Background: The aim was to investigate the relationship between diabetic peripheral neuropathy (DPN) and abnormalities in ganglion cell complex (GCC); specifically, focal loss volume (FLV) and global loss volume (GLV).
Methods: The ganglion cell complex was evaluated using optical coherence tomography on 193 individuals (84 with type 1 diabetes, 67 with type 2 diabetes and 42 without diabetes). In those with diabetes, 88 had diabetes but no diabetic retinopathy (no DR group) and 63 had diabetes with diabetic retinopathy (DR group). Seventeen individuals in the no DR group and 27 in the DR group had diabetic peripheral neuropathy according to the neuropathy disability score (NDS). The probability of FLV and GLV being abnormal was determined. Forty four individuals had diabetic peripheral neuropathy (NDS of three or greater). Binary logistic regression analysis was performed, adjusting for the presence of diabetic retinopathy, age, sex, type of diabetes, duration of diabetes and HbA levels.
Results: Twenty-five per cent of individuals with diabetic peripheral neuropathy had abnormal FLV compared to 11 per cent of those with diabetes but no diabetic peripheral neuropathy and five per cent in the control group (p = 0.011). Fourteen per cent of individuals with diabetic peripheral neuropathy, 10 per cent without diabetic peripheral neuropathy and two per cent in the control group had abnormal GLV (p = 0.185). For every unit increase in the neuropathy disability score, the odds of having an abnormal FLV increased by a factor of 1.25 (p = 0.007), after adjusting for potentially confounding factors. Abnormal GCC FLV is an independent predictor of diabetic neuropathy, (odds ratio = 2.94, 95 per cent CI [1.16, 7.40], p = 0.023).
Conclusion: Diabetic peripheral neuropathy is associated with abnormal GCC FLV at the macula, which is independent of diabetic retinopathy, age, sex, type of diabetes, duration of diabetes and HbA levels. An abnormality in GCC FLV is an independent predictor of diabetic peripheral neuropathy.
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http://dx.doi.org/10.1111/cxo.12379 | DOI Listing |
J Reconstr Microsurg
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Department of Plastic and Reconstructive Surgery, MedStar Georgetown University Hospital, Washington, District of Columbia.
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Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States.
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Department of Rehabilitation, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
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Department of Medical Biology, School of Medicine, Yeditepe University, Istanbul, Türkiye.
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Conjoint Endocrine Laboratory, Chemical Pathology, Pathology Queensland, Queensland Health, Herston, Qld 4029; School of Medicine, University of Queensland, Herston, Qld 4029; School of Biomedical Sciences, Queensland University of Technology, Brisbane, Qld 4000, Australia. Electronic address:
Transthyretin is a thyroid hormone binding protein with a major role in the distribution of thyroid hormones to peripheral tissues. In preeclampsia, the failing placenta releases soluble endoglin into the maternal circulation causing systemic vascular dysfunction. Our group has previously shown that transthyretin binds to soluble endoglin and is taken up as a complex into hepatocytes.
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