Primary nociceptive afferents mediate the blood flow dysfunction in non-glabrous (hairy) skin of type 2 diabetes: a new model for the pathogenesis of microvascular dysfunction.

Stansberry, Kevin B.; Peppard, H. R.; Babyak, L M; Popp, G M; McNitt, Patricia M; Vinik, A

doi:10.2337/diacare.22.9.1549

Cited by 97 publications

(61 citation statements)

References 18 publications

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“…Impaired vasodilatory response to plantar pressure causing tissue ischemia is the common final pathway, according to various theories, of the development of diabetic foot ulcers (Boulton et al, 2000). Diabetic patients (with or without peripheral neuropathy) suffer from various forms of microvascular dysfunction, including abnormal vasomotion (Benbow et al, 1995;Stansberry et al, 1996;Bernardi et al, 1997), impaired vasodilatory response to local heating (Malik et al, 1993;Stansberry et al, 1999), decreased blood flow under or after pressure loading (Fromy et al, 2002;Koitka et al, 2004), endothelial nitric oxide dysfunction (Veves et al, 1998), and attenuated response to sympathetic maneuvers (Aso et al, 1997).…”

Section: Microvascular Factors and Ulcerationmentioning

confidence: 99%

Diabetic foot ulceration and amputation

Burns¹,

Jan²

2012

Rehabilitation Medicine

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Section: Microvascular Factors and Ulcerationmentioning

confidence: 99%

Diabetic foot ulceration and amputation

Burns¹,

Jan²

2012

Rehabilitation Medicine

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“…A variety of abnormalities have been described, including impairment in vasodilatory responses to skin heating, needle injury, postocclusive hyperemia, and response to ion-tophoresis of vasoactive substances (22)(23)(24)(25)(26)(27)(28)(29). Of particular interest is the finding of reduced maximal vasodilation to injury, including thermal (heating 44°C) and lacerating (needle prick) injury in people with diabetes (30,31).…”

mentioning

confidence: 99%

Comparative Roles of Microvascular and Nerve Function in Foot Ulceration in Type 2 Diabetes

et al. 2004

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OBJECTIVE -To determine the relative roles of different modalities of sensory nerve function (large and small fiber) and the role of microvascular dysfunction in foot ulceration in type 2 diabetic subjects. RESEARCH DESIGN AND METHODS-A total of 20 control subjects and 18 type 2 diabetic subjects with foot ulceration and 20 without were studied. None of the subjects had clinical features of peripheral vascular disease. The Computer-Aided Sensory Evaluator IV (CASE IV) was used to determine vibration detection threshold (VDT), cold detection threshold (CDT), warm detection threshold (WDT), and heat pain onset threshold (HPO). Vibration perception threshold (VPT) was also assessed by a neurothesiometer. Microvascular function (maximum hyperemia to skin heating to 44°C) was assessed using laser Doppler flowmetry (mean maximum hyperemia using laser Doppler flowmeter [LDF max ]), laser Doppler imaging (mean maximum hyperemia using laser Doppler imager [LDI max ]), and skin oxygenation with transcutaneous oxygen tension (TcpO 2 ).RESULTS -VPT, VDT, CDT, and HPO were all significantly higher in individuals with ulceration than in those without (VPT and VDT: P Ͻ 0.0001) (CDT and HPO: P ϭ 0.01). LDF max , LDI max , and TcpO 2 were significantly lower in the two diabetic groups than in the control subjects, but there was no difference between individuals with and without ulceration. CONCLUSIONS -This study found that there was no additional value in measuring smallfiber function with the CASE IV over measuring vibration by either CASE IV or the inexpensive neurothesiometer in discriminating between individuals with and without ulceration. Furthermore, none of the tests of microvascular function including the TcpO 2 were able to discriminate between individuals with and without ulceration, suggesting that such tests may not be of benefit in identifying subjects at greater risk of foot ulceration. Diabetes Care 27:1343-1348, 2004T he incidence of diabetes-related lower-extremity amputations continues to increase in the developed and developing world; in the U.S., it has been estimated to cost nearly $2 billion and account for 2,600 patient-years of hospital stays per year (1). Up to 80% of these amputations are preceded by foot ulceration (2). Furthermore, between 1995 and 1996, the Medicare costs for patients with foot ulcers were on an average three times higher than those of Medicare patients in general (3). Thus, there is a pressing need for a better understanding of the etiopathogenic factors involved in foot ulceration so that robust screening and preventative measures can be developed.In the absence of macrovascular disease, impaired nerve function and deranged microvascular function have been implicated as important etiological factors (4 -10). With regard to neuropathy, clinical assessment using simple clinical tools such as the neuropathy disability score, neuropathy symptom score, pressure perception using Semmes-Weinstein monofilaments, and vibration sensation with the neurothesiometer (Horwell Scientific Labora...

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“…The ~35-min time delay between GA and GF under rapidly changing glucose concentrations observed by Jungheim and Koschinsky [29] may have been caused by the higher capillary circulation on the fingertip, which is 5-20 times higher than that at the forearm [32][33][34], thereby leading to a slower glucose dynamics. On the other hand, McGarraugh [35] compared GA and GF with and without rubbing the forearm, and found that when the forearm was rubbed, the comparison yielded a nearly ideal correlation between GA and GF in the rapidly changing hyperglycemia region.…”

Section: Discussionmentioning

confidence: 96%