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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparative prospective study of 120 adult diabetics (60 insulin dependent, 60 non-insulin dependent) and 120 non-diabetic adults as controls showed significantly higher incidence of Dupuytren's disease, limited joint motion, carpal tunnel syndrome, and flexor tenosynovitis in the diabetic population. Of the diabetic patients one third had a mild non-progressive form of Dupuytren's disease, which commonly involved the long and ring rays. Limited joint motion was noted in a third of diabetics, and carpal tunnel syndrome was observed in 15-25%, and flexor tenosynovitis in about a fifth. Limited joint motion co-existed with Dupuytren's disease in 57% of insulin-dependent diabetics. Diabetic polyneuropathy was found in two thirds of insulin-dependent diabetics and in one third of non-insulin dependent diabetics. All these hand changes were more marked in insulin-dependent diabetics and they showed a positive correlation with increasing age of the patient, duration of the diabetes, and the presence of a microangiopathy.
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PMID:Dupuytren's disease, carpal tunnel syndrome, trigger finger, and diabetes mellitus. 772 49

Diabetic polyneuropathy is a major complication of diabetes mellitus that frequently leads to foot ulceration. Because of economic impact of foot ulceration and subsequent amputation, major initiatives are under way in the United States and the United Kingdom to reduce their incidence by up to 50%. Although diabetic ulcers may have an ischemic and neuropathic component, the majority are neuropathic. Results from studies have shown a strong association between the neuropathy and the subsequent development of foot ulcers. However, other predisposing factors such as high foot pressures, inappropriate footwear, and other extrinsic pressure usually must be present, together with neuropathy, to cause foot ulcers. Therefore, the challenge to the physician is to identify the patient at risk and intervene so as to educate and prevent the occurrence of foot ulcers.
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PMID:End-stage complications of diabetic neuropathy: foot ulceration. 787 9

Diabetic polyneuropathy is a complex disease of progressive nerve fiber loss. Initial screening and diagnosis in clinical practice usually depend on assessment of subjective complaints. A need exists for objective, simple, and reproducible assessment tools that can be readily used in clinical practice. The importance of early diagnosis is highlighted by the recent North American Diabetes Control and Complications Trial where intensive insulin therapy reduced the risk of developing diabetic neuropathy by 61%. At the University of Michigan, we have developed an outpatient neuropathy program. Patients are given a questionnaire and a brief screening examination, designated the Neuropathy Screening Instrument. Diabetic neuropathy is confirmed and staged in patients with a positive Neuropathy Screening Instrument, by a quantitative neurologic examination and nerve conduction studies, designated the Diabetic Neuropathy Score. The Michigan program has been compared with well-established instruments and has been found to be sensitive and reproducible for screening and diagnosis. We believe the program provides a valuable tool for the clinician in the practice setting and should allow diagnosis and intervention earlier in the course of diabetic neuropathy.
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PMID:Clinical testing in diabetic peripheral neuropathy. 787 10

Epidemiologic studies have identified lipoprotein(a) (Lp(a)) as an independent risk factor for atherosclerosis, mainly for coronary heart disease. Atherosclerosis is the most common cause of death in diabetic patients, but there is little information available concerning the importance of Lp(a) in these patients. We compared the presence or absence of late diabetic complications with Lp(a) serum concentrations in 224 patients (82 IDDM, 142 NIDDM). Lp(a) distribution was skewed as described for non-diabetic patients. Despite highly significant differences for total cholesterol, total triglycerides, HDL-cholesterol, VLDL-cholesterol and VLDL-triglycerides (P < 0.001) and for LDL-cholesterol (P < 0.01) Lp(a) concentrations were similar in NIDDM and IDDM (mean: 27 vs. 30, median: 12 vs. 21 mg/dl, P = 0.10). Diabetic polyneuropathy, autonomic neuropathy, nephropathy, peripheral occlusive disease, diabetic gangrene and coronary heart disease were not associated with raised Lp(a) values. Non-insulin-dependent patients with retinopathy exhibited higher Lp(a) concentrations in serum than those without this complication. This significant association was lost when duration of diabetes was taken into account by logistic regression. We conclude, that other risk factors surpass the significance of Lp(a) in diabetic patients.
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PMID:Lipoprotein(a) in diabetes mellitus. 845 77

Diabetic polyneuropathy is a common, disabling chronic complication of diabetes mellitus. Previous studies have suggested that combined pancreas-kidney transplantation can ameliorate nerve conduction. The relative contribution of the correction of hyperglycaemia and uraemia on nerve function is still a matter of debate. Nerve conduction velocity (NCV) was assessed before and after simultaneous pancreas and kidney transplantation, and before and after pancreas graft failure in five insulin-dependent diabetic (IDDM) patients affected by severe diabetic polyneuropathy. Sensory and motor NCV were recorded in five nerves and expressed as a cumulative index for each patient. Metabolic control was evaluated by fasting blood glucose and glycosylated haemoglobin levels. NCV index was below normal values before transplant: -3.8 +/- 0.7 (normal value: 0.89), improved 1 and 2 years after transplant: -3.1 +/- 1.3 and -2.6 +/- 0.9 (p = 0.0019), stabilised until pancreas failure and deteriorated to pre-transplant values 2 years after pancreas graft failure: -3.6 +/- 1.0 (p = 0.034). Fasting blood glucose levels worsened after pancreas graft failure. HbA1c levels, in the normal range during functioning pancreas graft (6.6 +/- 0.6%), deteriorated after its failure (8.0 +/- 0.6%, p = 0.04). Kidney function was preserved. These data support a positive effect of pancreas transplantation per se on NCV in IDDM subjects with diabetic polyneuropathy, thus demonstrating that metabolic control provided by a self-regulated source of insulin not only halts but also ameliorates nerve function, even if polyneuropathy is advanced.
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PMID:Amelioration of nerve conduction velocity following simultaneous kidney/pancreas transplantation is due to the glycaemic control provided by the pancreas. 930 Feb 50

Diabetic polyneuropathy is a complication, that affects most patients with longstanding diabetes mellitus, deteriorating their quality of life. In the last few years, new therapeutic approaches have been developed that can improve symptoms and neurologic function, and which may prevent and in some cases stop nerve damage, and even, promote nerve fiber regeneration. These treatments are supported by several investigations in animals and humans: a) thigh glycemic control (insulin), b) aldose reductase inhibition (tolrestat), c) prevention of protein glycation (amino-guanidine), d) improvement of nerve ischemia (vaso-dilators, gamma-linolenic acid), and e) administration of neurotrophic factors (gangliosides). Most evidence support the usefulness for glycemic control. Early treatment is suggested, because marked nerve fiber loss is present in advanced neuropathy.
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PMID:[Treatment of diabetic neuropathy]. 965

Diabetic polyneuropathy is a serious complication in patients with diabetes mellitus. In addition to the maintenance of a sufficient metabolic control, alpha-lipoic acid (ALA) (Thioctacid, Asta Medica) is known to have beneficial effects on diabetic polyneuropathy although the exact mechanism by which ALA exerts its effect is unknown. In order to study the effect of ALA on microcirculation in patients with diabetes mellitus and peripheral neuropathy one group of patients (4 female, 4 male, age 60+/-3 years, diabetes duration 19+/-4 years, BMI 24.8+/-1.3 kg/m2) received 1200 mg ALA orally per day over 6 weeks (trial 1). A second group of patients (5 female, 4 male, age 65+/-3 years, diabetes duration 14+/-4 years, BMI 23.6+/-0.7 kg/m2) was studied before and after they had received 600 mg ALA or placebo intravenously over 15 minutes in order to investigate whether ALA has an acute effect on microcirculation (trial 2). Patients were investigated by nailfold video-capillaroscopy. Capillary blood cell velocity was examined at rest and during postreactive hyperemia (occlusion of the wrist for 2 minutes, 200 mmHg) which is a parameter of the perfusion reserve on demand. The oral therapy with ALA resulted in a significant decrease in the time to peak capillary blood cell velocity (tpCBV) during postocclusive hyperemia (trial 1: 12.6+/-3.1 vs 35.4+/-10.9 s, p<0.05). The infusion of ALA also decreased the tpCBV in patients with diabetic neuropathy (trial 2: before: 20.8+/-4,5, ALA: 11.74+/-4.4, placebo: 21.9-5.0 s, p<0.05 ALA vs both placebo and before infusions) indicating that ALA has an acute effect on microcirculation. Capillary blood cell velocity at rest (rCBV), hemodynamic parameters, hemoglobinA1c and local skin temperature remained unchanged in both studies. These results demonstrate that in patients with diabetic polyneuropathy ALA improves microcirculation as indicated by an increased perfusion reserve on demand. The observed effects are apparently acute effects. With the restriction of the pilot character of this investigation the findings support the assumption that ALA might exert its beneficial effects at least partially by improving microcirculation which is likely to occur also at the level of the vasa nervorum.
Exp Clin Endocrinol Diabetes 2000
PMID:Effects of alpha-lipoic acid on microcirculation in patients with peripheral diabetic neuropathy. 1092 11

Diabetic polyneuropathy (DPN) shows more severe functional and structural changes in type 1 than in type 2 human and experimental diabetes. We have previously suggested that these differences may be due to insulin and/or C-peptide deficiencies in type 1 diabetes. To further explore these differences between type I and type 2 DPN, we examined factors underlying nerve fiber regeneration in the hyperinsulinemic type 2 BB/Z-rat and compared these with previous data obtained from the iso-hyperglycemic, insulin and C-peptide-deficient type 1 diabetic BB/Wor-rat. The expression of neurotrophic factors and cytoskeletal proteins were studied in L4 and L5 dorsal root ganglia (DRG) at various time points after sciatic nerve crush. The data were compared to those of nondiabetes-prone BB-rats. Insulin-like growth factor 1 (IGF-1) and TrkA levels were lower in DRG from type 1 than from those of type 2 and control BB-rats. On the other hand, IGF-1 receptor expression was increased at baseline in type 1 BB/Wor-rats and decreased after crush injury, whereas its expression increased after crush injury in both control and type 2 BB/Z-rats. Following crush injury, betaII- and betaIII-tubulins were upregulated in type 2 BB/Z and control rats, which did not occur in type 1 BB/Wor-rats. Furthermore, type 2 BB/Z-rats showed the normal downregulation of low and medium molecular neurofilament (NF-L and NF-M, respectively), which did not occur in type 1 BB/Wor-rats. These findings were associated with significantly milder abnormalities in axonal elongation and caliber growth of regenerating fibers in type 2 compared to type 1 diabetic rats. These data suggest that impaired insulin signaling in type 1 diabetic nerve may be of greater significance in the regulation of neurotrophic and neurocytoskeletal protein synthesis than hyperglycemia in explaining the differences in nerve fiber regeneration between type 2 and type 1 diabetes.
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PMID:Insulin deficiency rather than hyperglycemia accounts for impaired neurotrophic responses and nerve fiber regeneration in type 1 diabetic neuropathy. 1263 30

Diabetic polyneuropathy (DPN) is the most common chronic complication of diabetes and affects Type 1 diabetic patients disproportionately. In the last two decades it has become increasingly evident that underlying metabolic, molecular and functional mechanisms and, ultimately, structural changes differ in DPN between the two major types of diabetes. In Type 1 diabetes, impaired insulin/C-peptide action has emerged as a prominent pathogenetic factor. C-peptide was long considered to be biologically inactive. During the last number of years it has been shown to have a number of insulin-like effects but without affecting blood glucose levels. Preclinical studies have demonstrated effects on Na(+)/K(+)-ATPase activity, endothelial nitric oxide synthase, expression of neurotrophic factors and regulation of molecular species underlying the degeneration of the nodal apparatus in Type 1 diabetic nerves, as well as DNA binding of transcription factors and modulation of apoptotic phenomena. In animal studies, these effects have translated into protection and improvement of functional abnormalities, promotion of nerve fibre regeneration, protection of structural changes and amelioration of apoptotic phenomena targeting central and peripheral nerve cell constituents. Several small-scale clinical trials confirm these beneficial effects on autonomic and somatic nerve function and blood flow in a variety of tissues. Therefore, evidence to date indicating that replacement of C-peptide in patients with Type 1 diabetes will retard and prevent chronic complication is real and encouraging. Large-scale clinical trials necessary to bring this natural substance into the clinical arena should, therefore, be encouraged and accelerated.
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PMID:C-peptide and diabetic neuropathy. 1294 92

Diabetic polyneuropathy is the most common complication of diabetes mellitus. Several interactive pathogenetic mechanisms have been identified mainly in streptozotocin-induced diabetes in rats and have been ascribed to hyperglycemia. Over the last number of years it is becoming increasingly clear that diabetic neuropathy differs in type 1 and type 2 diabetes in humans and in murine models that more accurately mimic the human disorders. Beside hyperglycemia, attention is increasingly being paid to the pathogenetic roles of insulin and C-peptide deficiencies, particularly in type 1 diabetic neuropathy. There is now evidence to suggest that insulin and C-peptide deficiencies are mainly responsible for perturbations of neurotrophic factors and contribute to oxidative stress in diabetic nerve. This may also be true for apoptotic phenomena afflicting both the peripheral and central nervous systems in diabetes. The new data have lead to re-evaluations of pathogenetic components in this complex disorder, and their further exploration is likely to form a more refined basis for future therapeutic and preventive measures.
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PMID:New insights into the metabolic and molecular basis for diabetic neuropathy. 1462 88


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