PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “LUPUS ERYTHEMATOSUS, SYSTEMIC”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,207 records · Page 67Linked to original sources
PubMed1983

Ethnic difference in the prevalence of systemic lupus erythematosus.

A retrospective study of systemic lupus erythematosus (SLE) was carried out in Auckland, New Zealand, for the years 1975 to 1980 inclusive. One hundred and fifty-one patients were found of which 106 fulfilled the American Rheumatism Association criteria. There were 15 deaths. Age-adjusted prevalence rates per 100 000 were estimated for all cases at the end of 1980 as follows: white 14.6, Polynesian 50.63, and other 19.11. There was a preponderance of females in each ethnic group, average 87% of all cases. Age-adjustment mortality rates per million patient years were: white 2.5 and Polynesians 13.0. Survival curves for both ethnic groups were similar. The prevalence rate in New Zealand Polynesian is significantly higher than in white counterparts which confirms the observation that the disease is commoner in the pigmented races.

Adolescent↗
PubMed1986

Thyroid disorders in systemic lupus erythematosus.

Of 319 patients with systemic lupus erythematosus (SLE), nine had thyrotoxicosis, three had hypothyroidism, and two had thyroiditis. This prevalence seems greater than that of similar thyroid disorders seen in the general population. It is suggested that patients with autoimmune thyroid disorders may develop SLE or vice versa. This association requires confirmation by prospective study.

Adult↗
PubMed1998

Late onset systemic lupus erythematosus in southern Chinese.

OBJECTIVE: Systemic lupus erythematosus (SLE) is a multisystem disorder that predominately affects women of the reproductive age. Onset of the disease beyond the age of 50 years is unusual. This study was undertaken to compare retrospectively the clinical and laboratory features between early and late onset (onset of disease beyond the age of 50 years) SLE patients in a Chinese population. METHODS: Case records of all SLE patients who attended our rheumatology clinics between 1971 and 1997 were reviewed. Patients with a disease onset beyond the age of 50 years were identified. One hundred consecutive SLE patients who had their disease onset before the age of 50 were recruited as controls. The presenting clinical features, autoantibody profile, number of major organs involved, number of major relapses, and the use of cytotoxic agents in the two groups of patients were obtained and compared. RESULTS: 25 patients with late onset SLE were identified. All the female patients in the late onset group were postmenopausal. The female to male ratio was 3.2 to 1, compared with 13.3 to 1 in the control group (p < 0.02). Both groups had a comparable duration of disease. There were no significant differences in the presenting features between the two groups except for a lower prevalence of malar rash (24% v 86%, p < 0.0001) and a higher prevalence of rheumatoid factor (32% v 1%, p < 0.0001) in the late onset patients. On subsequent visits, the late onset group had a lower prevalence of lupus nephritis (4% v 51%, p < 0.001), fewer major organs involved (mean number of major organs involved; 0.3 v 0.9, p < 0.02), fewer major relapses (mean number of major relapses/patient; 0.08 v 0.47, p < 0.002, number of major relapses/patient year; 0.009 v 0.12, p < 0.001), and required fewer cytotoxic agents for disease control (percentage of patients on cytotoxic agents; 32% v 79%, p < 0.002). CONCLUSION: Late onset SLE in Chinese tends to run a more benign course with fewer major organ involvement and fewer major relapses. The significantly higher incidence of male sex in late onset SLE and the milder disease course in the postmenopausal female patients suggest that oestrogen status may influence disease activity.

Adolescent↗
PubMed2001

Use of anti-citrullinated peptide and anti-RA33 antibodies in distinguishing erosive arthritis in patients with systemic lupus erythematosus and rheumatoid arthritis.

OBJECTIVES: Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) can both present with an erosive arthritis with the small joints of the hands affected. Therefore a serological marker would be useful to distinguish between these two diseases at onset. In this study anti-RA33 antibodies, which are found in patients with SLE and RA, and anti-citrullinated peptide antibodies (anti-CCP), which have recently been described as highly specific for RA, were assessed. METHODS: Two hundred and thirty one patients receiving long term follow up for SLE were evaluated for arthritis and classified as erosive and non-erosive disease. Sixty six patients were tested for anti-RA33 and anti-CCP antibodies. All the patients were tested for rheumatoid factor (RF) and HLA-DR4 status. RESULTS: Ten patients had erosive disease, six of whom were RF positive (60%), and six anti-RA33 positive (60%), whereas only two were anti-CCP positive (20%). Two hundred and twenty one patients had non-erosive disease, 40 of whom were RF positive (18%), 14 were anti-RA33 positive (6%), whereas only one patient was found to be anti-CCP positive (0.5%). CONCLUSION: The presence of anti-CCP antibodies may be useful in distinguishing RA from erosive SLE. Anti-RA33 antibodies and RF are unhelpful.

Antibodies, Antinuclear↗
PubMed2003

Abdominal pain as the initial and sole clinical presenting feature of systemic lupus erythematosus.

Classically, a diagnosis of systemic lupus erythematosus (SLE) is dependent on renal, rheumatological, cutaneous and neurological target organ damage with supporting serological markers. A previously healthy 26-year-old Japanese woman whose only manifestation of otherwise occult SLE was severe abdominal pain is reported. A computed tomographic scan of the abdomen revealed thickened loops of small bowel, endoscopic findings were nonspecific and jejunal biopsy revealed a nonspecific enteritis. Laboratory studies revealed lymphopenia, hypocomplementemia, a positive antinuclear antibody, a weakly positive anti-Smith and a strongly positive anti-double stranded DNA. There was a prompt symptomatic recovery with immunosuppressive therapy. The authors' experiences, and a review of the literature suggest that a diagnosis of SLE should be considered in young Asian women who present with significant but clinically enigmatic gastrointestinal illness.

Abdominal Pain↗
PubMedDate not supplied

Aseptic leptomeningitis in systemic lupus erythematosus. A case report.

OBJECTIVE: Systemic lupus erythematosus (SLE) with leptomeningeal involvement is a rare condition. We report a case in a 17-year-old woman. CLINICAL PRESENTATION AND INTERVENTION: The patient was admitted to hospital with the complaints of vertigo, nausea, vomiting, headache, diplopia, ptosis on the left and weakness of the left leg. A diagnosis of SLE was established, with diffuse leptomeningeal involvement demonstrated by cranial magnetic resonance imaging. When treated with steroids, the clinical problems resolved almost completely. CONCLUSIONS: Although rare, leptomeningeal involvement can complicate SLE. Cranial magnetic imaging can demonstrate tissue involvement. The condition responds to steroid therapy.

Adolescent↗
PubMed1992

Massive bilateral pleural effusion as the only first presentation of systemic lupus erythematosus.

A rare case of systemic lupus erythematosus (SLE), with massive bilateral pleural effusions as the first manifestation, is described. The patient was a previously healthy 20-year-old soldier. Initial investigations were unrevealing, but after 3 months the patient developed the full-blown syndrome. He responded well to corticosteroids and cyclophosphamide with resolution of the pleural effusions and improvement of the clinical picture. SLE should always be considered in cases of massive pleural effusions, even in the absence of other overt stigmata of the disease.

Adult↗
PubMed1977

Circulating anticoagulant against factor XI and thrombocytopenia with platelet aggregation inhibition in systemic lupus erythematosus.

In a patient with systemic lupus erythematosus, anticoagulant activity directed against factor XI was found together with thrombocytopenia. In the serum globulin fraction, antiplatelet antibodies and an activity-inhibiting platelet aggregation could also be found. A possible correlation between the inhibition of platelet aggregation and the anticoagulant activity directed against factor XI is discussed.

Adult↗
PubMed1994

Unusual coexistence of systemic lupus erythematosus and primary biliary cirrhosis.

Systemic lupus erythematosus (SLE) and primary biliary cirrhosis (PBC) are distinct clinical disorders which rarely occur in the same patient. We report on a 65-year-old woman with coexistence of both conditions. Diagnosis of SLE was ascertained by the presence of seven ACR criteria (cutaneous lesions, photosensitivity, antinuclear and anti-double-stranded-DNA antibodies, pancytopenia, arthritis, oral lesions). PBC was disclosed by clinical investigation, liver histology and highly positive antimitochondrial M2 antibodies. The most important differential diagnoses of lupus hepatitis are PBC and autoimmune hepatitis. Diagnostic criteria for these conditions are discussed, and previous reports on overlap between SLE and PBC are reviewed.

Aged↗
PubMed2005

Altered regulation of IL-2 production in systemic lupus erythematosus: an evolving paradigm.

In systemic lupus erythematosus (SLE), IL-2 production by T lymphocytes in vitro is impaired. Deficient IL-2 production may be an outcome of a primary SLE T cell disorder that is due to impaired signal transduction. In this issue of the JCI, evidence is presented that an anti-TCR/CD3 complex autoantibody present in SLE sera can bind to T cells and activate the Ca(2+)-calmodulin kinase IV (CaMKIV) signaling cascade, resulting in downregulation of IL-2 transcription and IL-2 production. Because IL-2 may contribute to the maintenance of T cell tolerance, deficient IL-2 production could promote a breach of T cell tolerance that results in autoantibody production in SLE.

Autoantibodies↗
PubMed1993

Prevalence of systemic lupus erythematosus in India.

Prevalence of systemic lupus erythematosus (SLE) was studied in the northern Indian population by means of a two-pronged approach: (a) antinuclear antibody (ANA) screening of the general population by a new well-standardized finger-prick 'filter paper' technique (sensitivity and specificity: 95.4% and 86.2%, respectively); and (b) a questionnaire survey carried out primarily by trained personnel in the community (sensitivity and specificity: 100% and 68.6% respectively). The low specificity of the two methods was improved by the introduction of a step of secondary screening by the authors, thus excluding false positives. ANA screening of 52,062 individuals yielded 13 positive results, of which only two were found to be true cases of SLE after secondary screening. Questionnaire survey of 39,826 individuals similarly yielded 3393 positive results. On secondary screening, only one of these persons was found to be a case of SLE. Thus, three cases of SLE were detected in a population survey of 91,888, giving a point prevalence of 3.2 per 100,000 (95% CI = 0-6.86 per 100,000). The reported prevalence of SLE ranges from 14 to 60 per 100,000. Thus, the prevalence of SLE in India is comparatively low. Although the reasons for low prevalence are not clear, the study used highly sensitive methodology and it is therefore unlikely that SLE cases were missed. It is hypothesized that SLE is a disease of modernization and therefore its prevalence in a predominantly rural population like that of India is low.

Antibodies, Antinuclear↗
PubMed2001

Polymorphisms of the human prolactin gene--implications for production of lymphocyte prolactin and systemic lupus erythematosus.

Hyperprolactinaemia is associated with systemic lupus erythematosus (SLE) but the mechanism is unknown. Prolactin is expressed not only by pituitary lactotrophic cells but also by T-lymphocytes under the control of an alternative upstream promoter region. T-lymphocytes from SLE patients have been shown to secrete more prolactin than controls, thus implying a possible underlying difference in regulation. This may be due to genetic polymorphism that can be determined by scanning for mutations and using a variety of methods to determine their function. A polymorphism may also be used in disease association studies as it may be in linkage disequilibrium with a disease gene on the same haplotype. Single nucleotide polymorphisms (SNPs) have been found across the prolactin gene region including the extrapituitary and the pituitary promoter regions. These SNPs have been examined for genetic association with SLE and potential effects upon the function of the gene. One SNP in the lymphocyte specific upstream promoter affects prolactin transcription and disease association studies in a cohort of SLE cases demonstrated an increased frequency of the PRL-1149 G allele compared to control subjects. This indicates a possible mechanism for the association of prolactin with SLE. Although prolactin is likely to be one of several predisposing factors in the pathogenesis and progression of SLE, this suggests that manipulation of lymphocyte prolactin production (rather than pituitary production) might be a useful therapeutic approach.

Gene Expression Regulation↗
PubMed2004

Autologous stem cell transplantation for systemic lupus erythematosus.

Some patients with severe systemic lupus erythematosus do not respond to conventional immunosuppression or suffer severe side effects from such treatment. In order to explore the concept of immunoablation followed by haematopoietic stem cell transplantation (HSCT) or 'rescue', an international collaboration has occurred over the past seven years. The European Group for Blood and Marrow Transplantation (EBMT) and The European League Against Rheumatism (EULAR) have analysed their collective phase I and II studies and found a remission rate (based on a reduction of the SLEDAI to < 3) in 66%, one-third of whom later relapsed to some degree. The most often used protocol was cyclophosphamide (CY) and G-CSF for mobilization and CY plus anti thymocyte globulin as conditioning. Procedure related mortality was 12% in this sick group of patients with major organ involvement. The North American, mostly single centre experience showed higher rates of remission and one procedure related death. Some relapse was also observed. Phase II studies designed to assess the role of post-HSCT maintenance therapy are being considered by the EBMT/EULAR group.

Clinical Trials as Topic↗
PubMed2006

Elevation of plasma interleukin-18 concentration is associated with insulin levels in patients with systemic lupus erythematosus.

We previously reported that systemic lupus erythematosus (SLE) patients have a higher risk of insulin resistance and abnormal insulin secretion. Recent studies demonstrated that interleukin (IL)-18, a novel pro-inflammatory cytokine, may be involved in triggering the inflammatory processes in SLE and the concentrations of circulating IL-18 in SLE patients were significantly higher than those in healthy subjects. IL-12 has a synergistic effect with IL-18, and both cytokines are inducers of interferon (IFN)-gamma. The objective of this study was to identify the effect of fasting insulin levels on circulating concentrations of IL-18, IL-12 and IFN-gamma in patients with SLE. Plasma levels of proinflammatory Th-1 cytokines were determined by enzyme-linked immunosorbent assay in a total of 70 female SLE patients and 34 age-matched healthy females. Insulin resistance (IR) and secretion were evaluated by homeostasis model assessment (HOMA). All patients were further classified into subgroups based on the quartiles of fasting insulin levels. SLE patients with fasting insulin levels in the top quartile compared with other quartiles had significantly higher plasma levels of IL-18. The presence of insulin auto-antibodies (IAA) in SLE patients had no influence on plasma levels of IL-18. In addition, fasting insulin levels and HOMA IR were positively correlated with IL-18 in all SLE patients, respectively. In conclusion, elevated circulating IL-18 concentrations corresponded with increases in fasting insulin levels and the status of insulin resistance in patients with SLE.

Adult↗
PubMed1998

Use of intravenous immunoglobulin therapy in pregnancy in systemic lupus erythematosus and antiphospholipid antibody syndrome.

Systemic lupus erythematosus and antiphospholipid antibody syndrome are associated with an increased risk of intrauterine growth restriction, miscarriage, stillbirth and premature delivery. Recent advances in therapy during pregnancy have improved the outcome but there is still significant fetal and maternal morbidity and mortality. Treatment of patients failing conventional therapy during the second half of pregnancy is difficult and may be complicated by the development of preeclampsia. The addition of intravenous immunoglobulin therapy offers a low risk strategy for reducing autoantibody mediated disease and improving placental function in severely compromised, growth restricted pregnancies.

Antiphospholipid Syndrome↗
PubMed2006

Intra-vascular ultrasound findings of diffuse coronary atherosclerotic change in systemic lupus erythematosus with secondary antiphospholipid syndrome.

Systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) are autoimmune inflammatory diseases associated with juvenile atherosclerosis and thrombosis, respectively. A 44-year-old woman who had SLE with secondary APS had been treated with corticosteroid therapy, however, her inflammatory marker had never been within a normal range in her clinical course, and finally acute myocardial infarction was developed. Intra-vascular ultrasound also revealed diffuse coronary atherosclerosis progression for her age, which might result from SLE and APS, including vascular inflammation.

Adrenal Cortex Hormones↗
PubMed1984

Aortic and mitral insufficiency complicating fulminant systemic lupus erythematosus.

The cardiac complications of systemic lupus erythematosus (SLE) include a multitude of valvular, myocardial, and pericardial abnormalities resulting from acute and chronic inflammation involving the endocardium, myocardium, and/or pericardium. A case of acute, severe, aortic, and mitral insufficiency occurring as discrete complications of consecutive flares of SLE in the same patient is described with particular emphasis on the clinical and gross pathologic findings. The cardiac complications of SLE, both from a pathologic and clinical standpoint, are reviewed in the context of the uniqueness of this case.

Adolescent↗