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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medical care of arteriopathy of leg in a diabetic patient involves control of diabetes combined with a series of non specific measures applicable to all atheromatous arteriopathies. Allowance must be made for the often silent nature of the arterial lesion, explicable by the associated peripheral neuropathy and the site of the lesions, generally more distal or staged than in non diabetics. A stable blood sugar level must be obtained to provoke improvement in hemorrheologic parameters and to slow the atheromatous process. A dietary regimen is associated with oral hypoglycemic agents or insulin therapy, the latter systematically for trophic disorders, administered as multiple injections or by insulin pump until complete healing is obtained. Insulin therapy normalizes abnormal blood lipid levels secondary to an uncontrolled diabetes. Other vascular risk factors (primary hyperlipoproteinemia, hypertension, smoking) must be allowed for. Of major importance in these patients at risk are foot hygiene, prevention of local trauma and correction of plantar anomalies. Aggravating factors in patients with arteritis are diabetic neuropathy and foot deformities. Regular walking is encouraged. Drug therapy (oral or injectable vasoactive agents, platelet antiaggregants, prostacyclin, normal blood volume restoration) depends on the severity of the arteriopathy and any complications. Analgesics are often required in advanced stages. Local therapy and sometimes antibiotics are necessary for trophic disorders. The frequent asymptomatic character up to the stage of gangrene should not, because of the diabetic diathesis, induce a wait and see attitude, and revascularization by angioplasty or shunt operation should be envisaged. A frequent complication of sugar diabetes, arteriopathy of the leg should be diagnosed early before it is revealed by a gangrenous lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Medical treatment of diabetic arteriopathy]. 847 10

Hypertension is a common comorbidity with non-insulin-dependent diabetes mellitus (NIDDM). Data are somewhat inconsistent as to whether hypertension exacerbates diabetic complications in this population. Therefore, we examined the relationship between hypertension and vascular complications of NIDDM in the 950 patients enrolled in the prospective and randomized Appropriate Blood Pressure Control in Diabetes (ABCD) study. We found both systolic and diastolic hypertension to be associated with diabetic nephropathy (P < .001) as well as with its macrovascular complications (P < .05). Our present results also demonstrated that there was a significant relationship between hypertension and peripheral vascular disease (P < .05), and left ventricular hypertrophy (P < .001). There was, however, no apparent relationship between hypertension and diabetic neuropathy. Thus, arterial pressure may be a major determinant of complications in NIDDM.
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PMID:Associations of hypertension and complications in non-insulin-dependent diabetes mellitus. 903 22

The pathogeneses of diabetic neuropathy is still unclear. This study prospectively investigated the risk factors for distal symmetrical polyneuropathy (DSP) in a cohort of childhood-onset IDDM patients. Subjects from the Epidemiology of Diabetes Complications (EDC) Study were clinically examined at baseline and then biennially. DSP was diagnosed by a combination of clinical criteria, symptoms and signs (Diabetes Control and Complications Trial [DCCT] exam), and quantitative sensory threshold (QST). Among the 463 (70.4%) subjects who were free of DSP at baseline, 453 (97.8%) participated in at least one biennial reexamination during the first 6 years of follow-up and were included in the current analysis. A total of 68 (15.0%) subjects developed DSP in 6 years, giving a cumulative probability of 0.29. The Cox proportional hazards model shows that longer IDDM duration, hypertension, poor glycemic control, height, and smoking were all independent predictors of the incidence of DSP (all P < 0.0001, except for smoking for which P = 0.03). Hypertension showed the greatest impact on the development of DSP for individuals with either short or long IDDM duration. This study confirms some risk factors for DSP found in cross-sectional studies and suggests a strong relationship between hypertension and DSP. The results indicate that in addition to good glycemic control, avoidance of smoking and good blood pressure control may be helpful in preventing or delaying the onset of DSP in IDDM patients.
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PMID:Hypertension as a risk factor for diabetic neuropathy: a prospective study. 907 9

Although simultaneous pancreas and kidney transplantation (SPK) achieves normoglycemia and correction of uremia in type I diabetic patients with renal failure, little data are available on long-term outcome and clinical determinants of recovery of peripheral neuropathy. In this prospective study, 219 electrophysiological studies using a standardized protocol were performed before and up to 8 years after SPK in 44 patients. Nine control diabetic recipients with functioning kidney but nonfunctioning pancreas transplants were studied on 35 occasions. Patients were 38.5+/-7.9 years old (mean+/-SD) with pretransplant diabetes present for 25.2+/-7.6 years. Significant polyneuropathy (total nerve conduction scores [NCS] <-1.0) was present in 89% before transplantation, which correlated with body weight (r=0.628, P<0.001). Two distinct patterns of neurological recovery were observed after SPK. Conduction velocity (CV) improved in a biphasic pattern, with a rapid initial recovery followed by subsequent stabilization. In contrast, the recovery of nerve amplitude was monophasic, and continued to improve for up to 8 years. Initial improvement in NCS was primarily due to an increase in CV (P=0.002 vs. baseline), and was best in shorter and younger patients. Recovery of total NCS at 6 months after SPK, assessed by multivariate analysis, was least in obese recipients and when performed in patients who had started dialysis before SPK, and was associated with lower transplant kidney isotopic glomerular filtration rate and HLA mismatch (P<0.05 to 0.001). Subsequent improvement was associated with less severe initial neuropathy, smaller body weight, and longer duration of diabetes (P<0.01 to 0.001). Fasting hyperinsulinemia was associated with impairment of initial recovery and subsequent NCS after SPK, but was worse in the control group. Recovery of nerve action potential amplitudes was predicted by better initial amplitudes and HLA mismatch, lower body weight, and the use of nifedipine (P<0.05 to 0.001). Nifedipine was used for hypertension in 33% of SPK and was associated with better CV and amplitudes, particularly in the upper limbs, where there was less neuropathy. The use of angiotensin-converting enzyme inhibitors also appeared beneficial, but this was confined to the lower limbs. SPK resulted in a gradual, sustained, and late improvement in nerve action potential amplitudes, consistent with axonal regeneration and partial reversal of diabetic neuropathy. These data suggest that early transplantation of uremic diabetic patients before onset of severe neuropathy, minimizing obesity and optimizing renal transplant function, maximizes neurological recovery after SPK. Furthermore, the preliminary data support randomized clinical trials for evaluation of nifedipine and angiotensin-converting enzyme inhibitors in diabetic neuropathy.
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PMID:Diabetic neuropathy after pancreas transplantation: determinants of recovery. 908 22

Living skin equivalents are the combination of the bioengineering and tissue-transplantation sciences. Their uses have applications in aiding wound healing for ulcerations caused by thermal injury, diabetic neuropathy, venous hypertension, and pressure. Products can be divided into keratinocyte sheets, dermal replacements, or composite material. Past and current studies give the Food and Drug Administration and health care providers valuable data relating to these products' efficacy in the wound healing arena.
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PMID:Living skin equivalents and their application in wound healing. 946 74

A large epidemiological study has documented that one-third of diabetic patients have peripheral neuropathy. Diabetes duration, poor glycaemic control, smoking and hypertension are all independent predictors of the incidence of diabetic polyneuropathy. High prevalence of autonomic dysfunctions, both sympathetic and parasympathetic, has been found in patients with nonalcoholic chronic liver disease. The pathogenesis of metabolic neuropathy is unclear; even immunologic factors might play a role in the development of diabetic autonomic neuropathy. No specific treatments are available for these neuropathies. Correction of metabolic derangement is fundamental, as shown by the amelioration of peripheral nerve function obtained after successful simultaneous pancreas-kidney transplantation. The therapeuthic potentials of neurotrophins for the prevention and treatment of diabetic neuropathy have to be confirmed in future studies.
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PMID:Metabolic neuropathies. 984 2

This review describes the cerebral complications of diabetes mellitus from a neuropsychological, neurophysiological and neuroradiological perspective. In addition, possible pathogenetic mechanisms are discussed. Neuropsychological studies of diabetic patients generally report modest deficits in learning and memory and information processing. Notably, in elderly diabetic patients cognitive deficits may be more prominent. Recent epidemiological studies show that in the elderly diabetes is associated with an increased risk for dementia. Neurophysiological studies show increased latencies of evoked potentials and event-related potentials. Neuroradiological findings are enhanced peripheral and central cerebral atrophy, as well as focal lesions. The pathophysiology of the effects of diabetes on the brain has not been fully elucidated. The putative involvement of cerebral metabolic and microvascular disturbances, similar to those implicated in the pathogenesis of peripheral diabetic neuropathy, is discussed. In addition, the role of repeated hypoglycaemic episodes, cerebrovascular disease and hypertension is addressed. Finally, the potential differential effects of insulin dependent and non-insulin dependent diabetes on the brain are discussed, as well as possible links with brain ageing.
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PMID:Cerebral complications of diabetes: clinical findings and pathogenetic mechanisms. 1007 78

The aim of our study was to estimate selected parameters of hemostasis and fibrinolysis in diabetic patients with vascular complications and obesity. The investigation was carried out in 23 type 1 diabetic subjects aged 17-56 ys, in 25 type 2 diabetic patients aged 41-69 ys and in 38 healthy persons: 16 "young"--aged 32.5 +/- 13.2 ys and 22 "old"--aged 56.2 +/- 9.4 ys. The following parameters were determined: glycaemia, HbA1c, blood level fibrinogen, euglobulin clot lysis time, plasminogen activator inhibitor (PAI-1) activity, microalbuminuria, triglyceride, total, HDL- and LDL-cholesterol concentration. Plasma fibrinogen level was elevated in type 2 diabetic subjects, and the highest concentrations were noted in patients with retinopathy or arterial hypertension, in overweight persons and--surprisingly--in type 1 diabetic subjects with nephropathy and coronary vascular disease (CVD). There were also positive correlations between fibrinogen level and systolic blood pressure (r = 0.3413, p < 0.02), diastolic blood pressure (r = 0.3809, p < 0.002) and microalbuminuria (r = 0.3552, p < 0.05). The mean euglobulin clot lysis time was prolonged in type II diabetics in comparison to the control group, especially in obese subjects. The highest activity of PAI-1 was found in overweight controls (28.87 +/- 6.24 Au/ml, p < 0.002). PAI-1 activity was also slightly increased in type 1 diabetic patients, especially with the symptoms of diabetic neuropathy, nephropathy or CHD, in comparison to the other groups. Our results seem to confirm the disturbed balance between coagulation and fibrinolysis--towards and increased risk of a prothrombotic state --in both--obese and diabetic patients--especially with advanced vascular complications.
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PMID:[Some parameters of hemostasis and fibrinolysis in diabetic patients]. 1010 28

Diabetes mellitus causes profound alterations in many body tissues. Microvascular diabetic complications include diabetic neuropathy, nephropathy and retinopathy. Nephropathy first becomes manifest with hyperfiltration and microalbuminuria. These functional changes evolve over several years to a stage of marked deterioration of renal function. The possible preventive measures are metabolic control, reduction of dietary protein intake and use of ACE-inhibitors. Metabolic control is also important for the prevention of diabetic retinopathy. In fact, patients with HbA1c higher than 10% have an increased risk of progression of retinopathy. Moreover, an accelerated progression of retinopathy has been observed in patients with systemic hypertension following the onset of microalbuminuria. It has been demonstrated that diabetic neuropathy can also be present during childhood; therefore, it is possible to detect electrophysiological abnormalities in children and adolescents with IDDM. Glycaemic and blood pressure control are, so far, the main means for possible prevention or modification of the natural history of diabetic microvascular complications. Tight glycaemic control may have beneficial effects for diabetic neuropathy. In addition, other preventive measures, such as aldose reductase inhibitors, gangliosides, neurotrophic vitamins, etc., have been studied in the last years. However, no conclusive results have been obtained so far.
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PMID:Prevention of microvascular complications in diabetic children and adolescents. 1019 52

Hypertension has been proposed as an independent risk factor for diabetic neuropathy. In insulin-dependent diabetic (IDDM) patients suffering from neuropathy, red blood cell (RBC) Na/K ATPase is decreased. Such a decrease might be involved in the physiopathology of hypertension and therefore be the link between hypertension and neuropathy. To confirm this hypothesis, we studied 104 IDDM patients with a long duration of disease by looking at the association between neuropathy and hypertension and by comparing RBC Na/K ATPase activity in subgroups. The independent risk factors associated with neuropathy were hypertension, triglyceride level, diabetes duration and low RBC Na/K ATPase activity. Contrary to our expectations, Na/K ATPase was not decreased in hypertensive patients (294 +/- 16 nmol Pi/mg prot/h vs 303 +/- 9), but those treated with angiotensin converting enzyme (ACE) inhibitor had higher RBC Na/K ATPase activity than those treated with calcium blockers (355 +/- 15 nmol Pi/mg prot/h vs 216 +/- 10). These results confirm the association between neuropathy and hypertension, on the one hand, and neuropathy and decreased Na/K ATPase, on the other, and show that hypertension in IDDM patients was not associated with decreased RBC Na/K ATPase. Moreover, ACE inhibitor treatment in IDDM patients, whether hypertensive or not, was associated with higher levels of RBC Na/K ATPase, which could account for its beneficial effect on diabetic neuropathy.
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PMID:Relationship between neuropathy, hypertension and red blood cell Na/K ATPase in patients with insulin-dependent diabetes mellitus. 1033 22


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