Mortality in Systemic Lupus Erythematosus: A 10-Year Review

During the years 1963-72 33 patients with systemic lupus erythematosus (S.L.E.) died. Of these 30 case records were available for analysis. For the same period 167 patients with S.L.E. were admitted. It was ascertained that of the 30 deaths 22 were directly attributable to the disease itself and 8 were related to complications of therapy. The three commonest causes of death were neurological involvement (11 patients), renal failure (9 patients), and infection (8 patients).     

Recurrent Talaromyces marneffei Infection Presenting with Intestinal Obstruction in a Patient with Systemic Lupus Erythematosus

Mycopathologia - Talaromyces marneffei is an important opportunistic pathogen mainly afflicting the HIV-infected patients, in rare instance, it could cause infection in non-HIV-infected...     

Acute Renal Failure in Systemic Lupus Erythematosus

Acute anuric renal failure complicating systemic lupus erythematosus does not usually respond to treatment with corticosteroids and immunosuppressive agents. We describe four cases treated by dialysis, corticosteroids, and heparin in anticoagulant doses in which there was remarkable improvement in renal function after prolonged anuria. One patient died later from a gastric haemorrhage. The other three were alive and well 55, 54, and 30 months from the onset of anuria. In two cases a second renal biopsy showed a striking improvement in the lesions. Large doses of corticosteroid and heparin may be the best treatment in acute anuric lupus nephritis.     

ANCA与SLE临床表现的相关性及其意义

目的:探讨系统性红斑狼疮(Systemic Lupus Erythematosus,SLE)患者抗中性粒细胞胞浆抗体(Anti-neutrophil Cytoplasmic Antibodies,ANCA)与肾炎及其他临床表现和实验室检查的相关性及其意义.方法:采用前瞻性研究收集77例系统性红斑狼疮患者,用间接免疫荧光法(IIF)检测患者血清ANCA、ELISA法检测ANCA抗原,检测其他免疫学指标如抗核抗体、抗dsDNA抗体等.结果:77例SLE患者中ANCA阳性28(36.4%)例,ANCA阳性组浆膜炎、肾损害、神经精神症状、皮肤血管炎、抗dsDNA抗体阳性、抗Sm抗体阳性、补体下降以及血清IgG升高的发生率明显高于阴性组(P＜0.05).52例LN患者中,25例(48.1%)ANCA阳性,其中P-ANCA阳性者22例(88%).3例(12%)为a-ANCA均出现在RPGN,无一例出现c-ANCA.非LN组25例患者中,仅3例(12%)p-ANCA阳性,且均为抗-MPO.正常对照组无一例ANCA阳性.77例SLE患者中,14例(18.2%)为抗-MPO;13例(16.9%)为抗LF,且只见于DPGN、FPGN和RPGN伴有新月体形成者;10例(13%)为抗-CG,但在非狼疮肾炎患者未检测到抗-LF及抗-CG.在各种临床表现中,抗-MPO与肾脏和皮肤表现有关;而抗-LF与肾脏、关节炎及浆膜炎有关;抗-CG可见于各种临床表现.结论:ANCA可作为评价SLE疾病及鉴别血管炎和狼疮肾炎的一个重要指标.     

系统性红斑狼疮伴发急腹症的诊治思考 一附18 例临床分析

目的：提高对系统性红疯狼疮（SLE）伴发急腹症临床表现的认识,总结诊断和治疗此类病例的经验。方法：对18例SLE伴发急腹症的病例进行回顾性分析。结果：SLE并发急腹症临床表现多样化,可以表现为消化道出血,肠梗阻。肠穿孔,急性胃肠炎,急性胰腺炎,急性腹膜炎等。治疗后16例病情得到控制,2例死亡。结论：SLE伴发急腹症预示病情危重,对此应提高认识,尽早诊断;应用大剂量肾上腺皮质激素和免疫抑制剂有良好的疗效。     

成年女性系统性红斑狼疮血清中抗黄体抗体与月经异常 的相关性研究

目的:探讨成年女性系统性红斑狼疮(SLE)血清中抗黄体抗体与月经异常的相关性。方法:收集SLE患者及正常对照者的临床资料,详细记录入选研究对象的月经及生育情况,同时记录抗核抗体(ANA)等自身抗体的测定结果。采用酶联免疫吸附试验(ELISA)法检测患者血清中抗黄体抗体。结果:在入选的69例成年女性SLE患者中,26(38%)例患者抗黄体抗体阳性。而在40例健康对照者中,仅2(5%)例出现抗黄体抗体阳性。在入选的69例SLE患者中,29(42%)例患者的月经正常,40(58%)例患者出现月经异常。在40例健康对照者中,31(78%)例患者的月经正常,仅9(21%)例患者出现月经异常。有月经异常的SLE患者中抗黄体抗体的阳性率显著高于无月经异常的SLE患者(66%vs 18%,P<0.01),而在健康对照者中则未见有显著性差异。结论:SLE患者中抗黄体抗体的阳性率为38%,并可能与SLE的月经异常相关。     

系统性红斑狼疮合并消化道损害32例临床分析

目的：探讨系统性红斑狼疮（SLE）合并消化道损害者的临床特点。方法：回顾性分析32例SLE合并消化道损害的患者,收集整理其临床资料,分析其临床特点。结果：食道受累者7例（21．9％）,胃肠道受累者25例（78．1％）其中假性肠梗阻10例（31．2％）,且以肠梗阻为首发症状的2例均误诊为急腹症收住外科,肾脏受累14例（43．8％）。治疗后,24例好转。4例死亡。结论：以消化道症状为首发表现的SLE极易误诊,特别是以吞咽障碍,肠梗阻为首发症状者最易误诊。对有消化道受损表现同时伴有其它脏器受损者应排除有无SLE可能。SLE消化道损害发生率高,对此应提高认识和警惕。     

Glycation end-products specific auto-antibodies in Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease, which is highly inflammatory. Compared to a healthy control group, SLE patients exhibit a higher concentration of advanced glycation end products (AGEs) and a lower concentration of receptors for AGEs (RAGE) in serum, however, the exact aetiology is still unclear. In the present study, non-enzymatic glycation induced modification of human serum albumin (HSA) has been studied by biophysical techniques. Glycated HSA (G-HSA) was used as an antigen, and serum autoantibody levels were estimated in SLE and normal humans (NH) against it, using direct binding ELISA and competitive inhibition ELISA. Compared to N-HSA, remarkable structural modifications were observed in G-HSA. Modified HSA also showed increased pentosidine fluorescence (213.7 ± 13.4 AU). Glycation of HSA induced a conversion of α-helix and random coil to β-sheet and β-turns. Serum immuno assays results exhibited significantly (p < 0.001) higher binding of G-HSA with serum autoantibodies from SLE patients when compared with native HSA (N-HSA). Furthermore, competitive ELISA results showed significantly (p < 0.001) high percent inhibition of serum IgG from SLE patients with modified antigen. Chronic inflammation with excessive oxidative stress in SLE patients could be a possible reason for structural alterations in blood proteins, generating highly immunogenic unique new-epitopes. These in turn induce the generation of specific autoantibodies against G-HSA that may serve as a potential biomarker for SLE pathogenesis.     

Serum and Lymphocytic Neurotrophins Profiles in Systemic Lupus Erythematosus: a Case-Control Study

Background

Neurotrophins play a central role in the development and maintenance of the nervous system. However, neurotrophins can also modulate B and T cell proliferation and activation, especially via autocrine loops. We hypothesized that both serum and lymphocytic neurotrophin levels may be deregulated in systemic Lupus erythematosus (SLE) and may reflect clinical symptoms of the disease.

Methods

Neurotrophins in the serum (ELISA tests) and lymphocytes (flow cytometry) were measured in 26 SLE patients and 26 control subjects. Th1 (interferon-γ) and Th2 (IL-10) profiles and serum concentration of BAFF were assessed by ELISA in the SLE and control subjects.

Findings

We have demonstrated that both NGF and BDNF serum levels are higher in SLE patients than healthy controls (p=0.003 and p<0.001), independently of Th1 or Th2 profiles. Enhanced serum NT-3 levels (p=0.003) were only found in severe lupus flares (i.e. SLEDAI ≥ 10) and significantly correlated with complement activation (decreased CH 50, Γ=-0.28, p=0.03). Furthermore, there was a negative correlation between serum NGF levels and the number of circulating T regulatory cells (Γ=0.48, p=0.01). In circulating B cells, production of both NGF and BDNF was greater in SLE patients than in healthy controls. In particular, the number of NGF-secreting B cells correlated with decreased complement levels (p=0.05). One month after SLE flare treatment, BDNF levels decreased; in contrast, NGF and NT-3 levels remained unchanged.

Conclusion

This study demonstrates that serum and B cell levels of both NGF and BDNF are increased in SLE, suggesting that the neurotrophin production pathway is deregulated in this disease. These results must be confirmed in a larger study with naive SLE patients, in order to avoid the potential confounding influence of prior immune-modulating treatments on neurotrophin levels.