Correlation of Diabetic Retinopathy and Corneal Neuropathy Using Confocal Microscopy

Nitoda, Eirini; Kallinikos, Panagiotis A.; Pallikaris, Aristofanis I.; Moschandrea, J.; Amoiridis, Georgios; Ganotakis, Emmanuel S.; Tsilimbaris, Miltiadis K.

doi:10.3109/02713683.2012.683507

Cited by 74 publications

(90 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the current study, several CCM measures correlated with IENFD and with median and ulnar motor and sensory NCV, as well as sural SNAP, in the entire study population, but the relationship was modest to moderate. This is in line with the aforementioned studies (12,32,34) supporting the notion that the pathophysiology underlying the manifestation of neuropathy in the cornea may be different from DSPN affecting the lower limbs. Indeed, vascular factors including reduced endoneurial blood flow and microvascular alterations appear to contribute to the pathogenesis of DSPN (35,36), whereas the normal cornea, albeit being the most densely innervated tissue in the human body (several 100-fold higher than skin) (37), is devoid of blood vessels.…”

Section: Discussionsupporting

confidence: 90%

“…Previous studies have shown correlations of CCM measures with VPT (31), clinical severity of DSPN (4,10,12,32,33), NCS (12,32), HRV (12,30), cold TDT (12,30), and IENFD (12) in longer-standing diabetes. In the current study, several CCM measures correlated with IENFD and with median and ulnar motor and sensory NCV, as well as sural SNAP, in the entire study population, but the relationship was modest to moderate.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Early Detection of Nerve Fiber Loss by Corneal Confocal Microscopy and Skin Biopsy in Recently Diagnosed Type 2 Diabetes

et al. 2014

View full text Add to dashboard Cite

We sought to determine whether early nerve damage may be detected by corneal confocal microscopy (CCM), skin biopsy, and neurophysiological tests in 86 recently diagnosed type 2 diabetic patients compared with 48 control subjects. CCM analysis using novel algorithms to reconstruct nerve fiber images was performed for all fibers and major nerve fibers (MNF) only. Intraepidermal nerve fiber density (IENFD) was assessed in skin specimens. Neurophysiological measures included nerve conduction studies (NCS), quantitative sensory testing (QST), and cardiovascular autonomic function tests (AFTs). Compared with control subjects, diabetic patients exhibited significantly reduced corneal nerve fiber length (CNFL-MNF), fiber density (CNFD-MNF), branch density (CNBD-MNF), connecting points (CNCP), IENFD, NCS, QST, and AFTs. CNFD-MNF and IENFD were reduced below the 2.5th percentile in 21% and 14% of the diabetic patients, respectively. However, the vast majority of patients with abnormal CNFD showed concomitantly normal IENFD and vice versa. In conclusion, CCM and skin biopsy both detect nerve fiber loss in recently diagnosed type 2 diabetes, but largely in different patients, suggesting a patchy manifestation pattern of small fiber neuropathy. Concomitant NCS impairment points to an early parallel involvement of small and large fibers, but the precise temporal sequence should be clarified in prospective studies.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Early Detection of Nerve Fiber Loss by Corneal Confocal Microscopy and Skin Biopsy in Recently Diagnosed Type 2 Diabetes

et al. 2014

View full text Add to dashboard Cite

show abstract

“…A study has shown progressive deterioration of corneal nerve fiber pathology with increasing severity of retinopathy [149]. Another group has shown progression of corneal nerve fiber pathology in parallel with diabetic retinopathy and DSPN [150].…”

Section: Retinopathymentioning

confidence: 99%

Risk Factors and Comorbidities in Diabetic Neuropathy: An Update 2015

2015

View full text Add to dashboard Cite

■ AbstractDistal symmetric sensorimotor polyneuropathy (DSPN) is the most common neurological manifestation in diabetes. Major risk factors of DSPN include diabetes duration, hyperglycemia, and age, followed by prediabetes, hypertension, dyslipidemia, and obesity. Height, smoking, insulin resistance, hypoinsulinemia, and others represent an additional risk. Importantly, hyperglycemia, hypertension, dyslipidemia, obesity, and smoking are modifiable. Stringent glycemic control has been shown to be effective in type 1, but not to the same extent in type 2 diabetes. Antilipidemic treatment, especially with fenofibrate, and multi-factorial intervention have produced encouraging results, but more experience is necessary. The major comorbidities of DSPN are depression, autonomic neuropathy, peripheral artery disease, cardiovascular disease, nephropathy, retinopathy, and medial arterial calcification. Knowledge of risk factors and comorbidities has the potential to enrich the therapeutic strategy in clinical practice as part of the overall medical care for patients with neuropathy. This article provides an updated overview of DSPN risk factors and comorbidities.

show abstract

“…Further, we studied the role of miR-182 in TG sensory neurons because 1) miR-182 had the minimum P value; 2) miR-182 is a sensory organ-specific miRNA (19); and 3) miR-182 has been implicated in diabetic retinopathy (26), which occurs in parallel with nerve fiber alterations of the subbasal nerve plexus of diabetic corneas (27).…”

Section: Mir-182 Is Regulated By Sirt1 In Hg Conditionsmentioning

confidence: 99%

microRNA-182 Mediates Sirt1-Induced Diabetic Corneal Nerve Regeneration

Wang

Zhao

et al. 2016

Diabetes

View full text Add to dashboard Cite

Sensory neurons are particularly susceptible to neuronal damage in diabetes, and silent mating type information regulation 2 homolog 1 (Sirt1) has been recently identified as a key gene in neuroprotection and wound healing. We found that the expression of Sirt1 was downregulated in trigeminal sensory neurons of diabetic mice. A microRNA microarray analysis identified microRNA-182 (miR-182) as a Sirt1 downstream effector, and the expression level of miR-182 was increased by Sirt1 overexpression in trigeminal neurons; Sirt1 bound to the promoter of miR-182 and regulated its transcription. We also revealed that miR-182 enhanced neurite outgrowth in isolated trigeminal sensory neurons and overcame the detrimental effects of hyperglycemia by stimulating corneal nerve regeneration by decreasing the expression of one of its target genes, NOX4. Furthermore, the effects of miR-182 on corneal nerve regeneration are associated with a functional recovery of corneal sensation in hyperglycemic conditions. These data demonstrate that miR-182 is a key regulator in diabetic corneal nerve regeneration through targeting NOX4, suggesting that miR-182 might be a potential target for the treatment of diabetic sensory nerve regeneration and diabetic keratopathy.

show abstract

Correlation of Diabetic Retinopathy and Corneal Neuropathy Using Confocal Microscopy

Cited by 74 publications

References 42 publications

Early Detection of Nerve Fiber Loss by Corneal Confocal Microscopy and Skin Biopsy in Recently Diagnosed Type 2 Diabetes

Early Detection of Nerve Fiber Loss by Corneal Confocal Microscopy and Skin Biopsy in Recently Diagnosed Type 2 Diabetes

Risk Factors and Comorbidities in Diabetic Neuropathy: An Update 2015

microRNA-182 Mediates Sirt1-Induced Diabetic Corneal Nerve Regeneration

Contact Info

Product

Resources

About