ABSTRACT
Background and Aims: A substantial number of diabetic patients, diagnosed at relatively younger age, who don’t fit to typical type 2 and type 1 class of diabetes. These patients usually present with very high level of glycemia. The uniqueness of this group of patient provide the opportunity to explore the pathophysiology of nerve functional status at an early stage of diabetes. The present study was aimed to determine markers of endothelial dysfunction and evaluate nerve functional status of a group of newly diagnosed clinically uncomplicated young diabetic patients. Material and Methods: A total number of 32 (male-13 and female-19) newly diagnosed young (diabetes diagnosed under 30 yrs) were consecutively recruited from BIRDEM Out-patient department and 30 age-, BMI-matched healthy subjects with no family history of diabetes up to second generation served as controls. Serum fructosamine was measured by reduction test with NBT method. Serum C-peptide, endothelin-1 and tissue plasminogen activator (t-PA) by ELISA and von Willibrand factor (vWF) by Radial Immunodiffusion (RID) methods. Urinary albumin measured by immunoturbidimetry method. Nerve functional status was evaluated by nerve conduction velocities (NCV), distal latencies (DL), compound muscle action potential (CAMP), F wave latencies (FWL), nerve action potential (SNAP) for motor and sensory nerve as appropriate following the standard protocol. Results: Severe hyperglycemia in the diabetic group was reflected in their mean (SD) fasting C-peptide and fructosamine level. Altered endothelial dysfunction, as evidenced by significantly high tissue plasminogen activator (t-PA) (p<0.001) in the diabetic group. Albumin creatinine ratio (ACR) was almost similar in the two groups. Ulnar distal latency was similar in both the groups. But its CAMP and NCV were significantly lower in the diabetic group (p<0.02-0.001). Ulnar F wave latency were significantly higher (p=0.016) in the diabetic group. Ulnar sensory conduction parameters did not show any difference between two groups. Peroneal motor and sural sensory functional status of the diabetic subjects showed similar trend like that of ulnar motor and sensory status. Peroneal nerve motor NCV was significantly negtively correlated with fasting glucose [r=- 0.456, p=0.001]. Peroneal motor distal latency was significantly correlated with fasting fractosamine [r=0.439, p=0.012]. Fasting fructosamine showed significant negative correlation with motor peroneal NCV [r=-0.572, p=0.001], motor ulnar NCV [r=-0.468, p=0.007], both ulnar and sural sensory NAP (p=0.02 for both]. On the basis of F wave latency 53% of diabetic subjects had diabetic neuropathy and markedly higher t-PA compared to nonneuropathy groups (p=0.001). Conclusions: The data suggest that (i) Young type 2 diabetic subjects had endothelial dysfunction at the time of diagnosis even in the presence of normoalbuminuria state; (ii) Motor nerve conduction parameters are affected more than the sensory component; (iii) F wave latencies are more frequently and early to be involved in these subjects and linked to high serum t-PA.
ABSTRACT
Aims: The present study was undertaken to explore the relationship of plasma homocysteine in the pathogenesis of neuropathy in diabetic patients. Subjects and Methods: Forty two type 2 diabetic patients [22 with neuropathy (DN group) and 20 without neuropathy (DNN group)], age range between 35-70 years had relatively controlled glycemia and duration of diabetes 7-15 years, were studied. Motor and sensory nerve conduction velocities and action potential amplitudes of peripheral nerves were determined by following standard protocol. HbA1c was estimated by modified HPLC (BIO-RAD Variant, USA). Serum C-peptide was measured by enzyme linked immunosorbentassay (ELISA), plasma total homocysteine by Fluorescent Polarization Immunoassay (FPIA). Results: Age, BMI and blood pressure of the study subjects were. Duration of diabetes between DN and DNN groups was comparable. DN group had significantly higher fasting glucose levels (9.8±3.8, mmol/l) compared to the DNN group (6.9±1.8, p=0.004). This trend was also reflected in the HbA1c level: 8.7± 2.1 vs 7.2±1.6 in DN group and DNN group respectively (p=0.009). The two diabetic groups had relatively higher absolute C-peptide level compared to the controls (p=ns). DN and DNN groups had significantly higher plasma homocysteine level compared to the Controls. But between the two diabetic groups no significant difference was observed. Ulnar and peroneal motor nerve conduction velocities and compound muscle action potentials in the diabetic neuropathy group significantly lower compared to diabetic counterpart and the controls. Ulnar and sural sensory nerve conduction velocities and action potentials were significantly lower in the diabetic neuropathy group compared to the diabetic counterpart and the controls. Plasma homocysteine did not show any correlation with nerve conduction velocities and action potential amplitudes. Conclusions: The data concluded that (i) Diabetic neuropathy may not be related to hyperhomocysteinemia in type 2 diabetic patients of Bangladeshi origin; (ii) Hyperglycemia, even at milder level, is related to neuronal dysfunction in these subjects; and (ii) Hyperinsulinemia don't seem to be prerequisite for neuropathy in these subjects.
ABSTRACT
F-wave latency measurement is a sensitive parameter of diabetic neuropathy than the conduction velocities. This study was carried out to measure F-wave latency and to see which conduction parameters are affected frequently and early. A total number of 62 patients of which 32 newly diagnosed and 30 controls were included in the study. Ulnar motor nerve conduction velocity was found slowed in 6(18.75%) diabetic subjects, but F-wave latency was found prolonged in 16(50%) diabetic subjects. 28(87.5%) diabetic subjects had normal peroneal nerve conduction velocity but peroneal F wave was found prolonged in 17(53.12%) diabetic subjects. This result suggests that F-wave latency is more frequently & early involved conduction parameter in diabetic subjects.