Correlation of acetylator phenotype with peripheral, autonomic and centralneuropathy in Northern Indian non-insulin-dependent diabetes mellitus patients

Objectives: Genetic susceptibility to diabetic neuropathy has been suspecte d and tentatively explored; however, diabetic autonomic and central neuropa thies are poorly investigated areas. Previous trials correlating types of d iabetes and diabetic neuropathy with acetylator dimorphisms have not been c onclusive. The present study was designed to test peripheral neuropathy, au tonomic neuropathy and integrity of central conduction pathways in patients of non-insulin-dependent diabetes mellitus (NIDDM), and to correlate the f indings with the acetylator phenotype. Methods: Twenty-six patients of NIDDM with stable glycaemic control and 11 age- and sex-matched control subjects were recruited, clinically examined a nd investigated with glycaemic and lipid profile, renal function tests, ner ve conduction studies (sensory and motor), auditory brain stem evoked respo nses (ABERs) and somatosensory evoked potentials (SEPs). Acetylator status of the subjects was determined by sulphadimidine test. Results: Out of 26 NIDDM patients, eight (30.7%; group 1A) were slow acetyl ators and 18 (69.3%; group 1B) were fast acetylators. The distribution of s low and rapid acetylators in both the groups was similar. Glycaemic and lip id profiles and 24-h urinary albumin excretion in groups IA and 1B were als o similar. Motor nerve conduction velocity, latency of F wave, sensory nerv e conduction and amplitudes of sensory nerve action potentials were not dif ferent between fast and slow acetylator NIDDM patients. On testing for ABER s, there were no statistically significant differences in peak latencies of waves I, III and V; interpeak latencies (IPLs) I-III, III-V and I-V; ampli tude of waves I, III and V on both sides between NIDDM patients and control s. However, peak latencies of wave III (P < 0.01), wave V (P < 0.005), IPLs I-III and I-V(P < 0.005), IPLs III-V (P < 0.05), and amplitudes of wave I( P < 0.05) and wave V (P < 0.05) on the left side were significantly differe nt in slow acetylator NIDDM patients. Increase on the right side for the sa me group was statistically significant for IPLs I-III and I-V (P < 0.05). S EPs showed no statistically significant difference between NIDDM patients a nd controls, and slow and fast acetylator NIDDM patients. Conclusions: No significant association of acetylator status with periphera l neuropathy in NIDDM subjects was observed in the present study. However, central neural conduction, primarily tested by ABERs, was significantly del ayed in slow acetylators compared with fast acetylator NIDDM patients. Henc e, there may be a predisposition to neuropathy in this group of patients, a nd such a predisposition may be better detected by studying central rather than peripheral nervous conduction pathways in NIDDM patients.