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

Microangiopathy is an important complication of diabetes mellitus and neovascularity is a feature of human diabetic retinopathy. The objective of this work was to evaluate numbers, areas and size distributions of whole nerve, endoneurial and dorsal root ganglia perfused microvessels in a detailed fashion using unfixed tissues from rats with experimental diabetes. Experimental neuropathy was studied in male Sprague-Dawley rats 12 weeks after streptozotocin or citrate buffer injection. Electrophysiological recordings of sciatic-tibial motor and caudal sensory fibers identified conduction slowing in diabetes indicating neuropathy. Diabetics had a rise in the numbers of whole nerve microvessels and endoneurial microvessels with associated rises in vessel densities and total vessel luminal areas. Increased vessel numbers in 15-30 microm diameter size ranges were particularly prominent. There was a rise in summed vascular areas in diabetics but the mean luminal area of vessels was not increased. Similar, but not significant trends were observed in a selective analysis of endoneurial vessels alone. In contrast, dorsal root ganglia microvessels were not increased in number. Early experimental diabetic neuropathy is associated with increased numbers of microvessels supplying the peripheral nerve trunk, likely representing neovascularity.
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PMID:Increased peripheral nerve microvessels in early experimental diabetic neuropathy: quantitative studies of nerve and dorsal root ganglia. 1046 98

Microangiopathy is the most frequent complication of diabetes mellitus. It frequently precedes metabolic and biohumoral pathology. The diabetic foot is a particular aspect of the disease. Capillary videomicroscopy has proven to be a valuable technique for detecting early morpho-functional changes in the microcirculation in vivo. It is performed at the fingers' nailfold, at conjunctiva, and on the skin. This study aims to propose a qualitative assessment of microvascular complications in elderly patients with diabetes mellitus by toe nailfold capillary microscopy.
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PMID:Diabetic Foot in the Elderly: Capillaroscopic Findings. 1062 28

Children with insulin-dependent diabetes mellitus have a lower salivary flow rate, pH and buffer capacity, but a higher glucose content and peroxidase, IgA, magnesium and calcium concentration, in comparison with healthy children. Nevertheless the incidence of caries is lower than normal in diabetic children with good metabolic control. Periodontal disease usually starts at puberty as mild gingivitis with bleeding and gingival recession, and it may develop into severe periodontitis, especially in children with poor control of diabetes. Microangiopathy, impaired immune response, different bacterial microflora and collagen metabolism are involved in the pathogenesis of diabetic periodontal disease. The gingival flora is mostly composed of Gram-negative, anaerobic bacteria, while collagen has a lower solubility and is atrophic and inadequate to support the occlusion forces. For these reasons, prevention of periodontitis is important in diabetic children; they should receive oral hygiene instruction and visit a dentist at least twice a year.
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PMID:Oral health in children and adolescents with IDDM--a review. 1070 31

The incidence of diabetes and its complications is increasing to staggering proportions. Presently the WHO estimates an overall prevalence of 130 million, but by 2025 there will be 300 million individuals with diabetes mellitus. The incidence of diabetic neuropathy approaches 50% in most diabetic populations; there is no treatment, and its consequences in the form of foot ulceration and amputation are financially punishing for health care providers. Attempts to develop treatments have faltered for want of an understanding of the aetiology of diabetic neuropathy. As a consequence, 1999 saw the demise of two further compounds: recombinant growth factor by Roche-Genentech and the aldose reductase inhibitor zopolrestat, by Pfizer, both had reached phase III clinical trials. They joined an impressive list of at least 30 other compounds which have reached phase III clinical trials and failed to establish efficacy. The need to establish a viable treatment for human diabetic neuropathy is absolutely paramount. To provide a rational answer as to whether angiotensin-converting enzyme (ACE) inhibitors can prevent human diabetic neuropathy, two major issues need addressing: 1) Does vascular dysfunction cause human diabetic neuropathy? 2) Can ACE inhibitors ameliorate diabetic vascular dysfunction and hence neuropathy? Epidemiological studies support a strong association between neuropathy, retinopathy and nephropathy. Microangiopathy is deemed as the root cause of both nephropathy, and retinopathy and mounting evidence provides support for a vascular basis of diabetic neuropathy. ACE inhibitors appear to correct many of the abnormalities associated with the vascular dysfunction found in diabetes. Thus effective ACE inhibition impacts very positively on cardiovascular outcomes in patients with ischaemic heart disease, particularly in diabetic patients. ACE inhibition also prevents the development and progression of incipient and established diabetic nephropathy and delays progression of background retinopathy. Quinapril improves measures of diabetic autonomic neuropathy. Our recent study has demonstrated a significant improvement in peripheral neuropathy following 12 months of treatment with the ACE inhibitor trandolapril.
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PMID:Can diabetic neuropathy be prevented by angiotensin-converting enzyme inhibitors? 1071 71

Children with insulin-dependent diabetes mellitus have a lower salivary flow rate, pH and buffer capacity, but a higher glucose content and peroxidase, IgA, magnesium and calcium concentration, in comparison with healthy children. Nevertheless the incidence of caries is lower than normal in diabetic children with good metabolic control. Periodontal disease usually starts at puberty as mild gingivitis with bleeding and gingival recession, and it may develop into severe periodontitis, especially in children with poor control of diabetes. Microangiopathy, impaired immune response, different bacterial microflora and collagen metabolism are involved in the pathogenesis of diabetic periodontal disease. The gingival flora is mostly composed of Gram-negative, anaerobic bacteria, while collagen has a lower solubility and is atrophic and inadequate to support the occlusion forces. For these reasons, prevention of periodontitis is important in diabetic children; they should receive oral hygiene instruction and visit a dentist at least twice a year.
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PMID:Oral health in children and adolescents with IDDM--a review. 1085 89

Diabetes mellitus is a metabolic disorder characterized by hyperglycemia and associated with a high incidence of complications affecting both the microvascular and the macrovascular systems. Macrovascular disease affects the coronary arteries, the cerebral vessels, and the large peripheral arteries of the lower extremities. Microangiopathy affects the kidneys, eyes, and nerves. Both forms of complication are major causes of death and disability in diabetes. The precise pathophysiology of these vascular complications is becoming better understood, but specific treatment and prevention remain complex.
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PMID:Protection from vascular risk in diabetic hypertension. 1098 Nov 42

The aim of this study was to evaluate the cochlear micromechanics in type 1 diabetic patients and to compare these findings with diabetic microvascular complications (retinopathy and nephropathy). Cochlear activity was evaluated by recording 2f1-f2 DPOAE. DPOAEs were performed using an ILO92 Otodynamics Ltd Analyser. DPOAEs were measured in 42 normally hearing IDDM patients aged between 21 and 42 years, and 33 age-and sex-matched non-diabetic control subjects. IDDM patients were divided into two groups: 17 patients without microangiopathy and 25 with microangiopathy. Microangiopathy was evaluated with ophthalmoscopy and 24-hour albumin excretion rate into urine. Both groups (diabetic and control) had normal and undifferentiated results in tonal and impedance audiometry. The mean amplitudes of various DPOAEs were significantly reduced in the diabetic groups (with and without microangiopathy) compared with control subjects. No correlation was found between diabetic microvascular complications and DPOAE amplitudes reduction. Our results indicate the existence of an alteration in cochlear micromechanics in diabetic patients with microangiopathy as well as in patients without microangiopathy. The lack of significant correlation between the degree of microvascular complications in the retina or kidneys and DPOAEs amplitude reduction suggest that the impaired functional properties of the outer hair cells are probably caused by early metabolic complications in diabetes (among other things non-enzymatic glycation related to hyperactivity of free oxygen radicals) and not directly by diabetic microangiopathy.
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PMID:Cochlear dysfunction and diabetic microangiopathy. 1131 68

To measure erythrocyte deformability in vitro, we made transparent microchannels on a crystal substrate as a capillary model. We observed axisymmetrically deformed erythrocytes and defined a deformation index directly from individual flowing erythrocytes. By appropriate choice of channel width and erythrocyte velocity, we could observe erythrocytes deforming to a parachute-like shape similar to that occurring in capillaries. The flowing erythrocytes magnified 200-fold through microscopy were recorded with an image-intensified high-speed video camera system. The sensitivity of deformability measurement was confirmed by comparing the deformation index in healthy controls with erythrocytes whose membranes were hardened by glutaraldehyde. We confirmed that the crystal microchannel system is a valuable tool for erythrocyte deformability measurement. Microangiopathy is a characteristic complication of diabetes mellitus. A decrease in erythrocyte deformability may be part of the cause of this complication. In order to identify the difference in erythrocyte deformability between control and diabetic erythrocytes, we measured erythrocyte deformability using transparent crystal microchannels and a high-speed video camera system. The deformability of diabetic erythrocytes was indeed measurably lower than that of erythrocytes in healthy controls. This result suggests that impaired deformability in diabetic erythrocytes can cause altered viscosity and increase the shear stress on the microvessel wall.
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PMID:Direct measurement of erythrocyte deformability in diabetes mellitus with a transparent microchannel capillary model and high-speed video camera system. 1133 34

Localized lesions at the foot skeleton are a serious and well recognized complication of diabetes mellitus which may impair the clinical outcome of the patients remarkably. In contrast, the presence of a generalized bone disease or osteoporosis related to diabetes mellitus is less acknowledged and its clinical relevance is less obvious. This paper is a clinically focused review of the literature on osteoporosis related to diabetes mellitus. Due to the different pathogenesis of diabetes mellitus type 1 and type 2 it is not surprising that there is no uniform entity of diabetic osteopathy. The majority of clinical studies in subjects with diabetes mellitus type 1 showed a moderately decreased bone mass at the forearm, while bone mass at the femur or lumbar spine was either decreased or not different from non-diabetic controls. In patients with diabetes mellitus type 2 the risk of osteopenia is not as clear as in type 1 diabetes. Bone mineral density at the forearm in patients with type 2 diabetes mellitus was decreased, unchanged or even increased in comparison to controls, while bone mineral density at the vertebrae or femoral neck was either not significantly different or increased, but rarely decreased. The underlying mechanisms triggering changes in bone mass in patients with diabetes mellitus type 1 and type 2 are not well known. In most studies there was no consistent relationship between the metabolic control of diabetes and bone mineral density. Biochemical parameters of the calcium and bone metabolism showed no clear relationship to the bone mineral density measurements. From few bone histology studies in humans and experimental studies there is evidence that a decreased bone formation is one major mechanism leading to reduced bone mass in diabetics. Microangiopathy at the bone tissue was also discussed as a possible reason for diabetic osteopenia. It was shown that insulin and insulin like growth factors (IGF-1, IGF-2) have an influence on bone metabolism itself and other growth factors, cytokines and hormones may determine changes in diabetic bone metabolism. Recent findings suggest that leptin is involved in the regulation of osteoblast function and bone mass, which is of special interest in diabetes mellitus type 2. The clinical relevance of osteoporosis or osteopenia is determined by the increased risk for insufficiency fractures. Few studies found an increased fracture risk, especially in older women with type 1 diabetes mellitus, while others did not show an increased risk for fractures or even found a decreased rate of fractures in women with diabetes mellitus type 2. There is a need for further longitudinal studies, including the incidence and risk factors for osteoporotic fractures. In clinical routine the extent of diagnostic and therapeutic activities in patients with type 1 or type 2 diabetes mellitus in respect to generalized bone disease or diabetic osteopenia should be based on individual conditions and risk profile for osteoporosis.
Exp Clin Endocrinol Diabetes 2001
PMID:Diabetes mellitus a risk for osteoporosis? 1146 May 94

The aim of this study was to evaluate the relations between left ventricular (LV) functional abnormalities, microangiopathy, and autonomic dysfunction in patients with non-insulin-dependent diabetes mellitus (NIDDM). We studied 66 normotensive patients with NIDDM of > or =4 years' duration (age, 51 +/- 4.5 years; 35 men) and no clinical evidence of cardiac disease. Twenty-one healthy subjects matched for age and sex served as a control group. Echocardiography and Doppler studies were performed to assess LV systolic and diastolic function. Microangiopathy was assessed by fundus examination. Autonomic function was assessed by standing blood pressure and heart rate response to Valsalva maneuver. Patients with NIDDM had a lower ejection fraction (58% +/- 11% versus 66% +/- 4%, P <.0001), E-F deceleration slope (382 +/- 75 versus 427 +/- 31 cm/s(2), P <.05), and E velocity (55 +/- 11 vs. 58 +/- 6 cm/s, P =.02) of the mitral diastolic flow, compared with control subjects, respectively. Patients with ejection fraction <50% had a higher prevalence of retinopathy (65% versus 29%, P <.005), abnormal blood pressure response to standing (53% versus 8%, P <.0005), and proteinuria (65% versus 27%, P =.006). An inverse correlation was found between the duration of diabetes and both the ejection fraction (r = -0.53, P <.05) and E/A ratio (r = -0.4, P <.005). E/A ratio <1 was associated with a higher prevalence of retinopathy (49% versus 20%, P =.01) and abnormal blood pressure response to standing (29% versus 4%, P <.005). Patients with NIDDM and no symptoms of cardiovascular disease have a reduced LV systolic and diastolic function as compared with healthy subjects. LV systolic and diastolic abnormalities are correlated with the duration of diabetes and with other diabetic microangiopathies such as diabetic retinopathy and neuropathy.
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PMID:Left ventricular systolic and diastolic functional abnormalities in asymptomatic patients with non-insulin-dependent diabetes mellitus. 1154 74


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