白三烯受体拮抗剂联合吸入糖皮质激素治疗儿童感染后咳嗽

目的：探讨白三烯受体拮抗剂孟鲁司特联合吸入糖皮质激素治疗儿童感染后咳嗽的临床效果。方法：选取我院儿科2009年6月～2010年12月收治的178例感染后咳嗽的患儿，按其所采用的治疗方法不同分为二组，观察组89例患儿采用白三烯受体拮抗剂孟鲁司特联合吸入糖皮质激素进行治疗；对照组89例患儿采用吸入糖皮质激素治疗，比较两组患...     

Black sheep get the blues: A psychobiological model of social rejection and depression

Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke depression. In this model, social rejection events activate brain regions involved in processing negative affect and rejection-related distress (e.g., anterior insula, dorsal anterior cingulate cortex). They also elicit negative self-referential cognitions (e.g., “I’m undesirable,” “Other people don’t like me”) and related self-conscious emotions (e.g., shame, humiliation). Downstream biological consequences include upregulation of the hypothalamic-pituitary-adrenal axis, sympathetic-adrenal-medullary axis, and inflammatory response. Pro-inflammatory cytokines play an important role in this process because they induce a constellation of depressotypic behaviors called sickness behaviors. Although these changes can be short-lived, sustained inflammation may occur via glucocorticoid resistance, catecholamines, sympathetic innervation of immune organs, and immune cell aging. This response also may be moderated by several factors, including prior life stress, prior depression, and genes implicated in stress reactivity.     

多发性硬化患者颅内深部灰质核团MRI的T2信号的定量分析及其临床意义

目的应用T2加权成像观察多发性硬化大脑深部灰质核团(丘脑,尾状核,壳核,苍白球)病变的特点,对MRI T2信号强度进行定量分析,并探讨多发性硬化患者颅内深部灰质核团改变与临床指标(病程,有无行走障碍,有无视神经受累,脑脊液寡克隆带是否为阳性)的相关性。经过糖皮质激素治疗后,对比治疗前后颅内深部灰质核团T2信号强度。方法依据Mc Donald 2010诊断标准,收集多发性硬化患者17例为实验组,选取17例同性别、同年龄的健康人作为对照组,实验组及对照组均行核磁共振,应用测量T2相对信号值的方法,对两组颅内深部灰质核团(丘脑,尾状核,壳核,苍白球)的MRI T2信号强度进行定量分析,对比组间是否有差异,同时搜集病程,有无行走障碍,有无视神经受累,脑脊液寡克隆带结果等临床指标,评价颅内深部灰质核团改变与临床指标是否有相关性。对比糖皮质激素治疗前后颅内深部灰质核团T2信号强度。结果与对照组相比,MS组各灰质核团的T2信号均有所减低,差异有统计学意义:丘脑(P=0.001),尾状核(P=0.047),壳核(P=0.041),苍白球(P=0.009)。行走受限与各灰质核团T2信号强度具有相关性,spearman相关系数分别为丘脑0.566(P=0.018),尾状核0.51(P=0.037),苍白球0.538(P=0.026),壳核0.481(P=0.051>0.05)。其余临床指标与T2信号相关系数差异无统计学意义(P>0.05)。糖皮质激素治疗前后,颅内深部灰质核团T2信号强度差异无统计学意义(P>0.05)。结论多发性硬化患者的灰质核团相比于正常组,T2信号值普遍偏低,提示灰质核团铁质沉积。行走障碍与各个灰质核团的T2低信号有显著相关性,而病程、脑脊液寡克隆带和视神经受累等临床指标均与T2低信号无关。激素治疗对灰质核团铁沉积无即时影响。     

补骨胶囊对SLE患者激素治疗后骨质疏松的作用及细胞因子表达的影响

目的探讨中成药补骨胶囊对系统性红斑狼疮(SLE)患者激素治疗后骨质代谢及细胞因子表达的影响。方法66例SLE患者随机分为两组,治疗组34例,采用糖皮质激素和补骨胶囊治疗;对照组32例,单纯采用糖皮质激素治疗,另设健康组30例。观察治疗前后两组病人IL-1,IL-6,TNF-α表达水平和血钙、磷、碱性磷酸酶、甲状旁腺素的变化以及三角区骨密度的改变,并与健康组对照比较。结果治疗前两组病人的各项指标差异均无显著性;治疗后两组患者的IL-1,IL-6,TNF-α表达水平和血钙、甲状旁腺素的变化以及三角区骨密度的改变,差异均有显著性(P<0.01或P<0.05)。结论中成药补骨胶囊能有效防治由糖皮质激素致患者骨质疏松的发生,其作用机制可能与调节患者体内细胞因子IL-1,IL-6,TNF-α表达水平和甲状旁腺素的分泌有关。     

重症药疹的护理

目的：探讨重症药疹的护理要点和方法。方法：进行暴露疗法护理,以及对皮肤、黏膜、眼部、口腔、心理等进行临床护理干预。结果：重症药疹患者通过激素治疗和各种护理措施,其发热消退时间、黏膜糜烂治愈时间、躯干四肢皮疹治愈时间、肝肾功能恢复时间明显缩短。结论：重症药疹患者早期、足量应用大剂量激素治疗和有效的综合护理,可缩短病程,提高治愈率,降低死亡率,对患者早日康复至关重要。     

激素药源性股骨头坏死及骨质疏松50例分析

目的探讨应用糖皮质激素的剂量和时间与发生股骨头坏死及骨质疏松的关系。方法通过采用对比分组的方法，分析对武警医学院附属医院因特殊情况需大量应用糖皮质激素而发生股骨头坏死及骨质疏松的患者，了解激素应用剂量及应用时间与发病结果之间的关系。结果在所选病例中，全部出现不同程度的骨质疏松，但发生股骨头坏死的病例仅占总数的30％，且激素应用总量小于2000mg的病例中，短期股骨头坏死的发生率为0；2000-5000mg的病例中，短期股骨头坏死的发生率为17．6％；激素用量在5000mg以上的病例中，股骨头坏死的发生率为43．5％；激素用量在10000mg以上的病例，股骨头坏死的发生率为80％。结论股骨头坏死发生率与糖皮质激素的总用量有关，与激素应用时间长短无关。     

糖皮质激素吸入对哮喘患者血清IL-8、TNF-α水平的影响

目的观察糖皮质激素吸入对哮喘患者血清白细胞介素-8(IL-8)、肿瘤坏死因子-α(TNF-α)水平和肺功能的影响。方法采用ELISA法分别检测轻、中度哮喘急性发作期患者(30例)吸入丙酸倍氯米松2周前后和健康对照组(25例)血清中IL-8、TNF-α水平,并同时测1 s用力呼气容积(FEV1)占预计值的百分比。结果急性发作期患者治疗前IL-8、TNF-α值明显升高,与健康对照组比较,差异有统计学意义(P<0.01);急性发作期及缓解期FEV1占预计值的百分比较健康对照组下降(P<0.01);急性发作期患者治疗后IL-8、TNF-α水平下降,FEV1占预计值的百分比升高(P<0.05)。结论哮喘患者急性发作期血清中IL-8、TNF-α水平升高,糖皮质激素可使其水平下降,并改善哮喘患者肺功能。     

特发性血小板减少性紫癜患者激素敏感性与糖皮质激素受体亚型的关系研究

目的探究特发性血小板减少性紫癜（ITP）患者对糖皮质激素敏感性与其外周血单个核细胞内激素受体亚型表达的关系。方法采用实时定量RT—PCR和免疫组化技术检测不同激素敏感性ITP患者（包括糖皮质激素抵抗和敏感病人）外周血单个核细胞内α和β亚型糖皮质激素受体（GRα和GRβ）mRNA和蛋白表达，并将检测结果与正常对照组进行比较。结果糖皮质激素抵抗组患者外周血单个核细胞GRβmRNA表达量和GRβ蛋白表达阳性的单个核细胞比率明显高于激素敏感组及正常对照组（P〈0．01），而GRα mRNA和蛋白表达水平，各组之间无显著差异。结论ITP患者糖皮质激素敏感性与其GRβ表达水平密切相关。     

Development of hyperthyroidism in a patient with idiopathic nephrotic syndrome

We present a 13-year-old boy who developed hyperthyroidism during the clinical course of idiopathic nephrotic syndrome treated with glucocorticoid. He had a second relapse of minimal change nephrotic syndrome, and complete remission of nephrotic syndrome was achieved immediately with oral glucocorticoid. However, when the steroid dosage was reduced, signs of hyperthyroidism such as systolic hypertension and tachycardia were observed. Laboratory findings revealed thyroid-stimulating hormone (TSH) below 0.05 μU/ml, free tri-iodothyronine of 16.1 pg/ml, free thyroxine of 5.6 ng/dl, and anti-TSH receptor antibody of 90%. Thus, a diagnosis of hyperthyroidism was made and treatment with thiamazol was started. Massive proteinuria may decrease the activity of hyperthyroidism due to urinary loss of thyroid hormones. A decrease in glucocorticoid dosage may also be involved in the development of hyperthyroidism due to a reduced immunosuppressive effect. Received: 11 July 2001 / Revised: 22 October 2001 / Accepted: 27 November 2001