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

Diabetic neuropathy accompanied by anomalies in pain perception is one of the most frequent complications in insulin-dependent diabetes in humans. Many clinical and experimental studies have suggested that diabetes or hyperglycaemia alters pain sensitivity. In humans, diabetic neuropathy can be associated with burning, tactile hypersensitivity. Behavioural reactions of hyperalgesia in animal models of diabetes have been described. However, the aetiology of these disturbances is still unknown, although metabolic factors such as hyperglycaemia or neurotransmitter alteration may be involved. Activation of protein kinase C (PKC) has been implicated in changes in pain perception. Phorbol esters, which activate PKC, enhance the thermal hyperalgesia in diabetic mice and enhance nociceptive responses after tissue injury induced by formalin. Electrophysiological experiments have shown that activation of PKC leads to long-lasting enhancement of excitatory amino acid-mediated currents in dorsal horn neurones and trigeminal neurones. Thus, activation of PKC may underlie the neuronal sensitisation that produces hyperalgesia in diabetic neuropathy.
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PMID:Therapeutic potential of PKC inhibitors in painful diabetic neuropathy. 1177 75

Diabetic neuropathy is a chronic complication of diabetes. It involves non-inflammatory damage of the function and structure of peripheral nerves by metabolic vascular pathogenic processes. In case of affection of vegetative nerves (small non-myelinated C fibres) autonomic neuropathy develops. It is a relatively frequent form of neuropathy which remains for a long time without clinical symptoms and therefore is rarely diagnosed and treated. Manifestations of the affection are encountered in all organs which are supplied by vegetative nerves. The presence of this complication of diabetes is signalized by tachycardia at rest, deterioration of gastric evacuation, diabetic diarrhoea or constipation, erectile dysfunction, impaired function of the sweat glans or impaired pupillary reaction. The advanced form involves the danger of latent myocardial ischaemia, serious postural hypotension and sudden death. It increases significantly the mortality of the affected patients. Similarly as the treatment of other complication of diabetes, treatment of autonomic neuropathy is difficult. The objective of the present paper is to review contemporary therapeutic possibilities. An essential prerequisite remain efforts to achieve optimal compensation. The authors draw attention to the effect of alpha-lipoic acid which exerts a positive effect not only on subjective symptoms but also on the objective finding. The other mentioned drugs are used either only experimentally or for purely symptomatic treatment.
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PMID:[Autonomic neuropathy in diabetics, treatment possibilities]. 1213 56

Diabetic neuropathy is a chronic progressive disease accounting for considerable morbidity and reduced quality of life among patients with diabetes. Accumulating evidence suggests that the clinical and neurophysiological markers used to assess neuropathy not only predict the development of neuropathic foot ulceration, one of the most common causes for hospital admission and lower limb amputations, but are also predictors of increased mortality in diabetic patients. In addition to metabolic control, drug treatment of both incipient and clinically manifest diabetic neuropathy will be necessary for the years to come. Because 1-2% of the whole population in western societies may be affected, the search for effective drug treatment is not only a very important goal for the patient suffering from diabetic neuropathy and for the practicing physician, but also an economic task for both the health care systems and pharmaceutical companies. The validity of inferences about the clinical consequences of the use of any given agent to induce a specific pharmacologic effect will depend not only on the extent to which it affects the targeted biological phenomenon, but also on the extent to which all of the actions of the agent have been defined and the extent to which all affect the entire organism, alone and in concert. The ultimate test of the usefulness of a drug or device depends on the determination of outcomes, ideally in randomized clinical trials (RCTs) of sufficient scope and duration. The efficacy and safety of a variety of drugs based on the different pathogenetic hypotheses proposed have been evaluated in RCTs since the 1970s. However, the quality of RCTs published between 1981 and 1992 that evaluated the effects of medical treatment in diabetic polneuropathy was poor. Adequate designs for RCTs in diabetic neuropathy must consider the following criteria: type and stage of neuropathy, homogeneity of the study population, outcome measures (neurophysiological markers, intermediate clinical end points, ultimate clinical outcomes, quality of life), natural history, sample size, study duration, reproducibility of neurophysiological and intermediate end points, nonspecific effects of treatment, measures of treatment effect, the extent to which the overall trail result applies to individual patients (external validity), and the reporting of the RCTs. Trials focusing preferentially on patients with mild or moderate early stages of neuropathy over long periods of 3-5 years aimed at slowing or prevention, rather than reversal, using end point measures that have clinical and prognostic significance are most likely to produce meaningful results.
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PMID:Clinical trials for drugs against diabetic neuropathy: can we combine scientific needs with clinical practicalities? 1219 20

Diabetic neuropathy is a most-convoluted complication. Diabetic gastropathy, ulcers, diarrhea, and bladder dysfunction are the major peripheral neuropathies. Peripheral neuropathies have been the primary neuroscience focus of diabetes research. In contrast to the periphery, the brain is not usually thought to be a target of chronic diabetic complications. However, the impact of diabetes mellitus on the central nervous system has recently gained attention. It is well known that diabetes or hyperglycemia influences the sensitivity of laboratory animals to various pharmacological agents. An increased sensitivity of hyperglycemic or diabetic animals to barbiturates and a decreased sensitivity of D-amphetamine, p-chloroamphetamine, and carbon tetrachloride have been demonstrated. Furthermore, it was reported that mice and rats with streptozotocin-induced diabetes and spontaneously diabetic mice are significantly less sensitive than non-diabetic mice to the antinociceptive effect of morphine. However, little information is available regarding the mechanism responsible for these changes. It is well established that anxiety and depression are common in patients with diabetes. Moreover, diabetic animals showed significantly more anxiogenic activity than non-diabetic animals did. However, the mechanisms through which diabetes may contribute to the development of, or be a risk factor for, psychiatric disorders are not clear. We provide an overview of our current understanding of the effects of streptozotocin-induced diabetes on the opioid receptor and the benzodiazepine receptor.
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PMID:[Modifications of several pharmacological actions by diabetes: effects on the opioid receptor agonist and benzodiazepines]. 1237 65

Diabetic neuropathy encompasses various disturbances concerning somatic and autonomic nervous system and has significant impact on prognosis and course of diabetes mellitus. The aim of the work is an evaluation of vestibulo-spinal reflexes in children and young adults suffering from diabetes mellitus type 1. Material--95 children and young adults aged from 6 to 28 years with diabetes mellitus type 1 diagnosed. The control group consisted of 44 otoneurologically healthy subjects aged from 6 to 28 years. After detailed medical history collection and physical ENT examination stato-posturography was performed in each case. Posturographer PE 62 Model 04 was applied in the studies. Static posturography as well as dynamic one (one leg standing test) was performed in each case. 6 patients belonging to diabetic group complained about vertigo or dizziness. There were worse stabilograms parameters in diabetic group in comparison to control one, statistically significant in younger children. There were better stabilogram parameters in diabetic patients with longer history of the disease. The parameters analysed were significantly worse in the subgroup with not compensated diabetes. The parameters were slightly better in relation to the presence of hypoglycaemic incidents. No apparent differences in stabilograms parameters were present in relation to the presence of diabetic complications. Diabetes mellitus type 1 with slight or without complications does not have significant influence on vestibulo-spinal reflexes and posture stability of the patients. Balance organ disturbances in diabetes mellitus type 1 in children and young adults despite their presence have subclinical course. Perhaps one should consider monitoring of those disturbances in the course of the disease.
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PMID:[The influence of metabolic disturbances present in diabetes mellitus type I on vestibulo-spinal reflexes in children and young adults]. 1237 5

Diabetic neuropathy is one of the most common and serious complications of diabetes both type 1 and type 2. Damage to autonomic nerves in the course of diabetes mellitus leads to diabetic autonomic neuropathy. There are three hypotheses explaining the pathogenetic mechanism of polyneuropathy: metabolic, vascular and immunological. Many diabetic patients have demonstrable abnormalities of autonomic function without any evidence of clinical disease.
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PMID:[Autonomic neuropathy in diabetic patients. Part I. Pathogenesis and clinical problems]. 1242 Mar 52

Diabetic neuropathy is the most common peripheral neuropathy in western countries. Although every effort has been made to clarify the pathogenic mechanism of diabetic neuropathy, thereby devising its ideal therapeutic drugs, neither convinced hypotheses nor unequivocally effective drugs have been established. In view of the pathologic basis for the treatment of diabetic neuropathy, it is important to enhance nerve regeneration as well as prevent nerve degeneration. Nerve regeneration or sprouting in diabetes may occur not only in the nerve trunk but also in the dermis and around dorsal root ganglion neurons, thereby being implicated in the generation of pain sensation. Thus, inadequate nerve regeneration unequivocally contributes to the pathophysiologic mechanism of diabetic neuropathy. In this context, the research on nerve regeneration in diabetes should be more accelerated. Indeed, nerve regenerative capacity has been shown to be decreased in diabetic patients as well as in diabetic animals. Disturbed nerve regeneration in diabetes has been ascribed at least in part to all or some of decreased levels of neurotrophic factors, decreased expression of their receptors, altered cellular signal pathways and/or abnormal expression of cell adhesion molecules, although the mechanisms of their changes remain almost unclear. In addition to their steady-state changes in diabetes, nerve injury induces injury-specific changes in individual neurotrophic factors, their receptors and their intracellular signal pathways, which are closely linked with altered neuronal function, varying from neuronal survival and neurite extension/nerve regeneration to apoptosis. Although it is essential to clarify those changes for understanding the mechanism of disturbed nerve regeneration in diabetes, very few data are now available. Rationally accepted replacement therapy with neurotrophic factors has not provided any success in treating diabetic neuropathy. Aside from adverse effects of those factors, more rigorous consideration for their delivery system may be needed for any possible success. Although conventional therapeutic drugs like aldose reductase (AR) inhibitors and vasodilators have been shown to enhance nerve regeneration, their efficacy should be strictly evaluated with respect to nerve regenerative capacity. For this purpose, especially clinically, skin biopsy, by which cutaneous nerve pathology including nerve regeneration can be morphometrically evaluated, might be a safe and useful examination.
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PMID:Diabetic neuropathy and nerve regeneration. 1275 48

Diabetic neuropathy (DN) is a complex set of clinical syndromes that affect distinct regions of the nervous system, either singly or combined. DN is the most common form of neuropathy in the developed countries of the world and is responsible for 50% to 75% of nontraumatic amputations. It is also the most life damaging--once autonomic neuropathy sets in, the mortality rate approximates 25% to 50% within 5 to 10 years. Distal symmetric polyneuropathy, the most common form of DN, usually involves both small and large nerve fiber damage. Small nerve fiber neuropathies occur early and are often present without objective signs or electrophysiologic evidence of nerve damage. The greatest risk is foot ulceration and subsequent gangrene. Large nerve fiber neuropathies, which involve the sensory and motor nerves, are generally neuropathies of signs rather than symptoms. Clinical presentation usually includes a "glove and stocking" distribution of sensory loss and the greatest risk is Charcot's neuroarthropathy. Diagnosis of DN relies heavily on a careful patient history and physical examination. Most critical is that both the patient and the patient's shoes should be examined and corrective measures taken. Several studies have shown that good diabetes control can significantly reduce neuropathy. As new drugs and ways to enhance nerve blood flow and block pain pathways at different levels are being explored, the effective treatment of DN and the reduction of its impact on quality of life as well as mortality will become a reality. Patient education and preventive strategies, however, are still the best ways to treat the complications of neuropathy and reduce the amputation rate.
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PMID:Management of neuropathy and foot problems in diabetic patients. 1280 Apr 79

The aim of the study was to evaluate the incidence of diabetic neuropathy. The examined group consisted of 32 patients (14 boys, 18 girls) 16 to 19 years old with diabetes duration of 5 till 17 years, treated actually with multiple injections of human insulin. Diabetic neuropathy was observed in 56% of patients. The incidence of neuropathy was higher after 15 years of diabetes duration, in patients with bad metabolic control - HbA1c>8%, multiple ketoacidosis (p=0.003) and higher total cholesterol levels (p=0.003), with microalbuminuria (64.3%) and macroalbuminuria (83.3%) and in patients with systolic and diastolic blood pressure equal and/or above 90 % percentyle.
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PMID:[The incidence of neuropathy in patients with diabetes type 1]. 1281 69

Diabetic neuropathy is a clinical state of nerve damage caused by hyperglicaemia, raised activation of polyol pathway, oxydative stress, changes in endoneurial arteries and myelinated fibres. Patient complains of pain and paresthesiae in hands and limbs. The feelings of pain, temperature, touch, vibration are significantly reduced. The changes may also concern cranial nerves (IIII, IV, VI, VII), intracostal nerves, hands and limbs (Garland and Tavemer syndrome). Autonomic neuropathy concerns the impairment of autonomic functions of cardio-vascular, gastro-intestinal, uro-genital and other systems. The treatment concerns the improvement of diabetes metabolic control. Antiinflammatory antisteroid drugs are widely used but their usefulness is limited. Antidepressive drugs are the most often used group. The improvement is observed after 6 months of treatment. The side effects - orthostatic hypotension, heart rhythm disturbation and obstipation are harmful for the patients with coronary heart disease. In the cases of persistent pain the oral antiepileptic drugs may be used or cream with capsaicin for skin surface.
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PMID:[Polyneuropathy in diabetes type 1]. 1281 21


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