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Keval A Ray, Danielle Verghese, Benjamin Bird, Martin Josef Schardt, Jose Calva-Moreno, Daniel Gritsyuk, Ajay Rao, Raul A DeLa Cadena, William J Foster; Changes in Clinical Laboratory Results with Rapid Correction of Hyperglycemia. Invest. Ophthalmol. Vis. Sci. 2017;58(8):76.
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© ARVO (1962-2015); The Authors (2016-present)
Rapid control of hyperglycemia in patients diagnosed with Type 2 Diabetes Mellitus (T2DM) has been hypothesized (based upon retrospective clinical data) to be accompanied by a progression in diabetic retinopathy (DR), but this phenomenon has yet to be well-characterized in a formal, prospective study. We are investigating: (1) how DR progresses when poorly controlled T2DM patients initiate intensive blood sugar control, and (2) if there are biomarkers that predict progression of diabetic retinopathy. What we present here are changes in clinical laboratory tests of patients who are undergoing correction of hyperglycemia as part of this study.
As of December 2016, we have enrolled 20 patients who exhibited features of uncontrolled T2DM. At each patients' first visit (V1) to their endocrinologist, patients were evaluated and pharmacological intervention was initiated to control hyperglycemia. Patients were tracked over a 3-month period for a total of four visits (V1-V4) with visits spaced 30 days apart. The following labs were assessed at each of 4 visits: HbA1c, fructosamine, basic metabolic panel, 24-hour urine creatinine, and urine sodium. At V1, aldosterone/renin ratio, fasting lipid panel, and microalbumin/creatinine ratio were also obtained. Blood samples for future miRNA analysis and fundus photos were collected at all visits.
Under usual clinical care from an endocrinologist specializing in diabetes, 12 of the 15 completed patients demonstrated a reduction in HbA1c from the beginning to end of the follow-up period (p < 0.08). Additionally, fructosamine levels were found to significantly decrease with improvement of glycemic control (p <0.01).
Our initial analysis of this ongoing study demonstrated a decrease in non-enzymatic glycosylation, as measured by both a 3-month glycemic marker (HbA1c) and a 1-month marker (fructosamine). Completion of enrollment and analysis of retinal images, patient laboratory data, and patient miRNA may permit an association to be drawn between changes in these clinical laboratory tests or patient miRNA and progression in diabetic retinopathy. Our ultimate goal is to analyze laboratory data, miRNA, and fundus photos to establish a link between one or more of the above biomarkers and rapid progression in DR. In doing so, these biomarkers may uncover new diagnostic and therapeutic targets in the prevention and treatment of diabetic retinopathy in T2DM.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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