Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with nephrotic syndrome (NS) are believed to be at increased risk of atherosclerosis and coronary heart disease (CHD), although existing evidence for this association has not been persuasive. The risk of CHD among 142 persons with NS documented by protein-uria > or = 3.5 g daily was compared with that among 142 matched controls randomly selected from the membership of a large Northern California health plan. Controls were matched for sex, year of birth, and presence in the health plan when the referent case was diagnosed. No diabetics were included in this study. Mean follow-up for nonfatal CHD events was 5.6 years for NS subjects and 11.2 years for controls. Among the NS subjects myocardial infarction (MI) developed in 11, and there were 58 deaths, seven because of CHD. Among the controls, there were four MIs and 10 deaths, three because of CHD. In matched-pair analysis, there were 11 MIs among NS subjects and none among controls [P = 0.001, lower bound of 95% confidence interval for relative risk (CI), 2.8]. In an unmatched analysis adjusted for hypertension and smoking at diagnosis of NS, the relative risk of MI was 5.5 (95% CI 1.6 to 18.3) and the relative risk of coronary death was 2.8 (95% CI 0.7 to 11.3). Omitting data of NS subjects with minimal change disease and systemic lupus erythematosus yielded similar results. These data suggest that persons with NS are at increased risk of CHD.
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PMID:The increased risk of coronary heart disease associated with nephrotic syndrome. 823 Oct 39

Raynaud's syndrome manifests as a progressive color change of the fingers in response to cold, vibration or stress; the digits first turn white, then blue and finally red. The condition is called Raynaud's disease when it is a benign, primary condition. When it is secondary to another disease, such as lupus, scleroderma or atherosclerosis, it is termed Raynaud's phenomenon. Laboratory tests, i.e., complete blood count, chemistry screen, antinuclear antibody, lupus erythematous test and rheumatoid factor, should be used to seek underlying diseases before the symptoms are manifest. Other tests should be selected as indicated by the history and physical. There are many adjustments in lifestyle and working conditions that the patient can use to minimize the symptoms of Raynaud's syndrome. The primary care provider has an important role in teaching patients to protect their hands from the effects of cold, stress, nicotine and vibration. Adaptive devices and protective clothing minimize the symptoms of Raynaud's syndrome.
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PMID:The diagnostic puzzle and management challenge of Raynaud's syndrome. 845 39

Thrombosis occurs when there is a breakdown in the balance between thrombogenic factors and protective mechanisms. The thrombogenic factors may be exogenous (e.g. trauma, surgery), endogenous (e.g. cancer, vascular diseases) or both (e.g. atherosclerosis, complicated pregnancy). Defects in the protective mechanisms may be congenital (e.g. factor V R506Q-mutation, deficiency of protein C, protein S or antithrombin) or acquired (e.g. lupus anticoagulans, deficiency of antithrombin in nephrosis). In recent years, research in thromboembolic diseases has been overwhelmed with new observations, rendering it worthwhile to put efforts into the evaluation of thrombotic mechanisms in individuals suffering from or predisposed to thromboembolic diseases. Such efforts will pave the way for more effective prophylaxis in thrombosis-prone patients, more specific treatment of thrombotic diseases, and the mastering of recurrent thrombosis.
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PMID:Thrombogenesis. 868 75

Gemfibrozil improves lipid and apolipoprotein profiles, particularly very low density lipoprotein (VLDL) triglyceride and high density lipoprotein (HDL) cholesterol levels, in patients with dyslipidaemia when administered at a total daily dose of 900 or 1200 mg. As demonstrated by the Helsinki Heart Study, these effects result in a reduction in some risk factors for coronary heart disease (CHD) and also a 34% reduction in the incidence of this disease after 5 years compared with placebo. Limited data suggest that gemfibrozil has beneficial effects on the fibrinolytic system and may slow the progression of atherosclerosis. Gemfibrozil has shown efficacy in the treatment of patients with type IIa, IIb, III, IV or V dyslipidaemia or hypoalphalipoproteinaemia, especially in patients with elevated triglyceride and low HDL cholesterol levels. It is also effective in patients with non-insulin-dependent diabetes mellitus (NIDDM) and dyslipidaemia and has no detrimental effects on glycaemic control. A small number of studies also showed gemfibrozil to be effective for the control of dyslipidaemia associated with renal failure, transplantation, nephrotic syndrome, arterial occlusive disease or systemic lupus erythematosus. However, patients with pre-existing CHD do not appear to derive the same benefits (reduced CHD mortality) from gemfibrozil therapy as these other patients, although results are based on studies of limited size and number. In general, gemfibrozil has at least similar efficacy to bile acid sequestrants and other fibric acid derivatives. Comparisons with HMG-CoA reductase inhibitors show these agents to produce different effects on lipid profiles from gemfibrozil. Thus, gemfibrozil would be expected to be superior in some patients (those with elevated triglyceride or VLDL cholesterol levels), but HMG-CoA reductase inhibitors should have greater benefits in those with elevated low density lipoprotein cholesterol levels. Thus, in patients with elevated triglyceride levels and low HDL cholesterol levels, and, particularly in patients with NIDDM, gemfibrozil is a useful treatment option, which has been shown to reduce the risk of CHD in middle aged men. However, limited available data prevents the accurate comparison of this agent with HMG-CoA reductase inhibitors in patients with this lipid profile.
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PMID:Gemfibrozil. A reappraisal of its pharmacological properties and place in the management of dyslipidaemia. 873 20

Vascular damage in systemic lupus erythematosus (SLE) occurs through vasculitis, premature atherosclerosis, and hypercoagulability (predominantly due to the antiphospholipid antibody syndrome). In the Hopkins Lupus Cohort, a prospective cohort study, the incidence of thrombosis is 2 per 100 person-years of follow-up. Markers of immune-complex mediated injury (high anti-dsDNA and low C3), atherosclerosis (hypertension, hyperlipidemia, homocysteine) and antiphospholipid antibodies (lupus anticoagulant or anticardiolipin) are independent predictors of thrombosis. Hydroxychloroquine use is protective against future thrombosis.
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PMID:Thrombosis and systemic lupus erythematosus: the Hopkins Lupus Cohort perspective. 879 94

The family of antiphospholipid antibodies includes antibodies binding to cardiolipin in serological test for syphilis, antibodies prolonging the clotting time in lupus anticoagulant test, antibodies reacting with plasma phospholipid-binding proteins, such as beta 2-glycoprotein I and prothrombin, and antibodies binding to oxidized low-density lipoprotein (LDL). Antiphospholipid antibodies are traditionally associated with arterial and venous thrombosis in patients with primary or secondary antiphospholipid syndrome. The recent studies, especially those on patients with myocardial infarction, extend the concept of antiphospholipid antibodies, and suggest that they play a role also in atherosclerosis. Based on the clinical studies and immunological findings, it seems that the differences in the specificity of antiphospholipid antibodies may reflect to their pathogenetic mechanisms and, finally, to their clinical consequences. The present review suggests that antibodies to oxidized LDL may not interfere directly with blood coagulation, but seem to have importance in the inflammation of the vessel wall in atherosclerosis and in vasculitis. Instead, antibodies to beta 2-glycoprotein I and to prothrombin show a closer association with thrombosis. It is possible that in the atherosclerotic plaque, the plasma proteins, such as beta 2-glycoprotein I or prothrombin, are bound to the endothelial surface and antibodies to cryptic epitopes revealed in these proteins are induced. These antibodies may contribute to the formation of atherosclerotic thrombosis by changing the balance of haemostasis toward hypercoagulative state.
Lupus 1996 Oct
PMID:Antiphospholipid antibodies and atherosclerosis. 890 78

Premature atherosclerosis is a recognized complication of systemic lupus erythematosus. Atherosclerosis begins in the pediatric age group, and interventions directed toward prevention should begin in childhood as well. A possible cause of premature atherosclerosis is dyslipoproteinemia from the underlying chronic inflammatory disease or from corticosteroid therapy. A relationship between dyslipoproteinemia and anticardiolipin antibodies has been demonstrated. Dietary therapy is helpful, but many patients continue to have significant dyslipoproteinemia after both dietary modification and fish oil supplementation. Lipid-lowering drugs may be indicated in this subgroup. Potential mechanisms of dyslipoproteinemia are discussed.
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PMID:Hyperlipidemia and the rheumatic diseases. 894 49

It is now known that human exposure to certain chemicals e.g. benzene, halocarbons, ketones, nitrosamines, etc. can result in adverse health effects that are often not easily recognised as manifestations of chemical toxicity. These are inflammatory states, such as hepatitis, nephritis, scleroderma, and lupus, due to production of reactive oxygen species (ROS) through activation of cytochrome P4502E1 by the chemical, or by metabolism of the chemical to reactive intermediates and neoantigens which initiate immunotoxic effects. Intracellular glutathione (GSH), vitamins C, E and A protect against this ROS toxicity and inflammation; fasting and consumption of alcohol exacerbate it. Chronic inflammatory states may subsequently develop, including rheumatoid disease, atherosclerosis, diabetes, infertility and birth defects, multiple system organ failure (MSOF), Alzheimer's disease, and cancer.
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PMID:Chemical-induced inflammation and inflammatory diseases. 897 63

We identified a group of 24 young (less than 50 years of age) women with isolated, premature atherosclerotic aortoiliac occlusive disease and attempted to identify distinguishing hemostatic characteristics. Most of these patients (62%) presented with acute thromboembolic events (blue toe syndrome, n = 6; macroemboli, n = 6; or aortoiliac thrombosis, n = 3). Aortoiliac reconstruction (aortoiliac endarterectomy, n = 10, aortobifurcation bypass grafts, n = 6; and percutaneous angioplasty, n = 4) was complicated by early thrombosis in 6 of 20 cases (30%), (1 of 10 endarterectomies, 4 of 6 bypass grafts, and 1 of 4 angioplasties). Fresh thrombus overlying an atherosclerotic plaque was a common finding at surgery. This observation and the relatively high incidence of thromboembolic events led us to hypothesize that a characteristic hemostatic profile might underlie the remarkably similar clinical presentations of these women. Levels of antiphospholipid antibodies (anticardiolipin antibodies and lupus anticoagulant), plasminogen activator inhibitor-1, fibrinogen, antithrombin III, protein C, protein S, plasminogen, prothrombin fragment F1 + 2, and D-dimer were determined for these young women and for 21 age-matched white female control subjects without vascular disease and nine white male patients with aortoiliac occlusive disease (mean 61 years, range 43 to 74 years). The incidence of anticardiolipin antibodies was 42% (8 of 19) in the female patients, which was significantly elevated (p = 0.028). The female (62.5%) and male (100%) patients had significantly elevated D-dimer levels (p < 0.001). Deficiencies of antithrombin III, protein C, and protein S were rare. A unique pattern of premature aortoiliac atherosclerosis exists in some young women. Intra-arterial thromboembolic events are common at presentation and complicate surgical management. The role of antiphospholipid antibodies remains uncertain.
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PMID:Young women with advanced aortoiliac occlusive disease: new insights. 898 71

Aortoiliac occlusion due to atherosclerosis is known to occur in elderly people. Two unique cases are documented here in which aortoiliac occlusion was observed in young men. These patients had no identifiable risk factors for developing atherosclerotic thrombosis except for the lupus anticoagulant, an immunoglobulin associated with thromboembolic episodes. Although previously the lupus anticoagulant has been reported to cause thrombosis only in relatively small-sized arteries or veins, it may also be associated with aortoiliac atheromatous occlusion in young men.
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PMID:Aortoiliac occlusion associated with the lupus anticoagulant. Report of two cases. 911 85


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