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

Rhodotorula species have been reported as a causative agent of opportunistic mycoses in immunocompromised hosts. We report a case of sepsis and meningoencephalitis caused by Rhodotorula glutinis in a 20-year-old female patient with systemic lupus erythematosus (SLE), which was diagnosed at autopsy. The patient presented with longstanding fever. She was diagnosed with SLE after admission to the hospital and died on day 5 of the hospital stay. Autopsy was performed to confirm the presence of infection. Sepsis and meningoencephalitis due to Rhodotorula glutinis was confirmed by postmortem blood cultures and histopathological examination of biopsies taken from the brain at autopsy. Infection by Rhodotorula spp. is rare but can be fatal in immunocompromised hosts. Infections by such uncommon yeasts may often be difficult to diagnose, especially in the setting of febrile neutropenia. This report also emphasizes the value of autopsy as a powerful educational tool.
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PMID:Sepsis and meningoencephalitis due to Rhodotorula glutinis in a patient with systemic lupus erythematosus, diagnosed at autopsy. 1792 63

Infection of germline cells with retroviruses initiates permanent proviral colonization of the germline genome. The germline-integrated proviruses, called endogenous retroviruses (ERVs), are inherited to offspring in a Mendelian order and belong to the transposable element family. Endogenous retroviruses and other long terminal repeat retroelements constitute ~8% and ~10% of the human and mouse genomes, respectively. It is likely that each individual has a distinct genomic ERV profile. Recent studies have revealed that a substantial fraction of ERVs retains the coding potentials necessary for virion assembly and replication. There are several layers of potential mechanisms controlling ERV expression: intracellular transcription environment (e.g., transcription factor pool, splicing machinery, hormones), epigenetic status of the genome (e.g., proviral methylation, histone acetylation), profile of transcription regulatory elements on each ERV's promoter, and a range of stress signals (e.g., injury, infection, environment). Endogenous retroviruses may exert pathophysiologic effects by infection followed by random reintegration into the genome, by their gene products (e.g., envelope, superantigen), and by altering the expression of neighboring genes. Several studies have provided evidence that ERVs are associated with a range of pathogenic processes involving multiple sclerosis, systemic lupus erythematosus, breast cancer, and the response to burn injury. For instance, the proinflammatory properties of the human ERV-W envelope protein play a central role in demyelination of oligodendrocytes. As reviewed in this article, recent advances in ERV biology and mammalian genomics suggest that ERVs may have a profound influence on various pathogenic processes including the response to injury and infection. Understanding the roles of ERVs in the pathogenesis of injury and infection will broaden insights into the underlying mechanisms of systemic immune disorder and organ failure in these patients.
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PMID:Endogenous retroviruses in systemic response to stress signals. 1831 6

Infection with hepatitis C virus (HCV) may be associated with a wide spectrum of immunological abnormalities. HCV tends to induce nonspecific autoimmune reactions, as demonstrated by the high prevalence of various autoantibodies, including antiphospholipid antibodies (aPL). The aPL antibodies (lupus anticoagulant and anticardiolipin antibodies) are a heterogeneous family of immunoglobulins reactive with complexes of phospholipids and plasma proteins (cofactors). The most important of these protein cofactors are beta2-glycoprotein (beta2-GPI) and prothrombin. The antiphospholipid syndrome (APS) is an autoimmune disorder characterized by arterial or venous thrombosis, recurrent fetal losses in association with the presence of antiphospholipid (aPL) antibodies. Increased prevalence of aPL antibodies in several bacterial, parasitic, and viral infections have been reported. Most of the published data agree that anticardiolipin antibodies are frequently found in patients with chronic HCV infection, but they do not appear to be of clinical importance. Some studies, however, have found an increased incidence of thrombotic disorders in patients with chronic hepatitis C virus (HCV) who manifest aPL positivity. More prospective, long-term studies are required in order to address whether HCV is involved or not in the etiopathogenesis of APS.
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PMID:[Antiphospholipid antibodies with HCV infection. Innocent proteins or risk factor?]. 1840 57

Infections can act as environmental triggers inducing or promoting systemic lupus erythematosus (SLE) in genetically predisposed individuals. The aim of the present study was to compare the titres of antibodies (Abs) to infectious agents with neuropsychiatric (NPSLE) clinical manifestations. The sera of 260 individuals (120 patients with SLE and 140 geographic controls) were evaluated for the titres of Epstein bar virus (EBV), cytomegalovirus (CMV), toxoplasma, rubella and syphilis Abs using the BioPlex 2200 Multiplexed Immunoassay method (BioRad) and by the ELISA method for Helicobacter pylori and Hepatitis B core Ag. All BioPlex 2200 kits used were in developmental stages. Data analysis was performed using SPSS 9.0 statistical analysis software (SPSS Inc., Chicago, IL, USA, 1999). Correlation analysis indicated that rubella IgM Ab titres were marginally, positively associated with psychosis (P = 0.09). No other associations were detected between the 17 infectious Abs and five NP manifestations. When the positivity cut-off for anti-rubella IgM Abs was set at three standard deviations above normal, three positive subjects were identified: one patient with psychosis and one with depression, for a total NPSLE prevalence of 33.3%. On the contrary, the prevalence of NPSLE in the remaining subjects was 6.5%. Marginally significant correlations between elevated titres of rubella IgM Ab with psychosis and depression were found. Although this nearly 5-fold increase is not statistically significant, it appears that in a larger sample size, significance would be reached. This is the first study reported that examined the correlation of NPSLE manifestations with anti-infectious Abs.
Lupus 2008 May
PMID:Neuropsychiatric lupus and infectious triggers. 1849 Apr 12

Glucocorticoids (GCs) have many complex quantitative and qualitative immunosuppressive effects which induce cellular immunodeficiency and increase host susceptibility to various viral, bacterial, fungal and parasitic infections. As cortisol secretion is inadequate in chronic immune/inflammatory conditions, and current therapies have the aim of providing adequate (low) compensatory doses, the timing of GC administration, such as during the nocturnal turning-on phase of tumour necrosis factor (TNF) secretion, can be extremely important. The use of the lowest possible GC dose, at night, and for the shortest possible time should therefore greatly reduce the risk of infections. Infection is a major co-morbidity in rheumatoid arthritis (RA), and conventional disease-modifying anti-rheumatic drugs (DMARDs) can increase the risk of their occurrence, including tuberculosis. TNF-alpha plays a key role in the pathogenesis of RA, and the data concerning infections in RA patients treated with anti-TNF agents are controversial. Patients and physicians should vigilantly monitor for signs of infection when using anti-TNF agents. Recombinant gene technologies now make it possible to produce protein drugs that are almost identical to naturally occurring human polypeptides, including antibody (Ab) constructs; unfortunately, all human biological agents are potentially immunogenic. An increasing number of recent studies have demonstrated the safety of influenza and pneumococcal vaccines administered to patients with systemic lupus erythematosus (SLE) or RA. These vaccinations are generally immunogenic (i.e., capable of inducing a protective level of specific antibodies) but may not induce an adequate response in a substantial proportion of patients.
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PMID:Infections and treatment of patients with rheumatic diseases. 1857 Jul 57

Mycophenolate mofetil (MMF) with prednisolone has been associated with high remission rates when used as induction treatment for lupus nephritis. This prospective, multicentre, cohort study investigates the efficacy and safety of this regimen over 24 weeks in 213 Chinese patients with active lupus nephritis (Classes III, IV, V or combination). Baseline activity index (AI) was 6.91+/-3.33 and chronicity index (CI) was 1.9+/-1.2. The remission rate was 82.6% at 24 weeks (complete remission, 34.3%; partial remission, 48.4%). There were significant (P<0.01) improvements in kidney function shown by reductions in proteinuria, serum albumin, serum creatinine and creatinine clearance, as well as in systemic lupus erythematosus disease activity index (SLEDAI) scores. Independent risk factors influencing remission were pathological classification (including Class V and III or Class V and IV nephritis) and elevated serum creatinine at baseline (OR 2.967, 95% CI: 1.479-6.332, P=0.001 and OR 1.007, 95% CI: 1.002-1.011, P=0.001, respectively). Patients with concomitant membranous features on biopsy had a lower remission rate than those with Class III and IV nephritis (66.7% vs 87.3%, P=0.002). Renal biopsy was repeated in 25 patients following treatment. There was a transition to less severe pathological morphologies in majority of subjects. Infections were monitored throughout treatment: eight patients (3.8%) experienced bacterial infections, whereas herpes zoster occurred in seven patients. Nine patients (4.2%) suffered from gastrointestinal upset, which resolved without discontinuation of MMF. One patient became leucopenic, whereas another died from active disease unrelated to kidney symptoms. MMF combined with prednisolone is an effective and well-tolerated induction treatment for patients with active lupus nephritis and for controlling SLE systemic activity.
Lupus 2008 Jul
PMID:A prospective multicentre study of mycophenolate mofetil combined with prednisolone as induction therapy in 213 patients with active lupus nephritis. 1862 34

A growing body of experimental and clinical evidence supports the pivotal role of infections in the induction or exacerbation of systemic lupus erythematosus (SLE). Infections can be responsible for aberrant immune response leading to a loss of tolerance towards native proteins. Molecular mimicry, especially between Sm or Ro autoantigens and EBV Nuclear Antigen-1 response, as well as the over-expression of type 1 INF genes are among the major contributors to SLE development. On the other hand infections are very common in SLE patients, where they are responsible for 30-50% of morbidity and mortality. Several factors, either genetic, including complement deficiencies or mannose-binding lectin deficiency or acquired such as severe disease manifestations or immunosuppressant use, predispose SLE patients to infections. All types of infections, including bacterial, viral and opportunistic infections, have been reported and the most frequently involved sites of infections are the same as those observed in the general population, including respiratory, skin, and urinary tract infections. Some preventive measures could be adopted in order to reduce the rate of infections in SLE patients: i.e. screening for Mycobacterium tuberculosis and for some chronic viral infections before immunosuppressive treatment; adequate prophylaxes or drug adjustments when indicated, and pneumococcal and influenza vaccinations in patients with stable disease.
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PMID:Infections as triggers and complications of systemic lupus erythematosus. 1870 74

Systemic lupus erythematosus (SLE) is known to occur in all populations across the globe. In many respects SLE is similar across regions in its spectrum of clinical features, but the severity of the disease and comorbidity are appreciably different in the developing and industrialized worlds. Although data on the prevalence of SLE among Africans and Asians living in the tropics are limited, SLE is reportedly more common and more severe in people of African and Asian extraction living in industrialized countries. Renal disease is especially common in SLE patients in the developing world and is a major cause of morbidity and mortality. Discoid lupus and lymphopenia are frequent clinical features of SLE in patients of African extraction. Thrombotic complications and associated anti-phospholipid antibodies are less common in the Chinese and Black African SLE patients than in Caucasian patients. High frequencies of antibodies to extractable nuclear antigens, especially anti-Sm and anti-U1RNP, have been reported in SLE patients in many developing countries. Infections, including tuberculosis, are among the most important causes of comorbidity and mortality in SLE across all regions of the developing world. With a few exceptions, survival rates for SLE patients in developing countries are substantially lower than those reported in industrialized countries, with early death from infection and active disease. The bimodal pattern of mortality observed in many industrialized countries, is also less evident. While the poorer outcome in developing countries is partly related to inherent genetic differences, better outcomes can be achieved if new initiatives are undertaken to define the burden of disease, increase public awareness, and establish algorithms for diagnosis and treatment based on the available resources and local health-care delivery systems.
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PMID:Lupus in the developing world--is it any different? 1878 42

Systemic erythematosus lupus (SLE) is a disease with wide range of clinical manifestations, signs and symptoms. Disease outcome depends mostly on the affection of kidneys and central nervous system by the disease. Very important cause of death in patients with SLE is infection. Infections are very common among these patients due to aggressive immunosuppressive treatment that is needed for the disease inflammatory activity control. In this case report we have presented a patient with SLE who initially had severe renal affection, but also complications of immunosuppressive therapy that was administered. Even though the disease was accidentally diagnosed, it had a severe clinical progress. Because of lupus nephropathy, in the early phase of the disease we administered aggressive immunosuppressive therapy (combined parenteral therapy of glucocorticoides and cyclophosphamide). As an outcome of the combined effect of disease and immunosuppressive agents used in the treatment of the disease, the patient had increased infective diathesis (repeated infections caused by S. enteritidis--urinary infections and sepsis). During one of the disease flares the patient was hospitalized an opportunistic infection developed. It was meningitis caused by C. neoformans. This opportunistic mycosis infection presented with clinically totally nonspecific signs and symptoms of CNS affection. Therefore, we suspected affection of CNS with SLE. Even though all diagnostic procedures were made on time and that adequate antifungal and supportive agents were applied very early after the infection onset, the outcome was fatal. Because of infective diathesis in patients with SLE, which present with common and opportunistic infections, and due to high mortality rates caused by these infections, we have tried to emphasise the importance of taking adequate specimens early after infection outcome for these rare infective agents like C. neophormans. In recent medical literature are dominant cases reported in Asia. Reports from Europe are very rare, and this case is the one of that kind in Croatia.
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PMID:[Cryptococcal meningitis as a diagnostic problem in a patient with SLE--case report]. 1879 61

The aetiology of systemic lupus erythematosus (SLE) is thought to involve both genetic and environmental factors. In other complex diseases, analysis of large multi-case families has resulted in insights into biological mechanisms. We have sought to characterise the members of an extended Indigenous family, five of whom have been diagnosed with SLE. Pedigree members were evaluated using the Lupus Screening Questionnaire, clinical interviews and medical records. Participants contributed blood and urine samples for laboratory analysis. A Mendelian pattern of inheritance was not observed. The five affected members (all female) shared two American College of Rheumatology criteria (positive ANA and arthritis) but showed a wide variety of other SLE manifestations. Disease onset, severity and progression were discordant. Including the five individuals with SLE, 15 blood relatives and two non-consanguineous spouses had autoimmune manifestations. Autoimmune haemolytic anaemia (one case), idiopathic thrombocytopenic purpura (ITP) (one case) and hypothyroidism (two cases) were observed in non-SLE affected individuals. Anti-nuclear antibodies were present in 12 blood relatives and one non-consanguineous spouse. Infections (especially of the skin) were observed to be common in the kindred. The lack of clear Mendelian inheritance or phenotypic concordance makes a rare monogenic explanation for SLE unlikely in this family. The finding of familial autoimmunity associated with SLE further supports the hypothesis that a common genetic pathway can precipitate autoimmunity, with further genes and possible environmental factors interacting to produce the eventual phenotype. Future genetic linkage studies may reveal a rare 'autoimmune gene' variant in this kindred.
Lupus 2009 Feb
PMID:The clinical characterisation of systemic lupus erythematosus in a Far North Queensland Indigenous kindred. 1915 Nov 16


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