ESPE Abstracts (2016) 86 P-P2-308

The Autoimmune Hypothesis for Acute Bilateral Cataract in Type 1 Diabetes

Dimitrios T Papadimitrioua, Christina Bothoua, Filippos Skarmoutsosa, Theodoros K Alexandridesc, Vassiliki Papaevangeloub & Anastasios Papadimitrioub


aAthens Medical Center, Athens, Greece; bAttikon University Hospital, Athens, Greece; cUniversity Hospital of Patras, Patras, Greece


Background: Cataract as a chronic complication of diabetes is well established in the literature and the risk factors are also well known. However, rare cases of acute bilateral cataract have been reported, all of them happening relatively shortly after diagnosis in T1DM. While the pathophysiology of this phenomenon remains unclear – as a lot of different theories proposed so far with the most accepted being the osmotic stress induced oxidative damage – fail to explain adequately the acuteness of bilateral cataract formation - there have also been reports of acute bilateral cataract as the first presentation of T1DM.

Objective and hypotheses: We have recently published a case of acute bilateral cataract in a paediatric patient with T1DM manifested 3 months after presentation with severe diabetic ketoacidosis and initiation of insulin treatment.

Method: The cataract being completely liquefied; no lens tissue could be sent to immunopathology in either of the two operations. The only remarkable change to his biology and autoimmune status were the previously negative at presentation of T1DM, now clearly elevated insulin autoantibodies (IAA): 1.4 (<1.1).

Results: Our ‘autoimmune hypothesis’ proposes that the timing of the cataract formation – usually few weeks or months after onset of insulin treatment, as in our case-suggests an autoimmune response. More specifically, the IAA became positive within 3 months after the beginning of insulin treatment and this period coincides with the cataract formation. Unfortunately, we were unable to measure the IRA, which might have strengthened the autoimmune hypothesis, as decreased immunoreactivity for the insulin receptor has been found in the lens when cataract is detected. The timing of the occurrence of acute bilateral cataract in patients with good metabolic control, who do not carry the burden of a chronic diabetic decay, clearly implies an autoimmune mechanism on the grounds of a possible genetic predisposition for cataract formation.

Conclusion: While previously reported theories fail to explain the acuteness of the phenomenon, there are indications to suggest a possible autoimmune mechanism for acute bilateral cataract in diabetes that warrants further investigation. Elucidation of a possibly autoimmune underlying mechanism could result in early detection and development of prevention strategies to avoid such a stressful complication.

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