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

---

Query: UMLS:C0024141 (systemic lupus erythematosus)
44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both epidemiological and experimental studies have shown that impaired growth in utero due to maternal malnutrition, resulting in low birth weight, is associated with a high incidence of glucose intolerance, insulin resistance, and type 2 diabetes in adult life. Maternal malnutrition is a worldwide problem and unavoidable; therefore, prevention of type 2 diabetes in low birth weight infants who reach adulthood is difficult to achieve. Administration of human umbilical cord blood (HUCB) mononuclear cells into type 1 and type 2 diabetic mice has been shown to improve both their blood glucose levels and survival. It has also been shown that the progenitor cells derived from HUCB improve not only glycemia but also other disease conditions, including systemic lupus erythematosis, amyotrophic lateral sclerosis, Alzheimer's disease, stroke, brain damage in animals and certain malignancies in humans. Transfusion of unrelated HUCB, although abundantly available, is underutilized as a therapeutic agent. Therefore, we propose the hypothesis that transfusion of HUCB to low birth weight infants be considered a therapeutic modality to prevent the development of type 2 diabetes in their adulthood.
...
PMID:Administration of human umbilical cord blood to low birth weight infants may prevent the subsequent development of type 2 diabetes. 1648 Nov 20

Idiopathic hypertrophic cranial pachymeningitis is a rare chronic inflammatory and fibrosing process of unknown etiology. This entity is characterized by fibrosis and thickening of the dura mater and resulting in neurological syndrome. The authors report a 72 year-old woman who presented with progressive bifrontal headache, bilateral visual loss and transient episode of confusion. Neurological examination revealed bilateral optic atrophy, apathy and no focal neurological deficit. Investigations showed anemia of chronic disease, elevated erythrocyte sedimentation rate and polyclonal hypergammaglobulinemia. No specific inflammatory diseases or malignancy such as systemic lupus erythematosus, syphilis, hematologic malignancy were found MRI of the brain revealed thickened and enhanced dura mater and leptomeninges at the inferior aspect of bilateral frontal lobes as well as vasogenic edema of the frontal lobes. Cerebrospinal fluid showed mild pleocytosis, high protein level and normal glucose level. Meningeal biopsy revealed nonspecific inflammatory process of the dura and leptomeninges. There was no granuloma formation or evidence of vasculitis. Special stain for tuberculous bacilli, fungus and malignancy were all negative. The diagnosis of "idiopathic hypertrophic pachymeningitis" was made. The patient was treated with oral prednisolone 45 mg/day. Her headache was improved, but the profound vision loss in both eyes remained unchanged after 2 years of follow-up. Prednisolone was tapered within 18 months. Idiopathic hypertrophic cranial pachymeningitis usually involves dura at tentorium cerebelli, cavernous sinus and base of the skull. The extensive involvement at the anterior cranial fossa is extremely rare.
...
PMID:Extensive anterior cranial fossa idiopathic hypertrophic pachymeningitis: a case report and review of the literature. 1651 96

Ibuprofen is a common nonsteroidal antiinflammatory drug that is the most frequent cause of aseptic meningitis induced by drugs. The incidence of this type of aseptic meningitis is increasing, mainly among patients with underlying autoimmune connective tissue disorder, but also among healthy people. We report 2 patients with recurrent meningitis caused by ibuprofen mimicking bacterial meningitis: the first patient a woman with dermatomyositis and the second patient a previously healthy woman who developed autoimmune thyroiditis a few months later. We then review 71 episodes of ibuprofen-related meningitis in 36 patients reported in the literature. Twenty-two patients (61%) presented with an autoimmune connective tissue disorder, mainly systemic lupus erythematosus, and 22 (61%) had recurrent episodes. Most episodes consisted of an acute meningeal syndrome with a predominance of neutrophils in cerebrospinal fluid (CSF) in 72.2% of episodes and elevated protein in the CSF, so the clinical presentation of this type of aseptic meningitis may be quite similar to that of acute bacterial meningitis. CSF glucose levels are usually normal, which may help to differentiate between these 2 types of meningitis. In some cases the clinical presentation is that of meningoencephalitis with neurologic focal deficits. Although based on the close relation between the administration of ibuprofen and the onset of symptoms, especially if previous episodes have occurred, the diagnosis of ibuprofen-induced aseptic meningitis is a diagnosis by exclusion. If the clinical picture is compatible with bacterial meningitis, empirical antibiotic therapy must be administered until negativity of cultures and other microbiologic tests is determined. Rechallenge to ibuprofen reproduces the symptoms and confirms the diagnosis, but is usually not advised. Whatever the clinical presentation, physicians must consider the possibility of ibuprofen-related meningitis or meningoencephalitis in patients taking ibuprofen, especially if they are suffering from an autoimmune connective tissue disorder. On the other hand, we think it would be appropriate to screen for autoimmune disease in previously healthy patients diagnosed with ibuprofen-related meningitis or meningoencephalitis. Finally, we propose that meningitis due to ibuprofen be included in the list of causes of recurrent aseptic meningitis.
...
PMID:Characteristics of meningitis caused by Ibuprofen: report of 2 cases with recurrent episodes and review of the literature. 1686 46

Accumulating data indicate that metabolic syndrome is an inflammatory condition. Systemic lupus erythematosus (SLE) is an autoimmune disorder associated with nephritis and cardiovascular disease. Evidence suggests that individuals with SLE are at risk for developing insulin resistance; however, this has not been directly examined. Using an established mouse strain with SLE (NZBWF1), we examined whether SLE is associated with increased body weight and fat deposition. Mean arterial pressure was significantly increased (140+/-4 versus 114+/-2 mm Hg; n > or = 5) in SLE mice by 36 weeks of age compared with control mice (NZW/LacJ). Body weight in SLE mice was higher at each age compared with controls by 12%, 22%, and 34% (n > 30). Visceral adipose tissue weight was increased in SLE by 44%, 74%, and 117% at 8, 20, and 36 weeks, respectively (n > or = 12). Plasma leptin was increased in SLE mice (8.6+/-1.0 versus 24.7+/-2.2 ng/mL; n = 5), and renal and adipose tissue exhibited macrophage infiltration. Fasted insulin was higher in SLE mice (0.6+/-0.1 versus 1.4+/-0.3 ng/mL; n > or = 10), but fasted glucose was not different (94+/-5 versus 80+/-9; n > or = 9). A glucose tolerance test caused a significantly greater and longer increase in blood glucose from mice with SLE compared with control mice. Food intake was not different between control and SLE mice. However, mice with SLE demonstrated lower levels of nighttime activity than controls. These data show that the NZBWF1 strain may be an important model to study the effects of obesity and insulin resistance on SLE-associated hypertension.
...
PMID:Insulin resistance and obesity in a mouse model of systemic lupus erythematosus. 1715 78

Autoantibodies to the insulin receptor have been demonstrated to antagonize the physiologic actions of insulin, most often resulting in hyperglycemia unresponsive to massive doses of insulin (type B insulin resistance). Patients with these anti-insulin receptor antibodies typically have a coexistent autoimmune disorder, most commonly systemic lupus erythematosus (SLE) or undifferentiated autoimmune syndromes. Attempting to determine the prevalence and significance of anti-insulin receptor antibodies, sera from consecutive patients with SLE and early undifferentiated connective tissue disease (UCTD) were tested for the presence of anti-insulin receptor antibodies by radio-immuno assay. Thirty-eight patients participated in the study. Twenty-six had SLE and 12 had UCTD. One patient with SLE (2.6%) was positive for anti-insulin receptor antibodies. None of the patients demonstrated evidence of insulin resistance, hypoglycemia, ovarian hyperandrogenism, or acanthosis nigricans, findings commonly linked with the presence of anti-insulin receptor antibodies. The results presented here indicate that the incidence of anti-insulin receptor antibodies in patients with SLE or UCTD, without associated history of altered glucose metabolism, is quite low. Because in most cases the disturbance of glucose metabolism dominates the clinical picture at presentation and the associated systemic autoimmune syndrome presents either simultaneously with or subsequent to the diagnosis of diabetes, the measurement of anti-insulin receptor antibodies should be reserved for patients with indications of disordered glucose homeostasis.
...
PMID:The prevalence of insulin receptor antibodies in patients with systemic lupus erythematosus and related conditions. 1703 74

Ischemic heart disease and myocardial infarction in patients with SLE--are usually secondary to early coronary atherosclerosis. Estimation if antiphospholipid syndrome and antiphospholipid antibodies are the risk factor for myocardial infarction and ischemic heart disease in patients with TRU. We examined 129 patients with SLE (114 women and 15 men). All the patients underwent comprehensive physical examination. ECG, ultrasound heart examinations were performed. They were followed by heart scintygraphic examination if indicated. Routine biochemical and hematological laboratory tests were performed including fasting glucose level, concentration of homocysteine, uric acid and lipids. Wide range of immunological essays were performed, testing for antinuclear antibodies (ANA), extractable nuclear antigen antibodies (ENA), antiphospholipid antibodies (anticardiolipin antibodies--aCL, lupus anticoagulant--LA, antiprothrombine antibodies aPT, anti-beta2glicoprotein-I antibodies), anti-dsDNA antibodies, anti-nucleosome antibodies, antihistone antibodies, antineutrophil cytoplasmic antibodies (ANCA) and antiendothelial antibodies (AECA). Statistical analysis was performed with chi2 Yates, chi2 Pearson and R rang Spearman tests. Multivariate regression analysis was also done. Ischemic heart disease was found in 20 (15.5%) SLE patients, myocardial infarctions were diagnosed in 9 (6.97%). Ischemic heart disease and myocardial infarction were significantly related to presence of secondary antiphospholipid syndrome (SAPS), OR: 4.21, p = 0.008 and OR: 12.8; p = 0.02 respectively). They were also related to high activity of SLE, OR: 7.18; p = 0.012 and OR: 27.3; p = 0.006 respectively. Ischemic heart disease was significantly more common in older patients (52.75 years versus 42.15 years; p = 0.0008) and in patients with hypertension (p < 0.05). Impaired glucose tolerance (OR: 8.44; p = 0.03), presence of aCL IgG (OR; 2.93; p = 0.05) and p-ANCA anti-MPO (OR: 6.08; p = 0.036) were found to be risk factors of ischemic heart disease. Myocardial infarction was significantly associated with high uric acid level (OR: 5.01; p = 0.052) and impaired glucose tolerance (OR: 7.42; p = 0.047) and with presence of the following antibodies: aCL IgG and/or aCL IgM (OR: 5.61; p = 0.039), ANCA in the indirect immunofluorescence essay (OR: 5.78; p = 0.035), anti-MPO antibodies (OR: 6.58; p = 0.051) and AECA (OR: 11.10; p = 0.026). Presence of antiphospholipid antibodies and SAPS are significant risk factors of ischemic heart disease and myocardial infarction in SLE patients. The risk factors of ischemic heart disease and myocardial infarction in SLE patients significantly differ from the ones in general population.
...
PMID:[Antiphospholipid syndrome and antiphospholipid antibodies as a risk factors of ischaemic heart disease and myocardial infarction in patients with systemic lupus erythematosus]. 1719 52

Cardiovascular disease is a major cause of death in patients with systemic lupus erythematosus (SLE) especially during the late phase of the disease. This study was conducted to evaluate B-type natriuretic peptide (BNP) levels in female SLE patients without cardiac symptoms and to investigate whether BNP levels correlated with echocardiographic findings. We studied 59 women with SLE and 33 healthy women. SLE patients with history of cardiac disease, diabetes mellitus, hypertension, and other inflammatory diseases were excluded from the study. All subjects had a complete history and physical examination. Overall disease activity assessment in SLE patients at the time of the study were derived by calculation of SLE disease activity index (SLEDAI). BNP levels were determined, and transthoracic echocardiography were performed in all subjects. There was no difference between SLE patients and controls in terms of age, blood pressure, smoking status, plasma glucose, creatinine levels, and lipid profiles. Nine patients had SLEDAI score greater than 5. All subjects had an EF greater than 55%. Diastolic dysfunction was more frequent in lupus patients than in controls (15 [25.4%] vs. 2 [6%]; p = 0.022). BNP levels of SLE patients were significantly higher than controls (median 17.9 range [5-211] pg/ml vs. median 14.7 range [5-39.7] pg/ml; p = 0.033). Twenty-seven of the SLE patients (46%) and seven of the controls (21%) had BNP levels greater than or equal to 20 pg/ml (p = 0.019). There were no differences in BNP levels of SLE patients with and without diastolic dysfunction (median 17.8 range [5-117] pg/ml vs. median 18.5 range [5-211] pg/mL; p = NS). BNP levels were positively correlated with left atrium diameter (r (2) = 0.39, p = 0.001). BNP levels did not correlate with erythrocyte sedimentation rate/C-reactive protein levels, SLEDAI scores, total steroid dosage used, or other echocardigraphic parameters. BNP levels were increased in female SLE patients without cardiac symptoms as compared to healthy controls. Although none of the SLE patients in our study had clinical signs of ischemic heart disease, increased levels of BNP in SLE patients might be a reflection of a ischemic myocardial tissue.
...
PMID:B-type natriuretic peptide (BNP) levels in female systemic lupus erythematosus patients: what is the clinical significance? 1731 74

Catastrophic longitudinal myelitis is an extremely rare neurologic manifestation of collagen vascular disease, described heretofore in 11 cases of SLE and 1 of Sjogren's Syndrome. This report documents markedly abnormal and worsening CSF findings on sequential CSF examinations over a period of three days (WBC >1500 cells/microL, >80% neutrophils, markedly elevated protein, and extremely low glucose levels) in the absence of infection. These abnormalities cleared rapidly with institution of immunosuppressive therapy so that a third CSF exam done within three days revealed almost complete normalization of CSF values. These findings suggest that in some cases of CLM a strong inflammatory component may be present, while in others, other pathogenic factors may predominate.
Lupus 2007
PMID:Marked inflammation in catastrophic longitudinal myelitis associated with systemic lupus erythematosus. 1789 6

This study has employed high-resolution NMR spectroscopy of kidney extracts to study alterations in the concentrations of amino acids and glucose in systemic lupus erythematosus (SLE). We used the well-established mouse model of SLE, MRL/lpr, and their congenic controls, MRL/+. There was a substantial increase in the tissue concentration of branched-chain amino acids (133%), aromatic amino acids (134%) and glutathione (122%) in the lupus mice, compared to the controls. Since increased glucose can lead to fibrosis, we used [1-(13)C] glucose as a tracer to study its transport into the kidney. Significant increases in the levels of [1-(13)C] glucose (200% of controls) were observed in the MRL/lpr mice 15 min after its injection. 13C NMR spectra demonstrated that the 13C-label from [1-(13)C] glucose was not incorporated into glycolytic and Krebs cycle related metabolites within 15 min. Furthermore, we found that the expression of the profibrotic cytokine, TGFbeta and the regulatory transcription factor Smad3 are significantly enhanced in MRL/lpr mice compared to the MRL/+ controls. The mRNA and protein expression of extracellular matrix proteins, fibronectin, laminin, and collagen IV were upregulated in the MRL/lpr mice compared to the controls. All these changes were significantly reduced by the complement (C) inhibitor, Crry. Our results suggest that C activation causes increased glucose concentration in the kidney, which can lead to the observed hyperglycemia. This may be one of the important factors that cause increased extracellular matrix (ECM) deposition through the TGFbeta signaling in lupus mice and thereby lead to glomerulosclerosis that translates into increased kidney disease.
...
PMID:Alteration in kidney glucose and amino acids are implicated in renal pathology in MRL/lpr mice. 1794 82

Genetic studies in several human autoimmune diseases suggest that the pericentromeric region of chromosome 16 might harbor an autoimmune modifier gene. We hypothesized that the sodium-dependent glucose cotransporter gene SLC5A11 is such a gene, and so might interact with immune-related genes. Herein, this hypothesis was tested in a genetic evaluation of the multiple gene effect in systemic lupus erythematosus (SLE). We used the case-control candidate gene association approach. Eight immune-related genes involved in inflammation and autoantibody generation and clear-up [interleukin 1 receptor antagonist (IL1RN), interleukin 1-beta (IL1-beta), tumor necrosis factor-alpha (TNF-alpha), lymphotoxin-alpha (LTA), tumor necrosis factor ligand superfamily, member 6 (TNFSF6), programmed cell death 1 (PDCD1), C2, and complement component 4 (C4)] were selected for study. Frequency of each candidate's genotype and allele between case and control were compared. Results were stratified by reanalyzing genotype data with relevant symptoms. Finally, improved computational data mining was used to analyze the phenotypes in a large data set. In the frequency analysis, only IL1-beta was significantly associated with SLE. Stratification analysis showed a significant association with SLE symptoms between SLC5A11 and the other immune-related genes, with the exceptions of TNFSF6 and C4. SLC5A11 was significantly associated with low C4 (as was TNF-alpha), anti-Smith antibody (anti-Sm) (as was C2), serositis, and alopecia. Finally, SLC5A11 interacted with PDCD1, TNF-alpha, LTA, and C4. After our study, we concluded that SLC5A11 is involved with some immune effects and interacts with immune-related gene(s), consistent with its function as an autoimmune modifier gene. Furthermore, SLC5A11 might induce apoptosis through the TNF-alpha, PDCD1 pathway. The present genotype-phenotype mapping approach should be applicable to genetic study of other complex diseases.
...
PMID:The sodium-dependent glucose cotransporter SLC5A11 as an autoimmune modifier gene in SLE. 1806 35


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---