目的 分析小剂量糖皮质激素（GCs）治疗类风湿关节炎（RA）的不良反应。为GCs的临床应用提供借鉴。方法 回顾性随机记录164例RA患者的用药史。并分析应用小剂量GCs（≤10m-d）与高血压、糖尿病、非外伤性骨折、消化道溃疡、白内障、青光眼和高脂血症等不良反应之间的相关性。结果164例RA患者中。曾使用过GCs治疗者68例。占4l.5%。其中。小剂量GCs治疗6个月以上者47例（287%）。长期应用中大剂量GCs治疗者8例（49%）。应用剂量不详者13例（79%）。与未用过GCs组相比。小剂量GCs组的高血压和糖尿病发生率无明显增加（P>0.05）。但高脂血症发生率明显较高（艮0.05）。发生非外伤性骨折、白内障及青光眼的患者例数较少。尚难评价其意义。结论初步研究提示。小剂量GCs治疗对血压和血糖的影响不显著。但可能增加高脂血症等不良反应的发生率。

目的 通过分析系统性红斑狼疮（systemic lupus erythematosus, SLE）病情活动和合并感染患者的临床和血清学特点，发现对疾病活动和感染有鉴别意义的指标。方法 对2003-2004年在我科住院的110例SLE患者进行回顾性分析，比较病情活动未合并感染者87例（未感染组）和合并感染者23例（感染组）的发热、皮疹、口腔溃疡、脏器损害等临床表现。同时分析患者的C反应蛋白（CRP）。血沉（ESR），血清蛋白电泳（白蛋白、α1球蛋白、α2球蛋白、β球蛋白、γ球蛋白），补体（C3、C4），免疫球蛋白（IgA、IgM、IzG）及免疫复合物（CIC）的变化。结果 感染组CRP、ESR及α1球蛋白高于未感染组（P<01）。通过比较CRP、ESR及α1球蛋白与其他临床指标的相关性，发现CRP受感染之外的影响较少，在未感染组CRP浓度的均数在正常水平。合并感染后明显升高。感染组患者的发热、口腔溃疡、雷诺现象、心脏损害及糖皮质激素用量均高于未感染组（P<05）。结论 （1）sLE合并感染时大部分患者的cRP明显升高。②在狼疮活动时CRP大多正常或略高，但少数患者。尤其合并浆膜炎者的CRP水平可较高。CRP对于鉴别狼疮活动与合并感染有重要的临床应用价值。

It has been reported that collagen II (CII)-derived peptide induced T-cell activation via its amino acids responsible for T-cell receptor (TCR) recognition. In this study, three altered CII263–272 peptide ligands (APL) containing multiple substitutions of TCR contact residues were synthesized. Their roles in inhibition of T-cell activation were evaluated in peripheral blood lymphocytes (PBL) of rheumatoid arthritis (RA) in vitro. It was shown that 41% (25/61) of RA patients were responsive to the wild-type antigenic CII263-272. In contrast, marginal or silent T-cell responses to the three APLs were found, accompanied by inhibitory effects on secretion of Th1 type cytokines and expression of cell surface markers, CD69 and CD25. In addition, T-cell activation induced by the wild-type antigenic CII263-272 was inhibited by all the three APLs in a dose-dependent manner. It is demonstrated that APLs with substitutions of TCR contact residues are capable of down-regulating T-cell responses in PBLs of RA, suggesting that the CII-derived APLs are potentially therapeutic in RA. D 2005 Elsevier Inc. All rights reserved.

Collagen (CII) 263-272 peptide, an autoantigen in rheumatoid arthritis, is a specific human leukocyte antigen (HLA)-DR1/4-binding peptide recognized by T-cell receptors (TCR). The affinity of influenza virus haemagglutinin (HA) 306- 318 peptide for the antigen-binding groove of HLA-DR1/4 molecules is higher than that of CII263-272. The HLA-DR1/4-binding residues of HA306-318 are located in the region 308-317. Altered HA308-317 peptides with substitutions of TCR-contact residues may inhibit HLA-DR1/4-specific T-cell activation by blocking the antigen-binding site of HLA-DR1/4 molecules. To evaluate the role of altered HA308-317 peptides in HLA-DR1-restricted T-cell activation, we synthesized three altered HA308-317 peptides. The specific binding of altered HA308-317 peptides to HLA-DR1 molecules was examined using flow cytometry. Effects of altered HA308-317 peptides on HLA-DR1-specific T-cell hybridoma were studied by measuring T-cell proliferation and surface expression of CD69 or CD25. The results showed that altered HA308-317 peptides were able to bind to HLA-DR1 molecules and competed with CII263-272 or wildtype HA308-317 peptide. Compared with wildtype CII263-272 or HA308-317, altered HA308-317 peptides did not stimulate significant T-cell proliferation and CD69 or CD25 expression. Furthermore, the altered HA308-317 peptides inhibited HLADR1-specific T-cell activation induced by CII263-272 or wildtype HA308-317 peptide, which may suggest an effective therapeutic strategy in inhibition of HLA-DR1-specific T-cell responses in autoimmunity.