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91.
目的探究百令胶囊联合来氟米特片和醋酸泼尼松片治疗狼疮性肾炎的临床疗效。方法选取2012年12月—2017年3月开封市中心医院收治的126例狼疮性肾炎患者作为研究对象,按随机原则将患者分为对照组(63例)和治疗组(63例)。对照组患者口服来氟米特片,2片/次,1次/d;同时口服醋酸泼尼松片,1mg/(kg?d),2个月后减量至10mg/d。治疗组在对照组的基础上口服百令胶囊,1g/次,3次/d。两组患者均连续治疗6个月。观察两组患者的临床疗效,同时比较治疗前后两组的白蛋白(ALB)、血肌酐(Scr)、24 h尿蛋白定量(24 h UP)、补体C3、红细胞(RBC)和β2-微球蛋白(β2-MG)水平、系统性狼疮性疾病活动度(SLEDAI)积分。结果治疗后,对照组和治疗组的总有效率分别为79.37%、92.06%,两组比较差异具有统计学意义(P0.05)。治疗后,两组ALB、补体C3和RBC较治疗前明显升高,而Scr、24 h UP和β2-MG较治疗前明显下降,同组治疗前后比较差异具有统计学意义(P0.05)。治疗后,治疗组ALB、补体C3和RBC较对照组明显升高,Scr、24hUP和β2-MG较对照组明显下降,两组比较差异具统计学意义(P0.05)。治疗后,两组SLEDAI积分较治疗前明显下降,同组治疗前后比较差异具有统计学意义(P0.05);且治疗后,治疗组SLEDAI积分较对照组显著降低,两组比较差异具有统计学意义(P0.05)。结论百令胶囊联合来氟米特片和醋酸泼尼松片治疗狼疮性肾炎具有较好的临床疗效,可改善肾脏功能,降低狼疮性肾炎活动度和不良反应发生率,具有一定的临床推广应用价值。  相似文献   
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94.
目的探讨系统性红斑狼疮(SLE)患者血清IL-10和IL-18的表达及其与疾病活动的关系。方法应用ELISA法检测104例SLE患者和100例健康体检者血清IL-10和IL-18的水平,其中SLE患者根据疾病活动性指数(SLEDAI)评分标准分为活动组(56例)和缓解组(48例),比较各组结果的差异,并分析SLEDAI与IL-10和IL-18的相关性。结果 SLE组IL-10和IL-18水平分别为(18.25±3.66)、(582.61±65.28)pg/ml,明显高于对照组的(7.12±2.36)、(186.24±60.39)pg/ml,差异有统计学意义(P〈0.01);SLE活动组IL-10和IL-18水平分别为(25.98±4.75)、(683.72±62.48)pg/ml,高于缓解组的(14.67±3.21)、(493.51±69.17)pg/ml,差异亦有统计学意义(P〈0.01);SLE患者血清IL-10和IL-18水平与SLEDAI呈正相关(P〈0.05)。结论 IL-10和IL-18在SLE发病机制中发挥重要作用,而且与疾病活动性相关。  相似文献   
95.

Objective

To determine the influence of the use of tibolone on the frequency of flares of systemic lupus erythematosus (SLE) in postmenopausal patients.

Methods

Thirty patients with inactive or controlled SLE were included in the study. Patients were randomized to receive a 12-month course of either tibolona (2.5 mg/day) or placebo. The following were investigated: hypoestrogenism symptoms by Kupperman index, weight; anti-dsDNA antibodies; SLE flares (frequency) assessed by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI); and biochemical profile (total cholesterol, high-density lipoprotein cholesterol [HDL-C], triglycerides, complement components [C3/C4], α1-acid glycoprotein, urea, creatinine, 24-h proteinuria, C-reactive protein and erythrocyte sedimentation rate).

Results

The reduction in Kupperman index was greater in the patients using tibolone than in those using placebo. The mean SLEDAI was not different between the groups during the study as well as SLE flare frequency (tibolone: 2/15 [13.3%] vs. placebo: 1/15 [6.7%]; p = 0.54). All cases of flares were considered mild to moderate. Although the groups were similar at the baseline evaluation, after 6 and 12 months of treatment lower values were found in the tibolone group for triglycerides (6 months: 161.6 ± 30.9 mg/dl vs. 194.4 ± 46.5; p = 0.04; 12 months 163.7 ± 29.8 mg/dl vs. 204.1 ± 49.9 mg/dl; p = 0.02; tibolone vs. placebo group, respectively) and for HDL-C (6 months: 40.7 ± 10.7 mg/dl vs. 53.4 ± 16.5; p = 0.02; 12 months: 47.2 ± 7.9 mg/dl vs. 63.2 ± 16.3 mg/dl; p < 0.01; tibolone vs. placebo group, respectively). There were no differences between the two groups in any of the remaining variables.

Conclusion

In patients with inactive or stable SLE, the short-term use of tibolone did not significantly affect the frequency of flares. In addition, tibolone was well tolerated and effective to control hypoestrogenism related symptoms in SLE patients.  相似文献   
96.
Deviating cytokine patterns, as a consequence of aberrant immunoregulation, is implicated to be of aetiopathogenetic importance in systemic lupus erythematosus (SLE). To evaluate the possibility of anti-cytokine autoantibody-mediated cytokine regulation/dysregulation, IgG class autoantibodies against cytokines (IL-1beta, IL-6, IL-10, TNFalpha and TGFbeta(1)) were analysed by enzyme-linked immunosorbent assay (ELISA) in serial serum samples from clinically well-characterized SLE patients and in normal human sera (NHS). Anti-TNFalpha autoantibody levels were lower in patients with active disease compared to inactive disease (P<0.001) as well as to NHS (P<0.001). The anti-TNFalpha antibody levels correlated inversely to the SLE disease activity index (SLEDAI) (r(2)=0.07, P<0.01), whereas anti-TGFbeta antibodies were raised in SLE and correlated positively to levels of complement factor C1q (r(2)=0.08, P<0.005). Generally raised anti-cytokine antibody levels and correlations to disease activity measures were found in one individual. Inverse correlations were found comparing SLEDAI scores and autoantibodies to TNFalpha (r(2)=0.92) and IL-6 (r(2)=0.86) and positive correlations were found between levels of anti-TNFalpha and C1q (r(2)=0.86) and C3 (r(2)=0.90). We show, for the first time, a coincidence between reduced anti-TNFalpha autoantibody levels and disease exacerbation in SLE, which is of interest regarding aetiopathogenesis and disease control.  相似文献   
97.
98.

Aim of the work

To assess the clinical significance of serum levels of tumor necrosis factor alpha (TNF-α) and its -863 C/A and 1031 T/C promoter polymorphism in systemic lupus erythematosus (SLE) patients and find any association to disease activity and damage.

Patients and methods

Forty-two female SLE patients and 30 age and gender matched healthy control were included. Systemic Lupus Erythematosus Disease Activity Index and the Systemic Lupus International Collaboration Clinics-damage index were assessed. Serum TNF-α levels were measured and genotyped for TNF-α-863 C/A and 1031 T/C promoters.

Results

The SLE patients had a mean age of 28.5 ± 7.6 years and disease duration 3.3 ± 2.9 years. The mean serum TNF-α level in the SLE patients (8.2 ± 9.8 pg/ml) was significantly higher than in the control (3.5 ± 2.6 pg/ml) (p = 0.005). The TNF-α-863AA genotype was significantly frequent (52.4%) in the SLE patients compared to control (23.3%) (p = 0.012). Those patients had a significantly increased proteinuria and a tendency to a higher serum TNF-α level. Patients with TNF-α-1031 CC genotype had a significantly increased serum TNF-α levels (p = 0.002) and frequency of mucocutaneous manifestations (p = 0.03) as well as a higher frequency of lupus nephritis (LN) compared to those with TT genotype (p = 0.04). Only serum TNF-α level would predict the disease activity.

Conclusion

TNF-α-863 promoter gene polymorphism may be considered as a genetic marker for SLE susceptibility and its AA genotype was associated with LN and with high serum TNF-α production. The TNF-α-1031 AA genotype was related to an increased serum TNF-α level as well as to mucocutaneous manifestations and LN.  相似文献   
99.
Aim of the workThis study was undertaken to evaluate cataract risk factors in Egyptian systemic lupus erythematosus (SLE) patients.Patients and methodsA cohort of 150 consecutive adult SLE patients was included. None of the patients was diabetic or had cataract before steroids treatment for SLE. Detailed medical and ophthalmological histories were taken. Thorough clinical examination was performed with assessment of SLE disease activity index (SLEDAI) and systemic lupus international collaborating clinics damage index (SLICC DI), along with routine blood tests. Slit lamp examination was done to assess the anterior segment of the eye especially the lens to detect the type and degree of cataract.Results150 SLE patients were studied with a mean age of 37.16 ± 11 years; 129 females and 21 males and a mean disease duration of 11 ± 5.7 years. Their mean SLEDAI was 4.1 ± 3.78 and SLICC/DI 2.1 ± 1.3. The frequency of cataract was 18% (n = 27); 22.2% of them were cortical and 77.8% were posterior subcapsular with mild-moderate degree. Glaucoma was present in only 2%. A significant increase in age, disease duration, age at onset, SLICC/DI, cumulative steroid dose and hydroxychloroquine (HCQ) dose was found in those with cataract compared to non-cataract patients (p < 0.05). The age, age at onset, disease duration, SLICC/DI and cumulative steroid dose were significant independent factors increasing the probability of cataract occurrence among SLE patients (p < 0.01).ConclusionAlthough corticosteroids are prescribed to control SLE symptoms, these results highlight potential risks associated with their use, especially cataracts, which require careful and routine ophthalmologic examination and follow up.  相似文献   
100.
We examined the prevalence of thyroid dysfunction and the production of anti-thyroid antibodies (ATA) in patients with systemic lupus erythematosus (SLE) and assessed the association between ATA production and SLE disease activity status. Seventy-seven patients who met the American College of Rheumatology classification criteria for SLE participated in the study. Fifty-two individuals served as a control group. Demographic, clinical information and SLE disease activity (SLEDAI) status were collected from all patients. The sera of all participants were tested for free thyroxine (FT4), thyroid-stimulating hormone (TSH), anti-thyroglobulin (ATg) and anti-thyroid peroxidase (TPO). A SLEDAI score of > or =6 was considered clinically significant. The results of the thyroid function tests and ATA were compared between the study group and the control group. ATA levels were compared between the patients with a SLEDAI score of > or =6 to those with a SLEDAI score of <6. Hypothyroidism was detected in 11.6% of SLE patients compared to 1.9% in the control group. None of the patients or controls had evidence of hyperthyroidism. No statistically significant difference was observed in the levels of ATg or TPO between the study group and the control group. No correlation was found between ATA levels and the degree of the disease activity. Among the different variables tested in this study, hypothyroidism was the only significant abnormal finding in SLE patients. No association was found between the SLEDAI score and the prevalence of ATA production. Larger controlled, longitudinal studies are necessary to confirm these findings and elucidate the role played by ATA in the pathogenesis of thyroid dysfunction in SLE patients.  相似文献   
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