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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The natural history of diabetic neuropathy and its risk factors are not well understood, apart from the recognition that prevalence increases with duration and, in many studies, degree of glycemia. The role of potential risk factors was therefore evaluated in a cross-sectional analysis from the baseline examination of the Pittsburgh Epidemiology of Diabetes Complications Study. We present results from the first 400 subjects seen at baseline examination. Neuropathy was determined by a trained internist with a standardized examination and was defined as the presence of at least two of three criteria: abnormal sensory or motor signs, symptoms consistent with neuropathy, and decreased tendon reflexes. The prevalence of neuropathy in this cohort was 34% (18%, 18-29 yr old, 58% greater than or equal to 30 yr old) with no difference by sex. By focusing on subjects greater than or equal to 18 yr old, all significant univariate variables (e.g., duration, glycosylated hemoglobin [HbA1]) were analyzed in 3 multiple logistic regression models: all subjects greater than or equal to 18 yr old and separating the same subjects into two groups based on age (18-29 and greater than or equal to 30 yr). Duration, HbA1, smoking status, and high-density lipoprotein cholesterol were found to be associated with neuropathy in the models for the greater than or equal to 18-yr-old group and the greater than or equal to 30-yr-old group. In the 18- to 29-yr-old group, duration, HbA1, and hypertension status were found to be significantly associated with neuropathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiological correlates of diabetic neuropathy. Report from Pittsburgh Epidemiology of Diabetes Complications Study. 262 Jul 81

The relationship between diabetic neuropathy on the one hand and microangiopathy and arteriosclerosis on the other was studied by determining plasma 6-keto-prostaglandin F1 alpha (PGF1 alpha) and plasma thromboxane B2 (TXB2) in diabetics with neuropathy. The subjects were 13 patients with insulin independent diabetes mellitus with polyneuropathy (DN+ group), 9 cases which had no neuropathy (DN- group) and 6 control cases. The patients with severe retinopathy, nephropathy and hypertension were excluded. Plasma 6-keto-PGF1 alpha and plasma TXB2 concentration were determined by radioimmunoassay. The motor neuron conduction velocity (M.C.V.) was measured through the tibial nerve in all diabetics. Plasma 6-keto-PGF1 alpha was 116.3 +/- 4.2 pg/ml (mean +/- SE) in the DN+ group and 139.9 +/- 3.0 in the DN- group, each group showing a significant fall over the control with 150.8 +/- 4.5. Plasma 6-keto-PGF1 alpha in the DN+ group showed a significant decrease in comparison with that in the DN- group. As to plasma TXB2, there was no significant difference among the three groups. The M.C.V. fell off significantly in the DN+ group with 52.9 +/- 3.2 m/sec. Furthermore, a significant positive correlation was observed between M.C.V. and plasma 6-keto-PGF1 alpha. The following is the summary of these results. A decrease in plasma 6-keto-PGF1 alpha was observed in diabetics with polyneuropathy. A decrease in the production of prostacyclin (PGI2) due to impairment of vascular endothelium in the nerve tissue was surmised. The decrease in plasma 6-keto-PGF1 alpha presumably stimulates the activity of platelet agglutination and causes an ischemic change in the nerve tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Evaluation of plasma 6-keto-prostaglandin F1 alpha and thromboxane B2 in diabetic neuropathy]. 355 71

The heart rate variability (HRV) signal carries important information about the systems controlling heat rate and blood pressure, mainly elicited by autonomic nervous system (sympathetic and parasympathetic) controls. The present paper illustrates methods of HRV signal processing by using autoregressive (AR) modeling and power spectral density estimate. The information enhanced in this way seems to be particularly sensitive in discriminating various cardiovascular pathologies (hypertension, myocardial infarction, diabetic neuropathy, etc.). This method provides a simple non-invasive analysis, based on the processing of spontaneous oscillations in heart rate. Particular emphasis is directed to the algorithms used and to their direct application by using proper computerized techniques: only a few paradigmatical examples will be illustrated as preliminary results.
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PMID:Heart rate variability signal processing: a quantitative approach as an aid to diagnosis in cardiovascular pathologies. 355 95

Serum immunoglobulin (G, A, M) levels were performed on 66 patients with non-insulin-dependent (type II) diabetes mellitus (NIDDM). When compared with 30 age-matched normal controls and 32 hospitalized controls there was no significant difference between the mean IgG and IgM levels. The IgA levels were significantly higher (P less than 0.005) in the diabetic group when compared with both control groups. This is true regardless of age, sex, duration of disease, and type of treatment (insulin/diet or oral hypoglycemic agents and/or diet). Thirty-six percent of the diabetic patients' IgA levels exceeded the mean +/- 2 SD of the normal control group. There were no significant differences in immunoglobulin levels between insulin-treated and non-insulin-treated diabetic groups. Since diabetic patients may have a number of secondary diseases, attempts were made to correlate the most common of these (acute and/or chronic bacterial infections, hypertension, arteriosclerotic heart disease, and diabetic neuropathy) with elevated IgA levels. Only IgA levels of diabetic patients with infections versus diabetic patients without infections were significantly different (P less than 0.05). However, IgA levels of uninfected diabetic patients remained significantly higher than those of normal controls (P less than 0.005), hospitalized controls (P less than 0.01), and hospitalized controls with bacterial infections (P less than 0.005). Possible reasons for the isolated elevations of IgA are discussed.
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PMID:Elevation of IgA levels in the non-insulin-dependent (type II) diabetic patient. 675 40

Investigations on the vitamin pattern of diabetic neuropathy: thiamine, riboflavin, pyridoxine, cobalamin and tocopherol. The contents of the vitamins mentioned above have been measured in the blood of 119 patients (53 diabetic neuropathies, 66 diabetics without neuropathy). The incidence of neuropathy shows a strong correlation with the duration of the diabetic state, but not with sex, nor with concomitant diseases such as adipositas, hypertension, heart and circulatory diseases, except retinopathia diabetica. Most of the diabetics in our study are well supplied with vitamins B1, B2, and E; B6 and B12 are occasionally low, but there is no statistically relevant difference between diabetic controls and neuropathies. Adipose patients have neither a markedly different vitamin content nor a different calory uptake from non-adipose patients. A general trend towards reduced total calory uptake is seen in old age, men (lower protein intake) and women (lower carbohydrate intake) obviously differing somewhat in their habits. The influence of therapy on the vitamin pattern is not clear cut, except for patients under diet and biguanide-therapy showing a higher proportion of low or subnormal B12 values. The increased frequency of neuropathies in patients treated with sulfonyl-urea approaches only the limits of significance and needs further investigations.
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PMID:[Vitamin status in diabetic neuropathy (thiamine, riboflavin, pyridoxin, cobalamin and tocopherol)]. 705 98

Erythropoietin was administered to five anemic azotemic diabetic subjects for 1 year to assess the effect of increasing red cell mass on clinical well-being and the course of renal functional decline. None of the subjects manifested worsened hypertension or cerebrovascular or cardiovascular complications despite an increase in mean hematocrit from a baseline mean of 29.6% to a mean of 39.5%. The serum creatinine concentration after 1 year of treatment with erythropoietin was 3.7 mg/dL, which was unchanged from the baseline value of 3.5 mg/dL. Plasma viscosity remained constant as red cell mass increased. Although the viscosity of whole blood rose as the hematocrit increased, it was within the range of normal blood viscosity for an equivalent hematocrit. The favorable impact of erythropoietin treatment on three diabetic subjects who had macular edema and anemia is described. One hypothesis to explain the benefit of a raised hematocrit on both diabetic nephropathy and retinopathy is that the metabolic, hormonal, and hemodynamic components of the diabetic syndrome, in concert, produce tissue and cellular hypoxia that is ameliorated in part by the greater oxygen-transporting capacity of a raised red cell mass. The pseudohypoxia of diabetes may be implicated in the pathogenesis of diabetic neuropathy, retinopathy, muscular dysfunction, and nephropathy.
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PMID:Erythropoietin in diabetic macular edema and renal insufficiency. 761 Dec 53

Previous studies have shown that the normal circadian blood pressure fall is absent in patients with diabetic autonomic neuropathy, while the reported rise in blood pressure during the night in the same patients is controversial. This study analyzed the circadian profile in 19 diabetic patients with established autonomic neuropathy. Twenty-four hour ambulatory systolic blood pressure, diastolic blood pressure, mean arterial pressure, and heart rate were recorded every 20 minutes during the day and every 60 minutes at night in 29 patients, 19 with diabetic autonomic neuropathy and 10 nondiabetic hypertensive patients as controls. Twelve diabetic patients with autonomic neuropathy with unknown hypertension were found to have hypertension based on 24 hour ambulatory blood pressure monitoring. Repeated measured analysis of variance (ANOVA) and trend analysis indicated that the linear systolic blood pressure increased from night to morning to afternoon while mean arterial pressure and diastolic blood pressure increased from night to morning but decreased from morning to afternoon. In practice, the early morning rise in systolic blood pressure in diabetic neuropathy is not different from that in normal or hypertensive patients and requires appropriate treatment. The absence of the nocturnal rise in the blood pressure revealed a subgroup of patients with diabetic neuropathy which demonstrated no fatal cardiovascular or renal events over 18 to 24 months of follow-up.
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PMID:Reassessment of circadian profile of blood pressure and heart rate in diabetic patients with autonomic neuropathy. 789 13

We prospectively determined the prevalence of morbidity from the various forms of diabetic neuropathy over one year in a population of 800 patients with diabetes mellitus (336 type 1, 464 type 2 DM). Symptoms documented were: pain/paraesthesia in the feet, loss of feeling and the restless legs syndrome. We also documented the prevalence of: neuropathic ulcers, amyotrophy, foot drop, and oculomotor palsy. Autonomic symptoms documented were: impotence, postural hypotension and diarrhoea. The only symptoms reported by 100 non-diabetic control subjects were: loss of feeling in 2% and restless legs syndrome in 7%. In the diabetics; pain/paraesthesia was present in 13%, feeling loss in 7% and neuropathic ulcers in 2%. The prevalence of Diabetic amyotrophy (proximal femoral neuropathy) was 0.8%, oculomotor palsy 0.1% and peroneal nerve palsy 0.1%. Erectile impotence was present in 20%, symptomatic postural hypotension in 1% and diabetic diarrhoea in 1%. Overall; 22.9% of the population was afflicted by one or more problems resulting from neuropathy. Neuropathy was associated with older age (p < 0.001), and serious retinopathy (p < 0.001) in both groups of diabetics and with duration of diabetes, proteinuria (p < 0.02), hypertension (p < 0.01) and ischaemic heart disease (p < 0.02) in type 1 diabetics.
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PMID:Prevalence and forms of neuropathic morbidity in 800 diabetics. 820 Jul 77

Orthostatic hypotension and related neurologic symptoms are frequently encountered in clinical practice. The maintenance of appropriate blood pressure and heart rate responses upon assuming the upright posture are dependent upon: 1. intact mechanical (venous valves) mechanisms, 2. functioning arterial and cardiopulmonary baroreceptors, 3. normal peripheral neural pathways, 4. normal central neural integration, and 5. appropriate neurohormonal secretion. Dysfunction at one or more of these loci may facilitate the occurrence of orthostatic hypotension and syncope. In general, the mechanisms of orthostatic hypotension may be divided into three categories. In the first category, processes interfere with normal compensatory responses to upright posture. Examples of this mechanism include age related autonomic changes, diabetic neuropathy and central nervous system disease such as Shy-Drager syndrome. The second principal mechanism involves overwhelming otherwise normal reflexes by an intense orthostatic stimulus. An obvious example of this mechanism is syncope related to hemorrhage. A final category of orthostatic hypotension relates to interference with reflex responses by drugs that may limit vasoconstriction, heart rate or cardiac output adjustments or exaggerate venous pooling. These are commonly used medications such as vasodilators, beta-adrenergic blockers and nitrates. The treatment of orthostatic hypotension revolves around the recognition of underlying causes or contributing factors amenable to correction or avoidance. Other helpful treatment options include nocturnal head-up tilting and mineralocorticoids, both of which help to expand blood volume. Many other therapeutic agents have been tried in small and selected patient populations, often with disappointing results. While many of the drugs available (phenylephrine, ephedrine, tyramine, dihydroergotamine) can improve upright blood pressure, side effects are common, and supine hypertension is problematic in many patients. Interventions of this type should be carefully initiated in a monitored setting. The carotid sinus is an important component of a neural control system responsible for heart rate and blood pressure homeostasis. Excessive heart rate and blood pressure responses to distortion of the carotid sinus are the basis for the carotid sinus syndrome (CSS). Patients with CSS tend to be elderly males and local pathology in the neck is frequently involved. Atherosclerotic coronary artery disease and hypertension are important clinical correlates. Two major categories of carotid sinus hypersensitivity (CSH) are recognized: cardioinhibitory and vasodepressor. Cardioinhibitory CSH is the most common, and in its purest form consists of sinus bradycardia or arrest, asystole or AV block during carotid sinus massage. This vagally-mediated response is eliminated by atropine. Cardiac pacing is nearly universally successful in preventing severe symptoms.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alterations in reflex function contributing to syncope: orthostatic hypotension, carotid sinus hypersensitivity and drug-induced dysfunction. 833 Aug 51

The prevalence of diabetic ocular complications and the correlation between diabetic retinopathy and systemic factors were examined in 2,300 cases (4,600 eyes) with non-insulin-dependent diabetes mellitus. The prevalence of cataract was 66.7%, of retinopathy 37.0%, of refractive and accommodative change 6.2%, of glaucoma 1.9% (rubeotic glaucoma was 1.0%), of rubeosis iridis 1.5%, of iridocyclitis 0.8%, of extraocular muscle palsy 0.2%, and of ischemic optic neuropathy 0.1%. Duration of diabetes mellitus, HbA1C value, methods of diabetic control, age, diabetic nephropathy, diabetic neuropathy, hypertension, systolic blood pressure, diastolic blood pressure, and arteriosclerosis obliterans were related with diabetic retinopathy. We suggest that the management of diabetic patients needs sufficient attention in the cases with oral administration of medication, insulin therapy, and diabetic nephropathy.
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PMID:[Prevalence of diabetic ocular complications and systemic factors]. 836 83


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