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

Vascular complications are the main cause of morbidity in diabetes mellitus. However, the risk factors for vascular disease remain incompletely elucidated. It has been previously suggested that factors other than glycemia may contribute to the development of vasculopathy. In this study we determined the prevalence of phospholipid-binding antibodies in uncomplicated and complicated diabetes. We studied 53 uncomplicated diabetic patients, with type 1 (n = 32) or type 2 (n = 21) diabetes; 23 diabetic patients with proliferative retinopathy; 28 diabetic patients with an overt nephropathy; 37 diabetic patients with macroangiopathy and 22 non diabetic control patients. Both lupus anticoagulant and anticardiolipin antibodies were determined. Other risk factors for macroangiopathy were analysed. The prevalence of phospholipid-binding antibodies was similar in uncomplicated diabetic patients and in controls (type 1 diabetes: 9.4%; type 2 diabetes: 9.5%; control group: 4.6%; P= 0.76). In complicated diabetes, the frequency of these antibodies was increased only in patients with overt nephropathy (32.1%, P=0.01) or with macroangiopathy (32.4%, P=0.01) while patients with isolated retinopathy were comparable with uncomplicated diabetic patients (4.3%, P= 0.66). Uncomplicated diabetes was not associated with phospholipid-binding antibodies. We found a higher prevalence of these antibodies in diabetic patients with macroangiopathy or nephropathy. These results suggest a potential role of phospholipid-binding antibodies in the progression of vascular complications in diabetes mellitus.
Lupus 1998
PMID:Vascular complications of diabetes mellitus: what role for phospholipid-binding antibodies? 979 49

Low-grade inflammation, enhanced oxidant stress and lipid peroxidation have been shown in association with increased cardiovascular risk associated with cardiovascular events. It has been hypothesized that the low-grade inflammatory state characterizing metabolic disorders such as obesity, hypercholesterolemia, type 2 diabetes mellitus and homozygous homocystinuria may be the primary trigger of thromboxane-dependent platelet activation mediated, at least in part, through enhanced lipid peroxidation. Interestingly, as the clinical course of systemic lupus erythematosus (SLE), in particular in the presence of antiphospholipid antibodies, may be complicated by vascular disease, several mechanisms contributing to vascular complications have been documented also in this setting, including enhanced lipid peroxidation and thromboxane biosynthesis. Although epidemiological studies show an inverse relationship between antioxidant vitamin intake and cardiovascular disease, several clinical trials have obtained conflicting results on the effects of vitamin E on the risk of cardiovascular events. The availability of analytical tools for measuring F2-isoprostane biosynthesis in man has improved our understanding of the interplay between lipid peroxidation and low-grade inflammation. The use of F2-isoprostane as a biochemical end-point for dose-finding studies may allow reassessing the adequacy of vitamin supplementation in different clinical settings.
Lupus 2005
PMID:Oxidant stress, inflammation and atherogenesis. 1621 83

Thiazolidinediones (TZDs) are selective ligands of peroxisome-proliferator-activated receptor gamma increasingly used in the treatment of type 2 diabetes. Both in vitro and in vivo studies provide evidence that TZDs have anti-inflammatory properties. TZDs inhibit macrophage activation and decrease inflammatory cytokine expression and release in macrophage and monocyte. In vivo, treatment with TZDs decreases circulating mononuclear cells nuclear NF-kB content while increasing, in the same cells, expression of IkB, an NK-kB inhibitor. Furthermore, TZD treatment results in decreased plasma levels of inflammation and cardiovascular risk markers such as CRP, MMP9, PAI-1 and sCD40 in both obese and type 2 diabetic patients. Finally, TZDs induce synoviocyte apoptosis and reduce secretion of TNFalpha, IL-6 and IL-8 in synoviocyte from rheumatoid arthritis patients. TZDs might thus be considered for use in clinical trials targeting prevention of atherosclerosis and cardiovascular diseases and in pilot trials exploring the possibility that TZDs might help in the treatment of rheumatic diseases.
Lupus 2005
PMID:Thiazolidinediones and inflammation. 1621 90

Metabolic syndrome (MetS) is a recently defined clustering of cardiovascular risk factors associated with insulin resistance and an increased risk of future type II diabetes mellitus and cardiovascular disease (CVD). Systemic lupus erythematosus (SLE) patients have an increased prevalence of MetS and an increased prevalence of insulin resistance. Chronic inflammation may predispose to these complications in SLE and there is also evidence that corticosteroid therapy also contributes, although this finding has not been as consistent as would be predicted from the known metabolic effects of corticosteroids. MetS may represent a good model in which to begin to understand how SLE drives an increased risk of CVD. For now, the utility of identifying MetS in patients is to identify a subset in which more focused lifestyle interventions should be targeted and in whom medication review and adjustment (especially corticosteroid doses) should be considered to help modify future CVD risk.
Lupus 2013 Oct
PMID:SLE and metabolic syndrome. 2409 98