Dysmetabolism-related Early Sensory Deficits and Their Relationship With Peripheral Neuropathy Development
Authors' conclusion
We demonstrate for the first time the utility of a standardized QST-based approach in identifying early sensory deficits in individuals with and without T2DM. These are associated with a dysmetabolic status signified by IR markers, metabolic syndrome, and higher AGEs, which in turn are shown to influence PN development.
Study context
- Population
- Individuals with and without T2D without peripheral neuropathy by clinical and electrophysiological criteria196 followed up
- Participants
- 225 individuals
- Exposure
- Early peripheral sensory dysfunction (EPSD) vs healthy, in individuals with and without T2D
- No T2Dn = 117reference
- T2Dn = 108
- Outcome
- Association of early peripheral sensory dysfunction (EPSD) on QST with dysmetabolic factors, and their impact on PN development
Methodological detailscross-sectional comparison and longitudinal follow-up, standardized quantitative sensory testing (QST) protocol
- Cross-sectional comparison and longitudinal follow-up
- Standardized QST protocol
Main finding
As reported in the abstract
Without T2DM: higher insulin resistance (IR), HOMA-IR, OR
1.70
P = .009
Without T2DM: McAuley index, OR
0.62
P = .008
T2DM: metabolic syndrome, OR
18.32
P < .001
T2DM: skin AGEs, OR
5.66
P = .003
Observational data: associations, not effects.
Further findings
Predictors of peripheral neuropathy (PN) development (longitudinal analysis) · mean 2.64 years
- T2DM vs no diabetes mellitus, HR
- 3.32; P < .001
- EPSD vs healthy, aHR (adjusted for diabetes mellitus and sex)
- 1.88; P = .049
- "Sensory loss" phenotype (most strongly associated of 3 EPSD-associated sensory phenotypes), aHR
- 4.35; P = .011
- Higher IR and AGEs predicted PN development
Original publication
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