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Continuum of sensory profiles in diabetes mellitus patients with and without neuropathy and pain

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F65269705%3A_____%2F22%3A00076257" target="_blank" >RIV/65269705:_____/22:00076257 - isvavai.cz</a>

  • Nalezeny alternativní kódy

    RIV/00216224:14110/22:00127722

  • Výsledek na webu

    <a href="https://onlinelibrary.wiley.com/doi/epdf/10.1002/ejp.2034" target="_blank" >https://onlinelibrary.wiley.com/doi/epdf/10.1002/ejp.2034</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1002/ejp.2034" target="_blank" >10.1002/ejp.2034</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Continuum of sensory profiles in diabetes mellitus patients with and without neuropathy and pain

  • Popis výsledku v původním jazyce

    Background Quantitative sensory testing (QST) assesses the functional integrity of small and large nerve fibre afferents and central somatosensory pathways; QST was assumed to provide insight into the mechanisms of neuropathy. We analysed QST profiles and phenotypes in patients with diabetes mellitus to study whether these could differentiate patients with and without pain and neuropathy. Methods A standardized QST protocol was performed and &apos;loss and gain of function&apos; abnormalities were analysed in four groups of subjects: diabetic patients with painful (pDSPN; n = 220) and non-painful distal symmetric polyneuropathy (nDSPN; n = 219), diabetic patients without neuropathy (DM; n = 23) and healthy non-diabetic subjects (n = 37). Based on the QST findings, diabetic subjects were further stratified into four predefined prototypic phenotypes: sensory loss (SL), thermal hyperalgesia (TH), mechanical hyperalgesia (MH) and healthy individuals. Results Patients in the pDSPN group showed the greatest hyposensitivity (&apos;loss of function&apos;), and DM patients showed the lowest, with statistically significant increases in thermal, thermal pain, mechanical and mechanical pain sensory thresholds. Accordingly, the frequency of the SL phenotype was significantly higher in the pDSPN subgroup (41.8%), than expected (p &lt; 0.0042). The proportion of &apos;gain of function&apos; abnormalities was low in both pDSPN and nDSPN patients without significant differences. Conclusions There is a continuum in the sensory profiles of diabetic patients, with a more pronounced sensory loss in pDSPN group probably reflecting somatosensory nerve fibre degeneration. An analysis of &apos;gain of function&apos; abnormalities (allodynia, hyperalgesia) did not offer a key to understanding the pathophysiology of spontaneous diabetic peripheral neuropathic pain. Significance This article, using quantitative sensory testing profiles in large cohorts of diabetic patients with and without polyneuropathy and pain, presents a continuum in the sensory profiles of diabetic patients, with more pronounced &apos;loss of function&apos; abnormalities in painful polyneuropathy patients. Painful diabetic polyneuropathy probably represents a &apos;more progressed&apos; type of neuropathy with more pronounced somatosensory nerve fibre degeneration. The proportion of &apos;gain of function&apos; sensory abnormalities was low, and these offer limited understanding of pathophysiological mechanisms of spontaneous neuropathic pain.

  • Název v anglickém jazyce

    Continuum of sensory profiles in diabetes mellitus patients with and without neuropathy and pain

  • Popis výsledku anglicky

    Background Quantitative sensory testing (QST) assesses the functional integrity of small and large nerve fibre afferents and central somatosensory pathways; QST was assumed to provide insight into the mechanisms of neuropathy. We analysed QST profiles and phenotypes in patients with diabetes mellitus to study whether these could differentiate patients with and without pain and neuropathy. Methods A standardized QST protocol was performed and &apos;loss and gain of function&apos; abnormalities were analysed in four groups of subjects: diabetic patients with painful (pDSPN; n = 220) and non-painful distal symmetric polyneuropathy (nDSPN; n = 219), diabetic patients without neuropathy (DM; n = 23) and healthy non-diabetic subjects (n = 37). Based on the QST findings, diabetic subjects were further stratified into four predefined prototypic phenotypes: sensory loss (SL), thermal hyperalgesia (TH), mechanical hyperalgesia (MH) and healthy individuals. Results Patients in the pDSPN group showed the greatest hyposensitivity (&apos;loss of function&apos;), and DM patients showed the lowest, with statistically significant increases in thermal, thermal pain, mechanical and mechanical pain sensory thresholds. Accordingly, the frequency of the SL phenotype was significantly higher in the pDSPN subgroup (41.8%), than expected (p &lt; 0.0042). The proportion of &apos;gain of function&apos; abnormalities was low in both pDSPN and nDSPN patients without significant differences. Conclusions There is a continuum in the sensory profiles of diabetic patients, with a more pronounced sensory loss in pDSPN group probably reflecting somatosensory nerve fibre degeneration. An analysis of &apos;gain of function&apos; abnormalities (allodynia, hyperalgesia) did not offer a key to understanding the pathophysiology of spontaneous diabetic peripheral neuropathic pain. Significance This article, using quantitative sensory testing profiles in large cohorts of diabetic patients with and without polyneuropathy and pain, presents a continuum in the sensory profiles of diabetic patients, with more pronounced &apos;loss of function&apos; abnormalities in painful polyneuropathy patients. Painful diabetic polyneuropathy probably represents a &apos;more progressed&apos; type of neuropathy with more pronounced somatosensory nerve fibre degeneration. The proportion of &apos;gain of function&apos; sensory abnormalities was low, and these offer limited understanding of pathophysiological mechanisms of spontaneous neuropathic pain.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    30210 - Clinical neurology

Návaznosti výsledku

  • Projekt

    <a href="/cs/project/ED1.1.00%2F02.0068" target="_blank" >ED1.1.00/02.0068: CEITEC - central european institute of technology</a><br>

  • Návaznosti

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Ostatní

  • Rok uplatnění

    2022

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    European journal of pain

  • ISSN

    1090-3801

  • e-ISSN

    1532-2149

  • Svazek periodika

    26

  • Číslo periodika v rámci svazku

    10

  • Stát vydavatele periodika

    US - Spojené státy americké

  • Počet stran výsledku

    15

  • Strana od-do

    2198-2212

  • Kód UT WoS článku

    000854563100001

  • EID výsledku v databázi Scopus

    2-s2.0-85138012435