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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two-hundred-and-two impotent diabetic patients gave their consent to be investigated. Impotence is linked to diabetes mellitus in 58.9% of patients so all the other etiologies have to be systematically eliminated. Neuropathy or arteriopathy, when isolated, are found with the same frequency, but these 2 etiologies are often associated (47 patients). No statistical difference between IDDM and NIDDM was found. Mercury strain gauge plethysmography and venous occlusion coupled to ECG allows detection of arterial lesions in diabetic impotence. Patients agreed to submit to all of the various therapeutic possibilities. Combination of alpha-blockade and good glycemic control induced the best results.
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PMID:[Impotence in the diabetic]. 275 49

Data from the clinical charts of 44 diabetic patients with oculomotor palsy were studied. The sixth cranial nerve was involved in 55 p. 100 of cases, the third in 39 p. 100 and the fourth in 6 p. 100 of cases. Forty three patients had type II diabetes mellitus; in 19 the oculomotor palsy revealed diabetes, while in 25 patients diabetes mellitus had been diagnosed for 9.5 +/- 6.2 years. The oculomotor palsy resolved within an average of 93 days on average (range 156-39 days). Twenty eight patients had arterial hypertension and 23 ischemic cardiopathy of peripheral arteriopathy. There appeared to be no correlation between oculomotor palsy and the quality of glycemia control, renal function, the presence of diabetic retinopathy, or other diabetic neurological complications.
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PMID:[Paralysis of oculomotor nerves in diabetes mellitus. A retrospective study of 44 cases]. 802 75

The clinical characteristics of 132 diabetic patients referred for treatment of foot lesions were surveyed. One hundred and sixty three lesions (n=163) concerned 88 men and 44 women during a five-year period (from January 1989 to December 1993). Hospitalisation rate equalled 9.16%, i.e. 11.17% for men and 6.82% for women (p <0.001); the men/women ratio was 1.64. Eighty nine per cent (89%) of patients presented type 2 diabetes and 11% of patients type 1 diabetes. Mean age at the first foot lesion was 59.64 +/- 11.74 years. The mean duration of diabetes was 10.95 +/- 6.80 years. The patients had a high prevalence of diabetic complications, particularly peripheral neuropathy (84.85%) and obvious peripheral arteriopathy (78.78%). Infection was almost constant. There was no significant difference between men and women as far as the prevalence of complications was concerned. Smoking habits were noticed only in men. Inadequate footwear was considered as the major exogenous risk factor leading to a foot lesion. The definitive results 6 months after hospitalisation were as follows: the death rate was 9.09% (n=2; 11 men and 1 women, NS); 15.90% of patients (n=12) underwent a major amputation (4 at the level of the thigh, 17 at the level of the leg), 14.39% of patients (n=19) underwent a minor amputation; in 59.09% of patients (n=78) there was no amputation. Two patients (1.51%) underwent two consecutive amputations, left hospital against medical advice during their second hospitalisation, and then were lost sight. The prevalence of foot lesions was more important in men. Moreover, seriousness of the lesions and consequently the rate of amputations were important in men; this was probably due to smoking habits. The factors that influence the outcome seem to be: male gender, delay of management, quality of medical treatment, surgical attitude, inadequate level of amputation and finally lack of structured prevention. Prevention then should be based on the patient's education, general practitioners' training and a better and more efficient cooperation between surgeons and diabetologists.
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PMID:Diabetic foot lesions: etiologic and prognostic factors. 1080 25

In Africa, a rise in complications of diabetes mellitus has gone in hand with the growing disease prevalence, clearly demonstrating the importance of assessing complications. Diabetes mellitus constitutes a major financial burden in developing countries in Africa with relatively limited resources. Ketoacidosis is observed in 24% of juvenile diabetes and is the inaugural sign in 76% of all cases, progressing to coma in 34%. Even in type 2 diabetes, acidoketosis occurs in 34% of the cases. Infection is particularly frequent and is often fatal in tropical Africa because of the involvement of Staphyococcus and Gram-negative microorganisms. Hyperleukocytosis and anemia are correlated with ineffective antibiotic therapy. Pulmonary tuberculosis is the ninth most frequent complication of diabetes. Overall mortality is 14.9 per 1000 person-years of diabetes. Mean age at death is 51.6 years for women and 57.6 years for men after a mean 12.5 year disease duration. Thirty percent of all deaths result from acute metabolic complications, infections and stroke. More than half of the patients with insulin-dependent-diabetes have retinopathy. Differences observed in patients with different ethnic origins is linked basically to unfavorable social and economic conditions that worsen the risk of poor blood glucose control. Retinopathy accounts for 32% of all ocular complications, similar to other African data and more generally in ophthalmology centers. The rate of neuropathy is high, reaching 70% in patients with microangiopathy. Impotence concerns 48.7% of the diabetic population with a mean age of 41.4+/-15.5 years. Coronary artery disease had a recognized influence on hemoglobin diseases, particularly when the coronarography is normal. Lower limb arteriopathy is observed in 18% of the diabetic patients.
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PMID:[Main complications of diabetes mellitus in Africa]. 1117 5

Arteriopathy is the principal complication of type 2 diabetes mellitus. It develops from endothelial dysfunction, which we have hypothesised occurs in diabetes primarily as a consequence of dyslipidaemia and oxidative stress. Fenofibrate and CoQ may improve endothelial function by regulating dyslipidaemia and oxidative stress, respectively. We therefore aimed to assess the independent and combined effects of fenofibrate and coenzyme Q(10) (CoQ) on endothelium-dependent and endothelium-independent vasodilator function of the forearm microcirculation in type 2 diabetes. Eighty dyslipidaemic type 2 diabetics were randomized to receive fenofibrate (200 mg/daily), CoQ (200 mg/daily), fenofibrate plus CoQ (200+200 mg daily), or placebo for 12 weeks. Forearm microcirculatory function was assessed with venous occlusion plethysmography during the infusion of acetylcholine (ACh), bradykinin (BK), sodium nitroprusside (SNP) and N(G)-monomethyl-L-arginine (L-NMMA) into the brachial artery. Blood flow responses were calculated as area under the curve (AUC). Fenofibrate significantly lowered plasma cholesterol, triglyceride and fibrinogen (P<0.001), and elevated HDL-cholesterol and homocysteine (P<0.001). CoQ did not change plasma isoprostanes, but significantly lowered systolic blood pressure and HbA(1c) (P<0.05). Fenofibrate plus CoQ significantly improved (P<0.05) the AUC for ACh, BK and SNP without significantly altering basal responses to L-NMMA. Fenofibrate or CoQ alone did not significantly alter blood flow responses. Improvements in blood flow were independent of changes in plasma lipids, blood pressure, homocysteine and isoprostanes, but were correlated (P=0.013) with HbA(1c). In conclusion, in this factorial trial we found that only the combination of fenofibrate and CoQ markedly improved endothelial and non-endothelial forearm vasodilator function in dyslipidemic type 2 diabetic patients. The favourable vascular effect of this therapeutic combination could be due to increase in the bioactivity of and/or responses to endothelium-derived relaxing factors, including nitric oxide, and this may entail synergistic stimulation of peroxisome proliferator-activated receptors.
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PMID:Combined effect of coenzyme Q10 and fenofibrate on forearm microcirculatory function in type 2 diabetes. 1273 1

In order to calculate the cardiovascular risk in patients with chronic renal failure (CRF), we retrospectively analyzed 1482 acute myocardial infarctions (AMIs) treated in the ICU at C. Poma General Hospital, Mantua, Italy, from 1 December 2004 to 31 July 2007. Of these patients, 133 suffered from CRF at hospital admission (eGFR <40 mL/min/1.73 m2 body surface and/or serum creatinine >2 mg/dL). During hospitalization for AMI, the CRF-affected patients showed a 2.7 times higher relative risk of mortality than patients without CRF (Yates chi square 14.46; p = 0.0001432). The evaluated comorbidities (hypertension, type 2 diabetes, supra-aortic vascular stenosis >70%, previous PTCA, COPD, previous AMI, previous coronary artery bypass and chronic obliterative peripheral arteriopathy) increased the relative risk of death 1.2- to 3.76-fold in those affected. In accord with recent evidence in the international literature, our results point to the importance of early assessment of CRF for the prognosis of patients with AMI.
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PMID:[Mortality triplicates in acute myocardial infarction patients affected by chronic renal failure]. 1938 88

The risk of peripheral vascular disease (PVD) is increased in diabetic patients, occurs earlier and is often more severe and diffuse. Endothelial dysfunction, vascular smooth muscle cell dysfunction, inflammation and hypercoagubility are the key factors in diabetic arteriopathy. The presence of PVD, apart from its increased risk of claudication, ischemic ulcers, gangrene and possible amputation, is also a marker for generalized atherosclerosis and a strong predictor for cardiovascular ischemic events. However, despite the recognition that PVD is associated with increased ischemic event rates and death, particularly in diabetic patients, this specific manifestation of systemic atherosclerosis is largely underdiagnosed and undertreated. In type-1 diabetes, early intensive insulin treatment reduces both microvascular (nephropathy, retinopathy and neuropathy) and macrovascular complications of diabetes (DCCT/EDIC study). In type-2 diabetes, UKPDS showed that tight glucose control reduces micro- and macrovascular complications, when therapy is started early after diagnosis and that early intervention has long lasting protective effects. However recently published trials (ADVANCE, ACCORD and VADT) pointed out that lowering glycemic targets to nearly normal glycaemia does not further reduce cardiovascular events in individuals with longstanding type 2 diabetes and that hypoglycaemia is to be avoided in individuals with ischemic heart disease. Finally, the small but important Steno-2 trial demonstrated that to significantly reduce peripheral vascular disease, ischemic events and mortality in type-2 diabetes, intensified multifactorial treatment of all modifiable risk factors is needed. Therefore, to prevent micro- and macrovascular complications, like PVD, in type-1 and type-2 diabetes, intensive therapy, targeting glycemia and all other modifiable cardiovascular risk factors, should be initiated as soon after diagnosis as possible and maintained in a safe way throughout life.
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PMID:Diabetes and peripheral vascular disease. 1999

OBJECTIVE The extracellular matrix protein fibulin-1 is upregulated in the arterial wall in type 2 diabetes (T2D) and circulates in increased concentrations in diabetes. Metformin is an antidiabetic drug with beneficial cardiovascular disease effects in diabetes. We hypothesized that metformin would influence the increased level of plasma fibulin-1 in diabetes. RESEARCH DESIGN AND METHODS After a 4-week run-in period, 371 eligible patients with T2D were randomized to treatment groups in a factorial design including insulin alone (control), +metformin, +rosiglitazone, or +both metformin and rosiglitazone. Plasma fibulin-1 was analyzed at the beginning of the study and after 18 and 24 months. RESULTS Plasma fibulin-1 increased in all groups throughout the 2-year period; however, the increase was strongly attenuated among patients treated with metformin. A highly significant difference was observed when the mean change in plasma fibulin-1 was compared between metformin- and non-metformin-treated individuals both at 18 and 24 months of treatment, but rosiglitazone had no effect. Metformin and rosiglitazone alone reduced the HbA1c levels to comparable levels and in combination even further. CONCLUSIONS Metformin attenuates the increase in plasma fibulin-1 concentrations in T2D, independently of glycemic effects. Changes in fibulin-1 may reflect an important element in diabetic arteriopathy that can be influenced by metformin.
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PMID:Metformin, but not rosiglitazone, attenuates the increasing plasma levels of a new cardiovascular marker, fibulin-1, in patients with type 2 diabetes. 2413 89

Glucokinase activators (GKAs) are being developed for the treatment of type 2 diabetes. The toxicity of 4 GKAs (PF-04279405, PF-04651887, piragliatin, and PF-04937319) was assessed in mice, rats, dogs, and/or monkeys. GKAs were administered for 2 to 8 weeks. Standard endpoints, glucose, and insulin were assessed. All compounds produced varying degrees of hypoglycemia in all species. Brain neuronal necrosis and/or peripheral neuropathy were observed with most compounds. These findings are consistent with literature reports linking hypoglycemia with nervous system effects. Arteriopathy, mainly of cardiac vessels, was observed at a low frequency in monkey and/or dog. Arteriopathy occurred only at doses that produced severe and prolonged periods of repeated hypoglycemia. Since this lesion occurred in multiple studies with structurally distinct GKAs, these results suggested arteriopathy was related to GKA pharmacology. The morphological characteristics of the arteriopathy were consistent with that produced by experimental catecholamine administration. We hypothesize that the prolonged periods of hypoglycemia resulted in increased local and/or systemic concentrations of catecholamines via a counterregulatory and/or stress-related mechanism. Alternatively, prolonged hypoglycemia may have resulted in endothelial dysfunction leading to arteriopathy. This risk can be managed in human patients in clinical studies by careful glucose monitoring and intervention to avoid prolonged episodes of hypoglycemia.
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PMID:The relationship of glucokinase activator-induced hypoglycemia with arteriopathy, neuronal necrosis, and peripheral neuropathy in nonclinical studies. 2477 Oct 80

Diabetic foot ulcerations have been extensively reported as vascular complications of diabetes mellitus associated with a high degree of morbidity and mortality. Diabetic foot syndrome (DFS), as defined by the World Health Organization, is an "ulceration of the foot (distally from the ankle and including the ankle) associated with neuropathy and different grades of ischemia and infection". Pathogenic events able to cause diabetic foot ulcers are multifactorial. Among the commonest causes of this pathogenic pathway it's possible to consider peripheral neuropathy, foot deformity, abnormal foot pressures, abnormal joint mobility, trauma, peripheral artery disease. Several studies reported how diabetic patients show a higher mortality rate compared to patients without diabetes and in particular these studies under filled how cardiovascular mortality and morbidity is 2-4 times higher among patients affected by type 2 diabetes mellitus. This higher degree of cardiovascular morbidity has been explained as due to the observed higher prevalence of major cardiovascular risk factor, of asymptomatic findings of cardiovascular diseases, and of prevalence and incidence of cardiovascular and cerebrovascular events in diabetic patients with foot complications. In diabetes a fundamental pathogenic pathway of most of vascular complications has been reported as linked to a complex interplay of inflammatory, metabolic and procoagulant variables. These pathogenetic aspects have a direct interplay with an insulin resistance, subsequent obesity, diabetes, hypertension, prothrombotic state and blood lipid disorder. Involvement of inflammatory markers such as IL-6 plasma levels and resistin in diabetic subjects as reported by Tuttolomondo et al confirmed the pathogenetic issue of the a "adipo-vascular" axis that may contribute to cardiovascular risk in patients with type 2 diabetes. This "adipo-vascular axis" in patients with type 2 diabetes has been reported as characterized by lower plasma levels of adiponectin and higher plasma levels of interleukin-6 thus linking foot ulcers pathogenesis to microvascular and inflammatory events. The purpose of this review is to highlight the immune inflammatory features of DFS and its possible role as a marker of cardiovascular risk in diabetes patients and to focus the management of major complications related to diabetes such as infections and peripheral arteriopathy.
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PMID:Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes. 2562 Dec 12


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