Distal symmetric polyneuropathy independently increased all-cause mortality in type 1 (HR 2.99) and type 2 diabetes (HR 1.32), while cardiovascular autonomic neuropathy increased mortality in type 2 (HR 1.44).
Cohort (n=1,142)
No
Does the presence of cardiovascular autonomic neuropathy or distal symmetric polyneuropathy increase all-cause mortality in patients with diabetes?
Both cardiovascular autonomic neuropathy and distal symmetric polyneuropathy are independently associated with increased all-cause mortality in type 2 diabetes, while DSPN is associated with increased mortality in type 1 diabetes.
Effect estimate: HR 2.99 (DSPN in Type 1); HR 1.32 (DSPN in Type 2); HR 1.44 (CAN in Type 2) (95% CI 1.4-8.63 (Type 1 DSPN); 1.07-1.64 (Type 2 DSPN); 1.17-1.76 (Type 2 CAN))
Background. People with diabetic cardiovascular autonomic neuropathy (CAN) have increased cardiovascular mortality. However, the association between distal symmetric polyneuropathy (DSPN) or CAN with all-cause mortality is much less investigated. Thus, we set out to examine the effect of CAN and DSPN on all-cause mortality in a well-phenotyped cohort. Methods. All diabetes cases ( n = 1,347 ) from the catchment area of a secondary diabetes care centre who had medical examination including neuropathy assessment between 1997 and 2016 were followed up for all-cause mortality in the NHS Hungary reimbursement database until 2018. We investigated the association of CAN (Ewing tests) and DSPN (Neurometer) with all-cause mortality using Cox models stratified by diabetes type. Results. Altogether, n = 131 / 1,011 persons with type 1/type 2 diabetes were included. Of the participants, 53%/43% were male, mean age was 46 ± 12 / 64 ± 10 years, diabetes duration was 13 ± 10 / 7 ± 8 years, 42%/29% had CAN, and 39%/37% had DSPN. During the 9 ± 5 / 8 ± 5 -year follow-up, n = 28 / 494 participants died. In fully adjusted models, participants with type 1 diabetes patients with versus without DSPN had an increased mortality (HR 2.99, 95% CI 1.4-8.63), while no association with CAN was observed. In type 2 diabetes, both DSPN and CAN independently increased mortality (HR 1.32, 95% CI: 1.07-1.64, and HR 1.44, 95% CI: 1.17-1.76). Conclusions. Our results are compatible with an increased risk of mortality in people with type 1 diabetes and DSPN. Furthermore, we report a similarly strong association between DSPN and CAN and all-cause mortality in type 2 diabetes mellitus.
Vági et al. (Fri,) conducted a cohort in Diabetes mellitus (Type 1 and Type 2) (n=1,142). Distal symmetric polyneuropathy (DSPN) and cardiovascular autonomic neuropathy (CAN) vs. Absence of DSPN or CAN was evaluated on All-cause mortality (HR 2.99 (DSPN in Type 1); HR 1.32 (DSPN in Type 2); HR 1.44 (CAN in Type 2), 95% CI 1.4-8.63 (Type 1 DSPN); 1.07-1.64 (Type 2 DSPN); 1.17-1.76 (Type 2 CAN)). Distal symmetric polyneuropathy independently increased all-cause mortality in type 1 (HR 2.99) and type 2 diabetes (HR 1.32), while cardiovascular autonomic neuropathy increased mortality in type 2 (HR 1.44).