Diabetes mellitus and refractive changes: analysis of three cases and review of the Literature
Necati Duru1 (necatiduru at gmail dot com) #, Döndü Melek Ulusoy2, Ayşe Özköse2, Zeynep Duru3, Hasan Altınkaynak1, Nilay Yüksel1, Mustafa Ataş2
1 Ankara Atatürk Education and Research Hospital, Department of Ophthalmology, Turkey. 2 Kayseri Education and Research Hospital, Department of Ophthalmology, Turkey. 3 Ankara Numune Education and Research Hospital, Department of Ophthalmology, Turkey
# : corresponding author
Cite as
Research 2014;1:1169

The human lens has a very sensitive structure, and even small changes in body fluids or eye fluids can cause changes in the lens. High blood glucose levels are known to cause reversible or irreversible changes in the labile lens structure and the mechanism of these changes have been researched extensively. Studies have shown that hyperglycemia causes myopia and hypoglycemia causes hypermetropia. It is also reported that rapid treatment of diabetes mellitus causes hypermetropia. In this paper, three cases of refractive changes due to hyperglycemia and insulin treatment are reviewed, and refractive changes occurring in diabetic patients are discussed with the data in the literature.


It has been known for years that high blood glucose levels cause reversible or irreversible changes in the labile lens structure. A lot of studies were conducted to research the mechanism of these changes [1] [2] [3]. It is reported that short or long term changes in blood glucose level especially affect refractive values. In hyperglycemia, hypermetropia or myopia, and in hypoglycemia, hypermetropia was observed. Also, hypermetropia could occur in cases in which blood glucose level is reduced a great deal [4] [5]. These changes are important clinically in refractive examination. For this reason, we address the question of 'when is it appropriate for refractive examination to be performed in diabetic patients?'

In this article, three cases who developed refractive changes because of hyperglycemia and insulin treatment were reviewed with the aim of discussing refractive changes occurring in diabetic patients with the data in the literature.

Case Reports
Case 1

Fifty-nine-year-old male patient presented to ophthalmology outpatient clinic with the complaint of blurry vision. It was learned that he changed his eyeglasses two times in the last six months and his vision was impaired more in recent times. His eyeglasses were -2.50 dioptre (D) in right, and -2.25 D in left eye. In the visual acuity examination, his visual acuity was 20/20 with -3.00 D in right and -2.75 D in left eye. Anterior and posterior segment examination of patient was normal bilaterally. The patient was referred to an internal medicine doctor because of the fact that refractive change of patient in a short time might be related to diabetes mellitus. Blood glucose level was measured as 592 mg/ml and patient diagnosed with diabetes was hospitalised by endocrinologist. Insulin therapy was started to patient and blood glucose level was regulated. The patient presented to the opthalmology outpatient clinic three days later, and he offered that he saw better without his eyeglasses and he had difficulty in near vision. His refraction was measured as +0.50 D in right and as +0.75 D in left eye. His visual acuity was 20/20 bilaterally without refractive correction. When blood glucose level was regulated, refractive examination of patient was the same in the first week, first month, and second month after diagnosis of diabetes mellitus.

Case 2

Fifty-two-year-old male patient presented to ophthalmology outpatient clinic with the complaint of blurry vision. His eyeglasses used for one year were -1.00 D in right and -1.25 D in left. Visual acuity was 20/20 bilaterally with +3.00 D glass in right and with +3.50 D in left eye. He reported that he was diagnosed with diabetes mellitus one week ago and he began to receive insulin therapy. Refractive change was thought related to insulin therapy and patient was called for control two weeks later. Visual acuity was 20/20 in control examination with +4.00 D in right and with +4.25 D in left eye. Refraction was +0.75 D in both eyes in the first month control examination, and it was +0.25 D in right eye and +0.50 D in left eye in the second month control.

Case 3

Fifty-six-year-old female patient was referred to ophthalmology outpatient clinic for fundus examination. Her blood glucose level was 390 mg/ml. She said that she had not any visual problem except impaired near vision. However, she reported that she had had some problems in far vision and better near vision for the last month. Her visual acuity was 20/20 in both eyes with -2.00 D refractive correction. Anterior and posterior segment examination was also normal. The refractive change in such a short time was thought related to hyperglycemia, and patient was called two weeks later for control. She said that she had near vision problems again in control two weeks later. She said that she started to use insulin and her blood glucose level was regulated. Refractive values were +1.50 D in right eye and +1,00 D in left eye. Her refractive measurement was +0.50 D in right, and there was no refractive error in left eye in examination two months later.


Although oxidative mechanisms are thought to be responsible for cataract formation in diabetic patients, refractive changes are mostly related to osmotic fluctuations. In a hyperosmotic media, firstly, lens volume decreases. Then, lens volume begins to increase with inflow of glucose and water into the lens. Simultaneously, permeability of lens to K+ increases. When osmolarity decreases, glucose entered into lens continues to pull water from outside of the lens, and volume increase of lens doesn't stop immediately. Lastly, decrease in volume occurs only when glucose exits the lens [6].

The changes in lens affect refraction in these ways: In the beginning of hyperglycemia, hypermetropia occurance is observed for a short time because of decrease in lens volume, and myopia occurs when lens volume starts to increase. When blood glucose level reduces rapidly, hypermetropia is seen related with decrease in lens thickness and refractive index. After regulation of blood glucose level, lens thickness decreases and hypermetropia is seen. Hypermetropia occuring in the first days after beginning of treatment comes to balance within one month [5] [7].

Saito et al. reported that hypermetropia occured immediately after the beginning of treatment because of the decrease in refractive index related to water entering into the lens in their study involving diabetic patients [5]. Similarly, Sönmez et al. reported that hypermetropia was observed generally in diabetic patients when treatment was started and blood glucose began to decrease [8]. Gwinup et al. found that intravenous injection of glucose solution caused myopia in phakic diabetic patients and hypermetropia in aphakic diabetic patients in their study [9]. Similarly, Furushima et al. showed that induced hyperglycemia caused myopia in their study involving healthy individuals [10]. Contrary to these studies showing hyperglycemia caused myopia, Tai et al. established that hypermetropia occured during hyperglycemia [11].

Furthermore, it was reported that changes occuring in the cornea could cause refractive alterations apart from functional and morphological changes in lens in diabetic patients. Repeated corneal erosions, healed corneal epithelial defects and changes in corneal endothelium are the principal reasons of refractive alterations [12] [13] [14] [15]. Also it was showed that high glucose concentrations in the aquous humor and cornea could change corneal topography by affecting corneal hydration [8] [16] [17].

In our study, myopic alteration was observed related to hyperglycemia in three cases. Then, refractive changes towards hypermetropia were observed when blood glucose decreased rapidly with insulin therapy, and in the second month, stable refractive error was proved.


Consequently; it is known that diabetic patients have more complaints about their eyeglasses. Understanding the clinical progress of these cases is so important for appropriate refractive examination of them.

Financial Disclosure

No author has a financial or proprietary interest in any material or method mentioned

  1. Malone J, Lowitt S, Cook W. Nonosmotic diabetic cataracts. Pediatr Res. 1990;27:293-6 pubmed
  2. Unakar N, Tsui J. Inhibition of galactose-induced alterations in ocular lens with sorbinil. Exp Eye Res. 1983;36:685-94 pubmed
  3. Brown C, Burman D. Transient cataracts in a diabetic child with hyperosmolar coma. Br J Ophthalmol. 1973;57:429-33 pubmed
  4. Duke-Elders: System of Ophthalmology. London: Kimpton. 1990;5:368-573.
  5. Saito Y, Ohmi G, Kinoshita S, Nakamura Y, Ogawa K, Harino S, et al. Transient hyperopia with lens swelling at initial therapy in diabetes. Br J Ophthalmol. 1993;77:145-8 pubmed
  6. Jacob T, Duncan G. Glucose-induced membrane permeability changes in the lens. Exp Eye Res. 1982;34:445-53 pubmed
  7. Okamoto F, Sone H, Nonoyama T, Hommura S. Refractive changes in diabetic patients during intensive glycaemic control. Br J Ophthalmol. 2000;84:1097-102 pubmed
  8. Sonmez B, Bozkurt B, Atmaca A, Irkec M, Orhan M, Aslan U. Effect of glycemic control on refractive changes in diabetic patients with hyperglycemia. Cornea. 2005;24:531-7 pubmed
  9. Gwinup G, Villarreal A. Relationship of serum glucose concentration to changes in refraction. Diabetes. 1976;25:29-31 pubmed
  10. Furushima M, Imaizumi M, Nakatsuka K. Changes in refraction caused by induction of acute hyperglycemia in healthy volunteers. Jpn J Ophthalmol. 1999;43:398-403 pubmed
  11. Tai M, Lin S, Chen J, Liang C, Chou P, Lu D. Sweet hyperopia: refractive changes in acute hyperglycemia. Eur J Ophthalmol. 2006;16:663-6 pubmed
  12. Tsubota K, Chiba K, Shimazaki J. Corneal epithelium in diabetic patients. Cornea. 1991;10:156-60 pubmed
  13. Larsson L, Bourne W, Pach J, Brubaker R. Structure and function of the corneal endothelium in diabetes mellitus type I and type II. Arch Ophthalmol. 1996;114:9-14 pubmed
  14. Taylor H, Kimsey R. Corneal epithelial basement membrane changes in diabetes. Invest Ophthalmol Vis Sci. 1981;20:548-53 pubmed
  15. McNamara N, Brand R, Polse K, Bourne W. Corneal function during normal and high serum glucose levels in diabetes. Invest Ophthalmol Vis Sci. 1998;39:3-17 pubmed
  16. Herse P. Corneal hydration control in normal and alloxan-induced diabetic rabbits. Invest Ophthalmol Vis Sci. 1990;31:2205-13 pubmed
  17. Wilson S, Ambrosio R. Computerized corneal topography and its importance to wavefront technology. Cornea. 2001;20:441-54 pubmed
ISSN : 2334-1009