Evidence map›Paper›PMID 38019287›Full record

ArticleDiabetologia2024

A diminished sciatic nerve structural integrity is associated with distinct peripheral sensory phenotypes in individuals with type 2 diabetes.

Christoph M Mooshage, Dimitrios Tsilingiris, Lukas Schimpfle, Lukas Seebauer, Omar Eldesouky, Taraneh Aziz-Safaie, Anja Hohmann, Stephan Herzig, Julia Szendroedi, Peter Nawroth and 6 more

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03022721 (Heidelberg Study on Diabetes and Complications), which is not on this map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT03022721 recruitingnot on this map

Heidelberg Study on Diabetes and Complications

TypeobservationalSponsorHeidelberg UniversityRan2016 to 2028Enrolled500ConditionsDiabetes ComplicationsArmsNo interventions are planned for this study.
3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 2 countries.

Christoph M MooshageDepartment of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.
Dimitrios TsilingirisDepartment of Endocrinology, Diabetology, Metabolism and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Heidelberg, Germany.
Lukas SchimpfleDepartment of Endocrinology, Diabetology, Metabolism and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Heidelberg, Germany.
Lukas SeebauerDepartment of Endocrinology, Diabetology, Metabolism and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Heidelberg, Germany.
Omar EldesoukyDepartment of Endocrinology, Diabetology, Metabolism and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Heidelberg, Germany.
Taraneh Aziz-SafaieDepartment of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.
Anja HohmannDepartment of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Stephan HerzigGerman Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Julia SzendroediDepartment of Endocrinology, Diabetology, Metabolism and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Heidelberg, Germany.
Peter NawrothDepartment of Endocrinology, Diabetology, Metabolism and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Heidelberg, Germany.
Sabine HeilandDivision of Experimental Radiology, Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.
Martin BendszusDepartment of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.
Felix T KurzDepartment of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.
Stefan KopfDepartment of Endocrinology, Diabetology, Metabolism and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Heidelberg, Germany.
Johann M E JendeDepartment of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.
Zoltan KenderDepartment of Endocrinology, Diabetology, Metabolism and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Heidelberg, Germany. zoltan.kender@med.uni-heidelberg.de.ORCID 0000-0003-0745-1587
Heidelberg University · DEDemocritus University of Thrace · GRGerman Cancer Research Center · DE

Funding

Deutsche Forschungsgemeinschaft SFB1118Deutsche Forschungsgemeinschaft SFB 1158
6 · The paper itself

Abstract

aims/hypothesisQuantitative sensory testing (QST) allows the identification of individuals with rapid progression of diabetic sensorimotor polyneuropathy (DSPN) based on certain sensory phenotypes. Hence, the aim of this study was to investigate the relationship of these phenotypes with the structural integrity of the sciatic nerve among individuals with type 2 diabetes.

methodsSeventy-six individuals with type 2 diabetes took part in this cross-sectional study and underwent QST of the right foot and high-resolution magnetic resonance neurography including diffusion tensor imaging of the right distal sciatic nerve to determine the sciatic nerve fractional anisotropy (FA) and cross-sectional area (CSA), both of which serve as markers of structural integrity of peripheral nerves. Participants were then assigned to four sensory phenotypes (participants with type 2 diabetes and healthy sensory profile [HSP], thermal hyperalgesia [TH], mechanical hyperalgesia [MH], sensory loss [SL]) by a standardised sorting algorithm based on QST.

resultsObjective neurological deficits showed a gradual increase across HSP, TH, MH and SL groups, being higher in MH compared with HSP and in SL compared with HSP and TH. The number of participants categorised as HSP, TH, MH and SL was 16, 24, 17 and 19, respectively. There was a gradual decrease of the sciatic nerve's FA (HSP 0.444, TH 0.437, MH 0.395, SL 0.382; p=0.005) and increase of CSA (HSP 21.7, TH 21.5, MH 25.9, SL 25.8 mm CONCLUSIONS/

interpretationThe most severe sensory phenotypes of DSPN (MH and SL) showed diminishing sciatic nerve structural integrity indexed by lower FA, likely representing progressive axonal loss, as well as increasing CSA of the sciatic nerve, which cannot be detected in individuals with TH. Individuals with type 2 diabetes may experience a predefined cascade of nerve fibre damage in the course of the disease, from healthy to TH, to MH and finally SL, while structural changes in the proximal nerve seem to precede the sensory loss of peripheral nerves and indicate potential targets for the prevention of end-stage DSPN.

trial registrationClinicalTrials.gov NCT03022721.

Indexed as

Diabetes Mellitus, Type 2Diabetic NeuropathiesCross-Sectional StudiesDiffusion Tensor ImagingHumansPhenotypeSciatic NerveDiabetic neuropathyDiffusion tensor imagingFractional anisotropyMagnetic resonance neurographyQuantitative sensory testingSensory profilingType 2 diabetes

Identifiers

PMID38019287
PMCPMC10789832
OpenAlexW4389147111

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.