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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 76-year-old female patient is presented who suffered from muscular weakness in arms and legs. She was obese and had a symmetric accumulation of fatty tissue with a bumpy structure at both arms which gave the patient a pseudoathletic appearance. Fatty tissue accumulations were present at both shoulders, arms, at both thighs, at the back and the abdomen. She suffered from benign symmetric lipomatosis (BSL), also called Launois-Bensaude syndrome (LBS), which is a rare disorder of unknown origin and poorly understood pathophysiology. It is believed to be a disease of disturbed lipogenesis induced by catecholamines. The syndrome is often associated with features of metabolic syndrome such as diabetes mellitus, hyperuricemia, hyperlipidemia and hypertension and is associated with polyneuropathy which is an integral part of the disease. Therapeutic options are pharmacological treatment with salbutamol and surgical procedures such as lipectomy or liposuction.
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PMID:Benign symmetric lipomatosis (Launois-Bensaude syndrome). A rare cause of muscular weakness. 1718 68

Length-dependent polyneuropathy has long been recognized as a frequent complication of diabetes. A decade of observational and epidemiologic studies support the concept that intermittent hyperglycemia or insulin resistance associated with prediabetes may be sufficient to damage distal nerves. Features of the metabolic syndrome have been implicated as independent neuropathy risk factors in large population-based studies of diabetic patients. Preferential injury to small unmyelinated nerves is suggested by prominent neuropathic pain, predominant sensory injury, and early autonomic dysfunction. Small uncontrolled trials suggest that diet and exercise may transiently improve distal nerve function and neuropathy symptoms in these patients. Patients with prediabetes neuropathy may permit greater insight into the balance between distal axonal injury and nerve regenerative capacity that determines neuropathy progression, and will be good candidates for evaluation of rational therapy based on known pathophysiology of hyperglycemic neuropathy.
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PMID:Neuropathy associated with prediabetes: what is new in 2007? 1825 3

Metabolic syndrome (MS) encompasses a series of diseases which, when combined, increase vascular risk more than the sum of their individual risks. Insulin resistance (IR) is one of the basic components of MS. - Abdominal fat distribution is an IR marker and is associated to factors increasing vascular risk such as dyslipidemia, high blood pressure, and hyperglycemia, components of the so-called metabolic syndrome. - IR is related to glomerular sclerosis and renal failure through several mechanisms, Including genetic and environmental factors, and stimulation of the renin-angiotensin-aldosterone system. - IR usually precedes development of DM, and therefore contributes to its early identification. MS increases the risk of chronic complications from DM and is associated to an increased prevalence of cardiovascular disease, particularly coronary heart disease, increasing mortality from this cause. - The presence of MS in DM2 is usually associated to a greater prevalence of microalbuminuria or proteinuria and peripheral polyneuropathy.
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PMID:[Metabolic syndrome and kidney disease]. 1901 36

Cardiac autonomous neuropathy (CAN) is a rare complication of diabetes mellitus (DM) that impairs the patient"s quality of life and prognosis. Despite evidence if common pathogenetic mechanism of metabolic syndrome (MS) and autonomous dysfunction, the relationship between CAN and MS in type 2 DM remains poorly known. We examined 157 patients with DM to study manifestations of CAN depending on the presence of MS components. MS was diagnosed using WHO criteria and CAN based on two or more pathologic results in Ewing"s cardiovascular tests (deep respiration test, Valsalva test, orthostatic test with estimation of HR and AP). The patients were allocated to 4 groups to evaluate clinical symptoms of CAN, cardiac rhythm variability and daily AP profile. Group 1 comprised 14 patients without CAN presenting with not more than one component of MS, group 2 16 patients without CAN with 2-3 components of MS, group 3 108 patients with CAN and not more than one component of MS, group 4 108 patients with CAN and 2-3 with component of MS. Overall CAN prevalence was 80.9%. The occurrence of CAN positively correlated with peripheral polyneuropathy, arterial hypertension, severity of DM, AP, and the number of MS components. The presence of CAN and/or 2 and more MS components associated with lowered index of cardiac rhythm variability (LF/HF) indicative of disturbed sympatovagal balance. The daily AP profile in patients with CAN and 2 or more MS components was characterized by anomalous nocturnal drop. Combination of CAN with 2 or more MS components was associated with the most unfavourable night time AP profile.
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PMID:[Cardiac autonomous neuropathy and metabolic syndrome in patients with type 2 diabetes mellitus]. 2108 55

Chronic idiopathic axonal polyneuropathy (CIAP) is referred to as axonal neuropathy after an adequate workup fails to determine a cause. A subgroup of patients with CIAP has impaired glucose tolerance (IGT). These patients have been considered by some investigators to have a neuropathy as a result of IGT and/or metabolic syndrome (MetS). Patients with CIAP usually suffer from chronic pain and associated depression, both of which have been proposed to cause insulin resistance (IR) by such mechanisms as a sustained increase in the corticosteroids and catecholamines, and chronic low grade inflammation. In a pilot study of 14 patients with CIAP+IGT and eight normal controls, we found a correlation between the number of features of the MetS with scores of pain and depression. There was no increase in the frequency of retinopathy and nephropathy in these patients, contrary to what would have been expected if chronic hyperglycemia was the cause of the neuropathy. We hypothesize that neuropathy has an unclear cause in the majority of patients with CIAP+IGT/MetS--and IGT/MetS are a result of comorbidities of CIAP, including chronic pain and depression.
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PMID:Impaired glucose tolerance and metabolic syndrome in idiopathic polyneuropathy: the role of pain and depression. 2125 40

Diabetic peripheral neuropathy is a prevalent, disabling disorder. The most common manifestation is distal symmetrical polyneuropathy (DSP), but many patterns of nerve injury can occur. Currently, the only effective treatments are glucose control and pain management. While glucose control substantially decreases the development of neuropathy in those with type 1 diabetes, the effect is probably much smaller in those with type 2 diabetes. Evidence supports the use of specific anticonvulsants and antidepressants for pain management in patients with diabetic peripheral neuropathy. However, the lack of disease-modifying therapies for diabetic DSP makes the identification of new modifiable risk factors essential. Growing evidence supports an association between components of the metabolic syndrome, including prediabetes, and neuropathy. Studies are needed to further explore this association, which has implications for the development of new treatments for this common disorder.
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PMID:Diabetic neuropathy: clinical manifestations and current treatments. 2260 66

Diabetes is associated with a variety of chronic and acute neuropathies. In this article, the authors summarize the clinical features of the most common diabetic neuropathies, focusing on those for which therapy is available or under active investigation. Distal symmetric polyneuropathy (DSP) is the most common form. Potential treatments for DSP are discussed in four broad themes: (1) medication and lifestyle therapy to improve hyperglycemia, insulin resistance, and attendant features of metabolic syndrome, including obesity and dyslipidemia; (2) pharmacologic therapy to alter neuropathy natural history aimed at rational targets from known pathophysiology; (3) symptomatic relief of neuropathic pain; and (4) treatment to prevent complications of neuropathy, including stasis ulcers and falls. The approach to the most common acute diabetic neuropathies is also reviewed.
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PMID:The diabetic neuropathies: practical and rational therapy. 2311 44

Although metabolic syndrome was not extensively studied in type 1 diabetes, higher insulin resistance, the core feature of the syndrome was found to be associated with increased risk of developing microvascular complications. As diabetic nephropathy may progress to advanced lesion before microalbuminuria appears, we investigated the association of the metabolic syndrome and estimated glucose disposal rate (eGDR) with urinary albumin excretion (UAE), retinopathy and neuropathy in normoalbuminuric type 1 diabetic patients. Two hundred and 98 patients (UAE < 30 mg / 24 h at three occasions) were divided according to the IDF metabolic syndrome; eGDR (mg kg(-1) min(-1)) was calculated: 24.31-(12.22 x WHR) - (3.29 x HT) - (0.57 x HbA1c), (WHR = waist-to-hip ratio, HT = hypertension). Patients with (n = 99) compared to those without metabolic syndrome (N = 199) showed higher UAE (15.96 +/- 9.10; 13.48 +/- 8.36 mg /24 h), C-reactive protein (2.39 +/- 4.09;1.12 +/- 2.03 mg/L), prevalence of retinopathy (70.7; 55.27%) and polyneuropathy (80.8; 68.3%), and lower eGDR (5.75 +/- 1.74; 8.96 +/- 1.9), (p > 0.05). In patients with high-normal UAE, retinopathy and polyneuropathy eGDR was significantly lower compared with patients with low-normal UAE, and without retinopathy and polyneuropathy. In multiple regression analysis UAE and retinopathy were associated with diabetes duration (beta = -0.20, beta = -0.62), eGDR (beta = - 0.106; beta = -0.041), metabolic syndrome (beta = 0.49, beta = 0.28), (p > 0.05). In type 1 diabetic patients insulin resistance and IDF defined metabolic syndrome are associated with high-normal UAE, retinopathy and polyneuropathy. The predictive value of the metabolic syndrome for development of microalbuminuria and retinopathy needs to be assessed in further follow-up studies.
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PMID:The metabolic syndrome is associated with high-normal urinary albumin excretion and retinopathy in normoalbuminuric type 1 diabetic patients. 2339 Aug 36

To establish the role of the metabolic state in the pathogenesis of polyneuropathy, an age- and sex-matched, longitudinal study in rats fed high-fat and high-sucrose diets (HFSD) or high-fat, high-sucrose and high-salt diets (HFSSD) relative to controls was performed. Time courses of body weight, systolic blood pressure, fasting plasma glucose (FPG), insulin, free fatty acids (FFA), homeostasis model assessment-insulin resistance index (HOMA-IR), thermal and mechanical sensitivity and motor coordination were measured in parallel. Finally, large and small myelinated fibers (LMF, SMF) as well as unmyelinated fibers (UMF) in the sciatic nerves and ascending fibers in the spinal dorsal column were quantitatively assessed under electron microscopy. The results showed that early metabolic syndrome (hyperinsulinemia, dyslipidemia, and hypertension) and prediabetic conditions (impaired fasting glucose) could be induced by high energy diet, and these animals later developed painful polyneuropathy characterized by myelin breakdown and LMF loss in both peripheral and central nervous system. In contrast SMF and UMF in the sciatic nerves were changed little, in the same animals. Therefore the phenomenon that high energy diets induce bilateral mechanical, but not thermal, pain hypersensitivity is reflected by severe damage to LMF, but mild damage to SMF and UMF. Moreover, dietary sodium (high-salt) deteriorates the neuropathic pathological process induced by high energy diets, but paradoxically high salt consumption, may reduce, at least temporarily, chronic pain perception in these animals.
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PMID:High energy diets-induced metabolic and prediabetic painful polyneuropathy in rats. 2345 Dec 27

The aim of the present study was to characterize the morphometry of the femoral nerve in aging rats with metabolic syndrome compared to controls. Systolic blood pressure and fasting plasma glucose were measured, and myelinated and unmyelinated fibers in the femoral nerves were quantitatively assessed under electron microscopy. Aging rats exposed to a regimen of metabolic syndrome developed elevation of plasma glucose concentration, mild hypertension and polyneuropathy characterized by a decrease in myelin fiber area, axon diameter, myelin sheath thickness and myelin fiber loss in the femoral nerve. The histogram of size distribution for myelinated fibers and axons from the aging rats of the control group was bimodal. For aging MS animals, the histogram turned out to be unimodal. The ultrastructure of unmyelinated fibers and of Schwann cells in 18-month-old rats was well preserved. Granules of lipofuscin were seen in unmyelinated fiber axons of 18-month-old rats with MS. The damage percentage of the large myelinated fibers has increased significantly in 18-month-old and 18-month-old (MS) rats in relation to the controls. No significant difference was observed among the groups for the g-ratio. Comparing the three groups, the number of neurotubules and neurofilaments in myelinated fibers of 18-month-old rats with MS was significantly smaller than for the groups of 18-month-old and 14-month-old rats. The overall changes seen in the femoral nerve from aging rats seem minor compared to the changes in the aging rats with MS, suggesting that long-term MS accelerates the progressive modifications in peripheral nerves that develop in old age.
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PMID:Effects of metabolic syndrome on the ultrastructure of the femoral nerve in aging rats. 2586 14


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