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Prediabetes is associated with a length-dependent polyneuropathy that typically is sensory predominant and painful. A diagnosis of prediabetes should be sought in patients with otherwise idiopathic sensory-predominant neuropathy by doing a 2-hour oral glucose tolerance test. Fasting plasma glucose of 100 to 125 mg/dL or 2-hour glucose 140 to 199 mg/dL (impaired glucose tolerance) constitutes prediabetes. Most patients with neuropathy associated with prediabetes (NAP) are obese and show metabolic manifestations of insulin resistance, including hyperlipidemia and hypertension. Appropriate treatment addresses hyperglycemia, insulin resistance, and neuropathic pain. Professionally administered individualized diet and exercise counseling (modeled on the Diabetes Prevention Program) has been shown to be more effective than glucose-lowering medications in preventing progression from impaired glucose tolerance to diabetes, and is the mainstay of treatment for all patients with NAP. The goals of this therapy should be a 5% to 7% reduction in weight and an increase to 30 minutes of moderate exercise five times weekly. Patients with prediabetes are at increased risk for myocardial infarction, stroke, and peripheral vascular disease. Therefore, risk reduction with control of hypertension and hyperlipidemia is essential. Neuropathic pain troubles nearly every patient with NAP, and often limits aerobic exercise. No trials have specifically addressed the patient population with NAP, and neuropathic pain treatment closely follows recommendations for diabetic neuropathy. Gabapentin, lamotrigine, and tricyclic antidepressants are well-validated first-line therapies. Adjunctive therapy with opioids, nonsteroidal anti-inflammatory drugs often are necessary. Diet and exercise seem to reduce neuropathic pain in patients with NAP.
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PMID:Polyneuropathy with Impaired Glucose Tolerance: Implications for Diagnosis and Therapy. 1561 Jul 5

A disturbingly high prevalence of single or bilateral lower extremity amputations in our program prompted us to conduct a study to identify the prevalence of risk factors that predispose patients on hemodialysis (HD) to foot problems. The study consisted of a one-time assessment of subjects' risk for and actual prevalence of amputation. The sample consisted of 232 subjects--56% male, 44% female. Ages ranged from 21-91 years, mean age 65.1 and median age 69 years. The most common comorbidities were hypertension (75%), coronary artery disease (50%), diabetes (42.2%), hyperlipidemia (34.9%), and peripheral vascular disease (27.2%), which are all established risk factors for peripheral arterial occlusive disease. Twenty-one percent of subjects were current smokers; 28% were former smokers. Nearly 13.4% of subjects had undergone amputations ranging from single toes to bilateral above knee amputations. Only 31% of subjects had both bilateral palpable pedal pulses present. Neuropathy, as evidenced by the inability to feel the application of monofilaments to 10 sites on each foot or the presence of symptoms, was present in 74.6% of subjects. Only 2.6% of subjects demonstrated comprehensive self-care behaviors (SCBs). With respect to subjects' ability for self-care, 75% of subjects had adequate vision, 60% adequate dexterity, and 55% adequate flexibility to perform self-care. Study findings confirmed impressions that patients are at considerable risk for foot complications. Implications for nursing practice include regular foot assessment, education for self-care, and referral to specialists when required.
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PMID:Prevalence of risk factors predisposing to foot problems in patients on hemodialysis. 1618 Jul 79

Peripheral neuropathy is a common problem encountered by neurologists and primary care physicians. While there are many causes for peripheral neuropathy, none can be identified in a large percentage of patients ("idiopathic neuropathy"). Despite its high prevalence, idiopathic neuropathy is poorly studied and understood. There is evolving evidence that impaired glucose tolerance (prediabetes) is associated with idiopathic neuropathy. Preliminary data from a multicenter study of diet and exercise in prediabetes (the Impaired Glucose Tolerance Neuropathy Study) suggests a diet and exercise counseling regimen based on the Diabetes Prevention Program results in improved metabolic measures and small fiber function. Prediabetes is part of the Metabolic Syndrome, which also includes hypertension, hyperlipidemia and obesity. Individual aspects of the Metabolic Syndrome influence risk and progression of diabetic neuropathy and may play a causative role in neuropathy both for those with prediabetes, and those with otherwise idiopathic neuropathy. Thus, a multifactorial treatment approach to individual components of Metabolic Syndrome may slow prediabetic neuropathy progression or result in improvement.
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PMID:Idiopathic neuropathy, prediabetes and the metabolic syndrome. 1644 68

Stroke and peripheral neuropathy are recognized neurological complications of diabetes. Increasing epidemiological evidence also implicates the prediabetic state of impaired glucose tolerance (IGT) as a risk factor for cerebrovascular events and peripheral neuropathy. Data linking IGT to cognitive decline or deficits, however, are less robust. IGT is one component of metabolic syndrome, together with central obesity, hypertension, hypertriglyceridemia and reduced HDL. Each component of metabolic syndrome is an independent risk factor for stroke, but hyperglycemia might be more important than other components in the pathogenesis of neuropathy. Goal-driven diet and exercise regimens, together with pharmacological treatment of hyperlipidemia and hypertension, reduce stroke risk, but the effect of these interventions on neuropathy has not been fully explored.
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PMID:Therapy insight: neurological complications of prediabetes. 1693 64

Poor glycaemic control and the duration of diabetes mellitus are known to accelerate development and progression of neuropathy. Diabetic co-morbidities: hypertension and hyperlipidaemia, have been postulated to associate with development of neuropathy. A diabetic foot with low temperature and frequent exposure to low temperature environment has recently been hypothesized to be at higher risk to develop early neuropathy. This cross-sectional study is undertaken to identify risk factors for diabetic neuropathy and the association between foot temperature and development of diabetic neuropathy by using simple clinical examination in the outpatient setting. From April 18, to April 30, 2005, universal sampling method was used to select 134 diabetic patients (type 1 or type 2 for >1 year) with peripheral neuropathy. Excluded are those with chronic alcoholism, drug-induced neuropathy, dietary history of vitamin B deficiency and family history of porphyria and hereditary sensorimotor neuropathy. The patient's duration of diabetes, glycaemic control status and the presence of co-morbids: hypertension and hyperlipidemia, were recorded. The temperature of the foot was measured by using thermo buddy. Of 134 patients representing Malaysian ethnic distribution with an equal number of males and females, 20.1% were in the age group of 61 to 65 years and, 85.1% and 67.9% belonged to lower socioeconomic and educational groups respectively. Associations between diabetic neuropathy and glycaemic control (p = 0.018) and duration of diabetes (p < 0.05) were significant. However, hypertension, hyperlipidaemia and low foot temperature were not significantly associated with development of diabetic neuropathy. Poor glycaemic control is significantly associated with diabetic neuropathy. Foot temperature alteration is merely an effect of autonomic neuropathy with a cold foot is attributed to co-existing peripheral arterial disease.
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PMID:Alteration of foot temperature in diabetic neuropathy: is it another piece of puzzle? 1704 21

The commonest cause of an optic neuropathy in Singapore is ischaemia, and ischaemic optic neuropathy (ION) is one of the commonest causes of permanent loss of vision in elderly patients, especially in those with diabetes mellitus, hypertension and hyperlipidaemia. ION in our practice is almost invariably of the anterior variety and non-arteritic in origin, i.e. NA-AION. Posterior ION comprises less than two percent of our cases. Three patients with different patterns of NA-AION are described, and in the discussion, how the condition can be distinguished clinically from optic neuritis. With respect to posterior ION, the necessity of excluding a compressive cause before this diagnosis can be made is emphasised.
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PMID:Ischaemic optic neuropathy: the Singapore scene. 1738 70

The peroxisome proliferator-activated receptors (PPARs) are a group of three nuclear receptor isoforms, PPARalpha, PPARgamma and PPARdelta, encoded by different genes, and they form a subfamily of the nuclear receptor superfamily. The clinical interest in PPARs originates with fibrates and thiazolidinediones, which, respectively, act on PPARalpha and PPARgamma and are used to ameliorate hyperlipidaemia and hyperglycaemia in subjects with type 2 diabetes mellitus (T2DM). PPARs play a central role in these patients due to their ability to regulate the expression of numerous genes involved in glycaemic control, lipid metabolism, vascular tone and inflammation. Abnormal angiogenesis is implicated in several of the long-term complications of diabetes mellitus, characterized by vasculopathy associated with aberrant growth of new blood vessels. This pathological process plays a crucial role in diabetic retinopathy, nephropathy and neuropathy, impaired wound healing and impaired coronary collateral vessel development. In recent years, there has been increasing appreciation of the fact that PPARs might be involved in the molecular mechanisms that regulate angiogenesis through the action of growth factors and cytokines that stimulate migration, proliferation and survival of endothelial cells. During the last few years direct comparative analyses have been performed, using selective PPARs agonists, to clarify the angiogenic properties of the different members of the PPAR family. Lately, the findings provide new information to order to understand the biological, clinical and therapeutic effects of PPARs, and the role of these nuclear receptors in angiogenesis, with potentially important implications for the management of subjects affected by T2DM.
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PMID:Peroxisome proliferator-activated receptors and angiogenesis. 1962 79

Type 1 diabetes mellitus (T1DM) results from autoimmune destruction of insulin-producing beta cells and is characterised by the presence of insulitis and &and beta-cell autoantibodies. Up to one third of patients develop an autoimmune polyglandular syndrome. Fifteen to 30% of T1DM subjects have autoimmune thyroid disease (Hashimoto's or Graves' disease), 5 to 10% are diagnosed with autoimmune gastritis and/or pernicious anaemia (AIG /PA), 4 to 9% present with coeliac disease (CD), 0.5% have Addison's disease (AD), and 2 to 10% show vitiligo. These diseases are characterised by the presence of autoantibodies against thyroid peroxidase (for Hashimoto's thyroiditis), TSH receptor (for Graves' disease), parietal cell or intrinsic factor (for AIG /PA), tissue transglutaminase (for CD), and 21-hydroxylase (for AD). Early detection of antibodies and latent organ-specific dysfunction is advocated to alert physicians to take appropriate action in order to prevent full-blown disease. Hashimoto's hypothyroidism may cause weight gain, hyperlipidaemia, goitre, and may affect diabetes control, menses, and pregnancy outcome. In contrast, Graves' hyperthyroidism may induce weight loss, atrial fibrillation, heat intolerance, and ophthalmopathy. Autoimmune gastritis may manifest via iron deficiency or vitamin B12 deficiency anaemia with fatigue and painful neuropathy. Clinical features of coeliac disease include abdominal discomfort, growth abnormalities, infertility, low bone mineralisation, and iron deficiency anaemia. Adrenal insufficiency may cause vomiting, anorexia, hypoglycaemia, malaise, fatigue, muscular weakness, hyperkalaemia, hypotension, and generalised hyperpigmentation. Here we will review prevalence, pathogenetic factors, clinical features, and suggestions for screening, follow-up and treatment of patients with T1DM and/or autoimmune polyglandular syndrome.
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PMID:Type 1 diabetes and autoimmune polyglandular syndrome: a clinical review. 2000 14

A 76-year-old woman with a history of percutaneous transvenous mitral commissurotomy and repeated hospital admissions due to heart failure was referred for an operation for severe mitral valve stenosis. She presented with hypertension, hyperlipidemia and cerebral infarction with stenosis of right internal carotid artery, retinopathy, neuropathy and nephropathy caused by long-term uncontrolled diabetes mellitus, hemoglobin A1c of 9.4%, and New York Heart Association (NYHA) functional classification of 3/4. Echocardiography revealed severe mitral valve stenosis with mitral valve area of 0.6 cm2, moderate tricuspid valve regurgitation, and dilatation of the left atrium. Taking into consideration the NYHA functional classification and severe mitral valve stenosis, an immediate surgical intervention designed to prevent mediastinitis was performed. The approach was via the right 4th thoracotomy, as conventional sternotomy would raise the risk of mediastinitis. Postoperative antibiotics were administered intravenously for 2 days, and signs of infection were not recognized.In patients with long-term uncontrolled diabetes mellitus, mid-line sternotomy can easily cause mediastinitis. The choice of operative approach plays an important role in preventing this complication. In this report, the importance of the conventional right thoracotomy for prevention for mediastinitis is reviewed.
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PMID:Mitral valve replacement via right thoracotomy approach for prevention of mediastinitis in a female patient with long-term uncontrolled diabetes mellitus: a case report. 2047 46

Diabetes is a debilitating chronic disease that has no cure and can only be managed by pharmaceutical or nutritional interventions. Worldwide, the incidence of diabetes and diabetic complications is dramatically increasing. This may reflect the incomplete knowledge base underlying the role of inflammatory or nutritional stresses to exacerbate diabetic complications. Despite the knowledge that hyperlipidemia is a cardinal feature of both Type 1 and 2 diabetes, the actual lipid species that contribute to complications such as diabetic nephropathy, retinopathy, neuropathy and cardiovascular disease have not been well defined, or have not elucidated new treatment strategies. Sphingolipids comprise only a fraction of total lipids but a body of evidence has now identified dysfunctional sphingolipid metabolism and/or generation of specific sphingolipid metabolites as contributors to diabetic complications. This review suggests that pharmacological therapies that target dysfunctional sphingolipid metabolism and/or signaling may prove beneficial in decreasing the chronic pathology of hyperglycemia and hyperlipidemia. Moreover, the review suggests that these treatment options may also prove beneficial to ameliorate or delay pancreatic beta cell failure.
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PMID:Therapeutic strategies for diabetes and complications: a role for sphingolipids? 2091 56


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