Clinical and Biological Markers of Conduction Slowing in Diabetic Distal Symmetrical Polyneuropathy: A Prospective Study
Kelly Saverino1, Joseph Wardell1, Kazim Jaffry1, Mustafa Jaffry1, Suhayb Islam1, Daniel Menkes2, Nizar Souayah1
1Rutgers New Jersey Medical School, 2Oakland University William Beaumont School of Medicine
Objective:
To investigate clinical and biological markers as well as comorbidities associated with conduction slowing (CS) in diabetic Distal Symmetrical Polyneuropathy (DDSP).
Background:
Diffuse CS has been frequently reported in DDSP and was attributed to demyelination with secondary axonal loss. However, specific clinical and biological markers of CS in DDAP are lacking.
Design/Methods:
We investigated the clinical and biological characteristics of 9 patients with DDSP with conduction slowing prospectively and compared them with 19 DDSP patients without conduction slowing. Significance was assessed with t-tests and Mann Whitney U-tests.
Results:
The incidence of diabetic nephropathy was significantly higher in the group with CS as compared to the group without conduction slowing (22.2 vs 0, p<0.05). No significant differences between the 2 groups were observed for age, gender, BMI, duration of diabetes, ROADS score and interleukins. There was a trend towards more diabetic retinopathy and HTN in the group with conduction slowing but this did not reach statistical significance. This was also true for average grip strength, INCAT score, ONLS score HbA1C, incidence of limb amputation and coronary artery disease.
Conclusions:
Patients with DDSP and CS had a more severe neuropathy and less diabetic control than DDSP patients without CS. Moreover, there was a trend to more severe disease in DDSP patients with CS that did not reach statistical significance, which may be related to small sample size. Future studies will expand sample size and will also incorporate diabetic patients without neuropathy and person with chronic inflammatory demyelinating polyneuropathy (CIDP) and diabetic without neuropathy to assess if CS in DDSP is attributed to a combination of impaired renal function and suboptimal diabetic control.