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

Several lines of evidence support peripheral nerve ischemia as a contributing factor in the etiology of human diabetic neuropathy. We questioned whether diabetic subjects with relatively normal nerve function in the baseline state would be more likely than healthy control subjects to show either improvement of ulnar nerve function with acute intraarterial infusion of nitroprusside (vasodilation) or be more sensitive than control subjects to worsening of nerve function with acute intraarterial infusion of norepinephrine (vasoconstriction). We measured forearm blood flow (FABF) using venous occlusion plethysmography and assessed ulnar nerve function at baseline and during two intrabrachial artery infusions. Six nondiabetic control subjects (mean age, 56 years) and 11 subjects with type 2 diabetes (mean age, 58 years) in good general health participated. Only three type 2 diabetic subjects had peripheral sensory neuropathy, which was mild. Among control subjects, there was no significant change in sensory distal latency, motor distal latency, motor proximal latency, or sensory or motor conduction velocity during norepinephrine infusion. In contrast, among type 2 diabetic subjects, there was a significant increase in sensory (baseline vnorepinephrine, 2.73+/-0.10 v 2.94+/-0.10 milliseconds [MS], P< or =.01) and motor distal latencies (baseline v norepinephrine, 2.90+/-0.06 v 3.18+/-0.1 ms, P< or =.001) and motor proximal latency (baseline v norepinephrine, 7.15+/-0.18 v 7.60+/-0.23 ms, P<.01) and a decrease in sensory conduction velocity (baseline v norepinephrine, 52.1+/-2.0 v 47.7+/-1.6 m/s, P<.01) during norepinephrine infusion. There were no consistent changes in nerve function during nitroprusside infusion in either group. In summary, we found that subjects with type 2 diabetes, but not control subjects, demonstrate a decrement in nerve function with vasoconstriction during intraarterial infusion of norepinephrine, but no consistent change during nitroprusside-induced vasodilation. These findings suggest there may be enhanced sensitivity of nerve function to ischemia in type 2 diabetic subjects with mild or absent clinical neuropathy.
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PMID:Acute effects of adrenergic-mediated ischemia on nerve conduction in subjects with type 2 diabetes. 1020 44

Estimates of the prevalence of diabetic neuropathy range from 10% to 90% of the diabetic population, depending on the criteria used to define neuropathy. Diabetic neuropathy encompasses a wide range of abnormalities affecting both the peripheral and autonomic nervous systems and causes considerable injury and death. Neurologic complications occur equally in type 1 and type 2 diabetes mellitus, as well as various forms of acquired diabetes. In this overview, we present and discuss the most recent approaches to the treatment of the common forms of diabetic neuropathy, including distal symmetric, proximal motor, and autonomic neuropathy. We also provide the reader with algorithms for recognition and management of common pain and entrapment syndromes, and a global approach to recognition of syndromes requiring specialized treatments based upon our improved understanding of their causes.
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PMID:Diagnosis and management of diabetic neuropathy. 1033 35

Even though autonomic diabetic neuropathy is highly prevalent and a noted risk factor for cardiovascular morbidity and mortality, very little is known about factors associated with it. We carried out standard autonomic nervous system function tests by means of a computerized portable system on 55 diabetic patients (22 with type 1 diabetes, 33 with type 2 diabetes) who had no signs or symptoms of autonomic diabetic neuropathy and on 10 age- and sex-matched healthy control subjects. Test results of patients with type 1 diabetes did not differ significantly from those with type 2 diabetes. Of the clinical, metabolic, and anthropometric variables considered, only the duration of diabetes was inversely and independently correlated to deep breathing test scores (E:I ratio value of deep breathing 1.38-0.009. years of diabetes; R2 = 0.25). The duration of diabetes was inversely correlated to variations in orthostatic systolic blood pressure (r = -0.37, p < 0.01). The prevalence of diabetic retinopathy (score: 1 = no; 2 = yes) was significantly higher in the diabetic group with lower deep breathing values (1.8 +/- 0.3 vs 1.0 +/- 0.0; p < 0.01). The prevalence of ischemic electrocardiographic alterations (score: 1 = no; 2 = yes) was significantly higher in the diabetic group with a poorer orthostatic systolic blood pressure response (1.4 +/- 0.1 vs 1.2 +/- 0.1; p < 0.01). This study suggests that 1) autonomic neuropathy is correlated to disease duration; 2) type of diabetes, present level of metabolic compensation, and anthropometric characteristics do not seem correlated to this complication; 3) diabetic retinopathy and ischemic cardiopathy may be correlated to autonomic neuropathy.
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PMID:Factors associated with autonomic nervous function in type 1 and type 2 diabetic subjects free of clinical manifestations of autonomic neuropathy. 1034 1

Patients with diabetic polyneuropathy are known to have an impaired neurovascular reflex arc compared to healthy controls. This is seen in a delayed decrease in microcirculation of the ipsilateral hand after cooling of the contralateral hand. The aim of this pilot study was to investigate whether intravenous alpha-lipoic acid (ALA) (Thioctacid, Asta Medica) therapy might be able to improve this impaired neurovascular reflex arc in patients with diabetic neuropathy. In addition, clinical effects were evaluated with the aid of the neuropathy symptom score (NSS) and the neuropathy disability score (NDS). Ten patients with diabetes mellitus and polyneuropathy (5 females, 5 males, 2 smokers, 5 IDDM, 5 NIDDM, body mass index 26.1 +/- 1.0 kg/m2, age 58.3 +/- 9.5 years, diabetes duration 15.7 +/- 11.2 years, Hb A1c 6.8 +/- 0.3%) were investigated by nail-fold capillaroscopy after contralateral cooling before and after intravenous therapy with 600 mg alpha-lipoic acid per day over 3 weeks. Cardiac autonomic neuropathy was excluded by beat-to-beat variation analysis. Symptoms of diabetic neuropathy were evaluated before and after therapy with the aid of the NSS and NDS. Capillary blood cell velocity (CBV) of the hand was determined before, during, and for the following 30 min after cooling (3 min at 15 degrees C) of the contralateral hand. Blood pressure, heart rate, and local skin temperature were monitored at 2-min intervals. ALA therapy resulted in a significant improvement of the microcirculatory response to cooling, as seen by an immediate decrease in CBV of 12. 3% (P < 0.02 vs before treatment), which was absent before therapy. Blood pressure, heart rate, and local skin temperature were not different between investigations. There was a significant improvement of the NSS after therapy (5.4 +/- 1.1 vs 8.6 +/- 1.1 points, P < 0.01). These results demonstrate that intravenous therapy with ALA has a positive influence on the impaired neurovascular reflex arc in patients with diabetic neuropathy.
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PMID:The effect of alpha-lipoic acid on the neurovascular reflex arc in patients with diabetic neuropathy assessed by capillary microscopy. 1038

The goal of this study was to identify risk factors for diabetic peripheral sensory neuropathy in type 2 diabetes mellitus in a Chinese population. Peripheral sensory neuropathy was detected by quantitative sensory testing (5.07/10 g monofilament, neurometer and 128-Hz Riedel Seiffert graduated tuning fork). Those who had two or more abnormal quantitative sensory testings were defined as having diabetic sensory neuropathy. Of the 558 non-insulin dependent diabetes mellitits subjects, 62 (11.1%) had peripheral neuropathy. In 59 (10.6%) detection was by monofilament testing, 45 (8.1%) by graduated tuning fork, and 189 (33.9%) by neurometer. In a multivariate logistic regression model, age and insulin therapy were significantly associated with peripheral neuropathy. Age, serum triglyceride, height, and fasting plasma glucose were independently associated with large fiber neuropathy. Our results confirm the previously identified multiple risk factors of diabetic neuropathy. Different quantitative sensory testings detect different nerve fiber defects. The weak correlation between these tests indicates the need to use more than one test in screening for diabetic neuropathy.
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PMID:Quantitative sensory testing and risk factors of diabetic sensory neuropathy. 1039 73

The mechanism of neuropathic pain in the diabetic limb is far from clear. Phantom limb pain likewise is of obscure aetiology. The development of typical pain in an absent leg in a patient with diabetes many years after the amputation stimulates thought as to the mechanism, not only of neuropathic pain, but also of phantom limb pain. A 58-year-old man was diagnosed with type 2 diabetes 44 years after having undergone left below knee amputation for congenital AV malformation, at the age of 13. Eight months before the diagnosis of diabetes he began to complain of pain in the leg on the amputated side-pain very similar to that described in typical diabetic neuropathy. This was followed by similar pain in the right leg. MR scan of the spine revealed a small syringohydromyelia of the thoracic cord in addition to a prolapse of disc at L(5)/S(1) level on the left side, which was first noted 5 years previously. There were no other features of S(1) compression. The typical neuropathic character of the pain involving both the amputated and the intact limbs that developed with the diagnosis of type 2 diabetes suggest that the neuropathic pain may originate from centres higher than peripheral nerves.
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PMID:Diabetic neuropathic pain in a leg amputated 44 years previously. 1056 72

Recent surveys in the US have indicated that 71% of the total diabetes care is delivered by primary care physicians, and that current management practices in terms of the point of initiation of pharmacological treatment fall considerably short of the American Diabetes Association's recommendations. In part, this delay in initiating treatment is due to a fear of provoking hypoglycaemia, which in itself results from a general avoidance of blood glucose monitoring on the part of patients. As a consequence of this apparent disregard for diabetes care, blood glucose concentrations are not adequately controlled in the US and this is reflected in a high incidence of chronic complications, particularly diabetic neuropathy. This is likely to have major cost implications in the future. In an effort to improve the standard of diabetes care, a number of US authorities have begun producing guidelines for primary care physicians, and in the State of Texas, treatment algorithms that incorporate recommendations based on the current US registration trial data have been developed. These recommendations, which have now been adopted by the State of Texas and form part of the minimum standard of care mandated by the State Department of Health's Diabetes Council, provide guidance on the selection and use of oral antidiabetic drugs (including sulphonylureas, metformin, troglitazone, repaglinide and acarbose) in patients with type 2 diabetes, both for glycaemic control and for prevention of cardiovascular complications. It is hoped that organised implementation of these treatment algorithms will produce better control of diabetes and its complications than the current ad hoc strategies used by individual practitioners.
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PMID:Strategies for better diabetes control in the US. 1057 28

Detailed clinicofunctional examination of anginal patients with NIDDM using variation pulsometry and electrophysiological cardiac tests in 110 patients (89 females and 21 males aged 36-79 years, mean 64.3 +/- 5.2 years) has revealed that atypical cardialgia, arterial hypertension, obesity was present in 28.1, 76.4 and 85.4% of anginal patients with NIDDM. Sympathicotonia was registered in autonomic heart regulation of 83% of them. Anginal patients exhibited also suppression of sinus node automatism and sinoatrial conduction. When NIDDM is severe, pacemaker activity of the sinus node intensified suggesting development of cardial diabetic neuropathy.
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PMID:[Features of angina pectoris in patients with non-insulin-dependent diabetes mellitus (NIDDM)]. 1068 14

We report a 61-year-old man with diabetic polyneuropathy and bilateral ulnar nerve palsy due to osteoarthrosis in the elbow. He was diagnosed as having non-insulin dependent diabetes mellitus (DM) at 40 years of age. At 56 years of age, he developed muscle atrophy and weakness predominantly in the distal parts of his upper limbs. A neurological examination showed him to have severe atrophy and weakness in the muscles innervated by the ulnar nerve bilaterally. He also had paresthesia on the distal parts of all four limbs. Superficial and deep sensory deficits were observed in the lower limbs. A motor nerve conduction study showed a marked reduction in the motor conduction velocity as well as in the amplitude of the action potentials of both ulnar nerves. Roentgenograms of the elbow joints and grooves for the ulnar nerve revealed marked osteophyte formation bilaterally. The bilateral ulnar nerve palsy was thus considered to be due to the entrapment of the nerve by the osteophyte. Since several studies have suggested the existence of a relationship between DM and osteoarthropathy, it is important to check for the possible presence of osteoarthrosis in cases of diabetic neuropathy complicated with entrapment neuropathy.
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PMID:[A case of diabetic polyneuropathy complicated with entrapment neuropathy of the bilateral ulnar nerves due to osteoarthrosis at the elbow]. 1082 94

We studied the effects of zenarestat, an aldose reductase inhibitor (ARI), on peripheral neuropathy in Zucker diabetic fatty (ZDF) rats, an animal model of type 2 diabetes. ZDF rats and their lean rats counterparts were fed a sucrose-containing diet, and zenarestat was given orally once a day for 8 weeks. Motor nerve conduction velocity (MNCV), F-wave minimal latency (FML), and sorbitol concentrations in the sciatic nerve were measured. In ZDF control rats, a remarkable accumulation of sorbitol, a delay in FML, and a slowing of MNCV were observed compared with lean rats. At a dose of 3.2 mg/kg, zenarestat had no significant effect on the delay in FML and the slowing of MNCV, although the sorbitol accumulation in the sciatic nerve was partially inhibited in ZDF rats. On the other hand, 32 mg/kg zenarestat treatment improved these nerve dysfunctions in ZDF rats, along with a reduction of nerve sorbitol accumulation almost to the level of lean rats. These data showed that zenarestat improved diabetic peripheral neuropathy in ZDF rats, a type 2 diabetes model, providing evidence for the therapeutic potential of zenarestat for the treatment of diabetic neuropathy.
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PMID:The effects of zenarestat, an aldose reductase inhibitor, on peripheral neuropathy in Zucker diabetic fatty rats. 1109


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