From the Departments of Pediatrics (VS, IU) and Ophthalmology (MI, RS, KB, DG), Split University Hospital Centre, Split, Croatia.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Veselin Skrabic, MD, PhD, University Hospital Centre Split, Spinciceva 1, 21000 Split, Croatia. E-mail: email@example.com
The occurrence of juvenile diabetic cataract is rare.1,2 However, several articles on development of cataract in children with newly diagnosed type 1 diabetes mellitus have been published.1–9 The course of juvenile diabetic cataract is variable. In some patients, changes are reversible and resolve with improved metabolic control.9 In other patients, cataract is permanent, irreversible, and requires surgical intervention.
Juvenile diabetic cataract is morphologically similar to cataract in an older adult. Changes are often found toward the rear and are subcapsular. Typically, cloudy opacities such as vacuoles have been found. The risk factors for cataract development are the duration of symptoms of type 1 diabetes mellitus prior to the diagnosis, poor metabolic control, high glycosylated hemoglobin, diabetic ketoacidosis, genetic factors, and treatment with glucocorticoids.1,2,6
The pathogenesis of diabetic cataract is poorly understood. The lens homeostasis is disturbed by a long-lasting hyperglycemia, followed by changes in polyol pathway, build up of sorbitol, and development of osmotic stress.10–12 Non-enzymatic glycation of lens protein and oxidative stress are added mechanisms in diabetic cataract development.11,12
A 16.6-year-old girl presented with hyperglycemia of 36.6 mmol/L, ketonemia of 4.3 mmol/L, glucosuria, ketonuria, and normal acid-base status. She had a 6-month history of typical, unrecognized type 1 diabetes mellitus symptoms of nocturia, polyuria, thirst, increased appetite, and 10-kg weight loss. On admission, her HbA1c level was 15.5%. GAD-65, ICA-512, and IA-2 antibodies were positive and C-peptide was 0.24 pmol/L. The basal/bolus insulin regimen with human analog was initiated as 1.1 U/kg/day. In addition, she had an enlarged thyroid with positive thyroglobulin and thyroid peroxidase antibodies. Thyroid ultrasound showed an inhomogeneous gland structure consistent with chronic lymphocytic thyroiditis. Family history was negative for autoimmune diseases or cataract.
Results of eye examination on admission were normal. However, within 2 months the patient’s sight deteriorated and bilateral visual acuity was 1/60. Examination with the biomicroscope through dilated pupils indicated bilateral subcapsular posterior cataract with cortical clouding. Despite proved metabolic control (HbA1c 7.9%) 3 months after diagnosis, the condition worsened and progressed to mature cataract and complete vision loss with visual acuity limited to hand motions in front of the face. The intraocular pressure in the left eye rose to 45 mm Hg and phacoemulsification with implantation of foldable artificial lens with safety filter was urgently performed (+23.0 diopter, AcrySof IQ SN60WF acrylic intraocular lens; Alcon Laboratories, Forth Worth, TX).
Swelling of the lens secondary to hyperglycemia caused shallowing of the anterior chamber, iris bombe, and acute angle-closure glaucoma. Within 24 hours, the intraocular pressure in the right eye increased to 53 mm Hg and a second phacoemulsification procedure with implantation of the same type of intraocular lens was performed (Figs. 1 and 2). Over the next 3 days, the visual acuity improved to 6/6 and bilateral intraocular pressure was 15 mm Hg. There were no signs of diabetic retinopathy. Optical coherence tomography was performed, resulting in normal retinal cross-section scans. The thickness of the middle part of the macula (190 μm) and the total macula volume (7 mm3) were normal.
Figure 1. Juvenile Diabetic Cataract in the Right Eye Before Surgery.
Figure 2. Juvenile Diabetic Cataract in the Left Eye Before Surgery.
The association of type 1 diabetes mellitus and cataract is clearly documented in the literature. However, cataract is rarely found in the pediatric population. In children and adolescents with type 1 diabetes mellitus, cataract is mostly acute and bilateral with opacities and subcapsularly located vacuoles.1,2
The retrospective analysis of 600 Finnish children and adolescents with type 1 diabetes mellitus reported the prevalence of cataract of 1%.1 Montgomery et al. reported a prevalence of 0.7%.2 There are a few published articles of bilateral cataract developing shortly after a type 1 diabetes mellitus diagnosis.5,6,11,13 A multicenter study in the United States reported 14 adolescents with type 1 diabetes mellitus developing cataract an average of 2.3 years after a type 1 diabetes mellitus diagnosis, with 7 patients diagnosed as having juvenile diabetic cataract and type 1 diabetes mellitus simultaneously.6 The average age of patients with cataract was 11.4 years and most (11 of 14) were female. Ehrlich et al. described a patient who developed cataract within 3 weeks of a type 1 diabetes mellitus diagnosis.13 Pakhetra et al. described bilateral cataract development at the time of diagnosis of type 1 diabetes mellitus in a young girl and development of juvenile diabetic cataract within a few months of type 1 diabetes mellitus diagnosis in an another patient.5 Costagliola et al. described three boys who developed irreversible cataract within 30 days of a type 1 diabetes mellitus diagnosis presenting with diabetic ketoacidosis.11
Different morphologic types of cataract have been described.11 Di Benedetto et al. reported a higher occurrence of lens opacities in patients with type 1 diabetes mellitus than in patients with cataract and without type 1 diabetes mellitus.14 The authors did not describe the presence of vacuoles in children and adolescents.
The pathogenesis of juvenile diabetic cataract has not been fully explained. One of the possible mechanisms is secondary to hyperglycemia.6,11 The natural course of cataract is variable and probably related to the hydration of the lens. Based on the osmotic hypothesis, long-lasting hyperglycemia could lead to an excessive accumulation of sorbitol in the lens, leading to an influx of water from the aqueous humor, resulting in an intracellular edema, broken or disrupted fibrils, and opacities.
Metabolic changes associated with diabetic ketoacidosis could further decrease the availability of antioxidants and promote cataractogenesis. Cataract is more often irreversible and rarely transient and reversible.9 With improved glycemia, it is possible that sorbitol is metabolized and excess water dissipates. The streak-like opacities are foci of light scattering at points of water accumulation. These opacities lead to reversible or transient cataract. If intracellular electrolyte and biochemical changes occur, breakage of protein and cellular death could lead to irreversible cataract.6
Risk factors for the development of juvenile diabetic cataract are prolonged preclinical type 1 diabetes mellitus course, poorly regulated glycemia (= high HbA1c), diabetic ketoacidosis, genetic factors, and treatment with glucocorticoids.1,2,11 It is unknown why juvenile diabetic cataract is mainly found in the female population.2,5,6,8
To the best of our knowledge, there have been no reports of patients with newly diagnosed type 1 diabetes mellitus presenting with acute bilateral cataract and subsequent phacomorphic glaucoma. Our patient had a long preclinical phase, a high HbA1c (15.5%) level, and no signs of diabetic ketoacidosis. Cataract surgery was mandatory and successful. Based on our patient’s clinical course, it is recommended to check both the retina and lens in patients with newly diagnosed type 1 diabetes mellitus.
- Falck A, Laatikainen L. Diabetic cataract in children. Acta Ophthalmol Scand. 1998;76:238–240. doi:10.1034/j.1600-0420.1998.760223.x [CrossRef]
- Montgomery EL, Batch JA. Cataracts in insulin-dependent diabetes mellitus: sixteen years’ experience in children and adolescents. J Paediatr Child Health. 1998;34:179–182. doi:10.1046/j.1440-1754.1998.00195.x [CrossRef]
- Vinding T, Nielsen TV. Two cases of acutely developed cataract in diabetes mellitus. Acta Ophthalmol. 1984;62:373–377. doi:10.1111/j.1755-3768.1984.tb08417.x [CrossRef]
- Suzuki Y, Atsumi Y, Matsuoka K, et al. Acute metabolic cataracts as a first manifestations of diabetes mellitus in a 12-year-old girl. Diabetologia. 2004;47:592–593. doi:10.1007/s00125-004-1333-7 [CrossRef]
- Pakhetra L, Co R, Jyotsna VP. Bilateral early cataracts in type 1 diabetes. Medical Journal Armed Forces India. 2009;65:71–72.
- Wilson ME Jr, Levin AV, Trivedi RH, et al. Cataract associated with type 1-diabetes mellitus in the pediatric population. J AAPOS. 2007;11:162–165. doi:10.1016/j.jaapos.2005.10.005 [CrossRef]
- Taskapili M, Gulkilik G, Ozsutcu M, Kucuksahin H. Acute bilateral cortical cataracts as a first manifestation of juvenile diabetes mellitus in 12-year-old girl. J Pediatr Ophthalmol Strabismus. 2008;45:177–178. doi:10.3928/01913913-20080501-20 [CrossRef]
- Datta V, Swift PGF, Woodruff GHA, Harris RF. Metabolic cataracts in newly diagnosed diabetes. Arch Dis Child. 1997;76:118–120. doi:10.1136/adc.76.2.118 [CrossRef]
- Sharma P, Vasavada AR. Acute transient bilateral diabetic posterior subscapsular cataracts. J Cataract Refract Surg. 2001;27:789–794. doi:10.1016/S0886-3350(00)00762-8 [CrossRef]
- Awan A, Saboor T, Buchanan LM. Acute irreversible diabetic cataract in adolescence: a case report. Eye. 2006;20:398–400. doi:10.1038/sj.eye.6701876 [CrossRef]
- Costagliola C, Dell Omo R, Prisco F, Iausco D, Landolfo F, Parmeggiani F. Bilateral isolated acute cataracts in three newly diagnosed insulin dependent mellitus young patients. Diabetes Res Clin Pract. 2007;76:313–315. doi:10.1016/j.diabres.2006.08.010 [CrossRef]
- Costagliola C, Iuliano G, Menzione M, Nesti A, Simonelli F, Rinaldi E. Systemic human disease as oxidative risk factor in cataractogenesis: I. Diabetes. Ophthalmic Res. 1988;20:308–316. doi:10.1159/000266734 [CrossRef]
- Ehrlich RM, Kirsch S, Daneman D. Cataracts in children with diabetes mellitus. Diabetes Care. 1987;10:798–799.
- Di Benedetto A, Aragona P, Romano G, et al. Age and metabolic control influence lens opacity in type 1, insulin-dependent diabetic patients. J Diabetes Complications. 1999;13:159–162. doi:10.1016/S1056-8727(98)00023-3 [CrossRef]