CASE REPORT

Two cases of diabetic zonular cataracts

Bronner, Aaron OD; Guzek, James P. MD; Leng, Jason MD

Author Information
doi: 10.1097/j.jcro.0000000000000020
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Abstract

Diabetes mellitus (DM) is a widespread disease with the potential for several well-described secondary complications, some of which involve the crystalline lens. These effects range from induced myopia and hyperopia, acceleration and exacerbation of age-related thickening of the lens and accelerated cataractogenesis, and specific cortical and subcapsular cataract changes that are occasionally seen in patients with diabetes.2–7 Many of these changes are transient and responsive to greater control of blood sugar, both chronically and acutely. Others, such as lens opacification in the form of cataract, require surgical care. Herein, we present 2 cases of, to our knowledge, previously undescribed zonular ridges in the eyes of 2 patients with diabetes, who had recently achieved control of previously uncontrolled type II DM.

CASE 1

A 74-year-old man presented for evaluation of cataracts. He had typical cataract symptoms of reduced vision and inability to correct vision to his satisfaction with spectacles, glare at night, and a rapidly changing spectacle prescription. In the previous year, he had been diagnosed with type 2 DM. At the time of diagnosis, his glycosylated hemoglobin was measured at 14.2%. Since diagnosis and with the initiation of metformin therapy 6 months previously, he had been able to reduce this number to 8.1%.

On examination, he was found to have had a +1.25 diopter (D) refractive shift on his right eye and a +1.00 D shift on his left eye from his spectacles, which had been made 12 months ago. There were 2+ nuclear sclerotic cataracts and what were described as zonular perinuclear ridges on the lenses of both eyes (Figure 1). Cataract surgery was discussed with the patient, and he proceeded through surgery and recovery uneventfully with both eyes.

Figure 1.
Figure 1.:
Patient 1: subtle circumferential ridges surrounding the fetal nucleus. Their depth is mid-lens, as demonstrated by the in-focus fetal suture.

CASE 2

A 64-year-old woman presented for evaluation of cataracts. She had noted a generalized reduction in visual performance in all lighting and an inability of her eye doctor to fully correct her vision with spectacles. She had been diagnosed with diabetes over 10 years ago and had previously been successfully managed with metformin alone. However, over the last 18 months, she lost control of her blood sugar, and as recently as 6 months previous to our examination, her glycosylated hemoglobin was 14.1%. Because of this, she had recently been started on Humalog insulin, which had an immediate positive effect in her blood sugar control, and her last glycosylated hemoglobin, taken 1 week before our examination, was 7.0%.

Comparing autorefraction with her habitual spectacle correction, which was 1 year old, she was shown to have a +1.37 D hyperopic shift on the right eye and +1.87 D hyperopic shift on her left eye. On examination, there were 1-2+ NS, 2-3+ peripheral cortical spokes and prominent zonular ridges (Figure 2). The ridges here were more dramatic than in case 1, but followed the same circumferential pattern and occupied the same lenticular space. The patient opted to pursue cataract surgery, which was performed successfully. Her follow-up was uneventful.

Figure 2.
Figure 2.:
Patient 2 shows much more dramatic perinuclear ridges, but in the same circular distribution in the same anatomic zone of the lens.

DISCUSSION

DM has long been recognized as a source of changes to the crystalline lens. In the 1920s, Duke Elder proposed that the refractive effect of hyperglycemia was to produce myopia.1 It has since been shown that induction of myopia occurred on both a chronic and an acute scale with fluctuations in refractive error demonstrable within minutes blood sugar spiking.2 Other studies have confirmed the increased thickness of the diabetic lens compared with normal.3 There have been further case series and research into hyperopic shifts occurring within diabetics as well, particularly around initiation of better glucose control.4,5 Beyond causing refractive changes, which have been felt to be lenticular in origin, DM has also been associated with increased rates of all 3 common cataract types (nuclear sclerotic, cortical, and posterior subcapsular) over chronic periods. In the Beaver Dam study, a 1.0% increase in glycated hemoglobin was associated with a 15% and 12% average change in risk for nuclear and cortical cataracts, respectively, at the study's 5-year review, and a study from the United Kingdom showed an approximate doubling of the detection of cataracts in a diabetic population compared with a nondiabetic population.6,7 Furthermore, specific cataractous changes such as snowflake cataracts have long been associated with diabetics.

In our cases, 2 patients with recently achieved dramatic improvement in blood sugar control shared ophthalmic findings of both a modest hyperopic shift and unusual circumferential perinuclear ridges. To our knowledge, the 2 cases presented represent the first anterior segment photographs of these lenticular changes. Although the changes in blood sugar control and hyperopia are almost certainly linked, it is more speculative as to whether the perinuclear ridges themselves are also related to the diabetic status and, if so, what their specific origin is.

A similar, if not identical, finding has been described previously.8 In 2005, a single case report published in the New England Journal of Medicine described a 62-year-old patient with recently achieved good control of their diabetes who developed interesting lenticular changes. The clinical description in this case seems to match our case, and high-quality dramatic Scheimpflug images are provided, but no anterior segment photographs are provided, making it difficult to interpret whether the case provided is indeed the same clinical entity as ours. In the previous case, the findings were dramatic enough to show up on Scheimpflug imaging as significant optical cavitations, which the authors termed sugar cracks. It seems possible, as the authors of the previous case describe the sugar crack as transient, that our cases may represent the resolution stage of the same phenomenon. Unfortunately, however, because both of our patients were complaining of cataract-induced vision loss, surgery was performed and so we are unable to comment on any possible evolution over time in our lens findings. In both the previous case and ours, the proposed mechanism would be a change in the lens osmotic gradient due to hyperglycemia leading to lenticular swelling. Rapid reduction in blood sugar likely led to a rapid restoration in the osmotic gradient in the lens with subsequent changes in hydration, which resulted in the ridges seen. We would propose the nomenclature of diabetic zonular cataract.

WHAT WAS KNOWN

  • Variations in blood glucose occurring in diabetes have the potential to cause refractive and cataract development in the crystalline lens.
  • Although both nonspecific (nuclear sclerosis, cortical cataracts, and posterior subcapsular changes) and unique (snowflake) cataracts may occur with diabetes, zonular ridges in patients with diabetes have not been previously described in the literature to the authors' knowledge.

WHAT THIS PAPER ADDS

  • The previously undescribed cataract type in 2 patients achieving rapid reduction in blood sugar will assist clinicians in identifying the issue and to query for the association with diabetes, if unknown at the time.

REFERENCES

1. Duke-Elder S. Changes in refraction in diabetes mellitus. Br J Ophthalmol 1925;9:167–187
2. Gwinup G, Villarreal A. Relationship of serum glucose concentration to changes in refraction. Diabetes 1976;25:29–31
3. Wiemer NG, Dubbelman M, Hermans EA, Ringens PJ, Polak BC. Changes in the internal structure of the human crystalline lens with diabetes mellitus type 1 and type 2. Ophthalmology 2008;115:2017–2023
4. Riordan Eva P, Pascoe PT, Vaughn DG. Refactive change in hyperglycaemia: hyperopia, not myopia. Br J Ophthalmol 1982;66:500–505
5. Saito Y, Ohami G, Kinoshita S, Nakamura Y, Ogawa K, Harino S, Okada M. Transient hyperopia with lens swelling at initial therapy in diabetes. Br J Ophthalmol 1993;77:145–148
6. Becker C, Schneider C, Aballea S, Bailey C, Bourne R, Jick S, Meier C. Cataract in patients with diabetes mellitus—incidence rates in the UK and risk factors. Eye (London) 2018;32:1028–1035
7. Klein BE, Klein R, Lee K. Diabetes, cardiovascular disease, selected cardiovascular disease risk factors and the 5-year incidence of age-related cataract and the progression of lens opacities: the beaver Dam eye study. Am J Ophthalmol 1998;126:782–790
8. Tangelder GJ, Dubbelman M, Ringens PJ. Sudden reversible osmotic lens damage (“sugar cracks”) after initiation of metformin. N Engl J Med 2005;353:2621–2623
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