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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

A double blind placebo controlled trial was performed to evaluate the effects of the aldose reductase inhibitor, ponalrestat, on symptomatic diabetic neuropathy. After a 4-week placebo run-in phase, 60 patients were 2:1 randomized to receive either 600 mg ponalrestat or placebo once daily over 12 months. Forty-six patients, 30 of whom were treated with ponalrestat and 16 with placebo, completed the study. Motor and sensory nerve conduction, thermal and vibration sensation thresholds, heart rate variation at rest, E/I ratio, pupillary dilation velocity and pupillary reflex latency were determined at baseline and after 6 and 12 months. Neuropathic symptom scores were assessed every 3 months. Among the fifteen nerve function parameters studied, only trends in favour of ponalrestat were noted for heart rate variation and E/I ratio after 6 months (P = 0.06), but no significant differences between the groups could be demonstrated during the study. No adverse reactions were observed. It is concluded that one-year treatment with ponalrestat has no beneficial effects on symptoms or electrophysiological parameters in diabetic neuropathy.
Diabetes Res Clin Pract 1991 Oct
PMID:One-year treatment with the aldose reductase inhibitor, ponalrestat, in diabetic neuropathy. 174 64

Quantitative light and electronmicroscopical morphometric techniques were used to determine the effect of pancreatic islet transplantation on experimental diabetic neuropathy. Groups of STZ-diabetic rats were given islet transplants at 3 weeks after diabetes onset (prevention) and at 6 months after diabetes onset (reversal). Comparisons were made with onset controls, age-matched non-diabetic controls and untreated diabetic controls 6 months later (n = 8 for all groups). Euglycaemia and normal levels of glycosylated haemoglobin were achieved in both groups of diabetics after islet transplantation. Loss of body weight in diabetic animals was prevented by early islet transplantation, but was only partially reversed following delayed islet transplantation. Normal growth of myelinated fibres and axons during development was retarded in untreated diabetics, but was normal in rats given islet transplants soon after the onset of diabetes (cross-sectional perimeter and area). Diabetics transplanted with islets after a delay had myelinated fibres and axons with diminished calibre. Teased fibre preparations of nerves from diabetics which had received islet transplants showed no excess of abnormalities. This study has shown that the development of certain structural abnormalities of peripheral nerve fibres is prevented in diabetic rats which receive transplants of islets of Langerhans soon after the onset of diabetes. However, once established abnormal fibre morphology can not be completely ameliorated merely by achieving and sustaining euglycaemia through delayed islet transplantation.
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PMID:The effect of pancreatic islet transplantation on experimental diabetic neuropathy. 175 93

Peripheral small-fibre denervation has been reported to result in decreased activation of eccrine sweat glands to muscarinic cholinergic agents. Using computerised image-analysis of pilocarpine-activated sweatspot prints of a 4 cm2 area of the dorsum of the foot in 79 randomly selected diabetic patients we have identified a group of neuropathic patients (18%) with decreased sweatspot activation (less than 20/cm2), and a smaller group (6%) of younger patients with less marked neuropathy who had increased activation (greater than 132/cm2), probably resulting from denervation supersensitivity. The associations between sweatspot density and other conventional tests of peripheral nerve function were weak. The prevalence of abnormal sweatspot density, 24%, was similar to that of other tests, except thermal thresholds at the feet (35-37%), which were not correlated with sweatspot activation, suggesting that diabetic neuropathy has differing effects on afferent and efferent small fibres. The method is rapid and reproducible (median coefficient of variation 14%) and its ability to identify patients with increased, as well as decreased, peripheral nerve function may be of value in the characterisation and longitudinal follow-up of small-fibre abnormalities in diabetes.
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PMID:Changes in cholinergic sweat gland activation in diabetic neuropathy identified by computerised sweatspot analysis. 176 39

We report the results of a study of serum antibodies to proteins of the nerve cytoskeleton in patients with Type I and Type II diabetes mellitus, both with and without clinical signs of diabetic neuropathy. In contrast to previous reports, elevated levels of antibody to tubulin or glycated tubulin were not associated with either diabetes or diabetes with related neuropathy. Similarly, clinical evidence of neuropathy in patients with diabetes did not relate to increased levels of antibody to native or glycated microtubule-associated proteins (MAPs). The levels of antibody to MAPs and glycated MAPs were higher in control subjects over the age of 45 years compared with younger control subjects. Increased levels of antibody to tubulin and glycated tubulin were found in the sera of patients with systemic lupus erythematosus, but not rheumatoid arthritis.
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PMID:Antibodies to tubulin and microtubule-associated proteins. A study in diabetes mellitus, systemic lupus erythematosus, and rheumatoid arthritis. 177 91

A 46-year-old man, presenting with headache, nausea, and lassitude, was diagnosed as having diabetes mellitus and hyponatremia, and admitted to Tohoku University Hospital. Insulin treatment improved the hyperglycemia but aggravated hyponatremia, which was proved to be elicited by the inappropriate secretion of antidiuretic hormone (SIADH). An acute water load failed to suppress ADH release in the supine posture but slightly increased plasma atrial natriuretic peptide (ANP). On the other hand, plasma ADH markedly increased in response to an upright posture, accompanied by a fall in blood pressure and a rise in heart rate. After treatment with droxidopa "a sympathomimetic drug", ambulatory blood pressure gradually increased and hyponatremia disappeared. However, blood pressure and ADH responses to upright posture were not improved by treatment with the drug. Moreover, plasma ADH was still not sufficiently suppressed by acute water loading in the supine position, but plasma ANP markedly increased, thereby resulting in urinary dilution and natriuresis. These results suggest that exaggerated ADH release (SIADH) was brought about by the baroreceptor reflex stimulated by the postural hypotension, and also by the impaired osmoregulation associated with diabetic neuropathy, and that droxidopa improved cardiovascular function and increased ANP release with resultant urinary dilution and natriuresis in spite of slightly increased ADH release.
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PMID:A case of syndrome of inappropriate secretion of antidiuretic hormone associated with diabetes mellitus. 179 39

This interactive demonstration provides a model for integrating information in a medical facility. By the use of networking computers, diagnostic data and scientific data are shared between geographically-separated clinical and research units. Data collected in a patient database in the outpatient clinic is sorted on specified qualifying criteria and the resulting subset further analyzed for research studies. To show the process of patient selection from a general database to a diabetes database, and further selection to a subset of diabetes, i.e., Diabetic Neuropathy, the authors used HyperCard. Firstly, HyperCard provided us with a flexible design allowing for both vertical and horizontal progressions. Because we wanted to include an educational component on diabetes and its complications, this flexibility was important. At any point in the demonstration, the viewer is able to access more information nested in several levels. Secondly, we wanted to be able to import a variety of programs that are used to translate diagnostic data into scientific data that is analyzed and prepared for publication in a medical textbook or journal. According to Douglas Adams, author of "Pathways and Relationships", HyperCard occupies the same niche in the evolution of software as human beings do in the evolution of life. "It's the fact that we are unspecialized but infinitely adaptable that has been our success as a species. In the same way, HyperCard is unspecialized but can turn its hand to any kind of task. And if the task is beyond it, HyperCard can use the phone, go for a ride on Excel, or go out and find a powerful graphics tool or sophisticated wordprocessing program!"
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PMID:"Medical informatics in a medical research facility. An interactive multimedia presentation". Diabetes as a model. 180 37

Abnormalities of eccrine sweating are thought to be common in diabetes. We describe a ventilated-capsule sudorometer for the continuous measurement of basal and stimulated sweat secretion. It is sensitive (detecting as little as 200 ng water vapour), precise, and stable. Since it measures dewpoint rather than relative humidity, it can be calibrated to read sweat volumes directly and independently of ambient temperature and humidity. Preliminary studies using this technique show that basal skin water loss is significantly diminished in patients with established diabetic neuropathy (0.91 +/- 0.18 g (+/- SD) cm-2 h-1) compared with normal subjects (1.21 +/- 0.39 g cm-2 h-1; p = 0.04) and non-neuropathic diabetic subjects (1.32 +/- 0.48 g cm-2 h-1; p = 0.04), and that local sweating induced by iontophoresis of 10 g l-1 acetylcholine is significantly reduced in diabetic subjects up to 5 min of recording (0.95 +/- 0.43 vs 1.26 +/- 0.40 mg; p = 0.02). In neuropathic subjects both low- and high-amplitude responses are seen, the latter probably representing denervation supersensitivity. Further studies with sensitive sudorometry should enable the mechanisms of these abnormal responses to be established.
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PMID:Assessment of basal and stimulated sweating in diabetes using a direct-reading computerized sudorometer. 182 65

A personal series of 6780 patients with diabetes mellitus is reported. Of these 1410 were thought to have insulin-dependent (Type 1) diabetes and 4926 non-insulin-dependent (Type 2) diabetes. Among the former, 128 patients were only diagnosed when in severe ketoacidosis or coma. In 116 patients the diabetes was diagnosed in pregnancy. Chronic alcoholism was an aetiological factor in 75 patients; in 52 it led to the diagnosis being made, and it complicated treatment in 129 additional patients. In the patients with Type 2 diabetes whose treatment was stabilized 23.5% were having insulin injections, 44.5% tablets, and 32.0% diet only. Sight-threatening retinopathy developed in 21.3% of patients with Type 1 and 7.9% of those with Type 2 diabetes. The rate of developing sight-threatening retinopathy was 1.1% of patients per year. Blindness occurred in 0.28% of patients with Type 1 diabetes per year and 0.097% per year in Type 2 diabetes. If the mean survival of patients with retinopathy going blind is 7.5 years, this would mean 7500 people in the UK blind from diabetic retinopathy. There was a striking drop in the annual incidence of blindness after 1970 coinciding with the introduction of specific treatment for diabetic retinopathy. Juvenile cataract developed in 1.7% of patients who developed Type 1 diabetes before 30 years of age. Clinically important diabetic neuropathy developed in 17.4% of patients with Type 1 and 11.6% of those with Type 2 diabetes. The main features were paraesthesiae and numbness (49%), neuropathic ulceration (37%), pain (5%), autonomic symptoms (5%), and amyotrophy (4%). Oculomotor palsies and mononeuropathies were noted. Foot ulceration occurred in 81 patients with Type 1 and 279 of those with Type 2 diabetes. Charcot changes in the feet were noted in 21 patients. Major amputations were needed in 18 patients with Type 1 and 60 with Type 2 diabetes. Proteinuria believed to be due to diabetic nephropathy developed in 12.8% of patients with Type 1 and 4.7% of those with Type 2 diabetes. The prevalence of early renal failure was 4.6% and 1.4%, respectively. Coronary artery disease was noted in 9% of patients with Type 1 diabetes, and was more common in those who developed diabetes after 20 years of age. Myocardial infarction was as common in women as in men. In Type 2 diabetes coronary artery disease gave rise to symptoms in 19.1%, and myocardial infarction was more common in men.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diabetes in the United Kingdom: a personal series. 182 47


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