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1.
To investigate the relationship between serum ferritin and disease activity in systemic lupus erythematosus (SLE), we enrolled 128 patients with SLE (18 males and 110 females). Twenty-eight patients (2 males and 26 females) with rheumatoid arthritis (RA) served as controls. The SLE patients were subdivided into three groups according to Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) scores: groups A (0-5), B (6-9), and C (> or =10). We prospectively evaluated 48 SLE patients before and after treatment. Serum ferritin and anti-dsDNA antibody were measured by radioimmunometric assay. C-reactive protein (CRP) was measured quantitatively by immunonephelometry. Complements 3 and 4 (C3 and C4) were measured by nephelometry. Serum levels of ferritin during the more active stage of SLE (group C) exceeded those of RA patients and patients at less active stages of SLE (groups A and B). There were no significant differences between RA patients and groups A and B. Serum ferritin was elevated especially in serositis and hematologic manifestation. In this prospective study, changes in SLEDAI scores before and after treatment correlated significantly with serum ferritin levels and inversely to C3 and C4 levels. We confirm that serum ferritin levels can be a useful marker of disease activity in SLE patients.  相似文献   

2.
BackgroundSerum ferritin is elevated due to various conditions as inflammation and malignancy and could be up regulated in systemic lupus erythematosus (SLE).Aim of workTo evaluate serum ferritin level in SLE patients and correlate it with different clinical and laboratory parameters as well as disease activity.Patients and methodsThe study was carried out on 46 SLE patients and 20 matched controls. SLE Disease Activity Index (SLEDAI) was assessed and patients subdivided into severe (SLEDAI ≥ 11) and mild to moderate (SLEDAI < 11) activity. Serum ferritin, iron and total iron binding capacity (TIBC) levels were assessed.ResultsThey were 40 females and 6 males with a mean age of 36.7 ± 10.3 years and disease duration of 4.9 ± 2.3 years. Serum ferritin was significantly higher in patients than controls (163.5 ± 27.8 vs. 47.1 ± 10.6 ng/ml, p = 0.009). In patients, serum iron (49.2 ± 4.5 mg/dl) and TIBC (284.2 ± 80.8 mg/dl) were comparable with those in controls. Serum ferritin was significantly higher in patients with severe (220.9 ± 50.7 ng/ml) than those with mild-moderate activity (122.9 ± 29.7 ng/ml; p < 0.001). Serum ferritin was significantly higher in patients with anemia (p < 0.001) and thrombocytopenia (p = 0.03) and lower in those with leucopenia (p < 0.001) compared to those without. Ferritin significantly correlated only with hemoglobin (r = 0.5, p = 0.02), platelet count (r = 0.65, p = 0.03) and inversely with leucocytic count (r = −0.08, p = 0.006).ConclusionSerum ferritin is elevated significantly in SLE patients especially those with severe activity. A remarkable difference in serum ferritin levels in patients with hematological manifestations was found making it a potentially useful inflammatory marker for disease activity in patients with blood dyscrasia.  相似文献   

3.
OBJECTIVE: To obtain insight in the acute-phase response in SLE. METHODS: The clinical history, SLEDAI, CRP and ferritin concentrations were analysed throughout the disease course of 10 SLE patients. RESULTS: During a mean follow-up of 4.8 years, 10 exacerbations (SLEDAI > or = 11) occurred. Throughout the disease course, CRP and SLEDAI correlated positively in 5 patients, whereas the correlation between SLEDAI and ferritin was positive in 7 patients. However, elevated CRP concentrations together with elevated ferritin levels were only observed during 4 exacerbations. Ferritin concentrations were exceptionately high (> 1500 microg/L) during 4 flare-ups. CRP and ferritin levels remained normal during 5 exacerbations. CONCLUSION: SLE is characterised by highly variable and unusual CRP and ferritin responses that do not always reflect the extent of inflammation in individual patients. Despite severe disease activity, ferritin levels can remain well within the normal range, limiting its clinical usefulness as a marker for disease activity.  相似文献   

4.

Objective

To evaluate serum free light chains (FLC) as a putative biomarker of systemic lupus erythematosus (SLE) activity.

Methods

Seventy‐five SLE patients and 41 age‐ and sex‐matched rheumatoid arthritis (RA) controls were enrolled. Disease activity was assessed using the Safety of Estrogens in Lupus Erythematosus: National Assessment version of the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) definition and physician global assessments for SLE and the Disease Activity Score in 28 joints for RA. Serum FLC levels were compared against other biomarkers (IgG, C3, C4, double‐stranded DNA [dsDNA] antibody). Nonparametric tests were used to compare 1) FLC and IgG in SLE versus RA and healthy controls, 2) FLC and IgG among different levels of activity in SLE, and 3) FLC in active versus nonactive RA. Correlation of FLC, C3, C4, dsDNA antibody, and IgG with the SLEDAI and modified SLEDAI (M‐SLEDAI) were obtained.

Results

FLC was higher in SLE than in RA; both were higher than referent healthy controls. Total FLC was significantly higher in subjects with greater SLE disease activity than lower/no activity. There were no significant differences in IgG, C4, or dsDNA antibody stratified by disease activity. Total FLC and C3 showed moderate to strong correlation with the SLEDAI and M‐SLEDAI. In RA, no differences were seen in FLC levels for different levels of disease activity. Similar results were seen after controlling for renal function, age, and sex. In multiple linear regression, FLC significantly explained 50% variance of the SLEDAI after adjusting for renal function, age, and sex.

Conclusion

Serum FLC levels correlate strongly with disease activity in SLE, but not in RA. Serum FLC may be used as a biomarker of SLE disease activity.  相似文献   

5.
Overexpression of B-lymphocyte activating factor (BAFF) results in arthritis, glomerulonephritis and autoantibody formation in mice, but its role in human autoimmune disease is less obvious. Serum BAFF levels in patients with systemic lupus erythematosus (SLE) (n=42) and rheumatoid arthritis (RA) (n=60) were related to levels of disease activity, anti-dsDNA Ab, anti-ENA Ab, rheumatoid factor (RF) and anti-CCP Ab. BAFF levels were also followed over time in 19 SLE patients. BAFF levels correlated inversely with age, were higher in SLE than RA (median 2.7 versus 1.4 ng/mL, P < 0.01) and more SLE than RA patients had increased BAFF levels (57% versus 10%, P < or = 0.01). In SLE, BAFF levels correlated with SLEDAI scores but not with anti-dsDNA Ab levels. SLE patients with increased BAFF levels had higher SLEDAI and CRP levels. In RA, BAFF levels correlated weakly with anti-CCP levels (Rs 0.27, P = 0.07), but not with joint counts, ESR, CRP or RF levels. Longitudinal BAFF levels remained unaltered in two thirds of SLE patients and changes in BAFF levels were unrelated to disease flares. These findings suggest that BAFF stimulation of B-cells may contribute to SLE by other mechanisms than autoantibody production.  相似文献   

6.
OBJECTIVE: To examine protein oxidation in systemic lupus erythematosus (SLE) and to correlate levels of protein oxidation products with disease activity. METHODS: Serum was collected from SLE patients and healthy control subjects. Protein-bound carbonyls and the pro-oxidant enzyme myeloperoxidase (MPO) were quantified by enzyme-linked immunosorbent assay. Protein thiols were quantified using 5,5'-dithionitrobenzoic acid. Protein-bound amino acids and methionine, tyrosine, and phenylalanine oxidation products were quantified by acid hydrolysis and high-performance liquid chromatography. Disease activity was assessed by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Levels of anti-double-stranded DNA (anti-dsDNA) antibodies were measured by radioimmunoassay. RESULTS: Compared with control subjects, SLE patients exhibited elevated levels of protein carbonyls (0.108 +/- 0.078 versus 0.064 +/- 0.028 nmoles/mg of protein; P = 0.046), decreased levels of protein thiols (3.9 +/- 1.1 versus 4.9 +/- 0.7 nmoles/mg of protein; P = 0.003), decreased levels of protein-bound methionine (P = 0.0007), and increased levels of protein-bound methionine sulfoxide (P = 0.0043) and 3-nitrotyrosine (P = 0.0477). SLE patients with high SLEDAI scores or elevated anti-dsDNA antibody levels exhibited increased oxidation compared with patients with low SLEDAI scores or low antibody levels. Serum MPO levels were decreased in SLE patients (P = 0.03), suggesting that this enzyme is not responsible for the enhanced protein oxidation. CONCLUSION: We found elevated levels of multiple markers of protein oxidation in sera from SLE patients compared with controls, and these levels correlated with disease activity. The findings suggest that protein oxidation may play a role in the pathogenesis of chronic organ damage in SLE.  相似文献   

7.
Aim: Recent research has shown that prolactin (PRL) may participate in the pathogenesis of systemic lupus erythematosus (SLE) and hyperprolactinemia may be related to disease activity. The current study investigated both serum and cerebrospinal fluid (CSF) PRL in SLE patients and their possible relationship to central nervous system (CNS) involvement. Methods: Prolactin levels were determined by immunoradiometric assay. Serum PRL levels were detected in 80 patients with SLE and 25 matched healthy controls. Disease activity was scored by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). CSF PRL levels were detected in seven cases of CNS involving SLE, eight cases of non‐CNS involved inactive SLE and eight cases of non‐SLE CNS disorders. Results: Hyperprolactinemia was present in 40% of SLE patients. Serum PRL levels were significantly correlated with SLEDAI scores. There was no significant difference in serum PRL levels between SLE patients with or without CNS involvement, but the mean CSF PRL levels were higher in CNS‐involved SLE patients than in non‐CNS‐involved SLE and non‐SLE patients. There was no significant correlation between serum and CSF PRL levels. Conclusions: Our results suggest that high serum PRL levels correlate with active disease in SLE, but not with CNS involvement. CSF PRL levels in SLE patients correlate with CNS involvement, which indicates that CSF PRL may be involved in the pathogenesis of CNS‐SLE.  相似文献   

8.
Aim: Recent research has shown that prolactin (PRL) may participate in the pathogenesis of systemic lupus erythematosus (SLE), and hyperprolactinemia may be related to disease activity. The current study investigated both serum and cerebrospinal fluid (CSF) PRL in SLE patients and their possible relationship to central nervous system (CNS) involvement. Methods: Prolactin levels were determined by immunoradiometric assay. Serum PRL levels were detected in 80 patients with SLE and 25 matched healthy controls. Disease activity was scored by SLEDAI. CSF PRL levels were detected in 7 cases of CNS‐involved SLE, eight cases of non‐CNS‐involved inactive SLE and eight cases of non‐SLE CNS disorders. Results: Hyperprolactinemia was present in 40% of SLE patients. Serum PRL levels were significantly correlated with SLEDAI scores. There was no significant difference of serum PRL levels between SLE patients with or without CNS involvement, but the mean CSF PRL levels were higher in CNS‐involved SLE patients than in non‐CNS‐involved SLE and non‐SLE patients. There was no significant correlation between serum and CSF PRL levels. Conclusions: Our results suggest that high serum PRL levels correlate with active disease in SLE, but not with CNS involvement. CSF PRL levels in SLE patients correlate with CNS involvement, which indicates that CSF PRL may be involved in the pathogenesis of CNS‐SLE.  相似文献   

9.
The aim of this study was to investigate the levels and clinical significance of serum soluble chemokine (C-X-C motif) ligand 16 (sCXCL16) in patients with systemic lupus erythematosus (SLE), as well as the sCXCL16 molecule’s associations with disease activity and organ damage. Thirty-five patients with SLE, 16 patients with rheumatoid arthritis (RA), and 15 healthy controls were included in this study. The demographic and clinical features of the patients were recorded. The serum levels of sCXCL16 were determined. Disease activity was assessed using the SLE Disease Activity Index (SLEDAI), and organ damage was evaluated with the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index (SDI). The serum levels of sCXCL16 in the patients with SLE were higher than those in the patients with RA (P?=?0.002) or healthy controls (P?P?=?0.008). Positive correlations were identified between serum sCXCL16 concentrations and both SLEDAI (r?=?0.564; P?r?=?0.396; P?=?0.018). Both SLEDAI (P?=?0.021) and serum levels of CXCL16 (P?=?0.023) decreased after conventional treatment in 12 initial onset cases of SLE patients. Elevated serum sCXCL16 levels were discovered in the SLE patients with cutaneous (P?=?0.006) and renal involvement (P?=?0.032). Soluble CXCL16 may become a useful serological marker of disease activity and skin and renal involvement in SLE patients; thus, it may be used for evaluation of therapeutic interventions.  相似文献   

10.
To evaluate the correlation between measurements of antinuclear antibodies serum levels by enzyme immunoassay (ANA-EIA), and the degree of systemic lupus erythematosus disease activity. To retest the performance of the test compared to measurement of antinuclear antibodies by immunofluorescence (ANA-IIF). Eighty-five sera from 71 patients with SLE were tested. Demographic, clinical, laboratory, and SLEDAI status were collected. The sera were tested for ANA-EIA and by ANA-IIF at 1:40 and 1:160 dilutions. Serum levels of ANA-EIA were compared to the overall SLEDAI score and to each of its components. A SLEDAI score of ≥6 was considered clinically significant. The sera of fifty-one healthy volunteers served as controls. Serum levels of ANA-EIA were significantly higher in patients with a SLEDAI score of ≥6 compared to the group of patients with a SLEDAI score of <6 (P = 0.004). High serum levels of ANA-EIA correlated significantly with elevated anti DS-DNA antibodies (P < 0.001), low C3 or C4 levels (P < 0.001), pyuria (P < 0.011), arthritis (P = 0.019), and new rash (P = 0.019). Levels of ANA-EIA were significantly higher in patients tested positive by IIF compared to those who tested negative. Higher serum levels of ANA-EIA correlated with clinically significant disease activity in patients with SLE. Higher serum levels of ANA-EIA also correlated with some single items of the SLEDAI. The results also reiterated the validity of ANA-EIA testing in patients with SLE. Further longitudinal studies are needed in order to test the hypothesis that serum ANA-EIA levels might reflect fluctuations in disease activity.  相似文献   

11.
目的 探讨趋化因子积分与系统性红斑狼疮(SLE)临床特征的相关性.方法 采用实时定量聚合酶链反应(PCR)技术检测60例SLE患者,20例类风湿关节炎(RA)患者及23名健康对照外周血白细胞中7个趋化因子[RANTES、单核细胞趋化因子(MCP)-1、CCL19、MIG、IP-10、CXCL11和白细胞介素(IL)-8]的mRNA表达水平,计算趋化因子积分,并将其与相应的临床资料进行统计学分析.结果 趋化因子积分在SLE患者中较疾病和健康对照显著增高(P=0.0112和P=0.0019);趋化因子积分与SLEDAl积分呈正相关(P=0.0061),与补体C3水平呈负相关(P=0.003);与无肾炎病史患者相比,趋化因子积分在活动性狼疮肾炎(LN)患者中显著增高,特别在泼尼松用量<30 mgCd时(P=0.0418及P=0.002);趋化因子积分还与慢性损伤指数(SDI)相关;此外,在抗Sm、抗RNP抗体阳性的患者中也存在趋化因子积分显著升高.结论 趋化因子积分与SLE的疾病活动性、脏器损伤的出现和严重程度以及特定的自身抗体表型相关,是SLE新的生物标志物.  相似文献   

12.
OBJECTIVE: T cell abnormalities, B cell hyperactivity and abnormal cytokine production have been implicated to be of pathogenic importance in systemic lupus erythematosus (SLE). The aim of this study was to investigate if ongoing production and serum levels of type 1 and 2 cytokines reflect disease activity and the presence of organ manifestations. METHODS: Fifty-two SLE patients and 29 healthy individuals were investigated. Blood samples were collected for assessment of anti-ds DNA antibodies, cytokine production and serum cytokine levels. Disease activity was simultaneously assessed using the Systemic Lupus Activity Measure (SLAM) index and SLE Disease Activity Index (SLEDAI). ELISPOT analysis of freshly isolated peripheral blood mononuclear cells (PBMC) was used to estimate the production of cytokines (gamma-interferon (IFN-gamma), interleukin-4 (IL-4), IL-6 and IL-10) using both unstimulated cells and cells stimulated with the T cell mitogen phytohaemagglutinin (PHA). Serum levels of IL-10 were determined using an ELISA method, serum levels of IL-6 were determined using a bioassay and anti-ds DNA antibodies were analysed by immunofluorescence. RESULTS: The SLE patient group had significantly increased numbers of cells spontaneously producing IL-10 and IL-6 as compared to healthy controls (P = 0.01 and 0.03, respectively). The number of cells producing IL-10 and IL-6 after PHA-stimulation was also increased in SLE patients (P = 0.01 and < 0.0004, respectively). Serum IL-10 and IL-6 levels were also significantly increased in SLE patients (P < 0.0004 and 0.0005, respectively). Serum IL-10 levels correlated with the titre of anti-ds DNA antibodies in the patients. No correlation was found between disease activity or clinical profiles and the production or serum levels of cytokines except for a weak correlation (not statistically significant) between levels of IL-10 in the sera and disease activity as measured by the SLEDAI but not by the SLAM index. CONCLUSION: Our results confirm earlier reports that SLE patients have an increased production as well as increased serum levels of the type 2 cytokines IL-10 and IL-6. We found no significant correlation between IL-6 and IL-10 and disease activity or clinical profiles. Serum IL-10 levels correlated with the titre of anti-ds DNA antibodies in the SLE patients. In summary, our result indicate that the increased IL-10 production in SLE could be constitutive.  相似文献   

13.

Objective

Free radical–mediated reactions have been implicated as contributors in a number of autoimmune diseases, including systemic lupus erythematosus (SLE). However, the potential for oxidative/nitrosative stress to elicit an autoimmune response or to contribute to disease pathogenesis, and thus be useful when determining a prognosis, remains largely unexplored in humans. This study was undertaken to investigate the status and contribution of oxidative/nitrosative stress in patients with SLE.

Methods

Sera from 72 SLE patients with varying levels of disease activity according to the SLE Disease Activity Index (SLEDAI) and 36 age‐ and sex‐matched healthy controls were evaluated for serum levels of oxidative/nitrosative stress markers, including antibodies to malondialdehyde (anti‐MDA) protein adducts and to 4‐hydroxynonenal (anti‐HNE) protein adducts, MDA/HNE protein adducts, superoxide dismutase (SOD), nitrotyrosine (NT), and inducible nitric oxide synthase (iNOS).

Results

Serum analysis showed significantly higher levels of both anti–MDA/anti–HNE protein adduct antibodies and MDA/HNE protein adducts in SLE patients compared with healthy controls. Interestingly, not only was there an increased number of subjects positive for anti‐MDA or anti‐HNE antibodies, but also the levels of both of these antibodies were statistically significantly higher among SLE patients whose SLEDAI scores were ≥6 as compared with SLE patients with lower SLEDAI scores (SLEDAI score <6). In addition, a significant correlation was observed between the levels of anti‐MDA or anti‐HNE antibodies and the SLEDAI score (r = 0.734 and r = 0.647, respectively), suggesting a possible causal relationship between these antibodies and SLE. Furthermore, sera from SLE patients had lower levels of SOD and higher levels of iNOS and NT compared with healthy control sera.

Conclusion

These findings support an association between oxidative/nitrosative stress and SLE. The stronger response observed in serum samples from patients with higher SLEDAI scores suggests that markers of oxidative/nitrosative stress may be useful in evaluating the progression of SLE and in elucidating the mechanisms of disease pathogenesis.
  相似文献   

14.
OBJECTIVE: To determine levels of the soluble form of the chemokine fractalkine (sFkn) and its receptor, CX(3)CR1, in patients with systemic lupus erythematosus (SLE) with neuropsychiatric involvement (NPSLE) and in SLE patients without neuropsychiatric involvement, and to assess their relationship with disease activity and organ damage. METHODS: Levels of sFkn in serum and cerebrospinal fluid (CSF) were measured by enzyme-linked immunosorbent assay. Expression of Fkn and CX(3)CR1 was quantified using real-time polymerase chain reaction. Surface expression of CX(3)CR1 on peripheral blood mononuclear cells (PBMCs) was determined by flow cytometry. Disease activity and organ damage were assessed using the SLE Disease Activity Index (SLEDAI) and the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index, respectively. RESULTS: Serum sFkn levels were significantly higher in patients with SLE than in patients with rheumatoid arthritis (RA) or healthy controls. In addition, significant correlations between serum sFkn levels and the SLEDAI, the SLICC/ACR Damage Index, anti-double-stranded DNA and anti-Sm antibody titers, immune complex levels (C1q), and serum complement levels (CH50) were observed. Expression of CX(3)CR1 was significantly greater in PBMCs from patients with active SLE than in those from RA patients or healthy controls. Levels of sFkn were also significantly higher in CSF from untreated patients with newly diagnosed NPSLE than in SLE patients without neuropsychiatric involvement; treatment reduced both serum and CSF levels of sFkn in patients with SLE. CONCLUSION: Soluble Fkn and CX(3)CR1 may play key roles in the pathogenesis of SLE, including the neuropsychiatric involvement. Soluble Fkn is also a serologic marker of disease activity and organ damage in patients with SLE, and its measurement in CSF may be useful for the diagnosis of NPSLE and followup of patients with NPSLE.  相似文献   

15.
OBJECTIVE: To evaluate whether the levels of soluble form of the Fas apoptosis antigen (sCD95/sFas) varied from those of healthy control subjects in a group of patients with systemic lupus erythematosus (SLE). This was done to determine whether sFas has a role in either the disease activity or the organ damage in SLE. METHODS: Serum levels of sFas were measured over a period of 4 y (277 determinations) in 39 Arab patients with SLE and 22 age-, gender-, and race-matched healthy controls using double antibody ELISA. SLEDAI scores for disease activity and SLICC/ACR scores for cumulative organ damage were determined. Serum levels of acute phase reactants, complement, inflammatory cell counts, levels of autoantibodies, and kidney and liver function test results were obtained retrospectively from clinical records. RESULTS: sFas levels were significantly higher in patients with SLE (n = 39, 277 determinations) (0.60 ng/ml +/- 0.38) than in healthy controls (n = 22) (0.26 ng/ml +/- 0.11) (P < 0.00001). The levels of sFas correlated with SLICC/ACR (r = 0.36; P < 0.02), but not with SLEDAI. sFas correlated with renal and liver function tests measured by s-creatinine (r = 0.38; P < 0.0001), creatinine clearance (r = -0.30, P < 0.001), s-albumin (r = -0.28, P < 0.0001), and ALT (r = 0.35; P < 0.00001), but did not correlate with the levels of acute phase reactants. CONCLUSION: sFas is elevated in sera of SLE patient. Since sFas correlates with indices of organ damage but not with disease activity, it may be a marker of organ damage in SLE and may act to protect certain organs from further damage by inhibiting Fas-mediated apoptosis.  相似文献   

16.
OBJECTIVE: To assess the bioactivity of circulating prolactin (PRL) in serum samples from patients with systemic lupus erythematosus (SLE) using 2 novel homologous in vitro bioassays, and to correlate PRL bioactivity with lupus activity. METHODS: Serum samples from 98 SLE patients with and without disease activity were tested for immunoreactive and bioactive concentrations of PRL. RESULTS: Patients with active disease exhibited higher bioactive serum PRL levels in homologous bioassays (p 相似文献   

17.
Cytokines play an important role in the pathogenesis of systemic lupus erythematosus (SLE). Among the cytokines that regulate B cell homeostasis is a proliferation-inducing ligand (APRIL). This study aimed to determine whether serum levels of APRIL are raised in patients with SLE and correlate with disease activity or proinflammatory cytokines production, or both. Serum APRIL, interleukin-17 (IL-17), IL-4 and interferon gamma (IFN-γ) levels were measured in forty patients with SLE and 30 healthy controls. Disease activity was assessed by SLE disease activity index (SLEDAI), and results were correlated with serum APRIL levels. Serum APRIL levels were significantly higher in patients with SLE than in healthy controls. Positive correlation was found between serum APRIL levels and total SLEDAI score and anti-dsDNA antibody titers. Moreover, serum APRIL levels was significantly higher in patients with arthritis, mucocutaneous manifestations and proteinuria. APRIL is increased in patients with active SLE accompanying the increase of IL-17 and IFN-γ. Significant positive correlations between serum levels of APRIL and IL-17 and IFN-γ and a negative correlation between serum levels of APRIL and IL-4 were found. The results suggest that APRIL may be an important marker of disease activity in patients with SLE. We provide the analyses of APRIL levels in patients with SLE, suggesting new tools for the diagnosis, prognosis and possible therapeutic management of SLE.  相似文献   

18.
Mok CC  Lau CS 《Lupus》2000,9(4):252-257
OBJECTIVE: To study the profile of sex hormones in male patients with systemic lupus erythematosus (SLE). METHOD: Serum prolactin (PRL), testosterone (T), estradiol (E2), follicle-stimulating hormone (FSII) and luteinizing hormone (LH) levels were obtained from 35 males with SLE and compared with 33 age-matched normal controls. RESULTS: No significant differences in serum T, E2, PRL levels and E2/T ratio were observed between male SLE patients and controls. However, patients with SLE had significantly higher levels of gonadotrophins (FSH, LH). Five (14%) SLE patients, but none of the controls, had both low testosterone and elevated LH. Hypoandrogenic male SLE patients did not have overt features of hypogonadism but had a higher prevalence of central nervous system disease and scrositis than those with normal androgen levels. Discase flares, on the other hand, were not significantly more frequent in these patients. Although PRL or T levels per se did not correlate with disease activity in our patients, the ratio of PRL to T showed a significant correlation with SLEDAI scores (p = 0.42. P = 0.01). CONCLUSIONS: Hypoandrogenism is present in some male patients with SLE and may be relevant in disease pathogenesis. However, whether these hormonal abnormalities are intrinsic to SLE or the consequence of any non-specific chronic disorders cannot be distinguished from the current data. Further studies involving a larger number of subjects and inclusion of other disease controls are needed.  相似文献   

19.
Aim: The purpose of the study is to measure serum and synovial fluid levels of activin A and inhibin A in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and osteoarthritis (OA) and correlate them with disease activity parameters. Subjects and methods: This study included 60 patients with various rheumatic diseases (20 with RA, 20 with SLE and 20 with OA), as well as 10 healthy controls. All of them were subjected to complete history‐taking, examination and estimation of disease activity index. The following investigations were done for all subjects: serum and synovial activin A, inhibin A, erythrocyte sedimentation rate (ESR), C‐reactive protein (CRP), anti‐dsDNA and complements 3 and 4. Results: Serum levels of activin A were significantly higher in RA, SLE and OA than controls and in RA and SLE versus OA The mean values of serum inhibin A were significantly higher in all studied groups than controls. Synovial activin A and inhibin A were significantly higher in RA than OA. Positive correlations were found between serum activin A and disease activity parameters of RA. In SLE, positive correlations were found between serum activin A and inhibin A with ESR and SLE Disease Activity Index. Conclusions: Serum activin A and inhibin A were significantly higher in RA and SLE. Serum levels correlated positively with disease activity parameters of RA and SLE. However, synovial levels were significantly higher in RA than OA but showed no correlation or negative correlation with disease activity. We recommend further studies to detect the exact role of activin A and inhibin A in these conditions.  相似文献   

20.
Abstract

Objective L-ficolin plays an important role in innate immunity and is involved in apoptosis. The objective of this study was to investigate the relationship between serum L-ficolin levels and clinical manifestations in patients with systemic lupus erythematosus (SLE).

Methods Serum L-ficolin levels were determined by enzyme-linked immunosorbent assay in 66 SLE patients and 50 healthy controls.

Results Median serum L-ficolin levels were 5.0 and 8.7 μg/ml in SLE patients and controls, respectively (p = 0.0001). There were no significant differences in serum L-ficolin levels between the active disease group [SLE Disease Activity Index (SLEDAI) > 6] and the inactive disease group (SLEDAI < 5). Decreased serum L-ficolin levels were associated with thrombocytopenia (median of with vs. without thrombocytopenia 3.4 vs. 5.3 μg/ml, p = 0.008). There were no correlations between serum L-ficolin levels and SLEDAI, serum C3, or serum C4 levels.

Conclusion The association between L-ficolin and thrombocytopenia suggests a pathogenic role for L-ficolin in thrombocytopenia in SLE.  相似文献   

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