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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral mononeuropathies may complicate distal arteriovenous fistulas for chronic renal dialysis. We observed three diabetic patients who developed pain, paresthesias, and weakness in the distribution of the median, ulnar, and radial nerves shortly after construction of proximal brachial artery-antecubital vein fistulas. EMG confirmed multiple distal nerve injuries. All three patients improved after shunt banding or ligation. Twenty additional patients with proximal shunts were examined for risk factors for brachial neuropathy. Although all patients had severe atherosclerosis and many had polyneuropathy, we identified no predictive risk factors other than diabetes.
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PMID:Brachial neuropathy after brachial artery-antecubital vein shunts for chronic hemodialysis. 303 8

The results of allogeneic clinical islet cell transplantation continue to be rather disappointing. However, results of clinical pancreatic transplantation in Type-I-diabetes are still improving: some centres (incl. the Munich centre) have reported a 1-year-graft survival rate of more than 70%. In 60-65% of successfully transplanted patients a normalisation of glucose tolerance can be achieved. There is accumulating evidence suggesting that successful pancreatic transplantation exerts a curative effect in Type I diabetes mellitus: Long term investigations have shown a subjective and objective improvement of diabetic retinopathy, nephropathy, polyneuropathy and peripheral microangiopathy.
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PMID:[Status of pancreatic organ and pancreatic islet cell transplantation]. 312 22

There is reason to believe that diabetic neuropathy may be related to the accumulation of sorbitol in nerve tissue through an aldose reductase pathway from glucose. Short-term treatment with aldose reductase inhibitors improves nerve conduction in subjects with diabetes, but the effects of long-term treatment on the neuropathologic changes of diabetic neuropathy are unknown. To determine whether more prolonged aldose reductase inhibition reverses the underlying lesions that accompany symptomatic diabetic peripheral polyneuropathy, we performed a randomized, placebo-controlled, double-blind trial of the investigational aldose reductase inhibitor sorbinil (250 mg per day). Sural-nerve biopsy specimens obtained at base line and after one year from 16 diabetic patients with neuropathy were analyzed morphometrically in detail and compared with selected electrophysiologic and clinical indexes. In contrast to patients who received placebo, the 10 sorbinil-treated patients had a decrease of 41.8 +/- 8.0 percent in nerve sorbitol content (P less than 0.01) and a 3.8-fold increase in the percentage of regenerating myelinated nerve fibers (P less than 0.001), reflected by a 33 percent increase in the number of myelinated fibers per unit of cross-sectional area of nerve (P = 0.04). They also had quantitative improvement in terms of the degree of paranodal demyelination, segmental demyelination, and myelin wrinkling. The increase in the number of fibers was accompanied by electrophysiologic and clinical evidence of improved nerve function. We conclude that sorbinil, as a metabolic intervention targeted against a specific biochemical consequence of hyperglycemia, can improve the neuropathologic lesions of diabetic neuropathy.
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PMID:Regeneration and repair of myelinated fibers in sural-nerve biopsy specimens from patients with diabetic neuropathy treated with sorbinil. 313 31

The time course of the blood level of C-peptide was studied in 20 patients with insulin dependent diabetes mellitus in the course of 1 year after human fetal pancreatic islet cell allotransplantation. All the recipients suffered from a labile type of diabetes complicated by polyneuropathy, glomerulosclerosis and progressive retinopathy. C-peptide concentration was determined by a radioimmunoassay using Behring-Werke AE kits (FRG). The recipient were divided into 3 groups with relation to the preoperative level of C-peptidemia (with a low level 0.17 +/- 0.06 ng/ml, a mean level 0.9 +/- 0.11 ng/ml and a high level 3.07 +/- 0.24 ng/ml). One-two days before cell culture allotransplantation the mean concentration of C-peptide was 0.3 +/- 0.02 ng/ml. One-two weeks after transplantation it rose up to 0.89 +/- 0.11 ng/ml (p less than 0.01), by the end of the 1st month it reached 2.85 +/- 0.54 ng/ml, in 2-3 months it was lowered up to 1.98 +/- 0.21 ng/ml and remained at this level in the next months decreasing up to 1.4 +/- 0.36 ng/ml and approximated the preoperative levels by the end of the year. The same time course was noted in all 3 groups irrespective of the preoperative levels and differed in quantitative indices only. Stabilization of a course of disease, normalization of some biochemical indices, disappearance or weakening of a degree of concomitant symptoms and a decrease in an exogenous dose of insulin were noted.
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PMID:[Changes in the C-peptide concentration in the blood of patients with diabetes mellitus after the transplantation of cultures of pancreatic islet cells]. 314 6

A new prostaglandin E1 analogue (TFC-612) was orally given to streptozocin-diabetic rats for 4 weeks after the induction of diabetes and its effects on motor nerve conduction velocity were studied. The compound significantly prevented a decrease of the velocity but did not reverse abnormal sorbitol and myo-inositol contents of the sciatic nerve. The results suggest that TFC-612 has a potent effect on diabetic nerve dysfunction via other mechanism than the correction of sorbitol and myo-inositol metabolisms and could be a potential compound for therapy of diabetic polyneuropathy.
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PMID:A new prostaglandin E1 analogue (TFC-612) prevents a decrease in motor nerve conduction velocity in streptozocin-diabetic rats. 327 9

Diabetic neuropathy is a common complication of diabetes that may be associated both with considerable morbidity (painful polyneuropathy, neuropathic ulceration) and mortality (autonomic neuropathy). The epidemiology and natural history of diabetic neuropathy is clouded with uncertainty, largely due to confusion in the definition and measurement of this disorder. We have reviewed a variety of the clinical manifestations associated with somatic and autonomic neuropathy and discussed current views related to the management of the different abnormalities. Although unproven, the best evidence suggests that near normal control of blood glucose in the early years following onset of diabetes may help delay the development of clinically significant nerve impairment. Intensive therapy to achieve normalization of blood glucose may also lead to reversibility of early diabetic neuropathy, but again this is unproven. Our ability to manage successfully the many different manifestations of diabetic neuropathy depends ultimately on our success in uncovering the pathogenic processes underlying this disorder. The recent resurgence of interest in the vascular hypothesis, for example, has opened up new avenues of investigation for therapeutic intervention. Paralleling our increased understanding of the pathogenesis of diabetic neuropathy, there must be refinements in our ability to measure quantitatively the different types of defects that occur in this disorder. These tests must be validated and standardized to allow comparability between studies and more meaningful interpretation of study results.
Diabetes Metab Rev 1988 May
PMID:Clinical aspects of diabetic neuropathies. 329 49

Previous trials have demonstrated a clinical and electrophysiological improvement of diabetic peripheral polyneuropathy in diabetic patients treated with cyclandelate at a dosage of 1600 mg/day. Hence, a double-blind randomised trial was started in 16 insulin-dependent diabetic patients presenting with symptoms of neuropathy, an increased vibration perception threshold (VPT), disturbed tendon reflexes at lower limbs and an EMG showing a significantly decreased motor nerve conduction velocity (MCV) of the peroneal nerves. The placebo-treated group and the cyclandelate-treated group were not significantly different regarding age, duration of diabetes and level of metabolic control (measured as total HbA1), which remained unchanged during the year of observation. In the cyclandelate-treated group, pathological sensation improved significantly in 7 of 8 patients. MCV, measured under standardised conditions, increased significantly during the first 6 months of treatment, while mean VPT did not change. In the placebo group 3 of 8 patients showed an improvement of sensation, 3 did not feel any change and 2 worsened. Neither mean MCV nor VPT changed significantly. No severe side effects were observed during the study period.
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PMID:Clinical experience with cyclandelate in insulin-dependent diabetic patients with neuropathy. 330 51

Twenty-nine diabetic patients (19 men, 10 women) aged 19-71 yr with newly developed painful polyneuropathy were studied prospectively for 12-18 mo. Pain remitted completely in 16 patients within 12 mo, but continued in the other 13 patients. At presentation, no differences were found in the type or prevalence of symptoms or neurophysiological measurements (electrophysiology and cardiovascular autonomic function tests) between the patients whose pain remitted and those whose pain continued. Most electrophysiological measurements improved slightly in remitting patients but deteriorated slightly in those whose pain continued to reveal a significant difference (P less than .05) between the groups on final review. Similarly, abnormal autonomic nerve function improved slightly when pain remitted but worsened or persisted in patients whose pain continued, again revealing a significant difference between the groups (P less than .05) on final review. We also observed that pain remission usually occurred if the onset of symptoms shortly followed some sudden metabolic change (e.g., rapid improvement in glycemic control, ketoacidosis, anorexia nervosa) when the duration of diabetes was relatively short or when considerable weight loss preceded the onset of pain. We suggest that remitting and chronic painful diabetic polyneuropathy have distinctive clinical features at presentation and detectable neurophysiological differences during their symptomatic evolution.
Diabetes Care 1988 Jan
PMID:Chronic and remitting painful diabetic polyneuropathy. Correlations with clinical features and subsequent changes in neurophysiology. 333 78

Diabetic neuropathy includes a heterogenous group of neuropathic syndromes associated with diabetes mellitus. One form of diabetic neuropathy is distal symmetric polyneuropathy, which is characterized at a late stage by intractable pain. This pain is generally refractory to present modalities of therapy except for narcotics. Pentoxifylline offers a new approach to therapy, reducing the blood viscosity and improving perfusion of ischemic microcirculation. A case report will be presented of intractable painful peripheral neuropathy responding dramatically to pentoxifylline therapy.
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PMID:Treatment of diabetic neuropathy with pentoxifylline: case report. 336 3

Sural nerve biopsies were obtained from 17 diabetic patients with neuropathy. All patients except three had both a symmetric distal sensory and autonomic polyneuropathy related to Type 1 (insulin-dependent) diabetes mellitus; 3 patients had a purely sensory polyneuropathy. Mean age was 34.5 years (range 18-53 years). The biopsies were compared with specimens from an age-matched control series. Myelinated fibre loss in the diabetic nerves was found to be nonuniform. Although patchy fibre loss has been considered to favour a vascular basis, an identical pattern of nonuniform loss was observed in a series of sural nerve biopsies from patients with Type I hereditary motor and sensory neuropathy, a subgroup within the spectrum of peroneal muscular atrophy, mainly of autosomal dominant inheritance, and a condition in which a vascular causation can be discounted. Possible reasons for nonuniform fibre loss other than vascular disease are discussed.
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PMID:Pattern of myelinated fibre loss in the sural nerve in neuropathy related to type 1 (insulin-dependent) diabetes. 337 77


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