Hypertension Contributes to Neuropathy in Patients With Type 1 Diabetes.


Journal

American journal of hypertension
ISSN: 1941-7225
Titre abrégé: Am J Hypertens
Pays: United States
ID NLM: 8803676

Informations de publication

Date de publication:
17 07 2019
Historique:
received: 26 01 2019
revised: 10 04 2019
accepted: 15 04 2019
pubmed: 24 4 2019
medline: 28 7 2020
entrez: 24 4 2019
Statut: ppublish

Résumé

Diabetic peripheral neuropathy (DPN) can lead to foot ulceration and amputation. There are currently no disease-modifying therapies for DPN. The aim of this study was to determine if hypertension contributes to DPN in patients with type 1 diabetes mellitus (T1DM). Subjects with T1DM (n = 70) and controls (n = 78) underwent a comprehensive assessment of DPN. Hypertension was present in 40 of 70 T1DM subjects and 20 of 78 controls. Hypertension was associated with abnormal nerve conduction parameters (P = 0.03 to <0.001), increased vibration perception threshold (P = 0.01) and reduced corneal nerve fiber density and length (P = 0.02) in subjects with T1DM. However, after adjusting for confounding factors only tibial compound motor action potential and nerve conduction velocity were associated with hypertension (P = 0.03) and systolic blood pressure (P < 0.01 to <0.0001). Hypertension had no effect on neuropathy in subjects without diabetes. This study shows that hypertension is associated with impaired nerve conduction in T1DM. It supports previous small trials showing that angiotensin-converting enzyme inhibitors improve nerve conduction and advocates the need for larger clinical trials with blood pressure lowering agents in DPN.

Sections du résumé

BACKGROUND
Diabetic peripheral neuropathy (DPN) can lead to foot ulceration and amputation. There are currently no disease-modifying therapies for DPN. The aim of this study was to determine if hypertension contributes to DPN in patients with type 1 diabetes mellitus (T1DM).
METHODS
Subjects with T1DM (n = 70) and controls (n = 78) underwent a comprehensive assessment of DPN.
RESULTS
Hypertension was present in 40 of 70 T1DM subjects and 20 of 78 controls. Hypertension was associated with abnormal nerve conduction parameters (P = 0.03 to <0.001), increased vibration perception threshold (P = 0.01) and reduced corneal nerve fiber density and length (P = 0.02) in subjects with T1DM. However, after adjusting for confounding factors only tibial compound motor action potential and nerve conduction velocity were associated with hypertension (P = 0.03) and systolic blood pressure (P < 0.01 to <0.0001). Hypertension had no effect on neuropathy in subjects without diabetes.
CONCLUSIONS
This study shows that hypertension is associated with impaired nerve conduction in T1DM. It supports previous small trials showing that angiotensin-converting enzyme inhibitors improve nerve conduction and advocates the need for larger clinical trials with blood pressure lowering agents in DPN.

Identifiants

pubmed: 31013342
pii: 5477297
doi: 10.1093/ajh/hpz058
pmc: PMC6636691
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

796-803

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : NINDS NIH HHS
ID : R01 NS046259
Pays : United States

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press on behalf of American Journal of Hypertension, Ltd.

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Auteurs

Georgios Ponirakis (G)

Weill Cornell Medicine-Qatar, Qatar Foundation, Education City, Doha, Qatar.

Ioannis N Petropoulos (IN)

Weill Cornell Medicine-Qatar, Qatar Foundation, Education City, Doha, Qatar.

Uazman Alam (U)

Institute of Cardiovascular Science, University of Manchester, Manchester, UK.
Eye and Vision Sciences, Institute of Ageing and Chronic Disease, University of Liverpool, UK.

Maryam Ferdousi (M)

Institute of Cardiovascular Science, University of Manchester, Manchester, UK.

Omar Asghar (O)

Institute of Cardiovascular Science, University of Manchester, Manchester, UK.

Andrew Marshall (A)

Institute of Cardiovascular Science, University of Manchester, Manchester, UK.

Shazli Azmi (S)

Institute of Cardiovascular Science, University of Manchester, Manchester, UK.

Maria Jeziorska (M)

Institute of Cardiovascular Science, University of Manchester, Manchester, UK.

Ziyad R Mahfoud (ZR)

Weill Cornell Medicine-Qatar, Qatar Foundation, Education City, Doha, Qatar.

Andrew J M Boulton (AJM)

Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester and NIHR/Wellcome Trust Clinical Research Facility, Manchester, UK.

Nathan Efron (N)

Institute of Health and Biomedical Innovation, Queensland University of Technology, Queensland, Australia.

Hitoshi Nukada (H)

Nukada Institute for Medical and Biological Research, Chiba, Japan.

Rayaz A Malik (RA)

Weill Cornell Medicine-Qatar, Qatar Foundation, Education City, Doha, Qatar.
Institute of Cardiovascular Science, University of Manchester, Manchester, UK.
Faculty of Science and Engineering, Manchester Metropolitan University, Manchester, UK.

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