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

The incidence and prevalence of diabetic neuropathies in Insulin Dependent (IDDM) and Non-Insulin Dependent (NIDDM) Diabetes Mellitus is not known because in previous studies the heterogeneity of diabetes and of the neuropathies was not taken into account, criteria for diagnosis and surveillance for neuropathy were variable, and studies were not prospective or population based. We have begun such prospective epidemiologic studies using a uniform algorithm for the classification of the diabetic disorders and uniform and validated approaches for the assessment of symptoms, neurologic deficits and various quantitative end-points of neural dysfunction. As regards cause, a key question which we are trying to answer is whether hyperglycemia and associated metabolic alterations affect neural tissue directly or whether there is an intervening tissue alteration between metabolic derangement and tissue change. Improved control of hyperglycemia does not appear to be associated with rapid neurologic improvement, possibly arguing for an intervening tissue alteration. The recently observed decrease in nerve oxygen tension and blood flow in streptozotocin diabetes suggests that an alteration of the nerve microenvironment may relate importantly to the cause of diabetic neuropathy.
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PMID:Diabetic neuropathy. 403 17

The prevalence of glaucoma and ocular hypertension was investigated in an epidemiological study of diabetics traced by registration of prescriptions on insulin and oral hypoglycaemic agents (OHA) on the island of Falster (inhabitants 44 498), Denmark. Among 533 diabetics (227 insulin- and 306 OHA-treated) the prevalence rate of primary open angle glaucoma and ocular hypertension was 6.0% and 3.0%, respectively. Neovascular glaucoma occurred in 2.1% of all diabetics and in 21.3% of diabetics with proliferative retinopathy. Open angle glaucoma was more prevalent (P less than 0.01) in type 2 diabetes mellitus compared with type 1 diabetes mellitus. No difference in the prevalence of neovascular glaucoma was found between type 1 and type 2 diabetics. The occurrence of open angle glaucoma correlated positively (P less than 0.01) to the current age (greater than 65 years) in both groups and the diabetes onset age (greater than 40 years) in insulin-treated diabetics. Neovascular glaucoma correlated positively (P less than 0.05) with diabetic macrovascular complications in total (myocardial infarction, ischemic heart disease, arterial hypertension, cerebrovascular stroke, gangrene/amputation), neuropathy and severe microvascular complications (proliferative retinopathy, retinovascular occlusion). Diabetics with open angle glaucoma and ocular hypertension showed a higher frequency (P less than 0.05) of ischemic heart disease, arterial hypertension and retinovascular occlusion compared with diabetics without glaucoma or ocular hypertension.
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PMID:The prevalence of glaucoma and ocular hypertension in type 1 and 2 diabetes mellitus. An epidemiological study of diabetes mellitus on the island of Falster, Denmark. 663 28

Human serum paraoxonase is physically associated with HDL and has been implicated in the detoxification of organophosphates and possibly in the prevention of LDL lipid peroxidation. We investigated the serum activity and concentration of paraoxonase in 78 patients with type 1 diabetes mellitus, 92 with type 2 diabetes, and 82 nondiabetic control subjects. Paraoxonase activity was generally lower in diabetics than in control subjects. This decrease was unrelated to differences in paraoxonase phenotype distribution or its serum concentration. Rather, the difference in paraoxonase activity was explained by its specific activity, which was lower in diabetics, indicating either the presence of a circulating inhibitor or disturbance of the interaction of paraoxonase with HDL affecting its activity. Paraoxonase specific activity was lowest in patients with peripheral neuropathy, suggesting an association of paraoxonase with neuropathy. In control subjects but not patients with diabetes, paraoxonase correlated with HDL cholesterol and apolipoprotein A-1. Our results indicate that the low paraoxonase activity in diabetes is due to decreased specific activity. In other studies low serum paraoxonase activity has been associated with increased susceptibility to atherosclerosis, and the present results also suggest an association with peripheral neuropathy, which could be due to reduced capacity to detoxify lipid peroxides in diabetes.
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PMID:Serum paraoxonase activity, concentration, and phenotype distribution in diabetes mellitus and its relationship to serum lipids and lipoproteins. 758 60

Management has changed dramatically: There is no doubt now that strict glycemic control protects against nephropathy, neuropathy, and retinopathy. Direct evidence comes from study of intensive insulin therapy in IDDM. The implication is that similar protection can be gained in NIDDM. Microalbuminuria mandates ACE inhibition and dietary protein restriction. Proliferative retinopathy can be arrested with laser photocoagulation.
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PMID:Taking control of diabetes. 759 89

Since diabetes is a major health problem in Malta a study was conducted to gain a better insight into one of its most common complications, that of retinopathy. A random sample of 200 cases of adult onset diabetes with retinopathy who attended the main hospital's diabetes clinic was assessed by an experienced ophthalmologist. Non-proliferative retinopathy was subdivided into three degrees of severity according to the number of microaneurysms, haemorrhages, exudates, and intraretinal microvascular abnormalities present while proliferative retinopathy included also advanced eye disease. Data on medical and family histories was gathered from personal interrogation and counterchecked from hospital files. A medical examination searched for other concomitant disease. The 124 females and 73 males were similarly aged with a mean of 59.5 +/- 11.5 years. The mean age at onset of diabetes was 44.4 +/- 7.9 years: no significant differences were seen between the grades of retinopathy or the sexes. Onset of eye disease was first detected at a mean age of 56.9 +/- 7.0 years. The great majority (82%) of retinopathy cases occurred after 10 years of diabetes. Males appeared to develop eye disease (especially non-proliferative) at a younger age (53.4 +/- 7.6 vs 58.9 +/- 6.6 years, p < 0.01) and after a shorter duration of diabetes (10.1 +/- 6.6 vs 14.0 +/- 7.8 years, p < 0.001) than females. Severity of retinopathy was strongly associated (p < 0.001), in females rather more than in males, with poor glycaemic control, use of insulin, presence of proteinuria and decreasing vision; and less markedly (p < 0.01) with duration of diabetes of more than 10 years, neuropathy and glaucoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Retinopathy in Maltese type 2 diabetic patients. 764 10

Basal and postprandial levels of gastrin, somatostatin, vasoactive intestinal polypeptide (VIP) and pancreatic polypeptide (PP) were followed up in 105 patients with non insulin dependent diabetes mellitus (20 with autonomic neuropathy only, 35 with peripheric neuropathy only, 30 with autonomic and peripheric neuropathy simultaneously and 20 without any sign of neuropathy) and in the control group of 40 individuals. Serum levels of gastrin, somatostatin, VIP and PP are determined by a RIA (used kits of Prof. SR Bloom, Hammersmith Hospital, London). The results of investigation showed significantly higher basal and postprandial levels of gastrin and VIP in patients with autonomic neuropathy in comparison with the group without neuropathy and with the control group (p < 0.001). The serum levels of somatostatin did not differ significantly between the groups of diabetics with and without neuropathy. Basal level of PP was significantly lower and postprandial PP levels remained low in patients with autonomic neuropathy in comparison with the group without neuropathy (p < 0.001). We postulate that basal and postprandial gastrin and VIP levels raised secondary to partial vagotomy in diabetics with autonomic neuropathy. Measuring PP serum levels in diabetics after a protein rich meal can be useful to check vagus nerve function in the gastrointestinal tract in order to detect autonomic neuropathy.
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PMID:[Association of autonomic neuropathies and gastrointestinal peptides in non-insulin dependent diabetics]. 773 57

Blood plasma concentrations of noradrenaline, dopamine, serotonin and their metabolites (DOPAC, HVA, 5HIAA) were measured in 28 patients with insulin-dependent and 32 with noninsulin-dependent diabetes mellitus (IDDM and NIDDM, respectively). The patients were divided into 4 groups. Group 1 were 15 patients without late diabetic complications, group 2 were 15 subjects with diabetic neuropathy, group 3 were patients with neuropathy and retinopathy (n = 16), and group 4 were 14 patients with neuropathy, retinopathy, and nephropathy. The results showed an increase of serotonin levels in IDDM patients vs. those with NIDDM, a positive correlation between serotonin and blood glucose levels in IDDM, increased concentration of dopamine and reduced plasma level of noradrenaline in patients with diabetic neuropathy vs. those without late diabetic complications. Plasma levels of dopamine were decreased in all the patients microvascular involvement. The findings indicate the development of changes in the sympathoadrenal system of patients with late diabetic vascular complications.
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PMID:[Status of the sympatho-adrenal system in patients with diabetes mellitus: dependence on the course of the disease and the presence of late complications]. 774 27

The microvascular complications of retinopathy, nephropathy, and neuropathy are less prevalent, and not as severe, in NIDDM as compared with IDDM for unknown reasons. Macrovascular disease is the greatest challenge in the management of NIDDM because it is the cause of death in 50% to 60% of this patient population. Control of the hyperglycemia is the most important because the prevention of complications is more effective than the treatment of them. Blood glucose control through diet, exercise, and medication is the key to reducing the previously identified complications. Lifestyle modifications of diet and exercise are the most effective treatment to reduce hyperglycemia. It is important to emphasize during the asymptomatic period the serious consequences of the complications and to set goals using the glycosylated hemoglobin. If these goals are not met, treatment should be intensified by more frequent visits or referral for the team approach. The time for intervention is before the complications are present, not after they occur. It is certainly reasonable to reduce as many risk factors as possible that adversely affect the complications of NIDDM. Hypertension can affect the course of coronary artery disease, retinopathy, nephropathy, and neuropathy and should be treated. The avoidance of tobacco is a must for the prevention of vascular disease and is associated with painful neuropathy. Dyslipidemia is seen frequently in NIDDM and should be assessed by fasting lipid panel and treated to lower the LDL cholesterol below 130 mg/dL. Reduction of individual risk factors is the most effective approach to this complex clinical syndrome until such time as a better understanding of the pathophysiology provides a more specific and effective intervention.
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PMID:Noninsulin-dependent diabetes mellitus. The prevention of complications. 787 91

A decrease in Na+,K(+)-ATPase activity is claimed to play a central role in the pathogenesis of electrophysiological and morphological abnormalities that characterize the neuropathic complications in different animal models of diabetes mellitus. The peripheral nerves from 17 patients with either type I or type II diabetes mellitus were studied to assess the importance of changes in Na+,K(+)-ATPase activity in chronic human diabetic neuropathy. Sixteen nerves from age- and sex-matched normal individuals, and 12 nerves from non-diabetic neuropathic subjects undergoing vascular or orthopedic surgery served as negative and positive controls, respectively. All specimens were processed blind. Ouabain-sensitive ATPase activity was measured by a modified spectrophotometric coupled-enzyme assay. Standard histology, fiber teasing and electron microscopy were used to establish the normal or neuropathological patterns of surgical material. Morphometric analysis permitted calculation of fiber density in each nerve specimen and correlation of this figure with the relevant enzymatic activity. Na+,K(+)-ATPase activity was approximately 59% lower in nerves from diabetic patients than in normal controls (P < 0.01) and approximately 38% lower in nerves from non-diabetic patients with neuropathy (P < 0.01). Although nerves from both neuropathic conditions had significantly fewer fibers than those from normal individuals (diabetic -33%, and non-diabetic -22%), the decreases in Na+,K(+)-ATPase activity and fiber density were not correlated only in specimens from diabetic patients (r2 = 0.096; P = 0.22). Taken together with data from experimental animal models, these results suggest that the reduction in Na+,K(+)-ATPase activity in diabetic nerves is not an epiphenomenon secondary to fiber loss; rather, it may be an important factor in the pathogenesis and self-maintenance of human diabetic neuropathy.
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PMID:Decrease of nerve Na+,K(+)-ATPase activity in the pathogenesis of human diabetic neuropathy. 813 5

Oral antidiabetic agents continue to play an important role in the treatment of type 2 diabetes. Of decisive importance is the timing of their use, together with a knowledge of their specific properties. Acarbose, which needs to be initiated at a low, slowly increasing dose, is noted for the fact that it has virtually no systemic side effects. Metformin reduces plasma glucose levels without inducing hyperinsulinemia, and carries virtually no risk of lactic acidosis. Glibenclamide can be used either alone to treat type 2 diabetes or in combination with other oral antidiabetics or insulin. Today, intensified insulin therapy represents the optimal standard of insulin replacement. It permits meal-oriented injection of normal insulin and the use of longer-acting insulin overnight. This form of treatment is now facilitated by the possibilities of plasma glucose selfmonitoring and the use of injection aids (pen). Intensified treatment should be initiated at the time type I diabetes is diagnosed. In the case of a particularly instable metabolic situation or neuropathy, it may become necessary to use insulin pumps.
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PMID:[Management of diabetes in general practice--current requirements. 2: Oral antidiabetics and insulin therapy]. 820 Jun 2


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