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Neuropathic Pain With and Without Diabetic Peripheral Neuropathy in Type 1 Diabetes

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posted on 2024-02-01, 18:17 authored by Barbara H. Braffett, Laure El ghormli, James W. Albers, Eva L. Feldman, William H. Herman, Rose A. Gubitosi-Klug, Catherine L. Martin, Trevor J. Orchard, Neil H. White, John M. Lachin, Bruce A. Perkins, Rodica Pop-Busui

Objective: Diabetic peripheral neuropathy (DPN) is common; however the features and burden of neuropathic pain in type 1 diabetes (T1D) are poorly understood. We evaluated the incidence of first occurrence, annual prevalence, remission, and risk factors for neuropathic pain during long-term follow-up of participants with T1D.

Research Design and Methods: The Michigan Neuropathy Screening Instrument was administered annually (1994-2020) in 1,324 participants in the Epidemiology of Diabetes Interventions and Complications (EDIC) study. Neuropathic pain (NP) with clinical signs of DPN (NP DPN+) was defined by self-reported neuropathic pain plus an examination score >2, while neuropathic pain without clinical signs of DPN (NP DPN-) was defined by self-reported neuropathic pain and an examination score ≤2.

Results: At EDIC year 1, participants had median [IQR] age 36 [30, 41] years, diabetes duration 13 [10, 18] years, and HbA1c 7.9 [7.2, 8.9]%. At year 26 (median diabetes duration 39 years), cumulative incidence of neuropathic pain was 57%, regardless of concomitant clinical signs of DPN (36% NP DPN+ vs. 46% NP DPN-). Neuropathic pain prevalence was 20% at 26 years (11% NP DPN+; 9% NP DPN-), suggesting frequent remission. Annualized remission rates were similar regardless of pain medication use. In addition to HbA1c, female sex was associated with NP DPN-.

Conclusions: Neuropathic pain incidence in T1D was high and frequently occurred in the absence of clinical signs of neuropathy, as assessed by the MNSI. Pain remission was not explained by pain medication use. Effective clinical strategies for identification and management are needed.

Funding

The DCCT/EDIC has been supported by cooperative agreement grants (1982-1993, 2012-2017, 2017-2022) and contracts (1982-2012) with the Division of Diabetes Endocrinology and Metabolic Diseases of the National Institute of Diabetes and Digestive and Kidney Diseases (current grant numbers U01 DK094176 and U01 DK094157), and through support by the National Eye Institute, the National Institute of Neurologic Disorders and Stroke, the General Clinical Research Centers Program (1993-2007), and Clinical Translational Science Center Program (2006-present), Bethesda, Maryland, USA. The sponsor of this study is represented by the NIDDK Project Scientist, who serves as part of the DCCT/EDIC Research Group and plays a role in the study design and conduct, as well as the review and approval of manuscripts. The NIDDK Project Scientist was not a member of the writing group of this paper. The opinions expressed are those of the investigators and do not necessarily reflect the views of the funding agencies.

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