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)

Glomerulonephritis is an important cause of end-stage renal failure, yet the pathogenetic mechanisms of most forms of glomerulonephritis are not clear. Renal fibrosis is the final common pathway for many kidney lesions that lead to chronic progressive organ failure. Recent study suggests that chemokines and chemokine receptors are involved in the resolution or progression of renal diseases. In view of the above we detected using immunohistochemistry the expression of RANTES, CCR5+ cells,TGF-beta1, alpha-SMA in renal biopsy specimens in 17 patients with IVG A/C class of lupus nephritis and in 10 normal kidneys. The correlative study was undertaken to evaluate the possible relationships between the immunoexpression of RANTES, the number of CCR5+ cells, the immunoexpression of TGF-beta1, alpha-SMA, the value of interstitial cortical volume and the serum creatinine level in patients with lupus nephropathy. Statistical analysis revealed significant increase in tubulointerstitial RANTES immunoexpression in lupus nephritis as compared to normal controls. In our study CCR5+ cells were detected in the interstitium in tissue samples in patient with lupus nephritis, meanwhile no CCR5+ cells were documented in normal controls. We found a strong positive correlation between tubulointerstitial immunoexpression of RANTES and the number of interstitial CCR5+ cells as well as between immunoexpression of RANTES and the immunoexpression of TGF-beta1, alpha-SMA, renal cortical volume and serum creatinine in patients with lupus nephritis. Moreover, the number of interstitial CCR5+ cells was positively correlated with tubulointerstitial alpha-SMA immunoexpression and renal cortical volume. In summary, the results suggest that in lupus nephritis RANTES may participate in interstitial lesions via CCR5+ cells.
Pol J Pathol 2007
PMID:The significant role of RANTES and CCR5 in progressive tubulointerstitial lesions in lupus nephropathy. 1758 40

Pregnancy in patients with systemic lupus erythematosus (SLE) is considered a high-risk pregnancy. It is complicated by preeclampsia, premature labour and miscarriage more frequently than in the general population. Improved prognosis depends on low disease activity during conception and on appropriate medical care (SLE activity monitoring, selection of therapy safe for the mother and the developing foetus, advances in neonatology). Because symptoms of physiological pregnancy and SLE exacerbation are similar, their correct interpretation is essential for skin lesions, arthralgias, arterial hypertension or results of laboratory tests: proteinuria, thrombocytopenia or leucopenia observed in the patient. In order to standardise the assessment of SLE activity during pregnancy, scores of this activity are used. In the past, scores validated on non-pregnant populations (including male patients) were used: Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), Systemic Lupus Activity Measure (SLAM), European Consensus Lupus Activity Measurment (ECLAM). Only recently have SLE activity scores been introduced that are specific for pregnant women: Lupus Activity Index In Pregnancy (LAI-P), Systemic Lupus Erythematosus Pregnancy Disease Activity Index (SLEPDAI), modified--Systemic Lupus Activity Measure (m-SLAM) and a visual three-grade score modified--Physician Global Assessment (m-PGA). So far, only scores LAI-P and m-PGA have been validated. According to the LAI-P score, clinical data are divided into 4 groups. Group 1 includes mild clinical symptoms, group 2--symptoms of involvement of internal organs, group 3 pertains to modifications of treatment and group 4 to laboratory parameters. Point values are ascribed to individual parameters depending on their intensity.
Pol Arch Med Wewn 2007 Jul
PMID:[Evaluation of systemic lupus erythematosus activity during pregnancy]. 1796 97

In the present work general characteristics and occurrence of TLR receptors have been presented. The participation of TLR receptors in kidney pathology in experimental models in the course of urinary system infection, acute renal failure and interstitial fibrosis has been discussed. In addition, the importance of TLRs in various forms of glomerular nephritis and in haemodialytic patients as well as in postrenal-transplant patients has been shown. It is believed that in lipopolysaccharide-induced renal failure in the course of infections caused by Gram negative bacteria TLR4 plays a fundamental role. In the event of damage of renal tubular epithelial cells by mechanical, toxic, or ischemic factors activation of TLRs induces inflammatory processes leading to acute renal failure. In the course of progressive fibrosis of renal interstitial tissue TLR 2 and 4 receptors are stimulated, which results in the fact that immunological and structural cells of renal tissue release chemokines and cytokines, which causes increased inflow of leucocytes and intensification of interstitial nephritis and progressive fibrosis. The study on experimental models on mice MLR (mixed lymphocyte reaction) with genetically conditioned lupus-like disease showed that, CpG-DNA stimulation as a TLR 9 specific agonist intensifies inflammatory symptoms in mice. Similarly in apoferritin induced glomerulopathy (model of immune complex disease) CpG-DNA nucleotide increased glomerulopathy symptoms. It has been proved that activation of mechanisms of inherent immunity through TLR4 receptors affects the frequency and intensity of acute rejections in human organ transplantations. Incidence of acute kidney and lung [transplant rejections was significantly lower in recipients with mutated variants of Toll-like receptor 4 (TLR-4 Asp 299Gly and TLR-4-Tyr399-IIe).
Pol Merkur Lekarski 2007 Nov
PMID:[Toll-like receptors (TLR) in the pathogenesis of kidney diseases]. 1836 25

Recently a role of the upregulation ofcyclooxygenase isoforms in renal injury and modulation the severity of the inflammatory reactions is suggested. Cyclooxygenase exists as two isoforms COX-1 and COX-2 which are poorly understood with regard to their roles in renal function. Thereby, the present study was undertaken to ascertain the immunoexpression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in lupus (LMGN) and nonlupus (NLMGN) membranous glomerulopathy and to examine the possible relationship between this immunoexpresion and inflammatory infiltrates. Eleven renal biopsy specimens from patients with class V lupus glomerulopathy and 16 from patients with primary (nonlupus) membranous glomerulopathy were examined by percutaneous renal biopsy. As a control 10 biopsy specimens of the kidneys removed because of trauma were used. In each specimen staining intensity of COX-1 and COX-2 in glomeruli, tubuli, arterioles and interstitial cells were recorded semiquantitatively whereas CD68+ cells, CD3+ cells and CD20+ cells were assessed quantitatively using computer image analysis system. Our study revealed that the mean scores of COX-1 immunoexpression did not differ significantly in all groups investigated whereas immunoexpression of COX-2 in LMGN was significantly stronger as compared with both NLMGN and controls. Moreover, in LMGN a significant positive relationship was noted between COX-2 immunoexpression and CD 68+ cells. In NLMGN and controls the correlations between COX-2 immunoexpression and CD 68+ cells were positive, but they have not reached statistical significance. In conclusion, our findings point that glomerular inflammation in lupus and non-lupus membranous glomerulopathy have different signalling pathways and suggest that in lupus nephritis COX-2 and monocytes/ macrophages but not COX-1 isoform are involved in the inflammatory process.
Pol J Pathol 2007
PMID:Analysis of renal immunoexpression of cyclooxygenase-1 and cyclooxygenase-2 in lupus and nonlupus membranous glomerulopathy. 1845 55

The antiphospholipid syndrome (APS) is a disorder of increased risk of thrombotic complications: venous thromboembolic disease, arterial thrombosis, and recurrent pregnancy loss. There is a much higher rate of recurrences of these thrombotic events as well. Some recent clinical trials have shown the superiority of the lupus anticoagulant and anti-beta2 glycoprotein-I antibodies assays over anticardiolipin determination for the identification of APS patients at risk for thromboembolic complications. The principles of the primary prophylaxis, treatment and secondary prophylaxis of thrombotic complications in patients with antiphospholipid syndrome has been also summarized.
Pol Arch Med Wewn 2007
PMID:[Antiphospholipid antibodies--risk factors for venous thromboembolism and arterial thrombosis]. 1877 19

Antiphospholipid syndrome (APS) is one of the most common reasons of thromboembolic complications in the course of connective tissue diseases. There is a strong relationship between presence of antiphospholipid antibodies and the risk of thrombosis. APS related thromboembolic complications range from superficial vein thrombosis up to rapidly developing, life threatening, multi-organ embolism. We present a case of a 21-year old female who presented with myocardial infarction as the first symptom of systemic lupus erythematosus and APS. Afterwards she was consequently treated with antithrombotic and anti-aggregation agents but it did not prevent her from reoccurrence of middle retinal vein. During the 10-year follow up she presented with reoccurring neurological symptoms i.e.: headache, memory deficits, concentration loss and impairment of the cognitive functions. She was found many times to be positive for IgG and IgM anticardiolipin antibodies, anti-beta2glicoprotein-I antibodies and lupus anticoagulant.
Pol Arch Med Wewn 2007
PMID:[Therapy resistance antiphosholipid syndrome in the course of systemic lupus erythematosus: case report]. 1877 25

Systemic lupus erythromatosus is often associated with an antiphospholipid syndrome (APS). A high prevalence of valvular heart disease in APS leads to increased risk of embolic events, particularly cerebrovascular. We present a patient with cerebral infarction, with positive lupus anticoagulant, anticardiolipin antibodies and factor V Leiden mutation. Echocardiographic examination revealed mitral valve anterior leaflet thickening and verrucous vegetations consistent with Libman-Sacks endocarditis, which is commonly associated with APS.
Kardiol Pol 2009 Jan
PMID:[Recurrent multi-focal cerebral stroke complicating Libman-Sacks endocarditis in a young woman with systemic lupus erythromatosus]. 1925 90

The presence of asymptomatic antiphospholipid antibodies (aAPA) creates many difficult diagnostic and clinical problems - they might be a cause either of incorrect hemorrhagic diathesis recognition or an unnecessary anticoagulant therapy. Patients with aAPA should be counseled individually regarding potential thrombotic and/or obstetric complications. An increased risk of these complications is particularly high when lupus anticoagulant (LAC) and IgG anti-beta2 glycoprotein antibodies coexist. The approaches to the diagnosis and management of treatment of patients with aAPA are also discussed.
Pol Arch Med Wewn 2008
PMID:[Clinically asymptomatic antiphospholipid antibodies--diagnostic and therapeutic problems]. 1956 75

A case of a 29-year-old woman 18 days after delivery with catastrophic antiphospholipid syndrome secondary (CAPS) due to undiagnosed systemic lupus erythematosus, leading to cardiogenic shock is reported. Laboratory evaluation revealed increased anticardiolipin antibodies, lupus anticoagulant, antinuclear antibody and thrombocytopenia. Left ventricular ejection fraction was 20%, neurologic deficit and acute renal failure were also present. Cardiac involvement is common in CAPS, but cardiomyopathy due to microvascular thrombosis is rare. CAPS should be considered as a cause of acute heart failure in a women with systemic lupus erythematosus. In the presented case early therapy with anticoagulants, steroids, immunoglobulins and plasmaferesis was beneficial.
Kardiol Pol 2009 Jul
PMID:[Catastrophic antiphospholipid syndrome complicated by cardiogenic shock - a case report]. 1965

Antiphospholipid syndrome (APS) is an autoimmune disease with clinical manifestations of arterial and venous thrombosis, concomitant fetal loss and the presence of antiphospholipid antibodies (APLA). This report focuses on the challenges of optimal treatment involving plasma exchange and intravenous human immunoglobulin infusions that is administered in patients with catastrophic APS (CAPS). CAPS is a rare variant of APS defined as acute failure of at least three tissues, organs or systems caused predominantly by small vessel thrombosis confirmed by histopathologic evidence. CAPS develops rapidly and leads to death in 50% of cases. We present the case of a 39-year-old male patient with APS with worsening renal function. Positive lupus anticoagulant, markedly high concentrations of anticardiolipin and anti-beta 2-glikoprotein I antibodies have been observed. According to the criteria introduced by Asherson, a catastrophic form of APS was diagnosed and the patient had been treated with low-molecular-weight heparin, glucocorticosteroids, and plasmapheresis. In order to maintain clinical improvement, the patient was given human immunoglobulins i.v. (1 g/kg body weight). After the procedure, gradual clinical improvement was observed and renal function remained stable (serum creatinine level of 1.5 mg/dl).
Pol Arch Med Wewn 2009 Jun
PMID:Catastrophic antiphospholipid syndrome. 1969 27


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