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

Diabetic neuropathy is a common and troublesome complication of diabetes mellitus. Vibration sensation is a measure of large fiber nerve conduction, which is very commonly affected in diabetes. The present study addresses the question of whether vibration perception threshold (VPT) measurement using a biothesiometer is reproducible under different levels of blood glucose at different hours of the day. Seventy-five diabetic patients, 31 insulin-dependent diabetes mellitus and 44 non-insulin-dependent diabetes mellitus, with mean age 50.33+/-14.22 years (21-70 years) and diabetes duration of 14.3+/-10.6 years (1-60 years) were included in the study. Forty-one patients were male and 34 were female. In conclusion, VPT was found to be reproducible under different blood glucose levels at different hours of the day, which is affected only by the height of the patient.
Diabetes Res Clin Pract 1999 Oct
PMID:Does instantaneous blood glucose affect vibration perception threshold measurement using biothesiometer? 1058 Jun 11

Diabetic neuropathy represents a major health problem, as it is responsible for substantial morbidity, increased mortality, and impaired quality of life. Near-normoglycaemia is now generally accepted as the primary approach to prevention of diabetic neuropathy, but is not achievable in a considerable number of patients. In the past two decades several medical treatments that exert their effects despite hyperglycaemia have been derived from the experimental pathogenetic concepts of diabetic neuropathy. Such compounds have been designed to improve or slow the progression of the neuropathic process and are being evaluated in clinical trials, but with the exception of alpha-lipoic acid (thioctic acid) which is available in Germany, none of these drugs is currently available in clinical practice. Here we review the current evidence from the clinical trials that assessed the therapeutic efficacy and safety of thioctic acid in diabetic polyneuropathy. Thus far, 15 clinical trials have been completed using different study designs, durations of treatment, doses, sample sizes, and patient populations. Within this variety of clinical trials, those with beneficial effects of thioctic acid on either neuropathic symptoms and deficits due to polyneuropathy or reduced heart rate variability resulting from cardiac autonomic neuropathy used doses of at least 600 mg per day. The following conclusions can be drawn from the recent controlled clinical trials. 1.) Short-term treatment for 3 weeks using 600 mg of thioctic acid i.v. per day appears to reduce the chief symptoms of diabetic polyneuropathy. A 3-week pilot study of 1800 mg per day given orally indicates that the therapeutic effect may be independent of the route of administration, but this needs to be confirmed in a larger sample size. 2.) The effect on symptoms is accompanied by an improvement of neuropathic deficits. 3.) Oral treatment for 4-7 months tends to reduce neuropathic deficits and improves cardiac autonomic neuropathy. 4.) Preliminary data over 2 years indicate possible long-term improvement in motor and sensory nerve conduction in the lower limbs. 5.) Clinical and postmarketing surveillance studies have revealed a highly favourable safety profile of the drug. Based on these findings, a pivotal long-term multicenter trial of oral treatment with thioctic acid (NATHAN I Study) is being conducted in North America and Europe aimed at slowing the progression of diabetic polyneuropathy using a clinically meaningful and reliable primary outcome measure that combines clinical and neurophysiological assessment.
Exp Clin Endocrinol Diabetes 1999
PMID:Alpha-lipoic acid in the treatment of diabetic polyneuropathy in Germany: current evidence from clinical trials. 1059 92

Diabetic neuropathy of can induce multi-organ dysfunction. The diabetes simultaneously has profound repercussions on gastrointestinal, sexual and erectile functions. One of the main sequelae of diabetic neuropathy is autonomic neuropathy affecting the vesicosphincteric control. The objective of this study was to review the epidemiological, clinical, laboratory and therapeutic data concerning voiding disorders observed in diabetes. Although the therapeutic management of an isolated voiding disorder in diabetics still remains symptomatic, it raises aetiological problems due to the comorbidity, particularly prostatic obstructive syndromes in men, pelvic dysfunction in women and ageing. Diabetic patients in renal failure also present specific vesicosphincteric disorders which are reviewed. Diabetic patients should be more systematically screened for the development of diabetic bladder disease, especially for associated factors which participate in its clinical expression. This implies extreme caution in the management of benign prostatic hyperplasia in the case of comorbidity, to avoid deteriorating a sometimes fragile detrusor-sphincter equilibrium. Diabetic detrusor hyperactivity must be better known in order to be more effectively detected. Pharmacological treatment of this condition raises problems related to detrusor hypocontractility also related to diabetic bladder disease. Clinical examination should be able to select those patients requiring further urodynamic studies in order to assess the individual detrusor-sphincter equilibrium. These investigations are required when surgical treatment of an associated urological or gynaecological disorder is considered.
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PMID:[Diabetes and urination disorders]. 1078 13

Diabetic neuropathy is common in patients with diabetes mellitus, and 7.5% of diabetics experience pain from diabetic neuropathy. Complications of diabetes mellitus are more common where control of the disease is not optimal. By improving the control of the disease, both the neuropathy and the pain it can produce may be improved. The pain of diabetic neuropathy can frequently be controlled using analgesics, antidepressants, anticonvulsants, topical capsaicin, and neuromodulation, either alone or in any combination.
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PMID:Treatment options in painful diabetic neuropathy. 1081 90

Diabetic neuropathy is a common complication of diabetes. Its commonest form is the bilateral, distal sensorimotor neuropathy and this has been associated with increased risk of disability from foot ulceration, inadvertent injury leading to gangrene as well as to amputation. The economic implications of the treatment of diabetic neuropathy and its consequences are enormous. In spite of this, there is no universally accepted method of treating it and efforts are still underway to find an adequate form of therapy. The following is a review of the outpatient management of peripheral diabetic neuropathy.
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PMID:The outpatient management of peripheral diabetic neuropathy. 1082 26

Diabetic neuropathy is a common complication of diabetes that is often associated both with considerable morbidity and mortality. The epidemiology and natural course of diabetic neuropathy is clouded with uncertainty, largely due to confusion regarding the definition and measurement of this disorder. The recent resurgence of interest in the vascular hypothesis, oxidative stress, the neurotrophic hypothesis and the possibility of the role of autoimmunity have 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, so that appropriate therapies can be targeted to specific fibre types. These tests must be validated and standardised to allow comparability between studies and a more meaningful interpretation of study results. 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.
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PMID:Diabetic neuropathies. 1099 72

Diabetic neuropathy traditionally is considered progressive and irreversible and will result in lower extremity ulceration and amputation in a segment of the diabetic population, despite the best efforts to control serum glucose levels. Restoration of sensation to the diabetic may prevent these complications of neuropathy. The present study was designed to evaluate whether decompression of a peripheral nerve at a known site of anatomic narrowing can restore sensibility to that nerve in the diabetic. Twenty diabetic patients ( 14 type I, 6 type II, with a mean duration of diabetes of 14.8 years) had surgical decompression of a median nerve at the wrist and an ulnar nerve at the elbow, or a decompression of the posterior tibial nerve at the ankle (total of 31 nerves). A therapist, in a manner blind to the operative site, evaluated two-point discrimination in the pulp of the appropriate digit. The postoperative sensibility was compared with that of the nontreated, contralateral extremity. At a mean of 23.3 months, 69 percent of the lower-extremity nerves and 88 percent of the upper-extremity nerves (79 percent overall) had improvement in sensibility. In comparison, 32 percent of the control (not decompressed) contralateral nerves had measurable progression of neuropathy. The hypothesis that decompression of a peripheral nerve in the diabetic will improve sensibility was confirmed at the p < 0.001 level.
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PMID:Results of decompression of peripheral nerves in diabetics: a prospective, blinded study. 1160 71

Diabetic neuropathy is the name used by clinicians to describe a heterogeneous group of diseases that affect the autonomic and peripheral nervous systems of patients suffering from diabetes mellitus. This article provides the pain management specialist with an overview of the pathophysiology and current trends in the diagnosis and treatment of these diseases. Because of the significant morbidity and suffering associated with diabetic neuropathy, this article emphasizes practical steps to prevent, treat, and manage diabetic neuropathy to assist the pain management specialist in caring for patients suffering from this common malady.
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PMID:Diabetic neuropathy: diagnosis and treatment for the pain management specialist. 1104 76

Bimoclomol, the recently developed non-toxic heat shock protein (HSP) coinducer, was shown to display multilateral protective activities against various forms of stress or injuries at the level of the cell, tissue or organism. The compound enhanced the transcription, translation and expression of the 70 kD heat shock protein (HSP-70) in myogenic and HeLa cell lines exposed to heat stress, and increased cell survival on exposure to otherwise lethal thermal injury. Bimoclomol increased contractility of the working mammalian heart, this effect was associated with the increased intracellular calcium transients due to increased probability of opening of ryanodine receptors in the sarcoplasmic reticulum (SR). In healthy tissues these cardiac effects were evident only at relatively high concentrations of the drug, while in the ischemic myocardium bimoclomol exerted significant cardioprotective and antiarrhythmic effects at submicromolar concentrations. It decreased ischemia-induced reduction of contractility and of cardiac output, and dramatically decreased the elevation of the ST-segment during ischemia as well as the occurrence of ventricular fibrillation upon reperfusion. Bimoclomol was also active in various pathological animal models subjected to acute or chronic stress. In the spontaneously hypertensive rats chronic pretreatment with bimoclomol restored sensitivity of aortic rings to acetylcholine; this effect was accompanied by accumulation of HSP-70 in the tissues. Bimoclomol pretreatment significantly diminished the consequences of vascular disorders associated with diabetes mellitus. Diabetic neuropathy, retinopathy, and nephropathy were prevented or diminished, while wound healing was enhanced by bimoclomol. Enhancement of wound healing by bimoclomol was observed after thermal injury as well as following ultraviolet (UV) irradiation. In addition to the beneficial effects on peripheral angiopathies, bimoclomol antagonized the increase in permeability of blood-brain barrier induced by subarachnoid hemorrhager or arachidonic acid. A general and very important feature of the above effects of bimoclomol was that the drug failed to cause alterations under physiological conditions (except the enhanced calcium release from cardiac sarcoplasmic reticulum). Bimoclomol was effective only under conditions of stress. Consistent with its HSP-coinducer property, bimoclomol alone had very little effect on HSP production. Its protective activity became apparent only in the presence of cell damage. Currently, bimoclomol reached the end of the Phase II clinical trial in a group of 410 patients with diabetic complications. Results of this trial will answer the question, whether a compound with promising in vitro and in vivo preclinical findings will produce the anticipated beneficial effects in humans. In the event of a positive outcome of this trial, the indications for bimoclomol will be substantially extended.
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PMID:Multilateral in vivo and in vitro protective effects of the novel heat shock protein coinducer, bimoclomol: results of preclinical studies. 1148 67

Diabetes mellitus is a major cause of peripheral neuropathy, commonly manifested as distal symmetrical polyneuropathy. This review examines evidence for the importance of vascular factors and their metabolic substrate from human and animal studies. Diabetic neuropathy is associated with risk factors for macrovascular disease and with other microvascular complications such as poor metabolic control, dyslipidaemia, body mass index, smoking, microalbuminuria and retinopathy. Studies in human and animal models have shown reduced nerve perfusion and endoneurial hypoxia. Investigations on biopsy material from patients with mild to severe neuropathy show graded structural changes in nerve microvasculature including basement membrane thickening, pericyte degeneration and endothelial cell hyperplasia. Arterio-venous shunting also contributes to reduced endoneurial perfusion. These vascular changes strongly correlate with clinical defects and nerve pathology. Vasodilator treatment in patients and animals improves nerve function. Early vasa nervorum functional changes are caused by the metabolic insults of diabetes, the balance between vasodilation and vasoconstriction is altered. Vascular endothelium is particularly vulnerable, with deficits in the major endothelial vasodilators, nitric oxide, endothelium-derived hyperpolarising factor and prostacyclin. Hyperglycaemia and dyslipidaemia driven oxidative stress is a major contributor, enhanced by advanced glycation end product formation and polyol pathway activation. These are coupled to protein kinase C activation and omega-6 essential fatty acid dysmetabolism. Together, this complex of interacting metabolic factors accounts for endothelial dysfunction, reduced nerve perfusion and function. Thus, the evidence emphasises the importance of vascular dysfunction, driven by metabolic change, as a cause of diabetic neuropathy, and highlights potential therapeutic approaches.
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PMID:Vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy. 1171 28


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