Pure cardiac autonomic neuropathy was not detected in any of the patients, and pure somatic neuropathy was detected in 5 patients (8.77%). From 28 patients with somatic neuropathy, 15 (53.5%) had parasympathetic neuropathy, 2 (7.14%) had impaired sympathetic neuropathy, and 8 (28.5%) had combined autonomic neuropathy. There was a significant correlation between CAN and somatic neuropathy (p<0.0001). From the 57 diabetic patients who completed questionnaries, 33 (57.8%) patients had no symptoms, 11 (19.2%) patients had only one symptom, and 13 (22.8%) patients complained of 1-4 symptoms. From 25 patients with CAN, 9 (36%) were asymptomatic, 7 had one or combination of two related gastrointestinal symptoms (44%), and 9 patients (36%) combination of three symptoms. The most common symptoms of diabetic autonomic dysfunction were gastrointestinal symptoms as nausea, vomiting, constipation, diarrhea (intermittent or alternate with constipation). Table IV presents the prevalence of autonomic symptoms. We found a significant linear trend toward more severe cardiac autonomic neuropathy (CAN) with increasing glycated hemoglobin level: p=0.014, R square=0.11, Slope=0.27 (one-way ANOVA with multiple comparisons, post test for linear trend) and increasing disease duration: p<0.0001, R square=0.333, Slope=2.,78 (one-way ANOVA with multiple comparisons, post test for linear trend). CAN in our patients involved both the parasympathetic and sympathetic nervous system, but the most frequently altered test was heart rate variability, which indicates an impairment of parasympathetic nervous system. Ewing's battery of tests were suggested as the diagnostic tool for CAN. Using this Ewing's methods the prevalence of CAN in this hospital-based study was 44%, which is consistent with a previous study on this type of patients, reported by Ziegler. Our data demonstrated strong correlations between CAN and HbA1c, as well as the duration of diabetes. Prolonged exposure to hyperglycemia is known to be a metabolic insult, which plays an important role in the pathogenesis of diabetic neuropathy. In addition, the impact of hyperglycemia on development and progression of chronic diabetic complications has been documented in large trials, as the DCCT and UKPDS studies. Obesity is a metabolic risk factor of many diseases, particularly diabetes and cardiovascular disease. Association of obesity with CAN has been observed by some authors. However, lack of association of BMI with CAN was found in our study. The relatively small group of patients investigated in our study could explain this discrepancy. Hypertension and hyperlipidemia are other cardiovascular risk factors shown to be associated with CAN in previous studies. In our study we did not find any significant association between systolic, diastolic BP, plasma lipid levels and CAN, however there was a trend toward higher values of cholesterol (p=0.18) and diastolic bood pressure (p=0.38). We considered that our group of patients was too small, and there is a need for further investigation on a greater number of diabetic patients. Our study results showed strong associations between parasympathetic neuropathy, sympatethic neuropathy and DPN. DPN represents a diabetic microangiopathy, and autonomic neuropathy and other diabetic microangiopathy often occur concurrently. The concurrent occurrence of these diabetic complications and CAN suggest that they may share some common pathogenic pathways. Poor glycemic control has been recognized as a common denominator in the development of various diabetic complications, particularly microangiopathy. The strong connections between CAN and DPN suggest that the impairment of microcirculation may play an important role in development of CAN, and diabetic microangiopathy could be a strong predictor for CAN. But this aspect must be the subject of future research, to examine the relationship between CAN and other microangiopathic complication related to DM (nephropathy, retinopathy). These data are not in accordance with a recent study performed in diabetes, which demonstrates a divergent development of autonomic and peripheral somatic neuropathy in diabetic patients. In this mentioned study, evaluation criteria for polyneuropathy included just clinical neurological examination and history of the patients. In our study the evaluation criteria for these patients was done on the base of neurophysiological data obtained from electroneurography, which probably detected the cases that would otherwise be considered asymptomatic. The basic mechanism underlying the damage of hyperglycemia on somatic and autonomic nerves is not dissimilar, and there is not a different susceptibility of autonomic (small and mostly unmyelinated) and peripheral somatic (large and myelinated) nerve fibers to hyperglicemia. In our study we observed that many patients with mild CAN (parasympathetic dysfunction) are asymptomatic, and the clinical manifestations of autonomic symptoms usually occur in more advanced stage of CAN. Symptoms-free patients cannot be excluded from having CAN, particularly in patients at an early stage of disease. The fact that the most common symptoms were gastrointestinal, suggests that in diabetic autonomic neuropathy, gastrointestinal autonomic dysfunction appears before cardiovascular autonomic dysfunction. Our results confirmed the association of CAN with the duration of diabetes, poorer glycemic control, but not with obesity, lipidic profile and blood pressure. Simultaneous appearance of CAN and DPN suggest that they may share some common pathogenic pathways. Prolonged exposure to hyperglycemia plays an important role in the pathogenesis of diabetic neuropathy. 7946
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