Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting connective tissue. It is characterized by a variety of clinical symptoms. In the pathogenesis of SLE, genetic as well as environmental and hormonal factors are considered to be responsible for the development of multiple immunological phenomena. Recently, the process of angiogenesis and vasculogenesis and their dysfunction has been considered in the pathogenesis of SLE. Vascular lesions seem to be responsible for the cutaneous, nephritic, cardiovascular, and gastrointestinal symptoms. Besides the typical antinuclear antibodies, anticardiolipin, anti-CRP, and antiendothelial cell antibodies are also present in the serum of SLE patients. Recently, antiendothelial cell antibodies (AECAs) have greatly aroused the interest of researchers. An increased titer of AECAs is assumed to be a vascular damage marker. It seems that AECAs can be responsible for vascular damage in SLE, thus confirming the strong relationship between SLE activity and AECA titers. In SLE patients' blood samples, increased levels of circulating endothelial cells (ECs) were also found. At the same time, higher adhesive molecule expression was detected at the inflammation site as well as in the healthy skin, which may indicate general endothelial cell activation. Positive correlation between EC count, C3 complement, and anticardiolipin antibodies and disease activity was also demonstrated. The above observations show the great impact of the vascular endothelium in the pathogenesis of SLE. There is an urgent need to continue further research on this subject.
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PMID:[The role of endothelial cells in the pathogenesis of systemic lupus erythematosus]. 1757 60

Apoptotic cells have been reported to down-regulate membrane-bound complement regulatory proteins (m-C-Reg) and to activate complement. Nonetheless, most apoptotic cells do not undergo complement-mediated lysis. Therefore, we hypothesized that fluid phase complement inhibitors would bind to apoptotic cells and compensate functionally for the loss of m-C-Reg. We observed that m-C-Reg are down-regulated rapidly upon apoptosis but that complement activation follows only after a gap of several hours. Coinciding with, but independent from, complement activation, fluid phase complement inhibitors C4b-binding protein (C4BP) and factor H (fH) bind to the cells. C4BP and fH do not entirely prevent complement activation but strongly limit C3 and C9 deposition. Late apoptotic cells, present in blood of healthy controls and systemic lupus erythematosus patients, are also positive for C4BP and fH. Upon culture, the percentage of late apoptotic cells increases, paralleled by increased C4BP binding. C4BP binds to dead cells mainly via phosphatidylserine, whereas fH binds via multiple interactions with CRP playing no major role for binding of C4BP or fH. In conclusion, during late apoptosis, cells acquire fluid phase complement inhibitors that compensate for the down-regulation of m-C-Reg and protect against excessive complement activation and lysis.
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PMID:C4b-binding protein and factor H compensate for the loss of membrane-bound complement inhibitors to protect apoptotic cells against excessive complement attack. 3262 Jun 91

We studied the large and small artery elasticity (AE) and systemic vascular resistance (SVR) of systemic lupus erythematosus (SLE) patients according to treatment profile. Forty-one SLE patients (90% female, mean age 48.7 +/- 2.4 years) were compared to 96 healthy controls. The large and small AE and the SVR were derived from radial artery waveforms (model CR-2000, HDI Inc.). Patients were categorized into groups according to treatment: steroid (12), hydroxychloroquine (HCQ) (9), steroid+HCQ (16), and no-steroids-no-HCQ (4). The steroid group had reduced large AE and increased SVR as compared to the HCQ group (8.3 mmHg x mL x 10 and 18.4 dyne x sec x 10(-3) versus 13.7 and 14.4, respectively). Mean large AE and the SVR of the HCQ group was similar to that of the controls (11.8 mmHg x mL x 10 and 14.5 dyne x sec x 10(-3), respectively). Mean large AE and SVR of the steroid+HCQ group were better than the steroid group (10.4 mmHg x mL x 10 and 16.0 dyne x sec x 10(-3)). Patients that received steroids had higher rates of hypertension (36%) and diabetes (1%) compared to rest of the patients (15% and 0%, respectively). Small AE, blood pressure, CRP, and SLEDAI were similar between the groups. Among SLE patients, steroid treatment was associated with the highest degree of vascular damage, and HCQ was associated with the lowest degree of vascular damage. It is possible that the steroids are responsible in part to the increased large-vessel manifestations observed in these patients, and that HCQ might have a protective effect on the vessel wall.
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PMID:Vascular elasticity of systemic lupus erythematosus patients is associated with steroids and hydroxychloroquine treatment. 1789 67

Excessive lipid peroxidation is a major factor of accelerated atherosclerosis, observed in patients with systemic lupus erythematosus (SLE). We aimed at the present study to determine the paraoxonasel (PON1) and arylesterase activities, and lipid-profile in 37 SLE patients and 30 age-/sex-matched controls. Association was analyzed between PON1 activity and SLEDAI, CRP, anti-oxLDL, and antiphospholipid antibody (aPL) levels, steroid dose, and atherothrombotic events. The age of patients was 40.8 +/- 13.9 year, follow-up time 6.7 +/- 6.2 year, SLEDAI 2 (0-15). PON1 and arylesterase activities were measured spectrophotometrically using paraoxon and phenyl acetate as substrates, respectively. Phenotypic distribution of PON1 was determined by dual substrate method. We measured antioxLDL and aPL levels by ELISA, the CRP by automated immunoassay. PON1 activity (121.9 +/- 65.9 U/mL) was reduced significantly (P < 0.001) in SLE as compared to control (188.1 +/- 78.9 U/mL), but arylesterase activity was not different. A negative correlation was found between PON1 activity and age. PON1 activity did not correlate with other measured parameters. Reduced PON1 activity associated with clinical atherothrombotic complications (P < 0.01). High activity BB phenotype was not present in SLE. Lipid parameters (TC, LDL-C, HDL-C, ApoAI, and ApoB) were within normal range in both groups. Results indicated reduced PON1 activity in lupus patients despite long disease duration and low inflammatory activity, and it was evidenced as a risk for atherosclerotic complications. As the arylesterase activity was normal, further examinations are required to find other mechanisms, such as anti-PON1 antibodies, genetic polymorphisms, and difference in distribution of HDL-subfractions or enzyme abnormalities in HDL remodeling.
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PMID:Reduced paraoxonase1 activity is a risk for atherosclerosis in patients with systemic lupus erythematosus. 1789 73

The aim of this study was to identify risk factors for lupus nephritis including clinical, laboratory, and ethnic factors in a cohort of lupus patients in New Zealand. A retrospective study of patients from two teaching hospitals in Auckland, New Zealand. Patients were selected if they had attended as either an inpatient, or a rheumatology outpatient between 2000 and 2005. 170 patients had SLE according to ACR classification. Lupus nephritis (LN) was diagnosed according to ACR criteria. Clinical, laboratory, and ethnic data were gathered from the patient notes. Twenty-four patients had LN at diagnosis and 32 patients developed LN after diagnosis. LN was associated with serositis (P = 0.008), cutaneous vasculitis (P = 0.026), anaemia (P = 0.005), CRP elevation >6 months (P < 0.001), hypocomplementaemia >6 months (P < 0.0001). Patients with elevated doublestranded DNA (dsDNA) (>5 x normal) were more likely to develop type IV LN (P = 0.0096). Forty-one percent of patients were Caucasian, 12% Maori, 23% Pacific People, 16% Asian, 6% Indian. Maori patients with SLE (odds ratio (OR) = 8.47, 95% confidence interval (CI) = 2.11-33.96, P = 0.002), and Pacific People (OR = 3.11, 95% CI = 1.29-11.48, P = 0.014) had increased risk for developing LN. Anaemia at presentation (hazard ratio (HR) 3.2, 95% CI = 1.4-7.1, P = 0.004), and low complement >6 months (HR = 3.4, 95% CI = 1.4-8.7, P = 0.008) were independent risk factors for developing LN after SLE diagnosis. In New Zealand, Pacific People and Maori patients with SLE have a higher incidence of LN, and patients with anaemia and hypocomplementaemia are more likely to develop LN after diagnosis. Patients with high dsDNA levels are more likely to develop Type IV lupus nephritis.
Lupus 2007
PMID:Ethnic, clinical and immunological factors in systemic lupus erythematosus and the development of lupus nephritis: results from a multi-ethnic New Zealand cohort. 1789 8

C-reactive protein CRP is an acute-phase protein known as a biomarker for inflammation. As such CRP levels have been traditionally used to detect and predict the outcome of infections inflammatory and necrotic processes and to monitor the efficacy of treatment in these conditions. With the development of high sensitivity assays CRP has resurfaced as a very strong predictor in cardiovascular disease and as a mediator of atherosclerosis. The Centers for Disease Control and American Heart Association have elaborated guidelines for the use of CRP in the primary prevention setting and in patients with stable coronary disease or acute coronary syndromes. CRP has been used for differentiation between Systemic Lupus Erythematosus activity and infection in individuals without serositis. More recently CRP has also elicited interest as a therapeutic option in lupus. Murine lupus models treated with CRP have been reported to present delayed Lupus onset decreased antibody levels enhanced survival and reversal of ongoing proteinuria. In this paper we reviewed the multiple roles of CRP particularly in lupus.
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PMID:C-Reactive protein and its implications in systemic lupus erythematosus. 1815 97

Patients with systemic lupus erythematosus (SLE) have accelerated atherosclerosis, but the underlying mechanisms are unclear. The size and number of lipoprotein particles may be better predictors of atherosclerosis than conventional cholesterol measurements. We measured lipoprotein subclasses by nuclear magnetic resonance spectroscopy (NMR), coronary artery calcification by electron beam computed tomography, and insulin resistance by homeostasis model assessment in 105 patients with SLE and 77 control subjects. VLDL particles were larger (50.0+/-8.5 versus 47.7+/-8.5 nm, P=0.01) and concentrations of large high-density lipoprotein (HDL) particles lower (10.1+/-5.3 versus 11.3+/-5.1 nmol/L, P=0.03) in patients with SLE than controls. In patients with SLE, small LDL concentration was associated with body mass index (rho=0.27), insulin resistance (rho=0.34), C-reactive protein (CRP; rho=0.30), and erythrocyte sedimentation rate (ESR; rho=0.20); all P<0.05. Large HDL concentration was inversely associated with insulin resistance (rho=-0.29), disease activity (rho=-0.23), and ESR (rho=-0.39); all P<0.05. VLDL concentrations correlated with CRP (rho=0.22), ESR (rho=0.24), disease damage (rho=0.20), and corticosteroid exposure (rho=0.29); all P<0.05. Neither the concentration of lipoprotein subclasses nor particle size was associated with coronary artery atherosclerosis. There were only minor differences in the NMR lipid profiles of patients with SLE and controls. Lipoprotein subclasses were associated with metabolic variables, inflammatory markers, and corticosteroid use but not with coronary artery atherosclerosis in SLE.
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PMID:Lipoprotein subclasses and particle size determined by nuclear magnetic resonance spectroscopy in systemic lupus erythematosus. 1842 45

A 47-year-old man was admitted to our hospital in January, 2006 because of a huge cutaneous ulcer in his lower limb. He was diagnosed with polyarteritis nodosa due to the cutaneous ulcer, mononeuritis multiplex, muscular pain, elevated serum CRP level and from histological findings of a skin biopsy. He was initially treated with 60 mg/day of prednisolone, followed by 1000 mg/day of intravenous cyclophosphamide (IVCY) therapy. In June, skin grafting to the cutaneous ulcer was carried out, although the graft did not survive. He revealed therapy-resistance to high dose corticosteroid and IVCY therapy, and so was treated with intravenous high dose immunoglobulin therapy. Serum CRP level then decreased and in October skin grafting was once again undertaken, this time the graft successfully survived. In December, serum CRP level increased again and cutaneous ulcer relapsed, thus he was treated with leukocyte apheresis therapy, although it was ineffective. In February 2007, he subsequently received rituximab (375 mg/m(2)/week x 3). Then, serum CRP level decreased rapidly, and cutaneous ulcer also improved. Recently the efficacy of rituximab against rheumatoid arthritis, systemic lupus erythematosus, polymyositis/dermatomyositis and ANCA-associated vasculitis has been recognized. This case suggests that rituximab is also effective against corticosteroid-resistant polyarteritis nodosa.
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PMID:[A case of polyarteritis nodosa successfully treated by rituximab]. 1844 15

The aim of this study is to evaluate the presence of antibodies to carbonic anhydrase I and/or II (ACAI and ACAII) in patients affected by connective tissue diseases (CTD) and to investigate their association with lung involvement evaluated by High resolution CT scan (HRCT). Ninety-six patients affected by CTD were studied, i.e. 33 rheumatoid arthritis (RA), 8 psoriatic arthritis (PA), 8 ankylosing spondilitis (AS), 23 Systemic Lupus Erythematosus (SLE), 10 Sjogren Syndrome (SS), and 14 Systemic Sclerosis (SSc). ACA were detected by ELISA. The lung involvement was evaluated by means of a previously described HRCT score. According to a receiver operator characteristic curve, patients were divided into those with HRCT score > or = 10 and those with HRCT score < 10, where HRCT score > or = 10 was predictive of interstitial lung disease. ACAI and/or ACAII were detected in 30/96 patients (31.2%) (P < 0.0001 in comparison with controls). In particular, the prevalence of ACAI and/or ACAII was significantly higher in patients with RA (P = 0.002), PA (P < 0.0001), SLE (P = 0.0003) and SSc (P < 0.0001). A positive correlation was found between HRCT scores and CRP or ACAI levels (P = < 0.0001 and P = 0.004, respectively). Thirty-nine of 96 patients (40.6%) showed a HRCT score > or = 10 and both their CRP and ACAI levels were significantly higher when compared with patients showing a HRCT score less than 10 (P < 0.0006 and P = 0.0009, respectively). Moreover, C3 and C4 complement fractions inversely correlated with HRCT scores (P = 0.0004 and P < 0.0001, respectively) and lower values of C3 and C4 complement fractions were found in patients with HRCT score > or = 10 than in those with HRCT score less than 10 (P = 0.014 and P = 0.007, respectively). Due to the lower levels of complement fractions detected in patients with HRCT score > or = 10, a possible immune-complex-mediated pathogenic mechanism of lung involvement could be suggested.
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PMID:Antibodies to carbonic anhydrase in patients with connective tissue diseases: relationship with lung involvement. 1883 34

Premature atherosclerosis (ATS) in SLE patients is an important clinical problem. It is explained not only by excess of traditional risk factors, but also by specific factors linked to disease activity and therapy. Such specific factors include the following: antioxLDL and anti CRP antibodies, immune complexes, mannose-binding lectin, disturbances of metabolism of annexin A5, antiphospholipid syndrome, immunologically determined dyslipidemia, influence of medication. As a conclusion,atherosclerosis in SLE patients results from an interplay between traditional and nontraditional risk factors. Therapeutic influences suggest antiatherogenic effects for hydroxychloroquine and immunosuppressants and a doubtful proatherogenic influence of cortisone.
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PMID:Traditional and nontraditional risk factors for atherosclerosis in patients with systemic lupus erythematosus. 1936 77


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