences.

One theory that can explain the fragility of the corneal endotheliumin eyes of diabetic patients is the polyol osmotic theory.2124 Indiabetic patients, the polyol pathway is enhanced, and excessive glucose isconverted to sugar alcohol, which accumulates in cells. Aldose reductase inthe polyol pathway is distributed in the corneal epithelium and endothelium.25,26 Accumulation of sugar alcohol mayinduce hyperosmolality, causing corneal endothelial fragility. Morphologicalabnormalities in the corneal endothelium have been reported to improve afteradministration of an inhibitor of this enzyme,27,28 whichsupports the involvement of this enzyme in the development of corneal endothelialabnormalities in eyes of patients with diabetes mellitus.

CONCLUSIONS

Compared with nondiabetic eyes, eyes of diabetic patients showed moredamage in corneal endothelial cells after cataract surgery and a delay inthe postoperative recovery of corneal edema. This suggests that eyes of diabeticpatients may be under metabolic stress and have corneal endothelium with lowerreserve ability than nondiabetic eyes. Although normal corneal stability ismaintained by the reserve function of corneal endothelial cells, surgicalinvasion destroys reserve ability, resulting in delay in postoperative recoveryof corneal edema compared with nondiabetic eyes. Because of advances in small-incisioncataract surgery, severe corneal edema rarely develops, but the protectionof the corneal endothelium is important for long-term corneal function afterintraocular surgery in eyes of diabetic patients.

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Article Information

Correspondence: Yoshio Akagi, MD, PhD, Division of Ophthalmology,School of Medicine, Fukui University, 23 Shimoaizuki, Matsuoka, Fukui 910-1193,Japan (akagiy@fmsrsa.fukui-med.ac.jp).

Submitted for publication August 4, 2003; final revision received December9, 2003; accepted January 9, 2004.

References
1.
Foulks  GNThoft  RAPerry  HDTolentino  FI Factors related to corneal epithelial complications after closed vitrectomyin diabetics. Arch Ophthalmol. 1979;971076- 1078
PubMedArticle
2.
Brightbill  FSMyers  FLBresnick  GH Postvitrectomy keratopathy. Am J Ophthalmol. 1978;85651- 655
PubMed
3.
Perry  HDFoulks  GNThoft  RATolentino  FI Corneal complications after closed vitrectomy through the pars plana. Arch Ophthalmol. 1978;961401- 1403
PubMedArticle
4.
Schultz  ROMatsuda  MYee  RWEdelhauser  HFSchultz  KJ Corneal endothelial changes in type I and type II diabetes mellitus. Am J Ophthalmol. 1984;98401- 410
PubMedArticle
5.
Yee  RWMatsuda  MKern  TSEngerman  RLEdelhauser  HF Corneal endothelial changes in diabetic dogs. Curr Eye Res. 1985;4759- 766
PubMedArticle
6.
Itoi  MNakamura  TMizobe  KKodama  YNakagawa  NItoi  M Specular microscopic studies of the corneal endothelia of Japanesediabetics. Cornea. 1989;82- 6
PubMedArticle
7.
Matsuda  MOhguro  NIshimoto  IFukuda  M Relationship of corneal endothelial morphology to diabetic retinopathy,duration of diabetes and glycemic control. Jpn J Ophthalmol. 1990;3453- 56
PubMed
8.
Keoleian  GMPach  JMHodge  DOTrocme  SDBourne  WM Structural and functional studies of the corneal endothelium in diabetes. Am J Ophthalmol. 1992;11364- 70
PubMed
9.
Larsson  LIBourne  WMPach  JMBrubaker  RF Structure and function of the corneal endothelium in diabetes mellitustype I and type II. Arch Ophthalmol. 1996;1149- 14
PubMedArticle
10.
Roszkowska  AMTringali  CGColosi  PSqueri  CAFerreri  G Corneal endothelium evaluation in type I and type II diabetes mellitus. Ophthalmologica. 1999;213258- 261
PubMedArticle
11.
Inoue  KKato  SInoue  YAmano  SOshika  T The corneal endothelium and thickness in type II diabetes mellitus. Jpn J Ophthalmol. 2002;4665- 69
PubMedArticle
12.
Goebbels  MSpitznas  M Endothelial barrier function after phacoemulsification: a comparisonbetween diabetic and non-diabetic patients. Graefes Arch Clin Exp Ophthalmol. 1991;229254- 257
PubMedArticle
13.
Herse  PHooker  B Corneal edema recovery dynamics in diabetes: is the alloxan induceddiabetic rabbit a useful model? Invest Ophthalmol Vis Sci. 1994;35310- 313
PubMed
14.
Saini  JSMittal  S In vivo assessment of corneal endothelial function in diabetes mellitus. Arch Ophthalmol. 1996;114649- 653
PubMedArticle
15.
Weston  BCBourne  WMPolse  KAHodge  DO Corneal hydration control in diabetes mellitus. Invest Ophthalmol Vis Sci. 1995;36586- 595
PubMed
16.
Diaz-Valle  DBenitez del Castillo Sanchez  JMCastillo  ASayagues  OMoriche  M Endothelial damage with cataract surgery techniques. J Cataract Refract Surg. 1998;24951- 955
PubMedArticle
17.
Walkow  TAnders  NKlebe  S Endothelial cell loss after phacoemulsification: relation to preoperativeand intraoperative parameters. J Cataract Refract Surg. 2000;26727- 732
PubMedArticle
18.
Dick  HBKohnen  TJacobi  FKJacobi  KW Long-term endothelial cell loss following phacoemulsification througha temporal clear corneal incision. J Cataract Refract Surg. 1996;2263- 71
PubMedArticle
19.
Matsuda  MSawa  MEdelhauser  HFBartels  SPNeufeld  AHKenyon  KR Cellular migration and morphology in corneal endothelial wound repair. Invest Ophthalmol Vis Sci. 1985;26443- 449
PubMed
20.
Furuse  NHayasaka  SYamamoto  YSetogawa  T Corneal endothelial changes after posterior chamber intraocular lensimplantation in patients with or without diabetes mellitus. Br J Ophthalmol. 1990;74258- 260
PubMedArticle
21.
Cogan  DGKinoshita  JHKador  PF  et al.  NIH conference: aldose reductase and complications of diabetes. Ann Intern Med. 1984;10182- 91
PubMedArticle
22.
Kinoshita  JH Mechanisms initiating cataract formation: Proctor Lecture. Invest Ophthalmol. 1974;13713- 724
PubMed
23.
Kador  PF The role of aldose reductase in the development of diabetic complication. Med Res Rev. 1988;8325- 352
PubMedArticle
24.
Kinoshita  JHNishimura  C The involvement of aldose reductase in diabetic complication. Diabetes Metab Rev. 1988;4323- 337
PubMedArticle
25.
Akagi  YYajima  YKador  PFKuwabara  TKinoshita  JH Localization of aldose reductase in the human eye. Diabetes. 1984;33562- 566
PubMedArticle
26.
Kern  TSEngerman  RL Distribution of aldose reductase in ocular tissues. Exp Eye Res. 1981;33175- 182
PubMedArticle
27.
Ohguro  NMatsuda  MOhashi  YFukuda  M Topical aldose reductase inhibitor for correcting corneal endothelialchanges in diabetic patients. Br J Ophthalmol. 1995;791064- 1065
PubMedArticle
28.
Matsuda  MAwata  TOhashi  YInaba  MFukuda  MManabe  R The effects of aldose reductase inhibitor on the corneal endothelialmorphology in diabetic rats. Curr Eye Res. 1987;6391- 397
PubMedArticle
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