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PubMed2005

Association between physician volume and in-hospital mortality in patients with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an uncommon, clinically complex disease for which prior experience treating similar patients may be particularly important. This study was undertaken to determine if physician volume is associated with the outcome of hospitalization of patients with SLE. METHODS: Data on in-hospital mortality in a population-based sample of 15,509 patients with SLE ages 18 years or older who were hospitalized in 2000, 2001, or 2002 in New York or Pennsylvania were obtained from state health planning agencies. Risks of in-hospital mortality were examined in relation to the average annual number of patients with SLE hospitalized by the admitting physician. RESULTS: Physician volume was inversely associated with mortality. Mortality was 4.1% among patients of physicians who treated <1 hospitalized patient with SLE per year, 3.5% among patients of physicians who treated 1-3 patients per year, and 2.5% among patients of physicians who treated >3 patients per year. After adjustment for demographic characteristics, severity of illness, and hospital characteristics, the mortality risk was 20% lower among patients in the middle category of physician volume (odds ratio 0.80, 95% confidence interval 0.66-0.96, P =0.02), and 42% lower among patients in the highest category of physician volume (odds ratio 0.58, 95% confidence interval 0.42-0.82, P = 0.002), compared with patients in the lowest category. The association was stronger among patients with nephritis (n = 2,673), for whom the adjusted odds of mortality were approximately 60% lower among those in the highest category of physician volume. CONCLUSION: Our findings indicate that higher disease-specific physician volume is associated with lower risks of in-hospital mortality in patients with SLE.

Female↗
PubMed2004

HLA class II haplotypes in Mexican systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is an autoimmune disease in which polymorphisms within the human leukocyte antigen (HLA) region have been associated to its etiology. For this study, HLA-DQB1, DQA1, and DRB1 genes were typed by polymerase chain reaction-sequence-specific primer in 237 individuals, taken from 74 families, who had a member with SLE, and who had their residence in the western region of Mexico; as well as in 159 ethnically matched healthy volunteers taken from 32 families. Genotype and allele frequency analysis was performed in 74 SLE patients and 54 unrelated controls. Precise three-loci identification of independent haplotypes was performed in 48 patients and 54 controls by familial segregation. Genotype distribution at each loci was concordant with Hardy-Weinberg's equilibrium in the control group. In general, no genotype effect was observed in SLE patients. Allele distribution comparison showed in the SLE group a significant increase of HLA-DQA1*0102, DQB1*0402, and DRB1*15; whereas alleles HLA-DQB1*0303 and *0501 were significantly decreased. SLE patients showed haplotype DQB1*0602-DQA1-*0102-DRB1*15 increased. As expected, patients with SLE have a reduced haplotype genetic diversity. The associations found in this study are related to an ancestral haplotype that has been observed in SLE populations of different origins.

Adolescent↗
PubMed2006

Differential expression of estrogen receptors in women with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an autoimmune disease primarily affecting women. T cell activation markers (calcineurin, CD154) increase in SLE T cells cultured with estradiol 17-beta. Biological effects of estradiol are mediated through 2 receptor proteins, estrogen receptor-alpha (ER-alpha) and estrogen receptor-beta (ER-beta). We compared the amount of estrogen receptor subtypes in T cells and measured the ability of receptor agonist-specific ligands to activate marker gene expression. METHODS: T cells were isolated from 22 female patients with SLE and 17 control women. The amount of ER subtypes was measured by immunoblotting. Some T cells were cultured with ER-alpha or ER-beta-specific agonists. Receptor activation was measured by increased expression of the T cell activation markers CD154 and calcineurin. RESULTS: Although the amount of ER-alpha appeared to be less in SLE T cells than in control T cells, the difference was not statistically significant (p = 0.081). The quantity of ER-beta was similar in SLE and control T cells. The expression of ER-alpha or ER-beta was independent of menstrual cycle phase, age, or SLE disease activity. Calcineurin and CD154 expression increased in SLE T cells cultured in medium containing ER-alpha and ER-beta agonists. CONCLUSION: These data indicate that both ER subtypes activate calcineurin and CD154 in SLE but not in normal T cells. Variation in the amount of ER-alpha in SLE T cells suggests this receptor subtype participates in the sensitivity of SLE T cells to estrogen.

Actins↗
PubMed2005

[Proinflammatory cytokines in inactive lupus erythematosus patients].

Systemic lupus erythematosus (SLE) is an autoimmune connective tisssue disease. Disregulation of proinflammatory cytokines' secrection plays a pivotal role in its etiopatogenesis. Most studies concerning serum levels of those cytokines were conducted in active SLE patients. To date, there are scarce date on proinflammatory cytokines' serum concentration in inactive SLE patients. The aim of the study was to evaluate serum level of IL-1beta, IL-6, IL-18 and TNF-alpha in inactive SLE patients. The study involved 25 SLE patients aged between 24-65 years (mean age 40.6 years) and 25 age- and sex-matched healthy volunteers. The activity of the disease was assesed by SLAM scale. Serum concentrations of IL-6 and IL18 were determined by ELISA while serum levels of TNF-alpha and IL-1beta were measured using chemiluminescensce assay. In all healthy volunteers and in 23 out of 25 SLE patients, serum level of IL-1beta was undetectable (< 5 pg/ml). Serum concentrations of IL-6, IL-18 and TNF-alpha were detectable in all SLE patients. In 9 out of 27 healthy subjects level of IL-18 was under detection limit. Serum levels of IL-6, IL-18 and TNF-alpha were significanly higher (p < 0.001) in SLE patients when compared to their concentrations in subjects from control group (3.45 pg/ml vs. 2.59 pg/ml for IL-6; 344.87 pg/ml vs. 50.31 pg/ml for IL-18; 7.72 pg/ml vs. 5.21 pg/ml for TNF-alpha, respectively). The evaluation of serum levels of proinflammatory cytokines may be a sensitive marker of disease activity which may be helpful in maintaining or withdrawing chronic therapy in SLE patients.

Adult↗
PubMed2006

Traditional risk factor assessment does not capture the extent of cardiovascular risk in systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is associated with accelerated atherosclerosis. However, the degree of endothelial dysfunction and its relationship to traditional and novel cardiovascular risk factors have not been examined in SLE. METHODS: In a case-control design, 35 patients with clinically stable SLE and 35 control subjects matched for age, sex, body mass index and smoking status were studied. Arterial elasticity, lipid profile, homocysteine, measures of inflammation and oxidative stress were determined. RESULTS: Among traditional vascular risk factors, there was a nonsignificant trend towards lower blood pressure in the control subjects, whereas low-density lipoprotein (LDL) cholesterol levels were significantly lower in the SLE group (2.5 vs 3.3 mmol/L, P < 0.001). Patients with SLE had significantly lower small artery elasticity (SAE; 4.9 vs 7.0 ml/mmHg x 100, P < 0.001) and higher plasma homocysteine (11.4 vs 8.3 mmol/L, P = 0.002) than control subjects. Levels of serum sVCAM-1 (614 vs 494 ng/mL, P = 0.002), oxidized LDL (144 vs 97, P < 0.001) and CD40 ligand (4385 vs 1373 pg/ml, P = 0.001) were significantly higher in SLE. Oxidized LDL levels, older age at SLE diagnosis and higher disease damage scores correlated inversely with SAE but not traditional risk factors. CONCLUSION: Impaired endothelial function as shown by decreased SAE, and an adverse profile of novel proatherogenic and prothrombotic vascular disease risk factors were prevalent in clinically quiescent SLE. These findings show the vulnerability of patients with SLE for atherosclerosis, and emphasize that assessments based on traditional risk factors alone may be inadequate.

Adult↗
PubMed2006

Relationship of plasma interleukin-18 concentrations to traditional and non-traditional cardiovascular risk factors in patients with systemic lupus erythematosus.

OBJECTIVES: Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis. Recent studies indicated that the concentrations of circulating interleukin (IL)-18, a novel proinflammatory T helper-1 cytokine, in SLE patients were significantly higher than those in healthy control subjects. The objective of this study was to examine the relationship between IL-18 and cardiovascular risk factors in patients with SLE. METHODS: Both traditional and non-traditional cardiovascular risk factors including body mass index (BMI), systolic blood pressure, diastolic blood pressure (DBP), fasting insulin and glucose, plasma lipid profile, plasma homocysteine, thiobarbituric acid-reactive substances, titres of autoantibodies against oxidized low-density lipoprotein, and brachial-ankle pulse wave velocity (baPWV) were determined in a total of 72 female SLE patients. All patients were further classified into subgroups based on tertiles of plasma IL-18 concentrations. RESULTS: Plasma concentrations of IL-18 were significantly higher in SLE patients than age-matched healthy controls. SLE patients with IL-18 concentration in the top tertile compared with the bottom tertile had significantly higher plasma levels of insulin, triglyceride, homocysteine and values of homeostasis model assessment insulin resistance (HOMA IR) and HOMA beta-cell. In addition, plasma concentrations of IL-18 correlated positively and significantly with BMI, insulin, HOMA IR, HOMA beta-cell, triglyceride, homocysteine, DBP and baPWV in all SLE patients. CONCLUSIONS: This is th first report showing the relationship between IL-18 and cardiovascular risk factors in SLE. In patients with SLE, the synergistic effects of hyperinsulinaemia, insulin resistance, hyperhomocysteinaemia, and vascular stiffness most likely contribute to the elevation of plasma IL-18 concentrations.

Adult↗
PubMed2001

Molecular heterogeneity of prolactin in the plasma of patients with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) has been associated with high levels of prolactin in the circulation of some patients. Although prolactin stimulates immune responses, the relationship between hyperprolactinemia and the pathophysiology of SLE remains controversial. This study was undertaken to investigate whether circulating bioactive prolactin isoforms are associated with the activity of SLE. METHODS: The molecular heterogeneity of prolactin was studied in the plasma of patients with active and inactive SLE and in healthy volunteers by radioimmunoassay (RIA), enzyme-linked immunosorbent assay (ELISA), Nb2-cell bioassay, and immunoprecipitation-Western blots. The specificity of the bioassay determinations was assessed by neutralization of growth-promoting effects with antiserum to human prolactin. RESULTS: Significantly higher prolactin levels were detected by bioassay and by ELISA than by RIA in both subsets of SLE patients and in normal individuals. Plasma prolactin levels in the SLE patients were significantly greater than those in the normal controls when measured by ELISA, but not by RIA or bioassay. The bioassay:ELISA and bioassay:RIA ratios were similar between SLE patients and controls, suggesting that prolactin biopotency was not altered with the disease, and none of the 3 assays detected a difference in prolactin levels between patients with active SLE and those with inactive SLE. However, the prolactin detected in plasma was associated with immunoreactive proteins of 130 kd and 23 kd, and the concentration of the 130-kd prolactin-like species was 10-fold higher in inactive SLE versus active SLE patients. CONCLUSION: Discrepancies among assays substantiate the molecular heterogeneity of circulating prolactin. The prolactin isotype that is found in association with inactive SLE could be of potential use as a marker for the inactive form of the disease and as an index for the efficacy of treatment.

Animals↗
PubMed2006

Novel cardiovascular risk factors and cardiac event predictors in female inactive systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is associated with severe and premature cardiovascular disease, which cannot be explained by traditional risk factors alone. This study aims to investigate novel cardiovascular risk factors and cardiac event predictors in inactive SLE female patients who do not have any major cardiovascular risk factors. Twenty-five inactive (SLE disease activity index score <4) SLE female patients and 22 healthy control women were studied. SLE patients with a history of diabetes mellitus, hypertension, hyperlipidemia, smoking, or coronary artery disease (CAD) were excluded. Venous blood samples were analyzed for lipid subfractions and novel cardiovascular risk factors such as lipoprotein (a), homocysteine, fibrinogen, high-sensitivity C-reactive protein (hs-CRP), and serum amyloid A (SAA) levels. Endothelial dysfunction was assessed by flow-mediated dilatation (FMD) from the brachial artery at baseline and during reactive hyperemia. SLE patients and controls were similar in terms of age (40+/-10 years vs 38+/-10 years, p = NS). No significant difference was found between the groups regarding family history of premature CAD, blood pressure, body mass index, lipoprotein (a), homocysteine, fibrinogen, SAA, apoprotein A-1 and B levels. Compared with the controls, SLE patients had higher levels of hs-CRP [median (range): 1.82 (0.02-0.98) vs 0.68 (0.02-0.35), p=0.04]. FMD was lower in SLE patients than controls (7.1+/-2.1 vs 11.4+/-1.2%, p<0.001). Increased levels of hs-CRP and decreased FMD were found in inactive SLE patients. Increased hs-CRP levels may reflect ongoing low-grade inflammation that could be a cause of impaired FMD in SLE patients. These findings suggest that SLE patients without traditional major cardiovascular risk factors may have increased risk of cardiovascular disease and future cardiac events.

Adult↗
PubMed1998

Lack of evidence of active lytic replication of Epstein-Barr and cytomegaloviruses in patients with systemic lupus erythematosus.

OBJECTIVES: Systemic lupus erythematosus (SLE) is a multifactorial disease. Environmental factors such as viral infection(s) have been proposed as pathaetiological factors. There are particular interests in studying lymphotropic viruses such as the Epstein-Barr virus (EBV) and cytomegalovirus (CMV). Although previous case reports and in vitro studies suggested that they may have a role, there is no direct evidence that onset of SLE or disease exacerbation is associated with active infection by these viruses. Using the very sensitive polymerase chain reaction (PCR) technique, we tried to find out evidence of active replication of these viruses in patients with SLE. METHODS: Thirty-four patients with SLE were compared with matched normal controls. Eleven patients were newly diagnosed to have SLE and 18 of the 34 patients had active disease as determined by a SLE Disease Activity Index (SLEDAI) score of > or = 10 at the time of study. RESULTS: Our results showed no evidence of active replication or reactivation of EBV in the leucocytes amongst the newly diagnosed SLE patients, established SLE patients, patients with SLEDAI > or = 10, patients with SLEDAI < 10, and control subjects. There was no evidence of CMV infection in any of the subjects studied. The IgG and IgA responses against EBV early antigen (EA) and viral capsid antigen (VCA) were also studied. The IgG and IgA responses against VCA of EBV were increased in patients with SLE when compared with controls. However, there were no differences in these responses among different subgroups of patients. The mechanism of these responses was not apparent but may represent non-specific hyperimmune responses in these patients. There were no differences in the titre of IgG and IgA against EBV EA between the patient groups and controls. CONCLUSION: There is no direct evidence that either EBV or CMV plays a direct role in the onset and/or exacerbation of SLE.

Antibodies, Viral↗
PubMed2026

Integrative post-GWAS analysis prioritizes immune regulatory pathways and candidate effector signals in systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) has a complex polygenic architecture, but translating genome-wide association signals into biologically interpretable candidates remains challenging. We applied an integrative post-GWAS framework to refine SLE-associated loci and prioritize candidate regulatory mechanisms. METHODS: European-ancestry SLE GWAS summary statistics from FinnGen and Bentham et al. were meta-analysed, comprising 8417 cases and 354,277 controls. After quality filtering, 6,782,131 SNPs were retained. Downstream analyses included LAVA regional prioritization, Bayesian colocalization with GTEx v8 whole-blood and spleen eQTLs, independent replication in the Juli&#xe0; et al. Spanish cohort, pathway enrichment, bivariate LAVA cross-trait local genetic correlation, and therapeutic annotation. RESULTS: The discovery meta-analysis identified 46 genome-wide significant SLE-associated loci, including putative novel signals requiring database/literature qualification. LAVA identified 14 candidate index variants across 12 high-confidence regions, of which nine index variants were retained as the primary prioritized set based on LAVA support and/or convergent regulatory evidence. The strongest association mapped to the chr6p21.3/MHC region (rs389884), where four genes showed colocalization support, including CLIC1 in whole blood and C4A in spleen. Because the chr6p21.3/MHC rs389884 region lead variant was unavailable for replication and no suitable proxy was identified, this signal was interpreted as an emerging candidate for functional validation rather than a replicated causal signal. Seven available variants replicated with concordant effects. An exploratory Roadmap immune chromatin-state overlap analysis placed 15 of 45 non-MHC lead variants (33.3%) directly, and 34 of 45 (75.6%) within &#xb1;10&#x202f;kb, in active immune enhancer/promoter states. Pathway analyses highlighted type I interferon, JAK-STAT signaling, cytokine regulation, and antigen presentation, while bivariate LAVA analyses supported shared local genetic architecture with rheumatoid arthritis, systemic sclerosis, and Sj&#xf6;gren syndrome. CONCLUSIONS: This integrative post-GWAS analysis refines SLE association signals into biologically interpretable candidate regions and supports interferon and JAK-STAT signaling as central genetically supported pathways in SLE.

CLIC1↗
PubMed2002

[Long-term analysis of clinical disease activity and chronic organ damage in patients with systemic lupus erythematosus].

BACKGROUND: Systemic lupus erythematosus is a chronic inflammatory and systemic disease with multiple symptoms which is often characterized by a course of exacerbations. Over the last few decades the prognosis of SLE considerably improved with >90% patients living more than 10 years with their disease. AIM OF THE STUDY AND METHODS: The aim of this retrospective-descriptive analysis of 65 patients with the diagnosis of SLE (based on the ARA criteria) was to investigate the symptoms and the laboratory values at the time of diagnosis (TD) and over a period of 10 years (10Y) in the outpatient university clinic of the Department of Nephrology and Rheumatology at Goettingen. In addition to symptoms and laboratory values, disease activity, exacerbations, chronic organ failure, and medical therapy were to be investigated. RESULTS: The long-term analysis revealed a decline in the prevalence of ANAs (TD: 95.6%; >10Y: 78.6%), ds-DNA antibodies (TD: 78.0%; >10Y: 46.7%) and pathological levels of the complement component C3 (TD: 72.7%; >10Y: 42.9%) over time. The symptoms most prevalent at the time of first diagnosis such as the typical butterfly rash (TD: 50.0,%; >10Y: 36.8%), discoid skin lesions (TD: 38.8%; >10Y: 23.5%) were noted less often after a 10 year-disease course. On the contrary the frequency of arthralgias (TD: 61.2%; >10Y: 57.9%), myalgias (TD: 26.1%; >10Y: 26.3%) and fatigue (TD: 63.0%; >10Y: 64.7%) remained stable over time. The prevalence of arterial hypertension (TD: 17.2%; >10Y: 54.5%), proteinuria (TD: 33.3%; >10Y: 66.7%) and erythrocyturia (TD: 27.8%; >10Y: 44.4%) remarkably increased during the disease course. Besides renal damage, coronary artery disease (TD: 6.0%; >10Y: 23.0%) and neurological disease (e.g., cerebrovascular insults) (TD: 10.9%; >10Y: 26.3%) were noted more often after 10 years. Of patients, 56.9% developed one or several exacerbations of the disease. In all cases, clinical symptoms correlated with an increase in the level of ds-DNA-antibodies and a decrease of C3-complement component. Other medications included immunosuppressants, antihypertensive drugs and NSAIDs. High-dose steroids were preferred as the first diagnosis (TD: 44.4%; >10Y: 11.1%), while low-dose steroids were more often prescribed after a 10-years diseases course (TD: 6.7%; >10Y: 27.8%). CONCLUSIONS: There is a shift towards secondary organ damage with a decline of the inflammatory activity in patients with SLE after 10 years of disease. These consecutive diseases are due to the primary damage of SLE as well as to medical treatment (e.g., with steroids).

Adolescent↗
PubMed2004

Pimecrolimus 1% cream for cutaneous lupus erythematosus.

Topical treatment of cutaneous lupus erythematosus usually includes potent glucocorticosteroids. However, prolonged use causes adverse side effects including skin atrophy as the foremost concern. In contrast to glucocorticosteroids, the anti-inflammatory and immunosuppressive macrolactam pimecrolimus has no atrophogenic potential. Affected areas of 11 patients with different forms of lupus erythematosus were treated with pimecrolimus 1% cream under semiocclusive conditions twice daily for 3 weeks. Skin involvement before and after therapy was assessed by means of a clinical score. In all patients, significant regression of skin lesions was observed after therapy (P <.001). This was an open and uncontrolled study on a limited number of cases. We suggest that pimecrolimus 1% cream could be an efficacious and safe treatment option for cutaneous lupus erythematosus.

Administration, Cutaneous↗
PubMed1992

Incidence of alopecia areata in lupus erythematosus.

BACKGROUND: A small percentage of patients with alopecia areata have connective diseases such as systemic lupus erythematosus, discoid lupus erythematosus, rheumatoid arthritis, and scleroderma. Lupus erythematosus is associated with a number of different types of alopecia, but the incidence of alopecia areata in lupus erythematosus has not been examined. OBSERVATIONS: Of our cohort of 39 patients with lupus erythematosus, alopecia areata developed in 10% (four patients), in contrast to 0.42% of general dermatologic patients. Biopsy specimens of alopecia areata lesions in each of our patients showed continuous granular deposition of IgG at the dermoepidermal junction, a finding usually found in only a minority of alopecia areata cases. Intralesional injections of corticosteroids were effective treatment. CONCLUSIONS: The incidence of alopecia areata in patients with lupus erythematosus is increased. Recognition of this form of alopecia allows for specific therapy with intralesional corticosteroids.

Adult↗
PubMed1993

Neonatal lupus erythematosus in Thailand.

Systemic lupus erythematosus (SLE) is not uncommon in Thai children and adults but neonatal lupus erythematosus has never been reported in Thailand. A case of NLE born of a mother without prior history of SLE was reported. He was initially misdiagnosed as congenital self-healing histiocytosis because of seborrheic dermatitis-like lesions, petechiae, hepatosplenomegaly and thrombocytopenia. Features supporting the diagnosis of NLE in this case were presented.

Humans↗
PubMed1997

Pathogenetic mechanisms and treatment of cutaneous lupus erythematosus.

The mechanisms of cutaneous lupus erythematosus are under active investigation, and important advances have been made. Humoral mechanisms are likely important in subacute cutaneous lupus erythematosus, the cutaneous subset most associated with the Ro antibody. Many advances have been made in understanding the various Ro epitopes and the specificities of the Ro antibody response. Lupus mice experiments have provided insight into the contributing roles of various T-cell subsets. Variations in cytokine production related to genetic polymorphisms and induction by ultraviolet light combined with alterations in selectins and adhesion molecules contribute to the accumulation of inflammatory cells in cutaneous lupus erythematosus. It is important to institute aggressive systemic therapy when there is widespread scarring disease. Antimalarial agents continue to be first-line systemic drugs, and our understanding of the use of combination antimalarial agents and proper dosing limits problems with toxicity and improves efficacy. Other therapies, including thalidomide, are helpful for patients with resistant disease.

Animals↗
PubMed2004

Socioeconomic factors in lupus erythematosus.

For a long time, systemic lupus erythematosus (SLE) was considered a potentially deadly disease. Since the introduction of immunosuppressive therapy, the life expectancy and the quality of life of patients suffering from lupus erythematosus has been dramatically improved. Today, the 5-year survival rate for SLE varies between 50% and 95%. Still, not all patients benefit equally from medical advances. Ethnic and/or socioeconomic minorities show severely disadvantageous prognosis or outcome in various studies. A substantial reduction in the quality of life as well as unemployment are other frequent side effects of this disease. Vocational handicaps related to discoid lupus erythematodes (DLE) was seen in nearly 45% of the patients. Therefore, the management of lupus erythematosus patients requires interdisciplinary cooperation between physicians, psychologists and social workers. The major aim of this article is to summarize the history of lupus erythematosus on the one and the other hand to consider the role of the socioeconomic factors influencing the prognosis of systemic and cutaneous lupus erythematosus.

Humans↗
PubMed1992

Incidence of and risk factors for hospitalizations in systemic lupus erythematosus: a prospective study of the Hopkins Lupus Cohort.

OBJECTIVE: To determine the incidence of and risk factors for hospitalization in systemic lupus erythematosus (SLE). METHOD: A prospective study of hospitalizations in 1989 and 1990 in the Hopkins Lupus Cohort was conducted. RESULTS: Of 261 patients with SLE in the Hopkins Cohort, 147 (56.3%) were hospitalized in 1989 or 1990. The incidence of hospitalization was 0.69 admissions/person-year. The mean length of stay was 9.6 days +/- 12.7 (SD). Activity of SLE accounted for 35% of admissions. Risk factors for hospitalization for active lupus in 1990 included activity of SLE in 1989 (measured by either the highest physician's global assessment in 1989, p = 0.004, highest lupus activity index (LAI) score in 1989, p = 0.002, or highest systemic lupus erythematosus disease activity index score in 1989, p = 0.008), an average prednisone dose greater than 10 mg in 1989 (p = 0.002), and the presence of neurologic lupus in 1989 (p = 0.02). Medical admissions other than for active SLE accounted for an additional 27% of admissions; one-half of these admissions (47%) were for complications of SLE and/or its treatment, with coronary artery disease the most common (21% of medical admissions). Infections were responsible for 14% of admissions. The majority of infections were bacterial (90%). Risk factors for hospitalization for infection in 1990 included active SLE in 1989 (p = 0.03), average prednisone dose of greater than 10 mg in 1989 (p = 0.04), immunosuppressive drug use in 1989 (p = 0.003), neurologic SLE in 1989 (p = 0.02) and previous hospitalization in 1989 (p = 0.03). CONCLUSION: Hospitalization is common in the Hopkins Lupus Cohort, with active SLE (35%), infection (14%, infection and/or active SLE; 11%, infection alone) and medical complications of SLE (13%) as the 3 most common causes.

Adult↗
PubMed2005

Immune cells and cytokines in systemic lupus erythematosus: an update.

PURPOSE OF REVIEW: Systemic lupus erythematosus is characterized by overactive B cells that differentiate into autoantibody-forming cells, aberrant T cell function that provides help to B cells, and the production of pro-inflammatory cytokines. This article reviews recent studies unraveling the complex interplay between cytokines and lymphocytes in systemic lupus erythematosus. RECENT FINDINGS: In systemic lupus erythematosus, T cells are characterized by heightened calcium responses early after activation of their surface receptor. Alterations of the T cell receptor/CD3 complex, namely the substitution of the FcepsilsonRgamma for the T cell receptor zeta chain, and increased mitochondrial potentials can account for this 'overexcitable' phenotype. At the same time, this heightened calcium signal leads to a block of the transcription of the IL-2 gene, a pivotal cytokine for the immune response. The end result is increased spontaneous apoptosis and decreased activation-induced cell death of T cells in systemic lupus erythematosus that in turn leads to enhanced help to B cells and potentially decreased regulatory function. The B cells, on the other hand, are shown to be directly activated by immune complexes by way of Toll-like receptors independently of T cells. Finally, recent studies have tried to elucidate the role of cytokines such as interferon-alpha in systemic lupus erythematosus and, following the paradigm of rheumatoid arthritis, to establish targets for treatment. SUMMARY: The increased apoptosis and aberrant T cell activation coupled with nonspecific activation of B cells lead to the production of auto-antigen: auto-antibody complexes that are the hallmark of systemic lupus erythematosus. Future treatments aiming at correcting the intracellular and intercellular signaling abnormalities may prove effective in restoring immune tolerance in systemic lupus erythematosus.

B-Lymphocytes↗