Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to assess the possible role of vascular endothelial growth factor (VEGF) in the pathogenesis of systemic lupus erythematosus (SLE) and primary antiphospholipid syndrome (PAPS). We studied 28 patients with SLE, 10 patients with PAPS, and 24 healthy controls. VEGF plasma levels were measured by ELISA. Immunolocalization of VEGF was done in renal tissue from SLE patients and cadaveric controls. Our results showed that VEGF plasma levels were increased in SLE patients compared with PAPS and controls. The correlation between clinical manifestations and VEGF levels revealed that SLE patients with renal failure had significantly increased plasma VEGF levels (134.1 + 91.0 pg/ml) compared with SLE patients with normal renal function (42.9 + 19.0 pg/ml), PAPS patients (41.9 + 26.6 pg/ml), and controls (36.2 + 27.0 pg/ml; P < 0.01). Immunostaining showed a strong expression of VEGF in SLE renal tissue samples. Our preliminary results indicate that VEGF is increased in plasma from patients with lupus nephritis and a moderate degree of renal failure and is overexpressed in renal tissue from these patients.
Lupus 2002
PMID:Vascular endothelial growth factor plasma levels in patients with systemic lupus erythematosus and primary antiphospholipid syndrome. 1189 14

Serum concentrations of three angiogenic cytokines: vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), interleukin-18 (IL-18) and antiangiogenic factor endostatin in the serum of 52 patients with systemic lupus erythematosus (SLE) and 20 healthy subjects were investigated. The possible association between serum levels of these proteins and SLE activity as well as correlation between the concentrations of angiogenic cytokines and the level of endostatin was also analyzed. VEGF and IL-18 were detectable in all SLE patients and healthy control group. bFGF was measurable in 71.2% of patients with SLE and 65% of healthy persons. Endostatin was detectable in 94.2% of SLE patients and 95% of normal subjects. The serum levels of endostatin and bFGF were not significantly different in SLE and healthy control (P > 0.05). The median concentration of VEGF was higher in active SLE (238.4 pg/ml) than in inactive disease (118.1 pg/ml, P < 0.05) or in control group (133.5 pg/ml, P < 0.04). The median serum level of IL-18 was higher in the SLE patients (595.2 pg/ml) than in the control group (252.7 pg/ml) (P < 0.001). The correlations between the levels of angiogenic cytokines and endostatin with clinical features, laboratory abnormalities and also with the type of treatment were analysed. We found a positive correlation between VEGF serum concentration and SLE activity according to SLAM score (p = 0.275, P < 0.05). The significant positive correlation was also found between IL-18 and endostatin (p = 0.289, P < 0.04). In contrast, the correlation between bFGF and endostatin was significantly negative (p = - 0.299, P < 0.04). In conclusion, serum levels of the angiogenic and antiangiogenic factors may play an important role in SLE pathogenesis.
Lupus 2002
PMID:Circulating angiogenesis inhibitor endostatin and positive endothelial growth regulators in patients with systemic lupus erythematosus. 1213 72

Reactive angioendotheliomatosis (RAE) is a very rare disorder characterized by marked proliferation of endothelial cells. It is often associated with infections, such as subacute bacterial endocarditis, but has also been described as an early sign of a developing hematological malignancy. We report the case of a 71-year-old Caucasian female who developed lupus-like RAE lesions. A thorough diagnostic workup and subsequent 3-year clinical follow-up revealed no sign of an underlying infectious or neoplastic disorder. Repetitive serum immunofixations were only once consistent with a monoclonal gammopathy of undetermined significance. In lesional skin, the pronounced bud-like endothelial cell formation was associated with an increased epidermal expression of vascular endothelial growth factor (VEGF), a potent angiogenic mediator. In accordance with the paracrine action of epidermally derived VEGF, vascular endothelial cells in lesional skin revealed increased expression of the VEGF receptor VEGFR-2 (KDR). This case suggests a possible role of epidermally derived VEGF in endothelial cell proliferation in RAE.
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PMID:Increased expression of VEGF in glomeruloid reactive angioendotheliomatosis. 1465 35

The angiogenic cytokine vascular endothelial growth factor (VEGF) may have a role in the pathogenesis of collagen diseases. We aimed to assess its serum levels in children and adolescents with systemic lupus erythematosus (SLE) and to elucidate its correlation with clinical features, laboratory parameters, and the overall disease activity. This study comprised 25 children and adolescents with SLE and 30 healthy controls. Disease activity was evaluated by SLE disease activity index (SLEDAI) score. Laboratory investigations included complete blood count, erythrocyte sedimentation rate (ESR), urine analysis, 24-h total urinary protein, assay of serum creatinine, ANA, anti-DNA, complement component C3, lupus anticoagulant, and VEGF. Serum levels of VEGF were significantly increased in SLE patients (579.5 +/- 184.7 pg/ml) when compared with controls (113.2 +/- 30.8 pg/ml) (p < 0.0001). VEGF serum levels were significantly increased in patients having renal involvement and neurologic symptoms than those who did not have them (p < 0.0001, p < 0.005, respectively). Serum levels of VEGF were higher in patients with antiphospholipid syndrome, vasculitis, and skin symptoms than those without, but the difference did not reach statistical significance. Meanwhile, they were similar in patients with and without arthritis (p > 0.05). VEGF serum levels were not correlated to age; inversely correlated to platelet count, serum C3 level; and positively correlated to ESR. SLEDAI score was positively correlated to VEGF serum level (r = 0.86, p < 0.0001). VEGF may be relevant to SLE pathogenesis. Its concentration seems to be a marker of SLE activity, which could help in disease monitoring and planning of treatment.
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PMID:Serum levels of vascular endothelial growth factor in children and adolescents with systemic lupus erythematosus. 1734 98

Individuals with systemic lupus erythematosus (SLE) have a striking increase in premature atherosclerosis of unclear etiology. Accelerated endothelial cell apoptosis occurs in SLE and correlates with endothelial dysfunction. Endothelial progenitor cells (EPCs) and myelomonocytic circulating angiogenic cells (CACs) are crucial in blood vessel repair after vascular damage, and decreased levels or abnormal function of EPCs/CACs are established atherosclerosis risk factors. We investigated if vascular repair is impaired in SLE. We report that SLE patients display abnormal phenotype and function of EPCs/CACs. These abnormalities are characterized by significant decreases in the number of circulating EPCs (310 +/- 50 EPCs/mL of blood in SLE versus 639 +/- 102 in controls) and significant impairments in the capacity of EPCs/CACs to differentiate into mature ECs and synthesize adequate levels of the proangiogenic molecules vascular endothelial growth factor (VEGF) and hepatic growth factor (HGF). These abnormalities are triggered by interferon-alpha (IFN-alpha), which induces EPC and CAC apoptosis and skews myeloid cells toward nonangiogenic phenotypes. Lupus EPCs/CACs have increased IFN-alpha expression and their supernatants promote higher induction of IFN-inducible genes. Importantly, neutralization of IFN pathways restores a normal EPC/CAC phenotype in lupus. SLE is characterized by an imbalance between endothelial cell damage and repair triggered by type I IFNs, which might promote accelerated atherosclerosis.
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PMID:Interferon-alpha promotes abnormal vasculogenesis in lupus: a potential pathway for premature atherosclerosis. 1763 46

Neonatal lupus erythematosus (NLE) is a passively acquired autoimmune syndrome resulting from transplacental passage of maternal anti-Ro/SSA and/or anti-La/SSB antibodies to the fetus. Characteristic manifestations of NLE include transient dermatitis, hepatic and hematologic abnormalities and congenital heart block. Skin lesions in NLE resemble subacute cutaneous lupus erythematosus and typically consist of annular, erythematous, scaly plaques. Telangiectasias, vascular abnormalities resulting from dilation of superficial dermal vessels, may also affect the skin in a minority of patients. The etiology of telangiectasias in NLE is unknown, but disordered angiogenesis likely plays a role. Hemangiomas are a common disorder of angiogenesis frequently encountered in infancy. There have been no reported cases of neonatal lupus associated with the development of hemangiomas. We present a case of an infant diagnosed with NLE after manifesting classic dermatitis, hepatic and hematologic abnormalities who later developed mucocutaneous and visceral hemangiomas. We further postulate that disordered angiogenesis, possibly dysregulated production of vascular endothelial growth factor, may play a primary role in the development of these cutaneous vascular lesions in NLE.
Lupus 2007
PMID:Neonatal lupus erythematosus complicated by mucocutaneous and visceral hemangiomas. 1797 65

A new entity was described by Crickx et al. in 1991, associating amicrobial pustulosis of the folds with systemic lupus erythematosus in young females. It is proposed to regroup this entity under the name of 'neutrophilic cutaneous lupus'. We report a case of a 13-year-old girl with a pustular eruption of the cutaneous folds and scalp associated with undetermined connective tissue disease. We performed a screening for the expression of 174 cytokines in the pustules and compared it with other pustular diseases (acne flare, acute generalized exanthematous pustulosis, pustulosis of Sneddon and Wilkinson). Matrix metalloproteinase 9 and Siglec-5 (CD170) were highly expressed in all types of pustules and reflect high neutrophil density. Amicrobial pustulosis of the folds was characterized by a higher expression of interleukin (IL) 1alpha, IL-2 receptor alpha, macrophage colony-stimulating factor, insulin-like growth factor binding protein 1, brain-derived neurotrophic factor, tumour necrosis factor (TNF) alpha and a lower expression of CD14, IL-1beta, IL-12, soluble TNF receptors I and II, growth-regulated oncogene alpha, fibroblast growth factor 4 and vascular endothelial growth factor as compared to the controls.
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PMID:Amicrobial pustulosis of the folds associated with auto-immune disorders. A case report with an analysis of cytokine expression profile in skin lesions of cutaneous neutrophilic lupus. 1823 Sep 75

Host responses to synthetic implants are analogous to healing, the process of repair that follows injury. Normally, the processes of wound healing follow well-established patterns but conditions such as autoimmune diseases profoundly affect tissue repair. We have analyzed sponge-induced wound healing responses in lupus-prone New Zealand White and control (Balb/c) mouse strains by measuring inflammation, extracellular matrix deposition, angiogenesis, and cytokine production in polyether-polyurethane sponge implanted subcutaneously in male mice of these two strains. Although there was no difference in the gross appearance of the implants, further analysis of the wound healing responses, induced from 7 to 21 days post implantation, disclosed important differences between the New Zealand White and Balb/c strains. The intensity of inflammation (circulating tumor necrosis factor-alpha and inflammatory leukocytes levels) was lower but implant fibrosis (collagen and transforming growth factor-beta1) was higher in New Zealand White, compared with Balb/c mice. Angiogenesis (hemoglobin, vascular endothelial growth factor, and vascularity) in New Zealand White implants peaked earlier than in Balb/c mice. In conclusion, we have shown that wound healing responses are clearly different in this strain of lupus-prone mice and suggest that this pattern of repair was critically influenced by impaired inflammation and accelerated angiogenesis in the New Zealand White strain.
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PMID:Mechanisms of wound healing responses in lupus-prone New Zealand White mouse strain. 1847 Dec 60

The aim of our study was to assess absolute counts of different subpopulations of circulating endothelial cells (CEC) in patients with active and inactive systemic lupus erythematosus (SLE). We have also investigated a potential correlation of CEC numbers with serum levels of angiogenic proteins as well as with clinical and laboratory symptoms of the disease. For the first time in SLE, CEC were enumerated directly, by the 'single platform' method. Resting (rCEC), activated (aCEC) and progenitor (pCEC) endothelial cells were identified in patients with SLE and healthy volunteers using four-colour flow cytometry. Serum concentrations of angiogenic proteins (vascular endothelial growth factor, placental growth factor (PIGF), soluble vascular cell adhesion molecule and endoglin) were evaluated by ELISA. The SLE activity was scored according to the Systemic Lupus Activity Measure system. We found that total CEC number in patients with SLE was significantly higher (median 14.2/microL) than in the control group (median 3.3/microL) (P < 0.0001). Absolute counts of aCEC, rCEC and pCEC (medians 4.9/microL, 6.8/microL and 2.3/microL, respectively) were also higher in patients with SLE than in healthy persons (medians 0.9/microL, 1.6/microL and 0.1/microL, respectively), with P < 0.0001 for all comparisons. There was no correlation between CEC or their subpopulations and SLE activity. Strong positive correlations were found between CEC, rCEC and pCEC numbers and serum levels of PIGF. Moreover, aCEC, rCEC and pCEC counts were significantly higher in SLE patients with leukopenia. In conclusion, our results show that absolute CEC counts and angiogenic proteins levels are elevated in patients with SLE as compared with healthy controls. These data may suggest that angiogenic process is involved in the pathogenesis of this disease.
Lupus 2009 Apr
PMID:Circulating endothelial cells and angiogenic proteins in patients with systemic lupus erythematosus. 1927 1

Angiogenesis plays a critical role in the pathogenesis of several connective tissue diseases. There is, however, relatively little information available on the role of angiogenesis in systemic lupus erythematosus (SLE). The aim of this study was to investigate the angiogenic activity in sera of patients with SLE and to determine the association between angiogenic activity and clinical complications. Sera from 66 Tunisian females with SLE and from 32 healthy blood donors were studied for their angiogenic activity using the in-vitro tube formation test on Matrigel. Samples were divided into five groups according to their angiogenic activity, which was scored from 0 (no angiogenesis) to 4 (high angiogenic activity). Samples from each group were then tested randomly to assess serum concentration of vascular endothelial growth factor (VEGF). No correlation was found between angiogenic activity scores and serum VEGF levels. Considering angiogenesis assessment in-vitro, sera of patients with SLE showed a much higher angiogenic activity than healthy controls since a high angiogenic score (score 4) is present in 43.9% of patients and in 6.3% of controls (P < 0.0002). This high angiogenic activity is not correlated with disease activity; however, SLE patients with anti-dsDNA antibodies and those with nephritis showed higher angiogenic activity compared with patients without these complications since score 4 is found in 50.9% and 67.9% versus 9.1% (P = 0.017) and 26.3% (P < 0.001), respectively. In conclusion, our study showed that high serum angiogenic activity in SLE was not correlated with the VEGF levels. We suggest the use of the 'in-vitro' tube formation test as a better tool to study the angiogenic potential of sera. We found that in patients with SLE, serum angiogenic activity is increased compared with healthy controls. This high angiogenic activity is associated with renal complications and with the presence of anti-dsDNA antibodies. These findings suggest an involvement of angiogenesis disturbance in the pathogenesis of SLE.
Lupus 2009 Jul
PMID:Angiogenic activity in sera of patients with systemic lupus erythematosus. 1950 66


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