The influence of isolated small nerve fibre dysfunction on microvascular control in patients with diabetes mellitus

Pfützner, Andreas; Forst, Thomas; Engelbach, M.; Margin, T.; Goitom, K.; Löbig, M.; Beyer, J.; Kunt, T.

doi:10.1046/j.1464-5491.2001.00524.x

Cited by 25 publications

(16 citation statements)

References 44 publications

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“…Similar results were observed during thermal hyperemia at 44 8C. Lower microvascular reactivity was found in the whole cohort of diabetic patients (Stansberry et al, 1997), whereas in other studies only in diabetic patients with neuropathy (Stevens et al, 1991;Young et al, 1996) or in those with isolated small nerve fiber dysfunction (Pfutzner et al, 2001). In diabetic patients with neuropathy flow, motion amplitude was reduced (Benbow et al, 1995).…”

Section: Discussionsupporting

confidence: 81%

Relationship Between Peripheral Diabetic Neuropathy and Microvascular Reactivity in Patients with Type 1 and Type 2 Diabetes Mellitus

Kasalova¹,

Prázný²,

Škrha³

2006

Exp Clin Endocrinol Diabetes

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The aim of the study was to evaluate differences in the relationship between peripheral diabetic neuropathy and microvascular reactivity in type 1 and type 2 diabetic patients. Twenty-eight type 1 and 37 type 2 diabetic patients were included in the study. Control groups consisted of 18 and 25, age and body mass index matched healthy persons. The presence of peripheral neuropathy was estimated by vibration perception threshold higher than 20 V evaluated by biothesiometry. Microvascular reactivity was examined by laser doppler fluxmetry using postocclusive reactive hyperemia and thermal hyperemia. The following variables of vascular reactivity were examined: peak flow after occlusion as a difference between maximal and basal perfusion (PORH (max)), mean velocity increase during postocclusive hyperemia (PORH (max)/t (1)), peak flow during thermal hyperemia (TH (max)) and the mean velocity increase in the perfusion during thermal hyperemia (TH (max)/t (2)). These parameters are expressed in perfusion units (PU) or in perfusion units per second (PU . s (-1)). The microvascular reactivity in type 1 diabetic patients without evidence of peripheral neuropathy was comparable with that in healthy persons and it was significantly higher than in type 1 diabetic patients with peripheral neuropathy in all tested parameters (PORH (max): 64 [40; 81] PU vs. 24 [17; 40] PU, p < 0.001, PORH (max)/t (1): 5.41 [2.69; 8.18] PU/s vs. 1.21 [0.69; 2.5] PU/s, p < 0.001, TH (max): 105 [77; 156] PU vs. 56 [46; 85] PU, p < 0.001 and TH (max)/t (2): 2.48 [1.67; 3.33] PU/s vs. 0.87 [0.73; 1.06] PU/s, p < 0.001). On the contrary, no difference in the microvascular reactivity parameters was found between type 2 diabetic patients with and without neuropathy (PORH (max): 48 [30; 60] PU vs. 49 [36; 57] PU, NS, PORH (max)/t (1): 3.46 [2.15; 5.19] PU/s vs. 3.29 [2.45; 4.8] PU/s, NS, TH (max): 95 [78; 156] PU vs. 97 [73; 127] PU, NS and TH (max)/t (2): 1.45 [0.95; 2.84] PU/s vs. 1.37 [1.12; 1.95] PU/s, NS). In both these groups microvascular reactivity was comparable with that estimated in the age and BMI matched healthy persons. An inverse relationship was observed between microvascular reactivity and vibratory perception threshold in type 1 diabetic patients, but it was not true in type 2 diabetic patients. We suppose that the pathogenesis of neuropathy and impaired microvascular reactivity may be differently influenced by metabolic factors in type 1 and type 2 diabetic patients.

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Section: Discussionsupporting

confidence: 81%

Relationship Between Peripheral Diabetic Neuropathy and Microvascular Reactivity in Patients with Type 1 and Type 2 Diabetes Mellitus

Kasalova¹,

Prázný²,

Škrha³

2006

Exp Clin Endocrinol Diabetes

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“…Characterizing these changes may be of particular importance for two reasons. First, it could provide a novel approach for the detection of early neuropathy, since small unmyelinated fibers specifically play an important role in thermoregulation (7,8) and are often the earliest nerve fibers affected in diabetic polyneuropathy (9). In addition, disruptions in normal temperature control may be central to the development of neuropathic pain and sleep disturbance, because neuronal activity itself is highly temperature sensitive (10) and distal extremity warming is critical to sleep onset and maintenance (11–13).…”

mentioning

confidence: 99%

Impaired Distal Thermoregulation in Diabetes and Diabetic Polyneuropathy

et al. 2009

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OBJECTIVE -To determine how thermoregulation of the feet is affected by diabetes and diabetic polyneuropathy in both wakefulness and sleep.RESEARCH DESIGN AND METHODS -Normal subjects, diabetic subjects without neuropathy, diabetic subjects with small-fiber diabetic polyneuropathy, and those with advanced diabetic polyneuropathy were categorized based on neurological examination, nerve conduction studies, and quantitative sensory testing. Subjects underwent foot temperature monitoring using an iButton device attached to the foot and a second iButton for recording of ambient temperature. Socks and footwear were standardized, and subjects maintained an activity diary. Data were collected over a 32-h period and analyzed.RESULTS -A total of 39 normal subjects, 28 patients with diabetes but without diabetic polyneuropathy, 14 patients with isolated small-fiber diabetic polyneuropathy, and 27 patients with more advanced diabetic polyneuropathy participated. No consistent differences in foot temperature regulation between the four groups were identified during wakefulness. During sleep, however, multiple metrics revealed significant abnormalities in the diabetic patients. These included reduced mean foot temperature (P Ͻ 0.001), reduced maximal temperature (P Ͻ 0.001), increased rate of cooling (P Ͻ 0.001), as well as increased frequency of variation (P ϭ 0.005), supporting that patients with diabetic polyneuropathy and even those with only diabetes but no diabetic polyneuropathy have impaired nocturnal thermoregulation.CONCLUSIONS -Nocturnal foot thermoregulation is impaired in patients with diabetes and diabetic polyneuropathy. Because neurons are highly temperature sensitive and because foot warming is part of the normal biology of sleep onset and maintenance, these findings suggest new potentially treatable mechanisms of diabetes-associated nocturnal pain and sleep disturbance.

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“…Prior pharmacokinetics studies showed after TDS application, serum concentrations of estradiol increase rapidly and reach maximal or near maximal values within 24 hours [2,6]. Percutaneous absorption is known to vary due to different factors such as skin thickness, blood flow, lipid content, and number of hair follicles [8].…”

Section: Discussionmentioning

confidence: 99%

Transdermal absorption of estradiol in normal subjects and in patients with peripheral neuropathies

2003

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The influence of isolated small nerve fibre dysfunction on microvascular control in patients with diabetes mellitus

Abstract: Our study confirms an association between small nerve fibre injury and skin microvascular dysfunction. It further underlines the concept of neurovascular disturbances in the pathogenesis of neurotrophic foot ulceration. Diabet. Med. 18, 489-494 (2001)

Cited by 25 publications

References 44 publications

Relationship Between Peripheral Diabetic Neuropathy and Microvascular Reactivity in Patients with Type 1 and Type 2 Diabetes Mellitus

Relationship Between Peripheral Diabetic Neuropathy and Microvascular Reactivity in Patients with Type 1 and Type 2 Diabetes Mellitus

Impaired Distal Thermoregulation in Diabetes and Diabetic Polyneuropathy

Transdermal absorption of estradiol in normal subjects and in patients with peripheral neuropathies

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