Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

215 children and adolescents with insulin dependent diabetes (age: 12(6)/12 +/- 3(9)/12 yrs; duration of diabetes 4(5)/12 +/- 3(9)/12 yrs, daily insulin requirement: 0.74 +/- 0.26 I.U./kg b.w.) were investigated for the presence of hand changes (cheiropathy) due to diabetes. Controls were 110 healthy persons of similar age (age: 11(5)/12 +/- 4(8)/12 yrs). Signs of cheiropathy were found in 44 (20.5%) of the diabetics. In 28 of these diabetics reduced mobility of the proximal and/or distal interphalangeal joints of one finger and in 16 others of at least two fingers was observed. No pathological alterations were found in the wrists, shoulder joints or spine. Mild signs of cheiropathy were seen in 5 (4.5%) of the controls. A significant positive relationship was found between age and duration of diabetes and the severity of cheiropathy. Diabetics with cheiropathy also had significantly higher daily insulin requirements than others. Of 49 patients with good diabetic control only one (2.0%) had signs of cheiropathy. In the group of 82 diabetics with fair control 12 (14.6%) showed hand changes, in the group of 84 patients with poor control 31 (36.9%). Cheiropathy must be considered to be a prognostic indicator of impending microangiopathy (retinopathy, nephropathy and neuropathy) in diabetic children and adolescents.
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PMID:[Diabetes specific hand changes (cheiropathy) in children and adolescents with insulin-dependent diabetes (type I)]. 635 9

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

Caucasian diabetic patients in Australian surveys showed a significant difference in the distribution of glyoxalase phenotypes. Insulin dependent diabetic patients with age of onset less than 40 years had a relative excess of glyoxalase homozygote 1-1 and a deficiency of types 2-1 and 2-2. Non-insulin dependent diabetic patients were not significantly different from non-diabetic subjects in the distribution of glyoxalase phenotypes. Insulin dependent diabetic patients without the complications of retinopathy or neuropathy also showed a significant excess of glyoxalase type 1-1 in relation to the control group. Genes controlling glyoxalase polymorphism appear to be associated with the variations of diabetes and its complications.
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PMID:Glyoxalase phenotypes in patients with diabetes mellitus. 703 Feb 93

Vascular complications are common in diabetics. Patients with type I diabetes mellitus may be more likely to suffer microvascular complications (retinopathy, nephropathy, neuropathy), whereas patients with type II diabetes may be more likely to have macrovascular complications (similar to atherosclerotic disease). Amputation rates are 10 to 15 times more common in the diabetic than in the non diabetic. A meticulous examination (historical and physical) combined with doppler ultrasonography will indicate the presence of peripheral vascular disease in the diabetic. Such an evaluation enables correct management of the risk factors and ensures an appropriate follow-up and treatment of the diabetes related lesions as soon as they occur.
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PMID:[Vascular complications of diabetes]. 748 Dec 39

The clinical and electro-neurographic examinations were carried out in 54 patients aged 21-67 years (mean = 41.8) with IDDM of at least 10-year duration, and 25 subjects aged 19-62 years (mean = 39.0) as a control group. The aim of the study was the determination of: 1) the frequency of polyneuropathy appearance in patients with IDDM of at least 10-year duration; 2) the usefulness of electroneurography for detection of subclinical impairment of peripheral nervous system in diabetics; 3) the characterization of electro-neurographic abnormalities in diabetic neuropathy; 4) the influence of diabetes duration and metabolic control on severity of peripheral nerves affection; 5) the relationship between polyneuropathy and retinopathy, nephropathy and cataract occurrence in diabetic patients. Polyneuropathy was diagnosed--clinically in 67% of patients, electro-neurographically in 85% of patients. The neurographic study proved high sensitivity for detection of subclinical affection of peripheral nerves in diabetics. The electro-neurographic abnormalities appeared more frequently and were more considerable in the group of patients with clinical polyneuropathy. Frequency of the sensory and motor nerve fibres involvement was similar. The electroneurographical abnormalities corresponded with the features of mixed--axonal and demyelinating type of neuropathy. It was disclosed that the degree of neurographical changes did not depend on duration and severity of hyperglycemia in late period of the disease. A moderate relationship between occurrence of polyneuropathy and retinopathy, nephropathy as well as diabetic cataract was revealed.
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PMID:[Clinical and electroneurographic changes in the peripheral nervous system of patients with chronic insulin-dependent diabetes (IDDM)]. 750 45

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

Patients suffering from the severe complications associated with both insulin- (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM): nephropathy, retinopathy, neuropathy, and atherosclerosis are still largely left without a prospect of an efficient treatment. This is the case even if it has been assumed for decades and now finally proved by the results from the Diabetes Control and Complications Trial (DCCT) that hyperglycemia is the single main cause of these complications. Improved glycemic control as a result of intensive insulin treatment has the potential to reduce the incidence and progression of complications, but implementation and monitoring of improved glycemic control in all groups of IDDM and NIDDM patients in different communities will be difficult and expensive. Results from the recently terminated DCCT have shown that even with intensive insulin treatment, there will be a significant burden of complications on the diabetic population. It will, therefore, still be of immense importance for the long-term quality of life for the diabetic patient that additional possibilities are developed for prevention and intervention against diabetic complications. Almost two decades of research, animal model testing, and clinical trials have been conducted on various efficient aldose reductase inhibitors. Now the concept of inhibition of formation of advanced glycosylation endproducts on proteins and lipids resulting from extra- and intracellular hyperglycemia is entering the scene as an alternative or perhaps supplementary approach to reduce the occurrence of diabetic complications. An overview of the results from these two fields of research and associated drug-development programs will be presented along with thoughts on possible future developments.
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PMID:Diabetic late complications: will aldose reductase inhibitors or inhibitors of advanced glycosylation endproduct formation hold promise? 759 49

Mitochondrial dysfunctions of the muscle in diabetic amyotrophy and of the liver in diabetic fatty liver have been reported. We investigated mitochondrial gene mutations in three cases: (1) a patient with diabetic amyotrophy in the muscles of the lower extremities, and neuropathy; (2) 5 diabetics with myoatrophy, diabetic nephropathy, and chronic renal failure; and (3) an IDDM patient with a diabetic fatty liver. We identified a 5778-bp deletion (8214-13991) in mitochondrial DNA from the muscle and liver biopsy specimens by the primer shift PCR and PCR-direct sequence methods. It is speculated that 5778-bp deletion is due to homogeneous recombination in the 7-bp repeat sequence of TCCTAGA flanking the region deleted in the mitochondrial DNA. Determination of respiratory chain enzyme activities in fresh muscle mitochondria demonstrated the defect in complex I activity. The deletion covers areas coding ND3, ND4, ND4L, and ND5 in complex I. The 5778-bp deletion might cause a defect in mitochondrial oxidative phosphorylation and contribute to the pathogenesis of diabetic amyotrophy, myoatrophy with diabetic nephropathy, and chronic renal failure, as well as diabetic fatty liver in IDDM.
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PMID:A new mitochondrial DNA deletion associated with diabetic amyotrophy, diabetic myoatrophy and diabetic fatty liver. 760 16

The Diabetes Control and Complications Trial (DCCT) has demonstrated that intensive diabetes treatment delays the onset and slows the progression of retinopathy, nephropathy, and neuropathy in patients with IDDM. A detailed description of the effects of this treatment on diabetic nephropathy is presented here. In the primary prevention cohort, intensive treatment reduced the mean adjusted risk of the cumulative incidence of microalbuminuria (> or = 28 micrograms/min) by 34% (95% CI 2, 56%; P = 0.04). Furthermore, intensive treatment decreased the albumin excretion rate (AER) by 15% after the first year of therapy (6.5 vs. 7.7 micrograms/min, P < 0.001). Thereafter the rates of change for AER within each treatment group were no different from zero, retaining a constant difference in AER between groups in the trial. In the secondary intervention cohort with baseline AER < 28 micrograms/min, intensive therapy reduced the mean adjusted risk of microalbuminuria (> or = 28 micrograms/min) by 43% (95% CI 21, 58%; P < 0.0001); the risk of a more advanced level of microalbuminuria (> or = 70 micrograms/min) by 56% (95% CI 26, 74%; P = 0.002); and the risk of clinical albuminuria (> or = 208 micrograms/min) by 56% (95% CI 18, 76%; P < 0.01). In the secondary intervention cohort, values for AER at year 1 were identical at 9 micrograms/min, but the 6.5% change per year in the conventional group greatly exceeded the rate of change of -0.3% in the intensive group (P < 0.001). Among the 73 secondary cohort subjects with AER levels > or = 28 micrograms/min but < or = 139 micrograms/min at baseline, the reduction of progression to clinical albuminuria with intensive therapy was not statistically significant. The longitudinal treatment effect of conventional versus intensive therapy (11.0% vs. 2.5% per year, respectively, P = 0.087) was similar in magnitude to that among patients with AER < 28 micrograms/min at baseline. For the primary, secondary and combined cohorts, there were no significant differences in the rates of change in creatinine clearance (CCr) between treatment groups during the study. Only seven subjects in the entire study (2 intensive, 5 conventional) developed urinary AER > or = 208 micrograms/min coupled with a CCr < 70 ml/min/1.73 m2. Neither the rate of change of blood pressure nor the appearance of hypertension (BP > 140/90 mm Hg) differed significantly between treatment groups in the primary, secondary or combined cohorts.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of intensive therapy on the development and progression of diabetic nephropathy in the Diabetes Control and Complications Trial. The Diabetes Control and Complications (DCCT) Research Group. 764 40


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