人工牙种植中牙槽骨骨量不足和颌骨缺损的处理

目的 探讨人工牙种植中牙槽骨骨量不足和颌骨缺损的处理。方法 总结32例多种原因、多种类型牙槽骨骨量不足和颌骨缺损，应用植骨、植入Bio-Oss、骨引导膜等方法，创造条件进行人工牙种植。结果 32例病例、48个牙位，除1例植骨行即刻种植2枚种植体失败外，其余均取得满意的种植效果。结论 传统意义上认为不适合种植的牙槽骨骨量不足和颌骨缺损病例，通过创造条件能够取得良好的种植效果。     

SARS感染对妊娠结局及胎、婴儿的影响

目的 观察中晚期妊娠合并严重急性呼吸综合征(severe acute respiratory syndrome，SARS)对妊娠结局及胎要儿的影响。方法 分析6例妊娠合并SARS的临床特征、妊娠结局，检测母儿SARS病毒抗体、RNA，随访要儿情况。结果6例(双胎妊娠2例)SARS患者娩出新生儿7例，其中早产2例，胎儿窘迫3例；1例双胎妊娠之一胎儿死亡，另一胎儿生长受限；新生儿均无窒息、SARS迹象。产妇冠状病毒抗体IgG均阳性，要儿4例阳性、3例阴性；母儿IgM抗体、病毒RNA均阴性。早产儿(3例)体格智能发育稍落后，足月儿(4例)正常。结论 中晚期妊娠合并SARS对围产结局有一定的不良影响，但未发现SARS病毒的垂直传播。     

强化极化液治疗冠心病并心功能不全的疗效观察

目的探索强化极化液治疗冠心病并心功能不全的临床价值。方法观察17例接受强化极化液治疗的冠心病并心功能不全患者的血压、心率、心功能的变化并设对照组。结果治疗组用药前后血压、心率、心功能变化明显(P<0.05或P<0.01)。对照组用药前后血压、心率、心功能变化亦显著(P<0.01或P<0.05)。两组治疗后疗效比较差异显著(P<0.05或P<0.01)。治疗组出现疗效时间为(2.5±0.7)d,对照组(10±2.5)d,治疗组明显短于对照组(P<0.01)。结论强化极化液对冠心病并心功能不全患者有良好的临床治疗效果。     

腭咽环扎术后阻塞性睡眠呼吸暂停低通气综合征上气道形态的研究

目的：探讨腭咽环扎术（VRLP）后阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者的上气道形态特征.方法：应用纤维鼻咽镜和头影测量技术检查了6例VRLP后并发OSAHS患者、6例VRLP后未发生OSAHS和6例未手术腭裂患者的上气道形态,测量了鼻咽腔直径、腭咽环扎处咽腔直径、口咽腔直径、舌根后咽腔直径、下咽腔直径、舌骨至下颌骨的距离等6个相关参数,并应用单因素方差分析进行组间比较.结果：未手术腭裂患者上气道形态光滑,VRLP后上气道在软腭后区和舌根后区出现2处狭窄,VRLP后OSAHS患者上气道鼻咽部明显狭窄变形,为腺样体肥大所致.结论：X线头影测量技术是一种简单实用的评估VRLP后OSAHS的方法,建议VRLP术前行此检查以排除腺样体严重增生患者.     

儿童急性肾功能不全临床分析

目的探讨儿童急性肾功能不全的病因、治疗和预后。方法回顾2002~2005年本院34例儿童急性肾功能不全住院患儿的临床资料,对其发病原因、临床表现、治疗和预后行归纳分析,并作进一步探讨。结果急性肾功能不全34例中男19例,女15例;起病年龄16.0 d~15.5岁。因急性肾功能发病占35.3%。药物引起占29.4%。药物致儿童急性肾功能不全死亡率为20%,转为慢性肾功能不全为30%。结论原发性肾小球疾病是儿童急性肾功能不全的最常见原因,药物致儿童急性肾功能不全预后差,应及早干预原发性肾小球疾病防止慢性化,充分重视肾毒性药物的临床应用。     

经皮肾一步扩张法在结石所致梗阻性肾功能不全中的应用

目的 探讨超声引导下经皮肾一步扩张法在结石性梗阻性肾功能不全中的临床效果.方法 选择我院2009年7月～2011年7月因结石所致上尿路梗阻,合并梗阻性肾积液、肾功能不全患者68例,随机分为一步扩张法( One-step)组和逐步式(Multi- step)组分别行经皮肾穿刺微造瘘引流术,每组各34例.One-step组在超声引导下一步式经皮肾穿刺微造瘘(PCN)直接穿刺引流,Multi-step组采用传统Seldinger法逐级扩张经皮肾通道实施造瘘引流.对比观察两组患者建立经皮肾通道的手术时间、术中出血量、成功率、术后并发症及肾功能的变化情况.结果 One-step组手术时间、扩张次数、术中出血量均少于Multi-step组,差异有显著性(P＜0.05).One-step组一次穿刺置入造瘘管的成功率明显高于Multi-step组,而术后并发症发生率明显低于multi-step组,差异均有显著性(P＜0.05).两组患者术后肾功能明显改善,术后2周尿素氮(BUN)、血肌酐(Cr)与术前相比,差异有显著性(P＜0.05),但术后2周两组间BUN、Cr比较,差异无显著性(P＞0.05).结论 一步扩张法经皮肾穿刺微造瘘操作简便、创伤小、出血量少和并发症少,有助于改善梗阻性肾功能不全.     

Abaloparatide in patients with mild or moderate renal impairment: results from the ACTIVE phase 3 trial

Abstract

Objective: To evaluate, post hoc, the efficacy and safety of abaloparatide by degree of renal impairment.

Methods: ACTIVE was a phase 3, 18-month, randomized, double-blind, active-comparator, placebo-controlled study of postmenopausal women with osteoporosis who received subcutaneous abaloparatide 80?µg, placebo, or open-label teriparatide 20?µg daily. Patients with serum creatinine >2.0?mg/dL or 1.5–2.0?mg/dL with an estimated glomerular filtration rate (eGFR) <37?mL/min, calculated by Cockcroft-Gault formula, were excluded.

Results: At baseline, 660 patients had eGFR ≥90?mL/min, 1276 had 60 to ?90?mL/min, and 527 had <60?mL/min. Older age and lower T-scores were associated with greater renal impairment. Among renal-function subgroups, there were no meaningful changes in bone mineral density, fracture risk reduction, or overall incidence of treatment-emergent adverse events in the active-treatment arms. Anemia, nausea, hypercalcemia, and upper-respiratory-tract infection tended to be more frequent with increasing renal impairment. Hypercalcemia measured by albumin-adjusted serum calcium occurred significantly less frequently with abaloparatide than teriparatide in patients with eGFR <60?mL/min (3.6% versus 10.9%; p?=?.008) and in the overall ACTIVE safety population (3.4% versus 6.4%; p?=?.006). Computed tomography scans in 376 patients revealed no evidence of increased renal calcification.

Conclusion: Increased exposure to abaloparatide and teriparatide in patients with renal impairment led to no meaningful differences in efficacy or safety. These results support the use of abaloparatide without dosage adjustment in patients with renal impairment, provided those with severe renal impairments are monitored for adverse events.     

Association of genetic polymorphisms and autoimmune Addison’s disease

Autoimmune Addison’s disease (AAD) is a complex genetic disease that results from the interaction of a predisposing genetic background with as yet unknown environmental factors. The disease is marked by the appearance of circulating autoantibodies against steroid 21-hydroxylase. Mutations of the autoimmune regulator gene are responsible for the so-called autoimmune polyendocrine syndrome type I (APS I), of which AAD is a major disease component. Among genetic factors for isolated AAD and APS II, a major role is played by HLA class II genes: HLA-DRB1^*0301-DQA1^*0501-DQB1^*0201 and DRB1^*04-DQA1^*0301-DQB1^*0302 are positively, and RB1^*0403 is negatively, associated with a genetic risk for AAD. The MHC class I chain-related gene A allele 5.1 is strongly and positively associated with AAD. Other gene polymorphisms contributing to genetic risk for AAD are MHC2TA, the gene coding for class II transactivator, the master regulator of class II expression, cytotoxic T lymphocyte antigen-4, PTPN22 and the vitamin D receptor.