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cohort·endocrinology, neurology, internal medicine, epidemiology, clinical trial·PMC10505541

Dysmetabolism-related Early Sensory Deficits and Their Relationship With Peripheral Neuropathy Development

The Journal of Clinical Endocrinology and Metabolism · 10 authors, 19 centres

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This prospective cohort study analyzed 225 individuals (117 without, 108 with type 2 diabetes) without clinical or electrophysiological peripheral neuropathy (PN) to identify early sensory deficits (EPSD) via quantitative sensory testing (QST). At baseline, in non-diabetic individuals, higher insulin resistance was independently associated with EPSD. Of 196 participants followed for a mean of 2.64 years, type 2 diabetes, EPSD (adjusted hazard ratio, 1.88), higher insulin resistance, and higher AGEs predicted PN development. The 'sensory loss' phenotype among EPSD was most strongly linked to PN (adjusted HR, 4.35). The study demonstrates the utility of QST for identifying preclinical sensory deficits linked to dysmetabolic states, which in turn influence PN progression. Limitations include the analysis of a convenience sample and the need for validation with other small fiber assessment methods.

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cohort

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endocrinology

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ORIGINAL PAPER

PMC10505541

Dysmetabolism-related Early Sensory Deficits and Their Relationship With Peripheral Neuropathy Development

The Journal of Clinical Endocrinology and Metabolism

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ABSTRACT

Abstract Aim To investigate the association of early peripheral sensory dysfunction (EPSD) identified through quantitative sensory testing (QST) with factors related to a dysmetabolic status in individuals with and without type 2 diabetes (T2DM) without peripheral neuropathy (PN), and the impact of those factors on PN development. Methods A total of 225 individuals (117 and 108 without and with T2DM, respectively) without PN based on clinical and electrophysiological criteria were analyzed. Comparative analysis was conducted between those identified as “healthy” and those with EPSD based on a standardized QST protocol. A total of 196 were followed-up over a mean of 2.64 years for PN occurrence. Results Among those without T2DM, apart from male sex, height, and higher fat and lower lean mass, only higher insulin resistance (IR; homeostatic model assessment for IR: odds ratio [OR], 1.70; P = .009; McAuley index OR, 0.62, P = .008), was independently associated with EPSD. In T2DM, metabolic syndrome (OR, 18.32; P < .001) and skin advanced glycation end-products (AGEs; OR, 5.66; P = .003) were independent predictors of EPSD. In longitudinal analysis, T2DM (hazard ratio [HR], 3.32 vs no diabetes mellitus; P < .001), EPSD (adjusted HR, 1.88 vs healthy; P = .049 adjusted for diabetes mellitus and sex), higher IR and AGEs predicted PN development. Among the 3 EPSD-associated sensory phenotypes, “sensory loss” was most strongly associated with PN development (adjusted HR, 4.35; P = .011). 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. Keywords: advanced glycation end products, diabetic polyneuropathy, early neuropathy, insulin resistance, metabolic syndrome, quantitative sensory testing

CITATION EXPORT

Dimitrios Tsilingiris, Lukas Schimpfle, Ekaterina von Rauchhaupt et al.. Dysmetabolism-related Early Sensory Deficits and Their Relationship With Peripheral Neuropathy Development. The Journal of Clinical Endocrinology and Metabolism. (2023). https://doi.org/10.1210/clinem/dgad248

AUTHORS

10 · 19 CENTRES

Dimitrios Tsilingiris, Lukas Schimpfle, Ekaterina von Rauchhaupt, Alba Sulaj, Lukas Seebauer, Hannelore Bartl, Stephan Herzig, Julia Szendroedi, Stefan Kopf, Zoltan Kender

1 Department for Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry, University Hospital Heidelberg, 69120 Heidelberg, Germany
2 German Center for Diabetes Research (DZD), 85764 Munich-Neuherberg, Germany
3 Department for Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry, University Hospital Heidelberg, 69120 Heidelberg, Germany
4 Department for Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry, University Hospital Heidelberg, 69120 Heidelberg, Germany
5 German Center for Diabetes Research (DZD), 85764 Munich-Neuherberg, Germany
6 Department for Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry, University Hospital Heidelberg, 69120 Heidelberg, Germany
7 German Center for Diabetes Research (DZD), 85764 Munich-Neuherberg, Germany
8 Department for Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry, University Hospital Heidelberg, 69120 Heidelberg, Germany
9 Department of General, Visceral and Transplant Surgery, University of Heidelberg, 69120 Heidelberg, Germany
10 German Center for Diabetes Research (DZD), 85764 Munich-Neuherberg, Germany
11 Joint Heidelberg-IDC Translational Diabetes Program, Helmholtz Center Munich, 85764 Neuherberg, Germany
12 Helmholtz Center Munich, Institute for Diabetes and Cancer, 85764 Munich-Neuherberg, Germany
13 Department for Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry, University Hospital Heidelberg, 69120 Heidelberg, Germany
14 German Center for Diabetes Research (DZD), 85764 Munich-Neuherberg, Germany
15 Joint Heidelberg-IDC Translational Diabetes Program, Helmholtz Center Munich, 85764 Neuherberg, Germany
16 Department for Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry, University Hospital Heidelberg, 69120 Heidelberg, Germany
17 German Center for Diabetes Research (DZD), 85764 Munich-Neuherberg, Germany
18 Department for Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry, University Hospital Heidelberg, 69120 Heidelberg, Germany
19 German Center for Diabetes Research (DZD), 85764 Munich-Neuherberg, Germany