Prevention of Deterioration of Renal and Sensory-Nerve Function by More Intensive Management of Insulin-Dependent Diabetic Patients

Holman, Rury R.; Mayon‐White, V. A.; Orde-Peckar, C.; Steemson, J; Smith, Beverly A.; McPherson, Kasi C.; Rizza, C. R.; Knight, A. H.; Dornan, Timothy; Howard-Williams, J.; Jenkins, L; Rolfe, Rena Clayton; Barbour, Deborah J.; Poon, P. Y. W.; Mann, J I; Bron, A. J.; Turner, R. C.

doi:10.1016/s0140-6736(83)92586-2

Cited by 174 publications

(47 citation statements)

References 26 publications

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“…The recently reported small deterioration in vibration perception associated with poor glycaemic control [13,14] is the only relationship between hyperglycaemia and sensory neuropathy hitherto identified. There have been no comparable studies of autonomic function.…”

Section: Discussionmentioning

confidence: 94%

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: 94%

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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“…It is however still uncertain whether strict control of hyperglycaemia can prevent the occurrence and progression of polyneuropathy in patients with long-standing diabetes [10,11]. Several short-term studies have demonstrated improvement of nerve conduction velocity in newly-diagnosed patients undergoing intensive insulin injection therapy [12][13][14] and in patients treated with continuous subcutaneous insulin infusion [15][16][17][18].…”

Section: Discussionmentioning

confidence: 99%

The effect of 8 years of strict glycaemic control on peripheral nerve function in IDDM patients: the Oslo Study

Amthor

Dahl-J�rgensen²,

Berg³

et al. 1994

Diabetologia

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SummaryWe have investigated the effect of long-term strict glycaemic control on peripheral and autonomic nerve function in 45 IDDM patients (age 18-42 years, diabetes duration 7-23 years) without clinical signs of neuropathy or other neurological disease. They were randomly assigned to treatment either with continuous insulin infusion, multiple injections (4-6 times daily), or conventional treatment (twice daily) for 4 years and followed prospectively for 8 years. Motor and sensory nerve conduction velocities were measured at the start and after 8 years. Autonomic nerve function tests were performed only once, after 8 years. A significant reduction of nerve conduction velocity was observed during 8 years in patients with mean HbA1 more than 10% (n = 12, group mean 10.9%, range 10.1-13.2%) compared to patients with HbAI less than 10% (n = 33, group mean 9.0 %, range 7.5-9.9 %). Change of motor nerve conduction velocity in the peroneal nerve was: -4.8 + 4.9 (SD) vs -2.2 + 5.3 m/s (p < 0.01). Change of motor nerve conduction velocity in the posterior tibial nerve was: -6.8 + 5.7 vs-3.9 +_ 5.1 m/s (p < 0.05). No significant changes were observed in the ulnar nerve. Change of sensoric nerve conduction velocity in the sural nerve was: -8.9 + 8.0 vs -4.6 + 5.3 m/s (p < 0.05). Multiple regression analysis showed that a change in HbA1 of 1% resulted in a 1.3 m/s change in nerve conduction velocity during 8 years. A significantly lowered heart-rate variation during deep breathing (p < 0.05) and heart-rate response to standing (p < 0.01) was found in patients with HbA1 more than 10 % compared to patients with HbA1 less than 10 %. This study confirms that the long-term lowering of blood glucose retards the deterioration in nerve conduction velocity observed in the diabetic nerve. [Diabetologia (1994) 37: 579-584]

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“…Impaired nerve function may be related to inadequate control of blood glucose levels [1,2]. Recently, improvement in glycaemic control using continuous subcutaneous insulin infusion [3,4] and intensive intermittent subcutaneous insulin injections [5] have been associated with an observed improvements in neurophysiological function. Unfortunately, there are many difficulties in implementing such regimens so that normal or near normal blood glucose levels cannot be achieved in many patients.…”

mentioning

confidence: 99%

Clinical and neurophysiological studies with the aldose reductase inhibitor, sorbinil, in symptomatic diabetic neuropathy

et al. 1984

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Summary. The effect of sorbinil (200 mg daily for 4 weeks) was examined in 13patients, mean age 59.7years (range 42-72 years), with symptomatic diabetic neuropathy of mean duration 6years (range 1-18years). In this double-blind, placebo-controlled crossover trial, studies were made of motor, sensory and autonomic nerve function, severity of painful symptoms and duration of sleep. One patient was withdrawn because of an adverse reaction to sorbinil. In the other 12, constant mean values for glycosylated haemoglobin A1 between 11% and 12% indicated stable though not ideal diabetic control throughout the study. Example values for nerve conduction velocity on placebo and active treatment were: 44.3 +_ 5.9 and 44.8 + 5.1 metres/s (mean + SD) for median motor nerve, 38.4+8.2 and 37.2+7.7metres/s for median sensory nerve. Thus there was no significant effect of sorbinil on conduction velocity in these or any other of the motor and sensory nerves tested. Abnormal autonomic function was not improved by sorbinil. Subjective pain scores on a 10 cm visual analogue scale were 4.2 + 2.4 on placebo and 4.3 + 2.4 after sorbinil. Duration of sleep on placebo and active treatment was 6.1 _+ 1.6 and 6.2 + 1.7 h/night, respectively. We were not able to detect any beneficial effect of sorbinil on painful diabetic neuropathy in our patients.Key words: Aldose reductase inhibitor, sorbinil, diabetic neuropathy.Peripheral neuropathy is a common complication of diabetes mellitus and in some patients severe pain may be experienced which is refractory to conventional treatments. Impaired nerve function may be related to inadequate control of blood glucose levels [1,2]. Recently, improvement in glycaemic control using continuous subcutaneous insulin infusion [3,4] and intensive intermittent subcutaneous insulin injections [5] have been associated with an observed improvements in neurophysiological function. Unfortunately, there are many difficulties in implementing such regimens so that normal or near normal blood glucose levels cannot be achieved in many patients. Effective alternative treatments for symptomatic diabetic neuropathy would therefore be valuable.Sorbitol and fructose accumulate in the nerves of diabetic animals and man in proportion to the degree of hyperglycaemia [6,7] and have been implicated in the impaired nerve conduction [8,9]. Inhibition of aldose reductase, the first and rate-limiting enzyme in the polyol pathway, has a beneficial effect on nerve conduction in rats with spontaneous galactosaemia and with streptozotocin-induced diabetes [6,/0]. Sorbinil, a non-competitive inhibitor of aldose reductase, has recently become available for use in man. Initial reports have suggested that treatment with this inhibitor may improve motor and sensory nerve conduction velocities [11] and reduce painful symptoms and weakness [12] in patients with diabetic neuropathy. In the present study we have examined the effects of this drug in patients with symptomatic diabetic neuropathy. Subjects and methods Subjects and study designA ran...

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Prevention of Deterioration of Renal and Sensory-Nerve Function by More Intensive Management of Insulin-Dependent Diabetic Patients

Cited by 174 publications

References 26 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)

The effect of 8 years of strict glycaemic control on peripheral nerve function in IDDM patients: the Oslo Study

Clinical and neurophysiological studies with the aldose reductase inhibitor, sorbinil, in symptomatic diabetic neuropathy

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