Neuropathy and Diabetic Foot Syndrome

Volmer-Thole, Maren; Lobmann, Ralf

doi:10.3390/ijms17060917

Cited by 303 publications

(251 citation statements)

References 54 publications

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“…In peripheral autonomic neuropathy, secretion of sweat becomes dysfunctional and there is reduced sudomotor response with atrophy of sweat glands [11, 12]. Dysfunctional sweating contributes to a loss of humidification and cooling by evaporation resulting in dry skin [12, 13].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Dysfunctional sweating contributes to a loss of humidification and cooling by evaporation resulting in dry skin [12, 13]. Patients consequently have reduced protective skin function which may lead to increased risk of injury and subsequent foot ulceration [12, 13]. In this study, SUDOSCAN® technology, based on electrochemical principles of reverse iontophoresis and chronoamperometry, was used to determine sweat gland function of the palms of the hands and soles of the feet [14].…”

Section: Discussionmentioning

confidence: 99%

“…Metabolic insults and compromised blood flow to the nerve vascular supply have been implicated in pathogenic mechanisms with several factors potentially involved (e.g., formation of oxygen radicals, enhanced activity of the polyol pathway in neurons and Schwann cells, non-enzymatic glycosylation of neuronal structural proteins, neurotrophic disorder, pro-inflammatory changes) [12, 16–18]. In a different cohort of individuals with T2DM, we recently showed that increased OPN levels and the interaction with age had a significant association with reduced parasympathetic nerve function particularly in younger individuals, while adjusting for 25-hydroxyvitamin D insufficiency [19].…”

Section: Discussionmentioning

confidence: 99%

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Osteopontin and clusterin levels in type 2 diabetes mellitus: differential association with peripheral autonomic nerve function

et al. 2017

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Osteopontin (OPN) and clusterin are secreted glycoproteins potentially associated with nerve function. Sudomotor dysfunction is associated with the development of foot ulcerations. The purpose of this study was to investigate the potential relationship of OPN and clusterin with sudomotor function (i.e., autonomic nerves that control sweating) in participants with type 2 diabetes mellitus (T2DM). Sudomotor function was assessed using SUDOSCAN® which measures electrochemical skin conductance (ESC) of the hands and feet. Demographics (e.g., age, gender, race, body mass index (BMI)), HbA1c, 25-hydroxyvitamin D, creatinine, OPN, and clusterin were also determined for the participants. Fifty individuals with T2DM (age = 59±11 years; 23/27 male/female; 13 African Americans) participated in this study. Lower ESC for the hands and feet were observed in African Americans versus Caucasians/Asians (p < 0.05). No significant ESC differences were observed for good [HbA1c <7%] versus poor [HbA1c ≥7%] glycemic control. With regard to gender, ESC values were lower for the hands for females (p < 0.05). In linear regression with ESC for the hands or feet as the dependent variable, increased OPN levels, but not clusterin, were independently associated with reduced sudomotor function while adjusting for age, gender, race, BMI, and glycemic control (ESC hands model R2 = 0.504, p < 0.001; ESC feet model R2 = 0.534, p < 0.001). The association between OPN and reduced sudomotor function found in our study warrants further investigation to delineate the underlying mechanisms and determine if OPN is neuroprotective, involved in the pathogenesis of sudomotor dysfunction, or simply a bystander.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Osteopontin and clusterin levels in type 2 diabetes mellitus: differential association with peripheral autonomic nerve function

et al. 2017

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“…Peripheral neuropathy, including sensory, motor, and autonomic deficits, is an underlying comorbidity in the majority of ulcers . Decreased sensation exacerbates minor traumas and motor weakness, especially in the anterior shins, and results in increased forefoot pressure, leading to tissue breakdown . Autonomic dysregulation leads to desiccation of the skin, and the resulting microfissures provide an entry portal for pathogens.…”

Section: Host Factors That Shape the Microbiome Of Dfusmentioning

confidence: 99%

The role of the microbiome in nonhealing diabetic wounds

Kalan

Brennan

2018

Annals of the New York Academy of Sciences

105

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Wound healing is a highly coordinated and complex process, and there can be devastating consequences if it is interrupted. It is believed that, in combination with host factors, microorganisms in a wound bed can not only impair wound healing but can lead to stalled, chronic wounds. It is hypothesized that the wound microbiota persists in chronic wounds as a biofilm, recalcitrant to antibiotic and mechanical intervention. Cultivation-based methods are the gold standard for identification of pathogens residing in wounds. However, these methods are biased against fastidious organisms, and do not capture the full extent of microbial diversity in chronic wounds. Thus, the link between specific microbes and impaired healing remains tenuous. This is partially because local infection and, more specifically, the formation of a biofilm, is difficult to diagnose. This has led to research efforts aimed at understanding if biofilm formation delays healing and leads to persistent and chronic infection. Circumventing challenges associated with culture-based estimations, advances in high-throughput sequencing analysis has revealed that chronic wounds are host to complex, diverse microbiomes comprising multiple species of bacteria and fungi. Here, we discuss how the use of genomic methodologies to study wound microbiomes has advanced the current understanding of infection and biofilm formation in chronic wounds.

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