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Diabetic neuropathy in some form or other afflicts a majority of patients with diabetes mellitus. Neuropathic disturbance of sensory, motor or autonomic nerves may occur singly or in combination. Cranial nerve and other mononeuropathies generally resolve spontaneously. Autonomic neuropathy which can result in orthostatic hypotension, gastroparesis diabeticorum, nocturnal diarrhea, atonic bladder and impotence, although chronic, may wax and wane in clinical severity. Neuritis, disesthesias and painful sensory neuritis may resolve with good diabetic control; on occasion, diphenylhydantoin has been of therapeutic benefit.
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PMID:Diabetic neuropathy, A review of clinical manifestations. 124 87

Diabetic neuropathy is a disease of peripheral nerves, characterized by axonal atrophy and degeneration that might be preceded by a marked impairment of axonal transport and by a reduced conduction velocity. Sensory nerves are particularly susceptible to diabetes. In the present report it is shown that experimental diabetes in rats causes a significant reduction of the content of the pain-related neuropeptide substance P in sciatic nerve and lumbar spinal cord. Such a loss of substance P is fully prevented by acetyl-L-carnitine treatment. The neuroprotective pharmacological effect is selective and takes place without significant changes of hyperglycaemia and without modifications of the reduced rate of body growth typical of diabetic animals.
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PMID:Acetyl-L-carnitine prevents substance P loss in the sciatic nerve and lumbar spinal cord of diabetic animals. 128 99

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 caused by confusion in the definition and measurement of this disorder. We have reviewed various clinical manifestations associated with somatic and autonomic neuropathy, and we herein discuss current views related to the management of the various abnormalities. Although unproven, the best evidence suggests that near-normal control of blood glucose in the early years after diabetes onset may help delay the development of clinically significant nerve impairment. Intensive therapy to achieve normalization of blood glucose also may 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, refinements must be made 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 Care 1992 Dec
PMID:Diabetic neuropathies. 146 46

Diabetic neuropathy is associated with some early defects of axonal transport in experimental animals. Axonal transport is dependent on intact microtubules, and unsubstituted lysine residues of tubulin are essential for microtubule polymerization. As lysine residues are the major target for the non-enzymatic attachment of glucose, the effect of diabetes on the extent of glycation of tubulin was investigated. There was a more than four-fold increase in the extent of glycation of tubulin in the sciatic nerve of rats with streptozotocin-induced diabetes of 2 weeks duration compared with control rats. In contrast, no such increase in glycation was observed in brain microtubule protein from diabetic rats at that stage of diabetes. Incubation of brain microtubule protein with glucose prior to in vitro polymerization showed that the early stages of glycation were not associated with inhibition of microtubule assembly. The observed glycation of peripheral nerve tubulin in early experimental diabetes may nevertheless contribute to axonal transport abnormalities through an as yet undetermined impairment of microtubule function.
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PMID:Glycation of rat sciatic nerve tubulin in experimental diabetes mellitus. 171 29

Although there is strong evidence that cigarette smoking is perhaps the major risk factor associated with peripheral occlusive vascular disease, there still appears to be little indication that clinicians in podiatric medicine and patients recognize this. When smoking is combined with other risk factors such as diabetes mellitus, the probability of developing peripheral arterial disease is greatly increased. In addition, smoking appears to accelerate the natural history of the process of atherogenesis and thrombosis. Diabetic neuropathy seems to have a greater prevalence when the patient has a history of an increased number of pack years smoked. By eliminating smoking, patients can often receive considerable relief from intermittent claudication and other sequelae of occlusive vascular disease, including the avoidance of amputation of the lower extremity. Patient care routinely should include efforts to prevent individuals from smoking as well as advice to smokers to stop. Podiatrists need to become a more prominent source of information about the hazards of smoking and should freely share this knowledge with their patients.
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PMID:Smoking and peripheral vascular disease. Podiatric medical update. 173 60

Late complications of diabetes mellitus include a variety of clinical pictures, mainly related to the involvement of the arterial wall both of large vessels (macroangiopathy) and small vessels (microangiopathy), and of the peripheral nervous system (neuropathy). Their presence in almost all types of diabetes indicates that there is a common pathogenetic mechanism, which can be substantially identified in high blood glucose levels and related alterations. Hyperglycemia, in fact, leads to some metabolic abnormalities, i.e. non-enzymatic glycosylation of proteins and polyol pathway activity; moreover it can negatively affect the pattern of some hormones, especially GH and sex steroids, and normal rheological and clotting properties of blood. These abnormalities, confirmed by experimental models, play a key role in the development of late diabetic complications. However some evidence indicates that a genetic background may predispose to their development or protect from their onset. The two main forms of diabetic retinopathy, non-proliferative and proliferative, show an incidence which increases with age and duration of diabetes, reaching 100% when diabetes lasts for more than 20 years. The risk of blindness, which is very high for the proliferative form, has been dramatically reduced by laser-photocoagulation. Diabetic nephropathy affects a lesser number of diabetics but, after a silent or preclinical stage, leads to renal failure and subsequent replacement therapy. Strict metabolic control in the silent stage and later rigid anti-hypertensive treatment can prevent or retard the evolution of this complication. A close association has been observed between diabetes and hypertension, which can directly affect the onset and evolution of diabetic nephropathy, probably through a common genetic mechanism. Diabetic neuropathy has a wide variety of clinical manifestations, at somatic, autonomic and central levels and can greatly modify the quality and expectancy of life. However, the major cause of death in diabetic subjects is large vessel disease or macroangiopathy, which is similar to non-diabetic atherosclerosis regarding the main histopathological and clinical manifestations but has a much higher prevalence and severity. Finally, a specific cardiomyopathy has also been described in diabetes mellitus and can account for the high rate of heart failure observed in these patients.
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PMID:The late complications of diabetes mellitus. 174 48

We report results from 120 (25- to 34-year-old) participants in a neuropathy substudy of subjects with insulin-dependent diabetes mellitus (IDDM) taking part in a cohort follow-up study. Diabetic neuropathy was evaluated by quantitative sensory testing, nerve conduction studies, and clinical examination. Mean quantitative sensory thresholds differed significantly by clinical category of abnormal sensation and ankle reflex activity. Mean sural and peroneal amplitudes and conduction velocities were also significantly lower for subjects classified as having abnormal ankle reflex activity. Modeling potential correlates in logistic analyses showed glycemic control, triglyceride levels, and hypertension status to be independently associated with clinically overt neuropathy. Similar lipid and hemodynamic parameters were associated with abnormality by any single assessment method used to define neuropathy. Although follow-up is needed to resolve the best assessment methods for determining neuropathy, these results suggest that good glycemic control as well as control of blood pressure and lipids is advisible.
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PMID:Measuring subclinical neuropathy: does it relate to clinical neuropathy? Pittsburgh epidemiology of diabetes complications study-V. 185 46

Diabetic neuropathy is an intriguing problem both for the patient and the clinician, however the clinical characteristics of type-II (non insulin-dependent) diabetics with peripheral neuropathy with special reference to gender differences is not paid much attention. We studied peripheral neuropathy and related complications in 179 type-II diabetics. Peripheral neuropathy was noted in 46 of 111 men and in 46 of 68 women. The age group of subjects did not differ significantly. Duration of diabetes differed between the groups with (n = 46) and without (n = 65) peripheral neuropathy (expressed in years and as mean +/- S.E: 7.7 +/- 0.7 vs 5.5 +/- 0.7; t = 2.2; P less than 0.05) in men, whereas in women it was not significant. Higher proportion (62.5% of 24) of men with proteinuria had neuropathy. Similar findings in women were not different. We conclude i) a large percent (51.4%) of the type-II diabetics had peripheral neuropathy than realised ii) duration of diabetes and proteinuria are important risk factors associated with neuropathy especially in men and iii) the gender differences need further clinicopathologic evaluation.
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PMID:Gender differences in the associated complications among type-II diabetics with peripheral neuropathy. 226 9

Diabetic neuropathy is probably the most frequent of the chronic complications of diabetes, and is usually found in association with diabetic retinopathy and/or nephropathy. We report seven patients with long-standing insulin-dependent diabetes mellitus in whom symptomatic peripheral neuropathy was the first and only documented complication. The diagnosis of peripheral symmetrical neuropathy was based on the presence of symptoms and abnormal physical findings, confirmed with abnormal electrophysiological and/or vibratory and thermal threshold measurements. Diabetic retinopathy and nephropathy were absent. We conclude that in some type 1 insulin-dependent diabetic patients, similar to what has been reported in type 2 non-insulin-dependent diabetes, peripheral neuropathy may be the first chronic complication to become manifest. This observation provides additional evidence to suggest that each of the diabetic complications may have a different pathogenic mechanism.
Diabetes Res Clin Pract 1989 Sep 18
PMID:Isolated symptomatic peripheral neuropathy in type 1 insulin-dependent diabetes mellitus. 255 8

Functional and structural neuropathy was examined in hyperglycemic (diabetic) BB rats maintained on small maintenance doses of insulin, hyperglycemic BB rats receiving no insulin, and BB rats in whom hypoglycemia was induced by the administration of excessive insulin doses. The data were compared with those of non-diabetic age- and sex-matched BB rats. Functional deficits and structural abnormalities were comparable in diabetic rats with and without insulin supplementation, suggesting that the generally necessary insulin dosing in this model does not per se account for the neuropathy. Hypoglycemic neuropathy was characterized by slowing of nerve conduction velocity, marked loss of anterior horn motoneurons and Wallerian degeneration, as well as loss of large myelinated fibers, suggesting a neuropathy involving predominantly motoneurons. Diabetic neuropathy was not associated with nerve cell loss but showed marked axonal atrophy involving predominantly sensory fibers. Thus, diabetic and hypoglycemic neuropathies are two distinguishable entities under strict experimental conditions, but may overlap in human diabetic subjects in whom tight insulin control is desirable.
Diabetes Res Clin Pract 1989 May 15
PMID:Diabetic and hypoglycemic neuropathy--a comparison in the BB rat. 275 83


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