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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 12 (1976), S. 237-243 
    ISSN: 1432-0428
    Keywords: Diabetes ; neuropathy ; intravascular coagulation ; diabetic neuropathy ; fibrin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sural nerve biopsy was performed in twenty-four diabetic patients, with clinical and electrophysiological evidence of diabetic neuropathy. Material from an autopsy case was also examined. Vessels plugged with fibrin were seen within nerve in nine cases. In three cases fibrin was observed tracking into the vessel wall and in four, older thrombus was observed in vessels. Areas of necrosis in nerve bundles were seen in two of the latter. In two patients there had been a preceding episode of intravascular coagulation. Fibrin deposition within small vessels could well play a part in damaging the diabetic nerve and a disturbance of the balance between deposition and removal by fibrinolysis could explain phasic variation in the symptoms of neuropathy.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 22 (1982), S. 141-147 
    ISSN: 1432-0428
    Keywords: Arteriovenous anastamoses ; blood flow velocity ; diabeticneuropathies ; electrophysiology ; ultrasonics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Many clinical problems arise as a result of tissue pathology in the diabetic leg. Neuropathic or vascular ischaemic syndromes are readily identified but on occasions differentiation of the two may be difficult. This survey reviews the aetiological background of neuropathy and ischaemia, examines the relationship of physiological blood flow abnormalities to both areas and comments on management of the clinical states encountered, including the common problem of the ulcerated diabetic foot.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; foot ulcers ; arteriovenous anastomoses ; venous oxygenation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Venous PO2 was measured in the feet and hands of four subject groups: 14 diabetics with neuropathy and foot ulceration; 12 diabetics with neuropathy but no ulceration; 11 diabetics with no evidence of microvascular complications; and 10 nondiabetic controls. Neither patients nor controls had clinical evidence of peripheral vascular disease. The mean venous PO2 in the feet of subjects with neuropathy and foot ulceration was significantly higher than in controls or the other two diabetic groups. Venous PO2 in the feet of the subjects with ulcers was also significantly higher than in their hands or in the hands of the other groups. These results provide further evidence of abnormal blood flow in the diabetic neuropathic foot and are compatible with arteriovenous shunting.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 24 (1983), S. 306-306 
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Keywords Insulin-dependent diabetes mellitus ; diabetic neuropathy ; prevalence ; glycaemic control ; microalbuminuria ; impotence ; epidemiology.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The EURODIAB IDDM Complications Study involved the examination of 3250 randomly selected insulin-dependent diabetic patients, from 31 centres in 16 European countries. Part of the examination included an assessment of neurological function including neuropathic symptoms and physical signs, vibration perception threshold, tests of autonomic function and the prevalence of impotence. The prevalence of diabetic neuropathy across Europe was 28 % with no significant geographical differences. Significant correlations were observed between the presence of diabetic peripheral neuropathy with age (p 〈 0.05), duration of diabetes (p 〈 0.001), quality of metabolic control (p 〈 0.001), height (p 〈 0.01), the presence of background or proliferative diabetic retinopathy (p 〈 0.01), cigarette smoking (p 〈 0.001), high-density lipoprotein cholesterol (p 〈 0.001) and the presence of cardiovascular disease (p 〈 0.05), thus confirming previous associations. New associations have been identified from this study – namely with elevated diastolic blood pressure (p 〈 0.05), the presence of severe ketoacidosis (p 〈 0.001), an increase in the levels of fasting triglyceride (p 〈 0.001), and the presence of microalbuminuria (p 〈 0.01). All the data were adjusted for age, duration of diabetes and HbA1c. Although alcohol intake correlated with absence of leg reflexes and autonomic dysfunction, there was no overall association of alcohol consumption and neuropathy. The reported problems of impotence were extremely variable between centres, suggesting many cultural and attitudinal differences in the collection of such information in different European countries. In conclusion, this study has identified previously known and new potential risk factors for the development of diabetic peripheral neuropathy. [Diabetologia (1996) 39: 1377–1384]
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Diabetes ; neuropathy ; microangiopathy ; heterogeneity ; morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Clinical, electrophysiological and ultrastractural morphometric observations were made in 5 diabetic non-neuropathic patients, 5 diabetic patients with mild neuropathy and 11 diabetic patients with severe neuropathy. Capillary abnormalities were assessed in simultaneous nerve, muscle and skin biopsies and compared with results from 6 age-matched, non-diabetic control subjects. Nerve capillaries demonstrated markedly greater pathology than skin and muscle capillaries. Endoneurial capillary density was significantly reduced in severely neuropathic diabetic patients (p〈0.01) when compared with control subjects. Capillary basement membrane (p〈0.002), endothelial cell (p〈0.003) and total diffusion barrier (endothelial cell, pericyte, basement membrane) (p〈0.001) thickness were significantly increased, and oxygen diffusing capacity was significantly reduced (p〈0.001) in the nerves of patients with severe diabetic neuropathy when compared to control subjects. Endothelial cell profile number and luminal perimeter were significantly increased in asymptomatic (p〈0.01), (p〈0.05) and severely neuropathic (p〈0.001), (p〈0.05) diabetic patients respectively. However, endothelial cell outer perimeter, a measure of capillary size, showed no significant increase in diabetic patients when compared with control subjects. An association was observed between neurophysiological and neuropathological measures of neuropathic severity. There was no significant correlation between the duration of diabetes and HbA1 levels with capillary pathology or with neuropathic severity. Very few abnormalities of muscle and skin correlated with neuropathic severity. However, all measures of nerve capillary pathology correlated significantly with neurophysiological and neuropathological measures of neuropathic severity.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; microangiopathy ; peripheral neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty diabetic patients with neuropathy underwent clinical and neurophysiological evaluation together with a detailed morphometric assessment of capillary pathology in endoneurial and epineurial microvascular beds of the sural nerve. Morphological data were compared with ten non-diabetic control subjects. There were no significant differences in control subjects between basement membrane area, endothelial cell area, endothelial cell profile number or luminal area of endoneurial when compared with epineurial capillaries. In contrast, when compared with epineurial capillaries, endoneurial capillaries from diabetic patients demonstrated a significant increase in basement membrane (p〈0.001) and endothelial cell (p〈0.001) area and a significant reduction in luminal area (p〈0.001). There was no significant difference in endothelial cell profile number between endoneurial and epineurial capillaries amongst diabetic patients. Previous studies have demonstrated a good correlation between the degree of microangiopathy and measures of neuropathic severity. In the present study increased endoneurial capillary basement membrane area was significantly related to reduced peroneal nerve conduction velocity (p〈0.001), myelinated fibre density (p〈0.001) and elevated vibration (p〈0.05) and thermal (p〈0.001) perception. Increased endothelial cell area and reduced luminal size were related to a reduced peroneal nerve conduction (p〈0.05, p〈0.01, respectively), reduced myelinated fibre density (p〈0.05, p〈0.01) and elevated thermal perception (p〈0.05, p〈0.001). Epineurial capillary basement membrane, endothelial cell and luminal area failed to relate to measures of neuropathic severity. This study has demonstrated more advanced microangiopathy and a more significant relationship to neuropathic severity in endoneurial compared with epineurial capillaries, thus providing further support for the role of microangiopathy in the pathogenesis of human diabetic neuropathy.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Phenformin ; lactic acidosis ; renal failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two cases of lactic acidosis are described in which the time sequence of events made it certain that phenformin was the precipitating cause. In one patient the condition arose because of self administration of an overdose; in the other, phenformin had been administered to a patient on maintenance dialysis. After recovery, and in the absence of phenformin therapy the second patient was able to clear an intravenous lactate load at a rate similar to that observed in other patients on chronic dialysis. — A review of the literature re-emphasizes the possible danger of phenformin in the presence of diminished renal or hepatic function, which should be shown to be normal before starting the drug and assessed periodically during therapy.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; nerve blood flow ; sural nerve ; sural sensory conduction velocity ; temperature ; exercise
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Severe microvascular disease exists at the stage of clinical diabetic neuropathy. A non-invasive test that will identify those diabetic subjects who will eventually develop neuropathy is essential for early intervention. Sural sensory conduction velocity was recorded (x 3) in 12 non-neuropathic diabetic subjects, 15 diabetic subjects with established neuropathy and 16 age-matched normal control subjects, before and after exercise to 80% age/sex predicted maximum heart rate. Fixed sural electrodes were used. Subcutaneous temperature was recorded by a needle thermocouple placed near the sural nerve. Sural sensory conduction velocity increased significantly after exercise in normal subjects (p〈0.01, mean increase 5.07 m/s) and non-neuropathic diabetic subjects (p〈0.02, mean increase 3.99 m/s) but not in neuropathic subjects (mean increase 0.99 m/s). Subcutaneous temperature rose significantly in normal subjects (p〈0.01, mean increase 2.07°C) and non-neuropathic diabetic subjects (p〈0.001, mean increase 2.52 °C) but not in neuropathic subjects (mean increase 0.15 °C). However, sural sensory conduction velocity increased by 1.2 m · s−1. °C−1 following direct warming of the limb in six neuropathic subjects which was comparable to that of normal and non-neuropathic subjects (1.49 and 1.48 m · s−1. °C−1). The impairment of exercise conduction increment in diabetic neuropathy suggests impaired nerve blood flow in diabetic neuropathy.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 847-854 
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; microangiopathy ; nerve ; hypoxia ; blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Despite considerable research we still do not have a comprehensive explanation for the pathogenesis of diabetic neuropathy. Although chronic hyperglycaemia is almost certainly involved, it is not known whether the primary pathology is metabolic, microvascular, or an interaction between the two. Hyperglycaemia-induced polyol pathway hyperactivity associated with nerve sorbitol accumulation and myo-inositol depletion may play a part in the genesis of diabetic neuropathy. The case for microvascular disease in diabetic neuropathy is now strong. Fibre loss in human sural nerve is multifocal, suggesting ischaemia. The degree of vessel disease has been related to the severity of neuropathy. People with chronic obstructive pulmonary disease develop the so called “hypoxic neuropathy” in which similar microvascular changes occur as in diabetic neuropathy. In rats with experimental diabetic neuropathy nerve blood flow is reduced and oxygen supplementation or vasodilator treatment improved the deterioration in conduction velocity and nerve blood flow. Similarly, in human diabetic neuropathy, there is impaired nerve blood flow, epineurial arterio-venous shunting and a reduction in sural nerve oxygen tension. At what stage during the development of nerve damage these changes occur is yet to be determined.
    Type of Medium: Electronic Resource
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