Statins do not increase risk of polyneuropathy

Warendorf, Janna K; Vrancken, Alexander F.J.E.; Eijk, Ruben P A van; Visser, Nora A.; Berg, Leonard H van den; Notermans, Nicolette C.

doi:10.1212/wnl.0000000000007148

Cited by 12 publications

(2 citation statements)

References 40 publications

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“…Statin use has been associated with a 35% lower risk of amputation in the elderly population [93]. In a literature review of 13 studies Warendorf et al found that the odds of polyneuropathy reduced with increasing time exposure to statins [94] whilst Davis et al showed that statin usage reduced incident polyneuropathy by 35% in dose dependent manner [95]. However, other studies have failed to report a protective effect of statins on neuropathy [90,[96][97][98].…”

Section: Lipid Therapeutics Targeting Neuropathymentioning

confidence: 99%

Lipids and peripheral neuropathy

Iqbal

Bashir

Ferdousi

et al. 2021

Current Opinion in Lipidology

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Purpose of review Hyperlipidaemia is associated with the development of neuropathy. Indeed, a mechanistic link between altered lipid metabolism and peripheral nerve dysfunction has been demonstrated in a number of experimental and clinical studies. Furthermore, post hoc analyses of clinical trials of cholesterol and triglyceride-lowering pharmacotherapy have shown reduced rates of progression of diabetic neuropathy. Given, there are currently no FDA approved disease-modifying therapies for diabetic neuropathy, modulation of lipids may represent a key therapeutic target for the treatment of diabetic nerve damage. This review summarizes the current evidence base on the role of hyperlipidaemia and lipid lowering therapy on the development and progression of peripheral neuropathy. Recent findings A body of literature supports a detrimental effect of dyslipidaemia on nerve fibres resulting in somatic and autonomic neuropathy. The case for an important modulating role of hypertriglyceridemia is stronger than for low-density lipoprotein cholesterol (LDL-C) in relation to peripheral neuropathy. This is reflected in the outcomes of clinical trials with the different therapeutic agents targeting hyperlipidaemia reporting beneficial or neutral effects with statins and fibrates. The potential concern with the association between proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor therapy and cognitive decline raised the possibility that extreme LDL-C lowering may result in neurodegeneration. However, studies in murine models and data from small observational studies indicate an association between increased circulating PCSK9 levels and small nerve fibre damage with a protective effect of PCSK9i therapy against small fibre neuropathy. Additionally, weight loss with bariatric surgery leads to an improvement in peripheral neuropathy and regeneration of small nerve fibres measured with corneal confocal microscopy in people with obesity with or without type 2 diabetes. These improvements correlate inversely with changes in triglyceride levels. Summary Hyperlipidaemia, particularly hypertriglyceridemia, is associated with the development and progression of neuropathy. Lipid modifying agents may represent a potential therapeutic option for peripheral neuropathy. Post hoc analyses indicate that lipid-lowering therapies may halt the progression of neuropathy or even lead to regeneration of nerve fibres. Well designed randomized controlled trials are needed to establish if intensive targeted lipid lowering therapy as a part of holistic metabolic control leads to nerve fibre regeneration and improvement in neuropathy symptoms.

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Section: Lipid Therapeutics Targeting Neuropathymentioning

confidence: 99%

Lipids and peripheral neuropathy

Iqbal

Bashir

Ferdousi

et al. 2021

Current Opinion in Lipidology

View full text Add to dashboard Cite

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“…All subjects underwent measurements in the University Medical Center Groningen (UMCG) as part of the TransplantLines Biobank and Cohort study, in which the living kidney donors serve as healthy controls [10]. We collected data on age, sex, height, weight, medical history, medication use [11][12][13], and co-morbidities from hospital records of the donor screening. Subjects were included between June 2016 and October 2017.…”

Section: Participantsmentioning

confidence: 99%

Vibration threshold in non-diabetic subjects

et al. 2020

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Measuring vibration perception threshold (VPT) accurately classifies and quantifies the severity of loss of vibration perception. A biothesiometer (Bio-thesiometer ® ; Bio Medical Instrument Co, Ohio, USA) appears to be the most suitable tool to determine VPT due to its low inter-rater variability and low occurence of adaption to the sensation. Different VPT values for a biothesiometer have been described, however, specification on age, height and different measurement locations is currently lacking. The objective of our study was to identify determinants of vibration perception in non-diabetic subjects, in order to provide individualized normal values of VPTs for clinical practice. Measurements of the vibration perception were performed on the big toes, insteps, lateral malleoli, and wrists. A total of 205 healthy subjects were included (108 (52.7%) males) with a median [interquartile range] age of 59 [51;64] (range 21-80) years. Mean height was 174.45 ± 9.20 cm and mean weight was 82.94 ± 14.84 kg, resulting in a mean BMI of 27.19 ± 4.00 kg/m 2. In stepwise forward linear regression analyses, age (st. β = 0.51, p < 0.001) and height (st. β = 0.43, p < 0.001) were found to be the independent unmodifiable determinants of the VPT at the big toe. Regression coefficients for quantiles of the determinants age and height were incorporated in the corresponding regression equations. This study provides equations to calculate age-and height-specific normal values for VPT that can be used in clinical practice and in large research studies.

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Cardiovascular autonomic neuropathy in diabetes: an update with a focus on management

Eleftheriadou,

Spallone,

Tahrani

et al. 2024

Diabetologia

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Cardiovascular autonomic neuropathy (CAN) is an under-recognised yet highly prevalent microvascular complication of diabetes. CAN affects approximately 20% of people with diabetes, with recent studies highlighting the presence of CAN in prediabetes (impaired glucose tolerance and/or impaired fasting glucose), indicating early involvement of the autonomic nervous system. Understanding of the pathophysiology of CAN continues to evolve, with emerging evidence supporting a potential link between lipid metabolites, mitochondrial dysfunction and genetics. Recent advancements, such as streamlining CAN detection through wearable devices and monitoring of heart rate variability, present simplified and cost-effective approaches for early CAN detection. Further research on the optimal use of the extensive data provided by such devices is required. Despite the lack of specific pharmacological interventions targeting the underlying pathophysiology of autonomic neuropathy, several studies have suggested a favourable impact of newer glucose-lowering agents, such as sodium–glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists, where there is a wealth of clinical trial data on the prevention of cardiovascular events. This review delves into recent developments in the area of CAN, with emphasis on practical guidance to recognise and manage this underdiagnosed condition, which significantly increases the risk of cardiovascular events and mortality in diabetes. Graphical Abstract

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Statins do not increase risk of polyneuropathy

Cited by 12 publications

References 40 publications

Lipids and peripheral neuropathy

Lipids and peripheral neuropathy

Vibration threshold in non-diabetic subjects

Cardiovascular autonomic neuropathy in diabetes: an update with a focus on management

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