暂时性骨质疏松症与股骨头坏死继发骨髓水肿临床分析

目的 探讨暂时性骨质疏松症(transient osteoporosis of the hip,TOH)与股骨头坏死继发骨髓水肿在临床症状及影像学上的差异. 方法 对2006年1月-2008年2月收治的5例(5髋)TOH及63例(67髋)股骨头坏死继发骨髓水肿患者分析其病因、发病诱因、疼痛程度、持续时间及病情转归等方面的差异,并分析X线片、MRI和ECT改变的异同点.5例TOH患者,男1例,女4例;年龄29～42岁.63例(67髋)股骨头坏死继发骨髓水肿患者,男53例,女10例:年龄18～70岁;根据ARGO分期标准,Ⅱ期23髋,Ⅲ期43髋,Ⅳ期1髋. 结果 TOH与股骨头坏死继发骨髓水肿患者在发病诱因、疼痛程度、关节积液和ECT改变上无差异.TOH患者发病前无股骨头坏死相关病因;发病前无不适症状;2髋X线片表现为密度降低;MRI水肿信号改变在股骨头颈的上方或整个股骨头;治疗后5～11个月疼痛消失后无残留症状.65髋股骨头坏死继发骨髓水肿患者有股骨头坏死的相关诱因:10髋表现为疼痛加重;59髋X线片上有硬化改变;MRI水肿信号改变在股骨头坏死灶的外侧,水肿信号消退后仍有轻度疼痛. 结论 TOH与股骨头坏死继发骨髓水肿在临床表现、X线片及MRI图像改变上存在差异.     

髋关节一过性骨质疏松症3例临床分析

目的 分析、总结髋关节一过性骨质疏松症(transient osteoporosis of the hip,TOH)的临床特点、影像学特点、诊断及鉴别诊断要点,以提高临床医师对TOH的认识和诊治水平。方法 回顾性分析我院骨科2012年5月至2014年3月诊治的3例 TOH患者的临床资料,包括临床表现、髋部影像学检查、实验室检查、病理学检查等资料,并进行分析、总结。结果 TOH临床特点为主要表现为患髋关节周围疼痛及因疼痛引起的跛行步态,负重时疼痛加重,关节内收、外展及旋转活动轻度受限,MRI 及X光片检查提示异常,3例患者均经MRI检查,1例病理学检查确诊为TOH。结论 熟练掌握TOH的临床特点、影像学特征、诊断及鉴别诊断要点,有助于TOH的早期诊断,可明显减少其误诊、误治率。     

8例髋关节暂时性骨质疏松症的临床诊断与治疗

目的探讨髋关节暂时性骨质疏松症（transient osteoporosis of the hip,TOH）的临床表现、诊断、鉴别诊断、治疗及预后。方法2003年8月至2009年8月治疗8例TOH患者,男2例,女6例;年龄22—43岁,平均34．9岁。患者均为单侧发病,左侧5例,右侧3例。患者的患髋均表现有不同程度的突发急性疼痛或渐进性疼痛,同时伴有显著的跛行。患髋内旋轻度受限是主要的体征。症状出现后3—6周,x线片可见股骨头均匀广泛的骨质疏松,MR表现为弥散且一致的等低T1、长T2异常信号,脂肪抑制序列呈高信号。嘱患者在疼痛可忍受的条件下半负重行走,避免出现骨折等并发症;口服二膦酸盐和钙剂;剧烈疼痛时,可口服非甾体类抗炎药物缓解疼痛。结果临床治疗3个月后疼痛明显减轻,10个月后疼痛完全缓解,复查MR示病变完全消失。结论TOH是一种少见的疾病,无原因出现的髋关节疼痛和跛行是主要症状,X线片和MR可分别看到暂时性的骨质疏松和骨髓水肿。此病具有自限性,保守治疗可获得良好的结果,明确诊断是治疗的关键。     

氧化应激介导绝经后骨质疏松发病机制的研究进展

研究证实氧化应激是绝经后骨质疏松症的重要发病机制。妇女绝经后受衰老和雌激素不足等因素的共同影响,体内氧化应激水平增高,使骨重建失衡,导致骨质疏松发病。其中衰老、雌激素缺乏、Fox O转录因子、Nox亚型与活性氧的产生和骨质疏松发病有着密切的关系。近年来,氧化应激导致骨质疏松发病机制方面的研究日益增多,并取得了一定进展,本文通过查阅国内外相关文献,对氧化应激介导绝经后骨质疏松发病机制的研究进展进行综述,总结了氧化应激导致绝经后骨质疏松发病的相关因素及机制,并结合抗氧化治疗骨质疏松的研究现状和远景提出了思考。     

异位骨化发病机制的研究进展

目的总结异位骨化(heterotopic ossification,HO)发病机制的研究进展。方法查阅近年有关HO危险因素及发病机制的文献,并综合分析。结果 HO发病机制尚未明确,但对HO相关的细胞外因子、信号通路、转录因子等有了更深入了解,如BMP、Smad信号通路、核心结合因子α1/成骨特异性转录因子2等可能参与了HO的形成,而一些相关的微小RNA也有可能参与HO形成。结论通过对HO发病机制进一步研究,为有效防治HO奠定基础。     

糖尿病肾脏疾病的发病机制研究进展

糖尿病肾脏疾病(diabetic kidney disease,DKD)是影响全世界的公共卫生问题,是糖尿病患者发病和死亡的主要原因,也是终末期肾病的主要原因。因其缺乏有效的治疗手段,对其机制的研究一直是临床研究的热点。肾脏血流动力学变化、氧化应激、炎症等都与DKD的发病机制有关,而相关研究指出代谢记忆和表观遗传学对DKD的进展中起着重要的作用,在这篇综述中,将结合目前的最新研究概述DKD发病机制的进展。     

腹主动脉瘤发病机制及药物治疗的研究进展

随着对腹主动脉瘤发病机制研究的不断深入,药物治疗成为研究热点.笔者就近年来该病发病机制及药物治疗的研究进展作一综述,后者主要包括MMPs抑制剂,NSAIDs,NF-kB抑制剂,RAS抑制剂等.     

程序性死亡在急性胰腺炎中的研究进展

目的了解现阶段程序性细胞死亡在急性胰腺炎发病机制中的研究进展,以希望为急性胰腺炎的发病机制及治疗提供参考。方法通过阅读近几年国内外的相关文献,对近年来急性胰腺炎与程序性细胞死亡的研究进展进行综述。结果程序性细胞死亡被定义为由细胞内程序执行的受控细胞死亡,包括凋亡、自噬、程序性坏死和焦亡。胰腺腺泡细胞的死亡模式主要包括细胞凋亡和坏死。虽然急性胰腺炎的发病机制尚未完全明确,但通过对程序性细胞死亡的研究,有助于我们对急性胰腺炎的发病机制和病程转归加深理解,以提供更有效的治疗方法。结论程序性细胞死亡在急性胰腺炎的发病中十分重要,研究程序性细胞死亡在急性胰腺炎中的机制对于急性胰腺炎的治疗、预防等有一定的必要性。     

基于代谢组学的子痫前期的研究进展

代谢组学是利用高通量技术对生物系统内由病理生理变化所产生的代谢物进行定量测量,研究生物体内某一时刻所有内源性小分子物质变化的一种研究方法。近年来,代谢组学在疾病分子标志物的发现、疾病的诊断和预测、发病机制的研究等方面发挥了重要作用。子痫前期(PE)是常见的妊娠期并发症,是围产期死亡和医源性早产的重要原因。目前,该疾病发病机制仍不明确,且缺乏有效的早期预测及诊断手段。本文就代谢组学在PE的分子标志物发现、PE预测及发病机制等方面中的研究进展进行综述。     

急性胰腺炎发病机制研究进展

急性胰腺炎(acute pancreatitis,AP)一直是基础与临床研究的热点与难点,其发病机制至今尚未完全阐明.随着研究的不断深入,除了传统的"胰酶自身消化"学说外,白细胞过度激活-炎性因子级联瀑布效应、胰腺微循环障碍、细胞凋亡、肠道细菌易位、"二次打击"学说等多种理论丰富了人们对AP发病机制的认识.本文就AP发病机制的研究进展作一综述.     

Distinguishing transient osteoporosis of the hip from avascular necrosis.

INTRODUCTION: To review the circumstances surrounding the misdiagnosis of transient osteoporosis of the hip (TOH) as avascular necrosis (AVN) and to increase physician awareness of the prevalence and diagnosis of this condition in young men, we reviewed a series of cases seen in the orthopedic unit at St. Michael's Hospital, University of Toronto. METHODS: We studied the charts of patients with TOH referred between 1998 and 2001 with a diagnosis of AVN for demographic data, risk factors, imaging results and outcomes. RESULTS: Twelve hips in 10 young men (mean age 41 yr, range from 32-55 yr) were identified. Nine men underwent magnetic resonance imaging (MRI) before referral, which showed characteristic changes of TOH. All 10 patients were referred for surgical intervention for a diagnosis of AVN. The correct diagnosis was made after reviewing patients' charts and the scans and was confirmed by spontaneous resolution of both symptoms and MRI findings an average of 5.5 months and 7.5 months, respectively, after consultation. CONCLUSIONS: Despite recent publications, the prevalence of TOH among young men is still overlooked and the distinctive MRI appearance still misinterpreted. Symptoms may be severe but resolve over time with reduced weight bearing. The absence of focal changes on MRI is highly suggestive of a transient lesion. A greater level of awareness of this condition is needed to differentiate TOH from AVN, avoiding unnecessary surgery and ensuring appropriate treatment.     

Transient osteoporosis of the hip: A case report

We report a case of transient osteoporosis of the hip (TOH) in a 59-year-old man including the clinical presentation, diagnostic studies, management and clinical progress. TOH is a rare self-limiting condition that typically affects middle-aged men or, less frequently, women in the third trimester of pregnancy. Affected individuals present clinically with acute hip pain, limping gait, and limited ranges of hip motion. TOH may begin spontaneously or after a minor trauma. Radiographs are typically unremarkable but MR imaging studies yield findings consistent with bone marrow edema. TOH is referred to as regional migratory osteoporosis if it travels to other joints or the contralateral hip. TOH often resembles osteonecrosis but the two conditions must be differentiated due to different prognoses and management approaches. The term TOH is often used interchangeably and synonymously with transient bone marrow edema.     

Review of past research and current concepts on the etiology of moyamoya disease

Research on moyamoya disease has progressed remarkably in the past several decades. Indeed, many new facts concerning the epidemiology of the disease have been revealed and surgical treatments have been drastically improved. However, despite extensive research, the mechanism of moyamoya disease is still unknown. Consequently, the cardinal treatment of this disease has not yet been developed. For further clarification of its etiology, innovative studies are therefore indispensable. The aim of this paper is to review research on the pathogenesis of moyamoya disease to identify milestones in the direction of its true solution. Many hypotheses of the pathogenesis of moyamoya disease have been proposed in the past half century, including infection (viral and bacterial), autoimmune disorders, proteins abnormality, and gene abnormality. Some of these are now considered to be historical achievements. Others, however, can be still subjected to contemporary research. Currently, several genetic abnormalities are considered to offer the most probable hypothesis. In addition, interesting papers have been presented on the role of the endothelial progenitor cell on the pathogenesis of moyamoya disease. Intuitively, however, it appears that a single theory cannot always explain the pathogenesis of this disease adequately. In other words, the complex mechanism of several factors may comprehensively explain the formation of moyamoya disease. The "double hit hypothesis" is probably the best explanation for the complicated pathology and epidemiology of this disease.     

Tyrosine hydroxylase activity in sympathetic nervous system of rats with streptozocin-induced diabetes

The activity of tyrosine hydroxylase (TOH), the rate-limiting enzyme in norepinephrine biosynthesis, was measured in selected sympathetic ganglia to develop a quantitative measure of sympathetic autonomic neuropathy in streptozocin-induced diabetic rats. Surprisingly, TOH activity was elevated twofold in diabetic prevertebral ganglia innervating the alimentary tract (i.e., superior mesenteric, celiac, and inferior mesenteric), which has terminal processes that develop neuroaxonal dystrophy in this model system. TOH activity of paravertebral ganglia (i.e., superior cervical and stellate) with nonalimentary targets was not increased in the same animals. Increased TOH activity in the prevertebral ganglia 1) developed within the 1st wk of diabetes and persisted for 10 mo, 2) did not represent a change in TOH affinity for d-1,6-methyl-5,6,7,8- tetrahydropterine cofactor, 3) was prevented by both nicotinamide pretreatment and early institution of insulin therapy, and 4) did not develop as a result of classical transsynaptic induction. Pair-feeding experiments confirmed that the most likely cause of increased TOH activity in this system was the marked hypertrophy and hyperplasia of the diabetic bowel resulting from compensatory hyperphagia. We conclude that TOH activity does not represent a suitable marker for sympathetic autonomic neuropathy in this experimental system. Rather, the increase appears to be an example of a selective increase in the synthesis of neurotransmitter enzymes, possibly in response to increased trophic support provided by the expanded target, i.e., the hypertrophic gut. The additional synthetic stress imposed on prevertebral neurons by the expansion of the innervation of the alimentary target coupled with the complex diabetic metabolic milieu may contribute to the development and selective distribution of dystrophic axonopathy to the innervation of the alimentary tract.     

Transanal hemorrhoidopexy: Why it makes sense

AimTransanal open hemorrhoidopexy (TOH) was developed as an alternative to stapled hemorrhoidopexy and THD/mucopexy. The aim of this article is to review the technical aspect and results of this technique.MethodsA single coloproctology center experience with this technique was reviewed retrospectively. All consecutive patients who underwent TOH were analyzed. Short and long-term results are reported. TOH involves placing a Z-suture in the low rectum above the hemorrhoidal cushions and excising a 1 centimeter strip of rectal mucosa between the upper and lower aspects of the suture. Tightening of the suture provides an effective upward life of the hemorrhoidal bundle. The procedure is performed in 3 or 4 quadrants of the anal canal (as needed) at the point of maximal prolapse.ResultsFrom 2006 until 2013, 217 patients with 2nd and 3rd degree internal hemorrhoids were operated. Short-term complications included major bleeding in 5 patients (2%) and severe pain in 19 patients (9%). Long-term follow-up was obtained in 169 of 217 patients (78%) either through clinic visits or phone interview. Available patients were followed up for a minimum period of 60 months after TOH (median 113 months). 109 patients (64%) were symptom free and 147 patients (87%) indicated that they would consent to TOH again.ConclusionsTOH is a safe operation for hemorrhoidal prolapse with encouraging short and long-term results. It is a safe and inexpensive alternative to stapled hemorrhoidopexy or THD/mucopexy and it should be included in the treatment algorithm of patients with symptomatic hemorrhoidal prolapse.     

Radiological morphology variances of transient osteoporosis of the hip

Background

Although several morphological abnormalities or variances of the hip joint have been proposed to be associated with hip joint degeneration, few studies have investigated any radiological features in patients with transient osteoporosis of the hip (TOH). The purpose of this study is to evaluate the morphological variances of the hip joint in TOH patients radiographically.

肠道菌群在HIV相关骨质疏松症中的影响

HIV/AIDS患者在HIV、ART、免疫功能改变等多种因素影响下,常导致骨骼、心血管、消化等系统疾病,骨质疏松症是其常见并发症之一,目前发病机制尚不完全明晰。随着对肠道微生态的不断深入研究,肠道菌群的失调被认为是骨质疏松症的发病机制之一。因此,本文拟对HIV/AIDS患者肠道菌群及肠道菌群失调致骨质疏松的发病机制相关研究进展进行概述,以期能为HIV相关骨质疏松症的治疗和预防提供新思路。     

类风湿关节炎骨破坏作用机制及中医药治疗研究进展

类风湿关节炎(RA)是一种累及多个关节的全身性自身免疫性疾病,常累及小关节,病变呈对称性、侵袭性和致残性,发病后期常易造成不可逆转的软骨、骨和其他邻近组织的破坏,最终导致严重的关节畸形甚至残疾,给患者及其家庭造成严重的身体和心理损害,严重影响生活质量。迄今为止,虽然治疗RA的药物很多,但RA仍然无法完全得到彻底根治,究其原因在于RA及其骨破坏的发病机制仍未完全明确。因此,对于RA骨破坏的发病机制及如何治疗显得格外重要。RA骨破坏的发病机制总的来说是成骨细胞与破骨细胞之间的失衡导致的,本文通过整理近年来参与RA关节软骨破坏及骨侵蚀病程的相关研究文献进行综述和讨论,分别从细胞因子/趋化因子、非编码RNA、信号通路等三个不同方面阐述了对成骨细胞与破骨细胞之间的作用造成RA骨破坏的发病机制,以期为RA骨破坏发病机制研究提供新的思路。中医药在预防RA骨破坏的发病过程中起着重要的作用,在保证疗效的前提下还能保证其安全性。因此,对于RA骨破坏的发病机制进行深入地研究及研究中医药在其治疗中的作用,为其治疗能够提供新的研究思路。     

Current progress in metabolomics of gestational diabetes mellitus

Gestational diabetes mellitus (GDM) is one of the most common metabolic disorders of pregnancy and can cause short- and long-term adverse effects in both pregnant women and their offspring. However, the etiology and pathogenesis of GDM are still unclear. As a metabolic disease, GDM is well suited to metabolomics study, which can monitor the changes in small molecular metabolites induced by maternal stimuli or perturbations in real time. The application of metabolomics in GDM can be used to discover diagnostic biomarkers, evaluate the prognosis of the disease, guide the application of diet or drugs, evaluate the curative effect, and explore the mechanism. This review provides comprehensive documentation of metabolomics research methods and techniques as well as the current progress in GDM research. We anticipate that the review will contribute to identifying gaps in the current knowledge or metabolomics technology, provide evidence-based information, and inform future research directions in GDM.