Electron microscopical studies of vessels in diabetic peripheral neuropathy.

Williams, Edward H.; Timperley, W R; Ward, J. D.; Duckworth, T.

doi:10.1136/jcp.33.5.462

Cited by 97 publications

(38 citation statements)

References 14 publications

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“…Secondly, the association of neural and microvascular complications, independent of glycaemia, also implies that there is either parallel development of abnormalities in different tissues, or an interdependent pathogenesis. However, from our data it is not possible to deduce which abnormalities; thus associations between developing complications could be due to such mechanisms as severe microangiopathy causing neuropathy [35], autonomically induced abnormalities of vascular autoregulation causing microangiopathy [36] or common activation of the sorbitol pathway [37] causing neural and microvascular damage in parallel.…”

Section: Discussionmentioning

confidence: 67%

Progression of subclinical polyneuropathy in young patients with Type 1 (insulin-dependent) diabetes: associations with glycaemic control and microangiopathy (microvascular complications)

Young

MacIntyre

Martyn³

et al. 1986

Diabetologia

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Summary. The progression of subclinical polyneuropathy over 2.5 years has been studied in a representative group of 75 young patients with Type I (insulin-dependent) diabetes (initial age 16-19years). The relationships between changes in nerve function, glycaemic control and concurrently developing microvascular complications (retinopathy, microproteinuria) were investigated. Deterioration of motor, sensory and autonomic nerve function, retinopathy and microproteinuria was related to poor glycaemic control. In addition, there was an association between developing neural and microvascular complications which was not diminished when their common relationship to hyperglycaemia was taken into account. These findings suggest that, although poor glycaemic control is an essential permissive factor in the early development of diabetic polyneuropathy, other influences, shared with microvascular complications, must also be important.

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Section: Discussionmentioning

confidence: 67%

Progression of subclinical polyneuropathy in young patients with Type 1 (insulin-dependent) diabetes: associations with glycaemic control and microangiopathy (microvascular complications)

Young

MacIntyre

Martyn³

et al. 1986

Diabetologia

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“…In the critically ill, this may contribute to the risk of organ failure. Putative causes in diabetes include vascular endothelium dysfunction (79), increased circulating levels of several clotting factors (80, 81), elevated platelet activation (82,83), and inhibition…”

Section: Other Nonmetabolic Effects Of Insulin In the Critically Illmentioning

confidence: 99%

How does blood glucose control with insulin save lives in intensive care?

Berghe¹

2004

J. Clin. Invest.

470

247

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Patients requiring prolonged intensive care are at high risk for multiple organ failure and death. Insulin resistance and hyperglycemia accompany critical illness, and the severity of this "diabetes of stress" reflects the risk of death. Recently it was shown that preventing hyperglycemia with insulin substantially improves outcome of critical illness. This article examines some potential mechanisms underlying prevention of glucose toxicity as well as the effects of insulin independent of glucose control. Unraveling the molecular mechanisms will provide new insights into the pathogenesis of multiple organ failure and open avenues for novel therapeutic strategies.

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“…Fagerberg [16] was the first to postulate sclerotic small vessels as a cause of nerve damage. The demonstration of platelet abnormalities in diabetes and in diabetic neuropathy [17] and the occurrence of cerebral small vessel damage in ketoacidosis [18] led to a reappraisal of the vascular hypothesis and indeed occlusion of small vessels with fibrin and platelets has been demonstrated in one-third of nerves studies [19,20]. Fresh fibrin deposits in vasa nervorum following ketosis point to the dynamic changing nature of vessel status within nerve although it must be admitted that the presence of some occluded vessels does not neces-sarily mean that such obstruction is a direct cause of nerve pathology.…”

Section: Neuropathic Problemsmentioning

confidence: 99%

The diabetic leg

Ward

1982

Diabetologia

100

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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.

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Electron microscopical studies of vessels in diabetic peripheral neuropathy.

Abstract: We present the results of an electron microscopical study of a further series of sural nerve biopsies from patients with diabetic neuropathy and attempt to clarify some of the mechanisms by which abnormali-

Cited by 97 publications

References 14 publications

Progression of subclinical polyneuropathy in young patients with Type 1 (insulin-dependent) diabetes: associations with glycaemic control and microangiopathy (microvascular complications)

Progression of subclinical polyneuropathy in young patients with Type 1 (insulin-dependent) diabetes: associations with glycaemic control and microangiopathy (microvascular complications)

How does blood glucose control with insulin save lives in intensive care?

The diabetic leg

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