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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty patients with "idiopathic" bone infarction were studied. There were 18 men and 2 women, age 30 to 69 years, at the time of the diagnosis (mean age = 49 years). Sixty-five lesions were recorded with a marked predominance to the lower extremities (77 p. cent are located around the knees) and to the metaphysis (only three pure diaphyseal lesions). Considered asymptomatic, these lesions were painful in 6 patients. They are multiple, and in this case symmetrical, in 12 patients (60 p. cent). X-Rays disclose the classic heterogeneous ball-like, smoke twirled or encapsulated calcifications. A periosteal thickening opposite the lesions was observed in 6 patients; this may be the only radiological sign. Finally, 18 of the 65 lesions were not visible on standard X-Rays, and obvious on MRI. The MRI aspect is characteristic and may be superposed on the basic lesions already described in the course of aseptic osteonecroses of the femoral head. This is, besides, the most sensitive test, snowing a larger number of more extended necroses than the other examinations. CT scanning as well as scintigraphy present a limited advantage. More than half of the patients also present epiphyseal aseptic osteonecroses, often multiple (55 sites for 13 patients), and often unrecognized. The etiological factors are in fact common to both of these diseases: steroid therapy, alcoholism, dyslipidemia, idiopathic forms. Among the possible causes, the literature mentions lupus erythematosus, renal transplant, cytosteatonecrosis, arteriopathies while there is no post-traumatic form. All of the characteristics of these bone infarctions determine a topographic form of the osteonecrotic disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bone infarction, or idiopathic metaphyseal and diaphyseal aseptic osteonecrosis of the long bones. Update and contribution of new imaging technics]. 219 73

Non-immune mechanisms appear to be important in the majority of patients with lupus nephritis and progressive renal injury. Proteinuria, hypertension and dyslipidemia are associated non-immune risk factors often implicated in the deterioration of kidney function. There is ample animal experimental evidence that they are independent risk factors for progressive renal injury and their treatment results in amelioration of renal function. Proteinuria and hypertension, unlike dyslipidemia, have been shown to be independent risk factors for progressive renal injury in patients with lupus nephritis. Treatment of hypertension and proteinuria in the diabetic and non-diabetic progressive renal disease population results in stabilization of kidney function. Response to treatment should target both blood pressure of 120/80 and significant reductions in protein excretion. If protein excretion rate is unaltered by use of an angiotensin-converting enzyme inhibitor and salt restriction, one might resort to the use of an angiotensin II antagonist. Treatment of the dyslipidemia following good control of proteinuria, blood pressure and dietary change may not alter renal progression but should provide similar protection from accelerated vascular disease to the non-renal dyslipidemia population.
Lupus 1998
PMID:Management of chronic renal insufficiency in lupus nephritis: role of proteinuria, hypertension and dyslipidemia in the progression of renal disease. 988 5

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease marked by immune-complex mediated lesions in small blood vessels of various organs, especially the kidneys, although other factors may also be implicated in the pathogenesis of the disease. This article focuses on the role of lipids in the progression of glomerular, vascular and tubulo-interstitial lesions in two patients with lupus nephritis associated with pronounced hyper- and dyslipidemia. The pathogenesis of progressive glomerulosclerosis in both patients appears to be multifactorial. In addition to immune complex mediated lupus glomerulonephritis, progressively active in the first patient, severe nephrotic-range persistent proteinuria, arterial hypertension associated with hyperfiltration and hyperperfusion injuries and, to a minor extent, hyper- and dyslipidemia were observed. Immunological and non-immunological factors were shown to contribute to the development of tubulo-interstitial lesions. In both patients, in addition to local immune deposits, prominent tubulo-interstitial lipid deposits were probably causally related to both hyperlipidemia and the increased permeability of the glomerular filtration barrier. Tubular lesions were highlighted by intracytoplasmic lipid droplets as well as small cleft-like spaces found to be impacted in the tubular lumina. They were seen to penetrate tubular epithelial cells and eventually lodge in the interstitium, surrounded by mononuclear cell infiltrates and foam cells. In both patients, hypertensive angiopathy and extraglomerular vascular immune deposits were demonstrated. In addition, in the second patient, arteriolar and small arterial hyaline was found at the age of 28 years to be full of lipids and calcium precipitates, suggesting a peripheral atherosclerosis-like process which never occurs as a natural age-related condition. In conclusion, all parts of the nephron may be involved in the pathogenetic process causally related or influenced by hyper- or dyslipidemia. Associated either with endothelial cell injury and consequent insudation of lipids in the vascular walls, glomerular filtration barrier injury with hyperfiltration, or tubulo-interstitial lipid deposition, the mechanism of tissue damage by lipids in all parts of the nephron shares similarities with the pathogenesis of systemic atherosclerosis.
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PMID:Role of lipids in the progression of renal disease in systemic lupus erythematosus patients. 1102 Sep 63

The femoral head is the main location of avascular osteonecrosis. The lesion remains asymptomatic for several months or years before causing non specific hip pain. Risk factors have been identified, mainly femoral neck fractures, corticosteroid therapy and related conditions (lupus erythematosus, organ transplantations), alcohol abuse, dyslipidemia, sickle cell disease, HIV infection, caisson workers, Gaucher's disease, male sex. When typical radiological signs are lacking, MRI is the best investigation. Progression toward hip joint damage highly depends on the necrotic volume assessed at MRI. The combination of plain radiographs which help staging the severity of osteonecrosis, and MRI which indicates the prognosis of the lesion, determines the therapeutic options: symptomatic pain relief therapies or surgical treatment (core decompression, osteotomy or total hip replacement).
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PMID:[Osteonecrosis of the femoral head]. 1200 11

Atherosclerosis is the major cause of cardiovascular disease (CVD) and in addition to established risk factors as smoking, hypertension, diabetes and dyslipidemia, inflammation and autoimmune reactions have been much discussed recently. Several lines of evidence indicate that also inflammation and autoimmune reactions are highly relevant in atherosclerosis and CVD. Inflammatory cells and cytokines are present in lesions, already at an early stage; animal experiments suggest that immune reactions, though not necessary for development of atherosclerosis, can modulate disease development and systemic inflammation is associated with an enhanced risk of CVD. The enhanced risk of CVD in a major autoimmune disease, systemic lupus erythematosus (SLE), is therefore highly relevant, and in addition to being an important clinical problem, SLE-related CVD could give insights into the nature of autoimmunity in atherosclerosis and CVD in general. We recently defined traditional and non-traditional risk factors for CVD in SLE. These include increased atherosclerosis (as determined by intima-media thickness of carotid artery); raised oxidized low density lipoprotein (OxLDL) and autoantibodies to OxLDL; dyslipidemia with raised triglycerides and Lp(a) and decreased HDL-cholesterol concentrations; raised systemic inflammation; presence of anti-phospholipid antibodies including lupus anticoagulant, homocysteine-levels and more frequent osteoporosis. Disease duration, smoking, blood pressure or diabetes mellitus did not differ significantly between the groups. Taken together, immune reactions are highly relevant in atherosclerosis, and patients with autoimmune disease like SLE are at high-risk of CVD. If confirmed prospectively, non-traditional risk factors like OxLDL in the circulation, autoantibodies against OxLDL and phospholipids and inflammation could lead to new therapeutic strategies and insight into disease mechanisms.
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PMID:Autoimmunity, oxidized LDL and cardiovascular disease. 1284 1

The increased risk of premature cardiovascular disease (CVD) in rheumatoid arthritis (RA) patients may depend on traditional risk factors but may also be attributable to RA-specific risk factors such as disease-related dyslipidemia, or cytokines such as tumor necrosis factor-alpha (TNF-alpha). TNF-alpha is a proinflammatory cytokine that can produce widespread deleterious effects when expressed in large amounts. It is produced in the heart by both cardiac myocytes and resident macrophages under conditions of cardiac stress, and is thought to be responsible for many of the untoward manifestations of cardiac disease. TNF-alpha may play a role in the triggering and perpetuation of atherosclerosis. Treatment with biologic agents directed against TNF-alpha has significant clinical benefits in inflammatory diseases such as RA and may be able to reduce cardiovascular risk. The disappointing results of the recent studies to antagonize TNF-alpha in CVD may have various explanations. However, the effects of TNF-alpha blockers on incident cases of congestive heart failure (CHF) in RA remains controversial. Due to the lack of evidence of a beneficial effect of anti-TNF-alpha agents in treatment of CHF, they should not be used to treat patients with New York Heart Association (NYHA) class III or IV heart failure.
Lupus 2005
PMID:Tumor necrosis factor-alpha, biologic agents and cardiovascular risk. 1621 87

Dyslipoproteinemia is common in lupus patients. In this study, we investigated the pattern of dyslipoproteinemia in the course of active systemic lupus erythematosus (SLE) in possible association with anti-double-stranded DNA (anti-dsDNA) antibodies. Forty-six lupus patients under 45 years old who fulfilled the American College of Rheumatology revised criteria for the classification of SLE were selected. The exclusion criteria were renal failure, nephrotic syndrome, thyroid or liver disease, diabetes mellitus, obesity, pregnancy and taking drugs that induce dyslipidemia. Disease activity was measured by Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Comparison of the lipid profiles, between active and inactive groups determined high levels of serum TG and VLDL and low levels of serum HDL in active group in comparison with inactive group (P < 0.05). The results indicated that the levels of TG and VLDL were significantly elevated in the patients with positive anti-dsDNA (P < 0.05). Although, the mean of serum HDL levels was also lower in patients with positive anti-dsDNA, the difference was not significant. This pattern of dyslipoproteinemia in active SLE may be associated with the autoimmune mechanisms especially in relation to the presence of anti-dsDNA antibodies.
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PMID:Dyslipoproteinemia during the active course of systemic lupus erythematosus in association with anti-double-stranded DNA (anti-dsDNA) antibodies. 1694 55

Systemic lupus erythematosus (SLE) is an independent risk factor for atherosclerosis, placing children and adolescents with SLE at great risk for developing cardiovascular sequelae, including myocardial infarction, in adulthood. Dyslipidemia and other traditional cardiac risk factors occur frequently in pediatric SLE and are often under-recognized and under-treated. Two dyslipidemia patterns are evident in pediatric SLE. Active disease is characterized by elevated triglycerides (TG) and low high density lipoprotein (HDL). With SLE treatment HDL and TG often normalize, while total cholesterol and low density lipoprotein (LDL) rise. The complex pathophysiology of dyslipidemia in SLE involves cytokines, autoantibodies, disease activity, medications, diet, and physical activity level, as well as other factors. Routine screening for dyslipidemia with fasting lipid profiles is indicated for children and adolescents with SLE. If lipoprotein levels are abnormal, first line therapy involves diet and exercise interventions for a minimum of six months. For persistent dyslipidemia, several pharmacologic therapies are available. Hydroxychloroquine, a common treatment for SLE, can improve lipid profiles and should be considered for all patients with SLE. Statins and bile acid sequestrants are typically added first for dyslipidemia, while niacin and fibrates are reserved for refractory disease and optimally prescribed in a multidisciplinary lipid clinic. Future research is needed to further illuminate the mechanisms of dyslipidemia in pediatric SLE with well designed clinical trials to determine the safest and most effective interventions to correct lipid profiles and prevent atherosclerosis.
Lupus 2007
PMID:Management of dyslipidemia in children and adolescents with systemic lupus erythematosus. 1771 98

With increasing longevity of lupus patients, peripheral vascular disease (PVD) has become an important cause of morbidity. With no systematic study of PVD in systemic lupus erythematosus (SLE), this study was undertaken to define the frequency and spectrum of PVD in SLE and factors affecting such an occurrence. All medium-sized peripheral arteries of bilateral upper and lower extremities were studied in 50 SLE patients using Doppler ultrasonography. PVD was defined clinically as one or more of intermittent claudication, absent/unequal pulses, gangrene or ischemic ulcers and sub-clinically as asymptomatic patients with Doppler abnormalities, with > or =50% reduction in diameter considered hemodynamically significant. Mean (SD) age of the patients was 31.6 (10.1) years. Forty-one percent were hypertensive. Dyslipidemia was found in 62%. Fifteen (30%) had Raynaud's phenomenon. Fourteen (28%) patients had PVD, of whom three had positive markers for antiphospholipid antibody (aPL) and six were asymptomatic. Ischemic ulcers were seen in eight (16%), gangrene in three (6%), femoral artery plaques in two (4%), stenosis in four (8%) and intermittent claudication in none. Dyslipidemia was found to independently affect occurrence of PVD (OR = 5.37, [95% CI 1.05-27.5], P = 0.05). The causes of PVD overlap significantly and further studies are needed to ascertain the relative contribution of each.
Lupus 2007
PMID:Peripheral vascular disease in systemic lupus erythematosus. 1772 65

Atherosclerosis is an inflammatory disease characterised by presence of activated immune competent cells in middle-sized and large arteries and is the major cause of cardiovascular disease (CVD). The risk of CVD is very high in systemic lupus erythematosus (SLE). SLE-related CVD and atherosclerosis are, therefore, important clinical problems but may in addition also have implications for the role of immune reactions in CVD in general. Others and we have recently demonstrated that risk factors for CVD in SLE are both traditional and non-traditional acting in concert. Traditional risk factors implicated in SLE include, for example, dyslipidemia (especially high triglycerides), hypertension, renal disease, non-traditional as inflammation, antiphospholipid antibodies (aPL) and low-density lipoprotein (LDL) oxidation are also associated with CVD in SLE. Atherothrombosis is likely to be a major underlying mechanism and is not only an increased risk of thrombosis per se. It is possible that factors like proinflammatory reactions or prothrombotic factors, such as aPL, make atherosclerotic lesions in SLE more prone to rupture than in 'normal' atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients is presently not clear. Treatment of patients with SLE should include a close monitoring of traditional risk factors and also the above-mentioned non-traditional for CVD.
Lupus 2008 May
PMID:Systemic lupus erythematosus and cardiovascular disease. 1849 Apr 8


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