痛风患者要护好肾

<正>痛风的罪魁祸首为嘌呤及尿酸代谢障碍,表现为高尿酸血症、反复发作的急性关节炎、痛风石和痛风石引起的慢性关节炎。而长期高尿酸血症导致的肾脏损害远远没有引起痛风患者的重视,因此导致的尿毒症正在逐年增加。痛风肾损害主要表现为痛风性肾病、急慢性肾功能衰竭和尿路结石。其发生主要是由于尿酸盐结晶在肾脏沉积,并引起炎症反应,或尿酸结晶沉积引起尿路阻塞。痛风性肾病的临床表现可有尿酸结石、小分子蛋白尿、水肿、夜尿、高血压、     

痛风的药物防治

痛风是嘌呤代谢紊乱或尿酸排泄减少引起的一种临床综合征。其特点为高尿酸血症、特征性急性关节炎反复发作、痛风石沉积、痛风石性慢性关节炎，且常累及肾脏［1］。关节滑液尿酸盐晶体的检出或痛风石的出现为确诊的依据。随着饮食结构和环境因素的改变、经济的发展及人类寿命的延长，痛风的发病率日益增高，成为当今世界尤其是中老年男性的常见病［2，3］。临床治疗痛风需要达到两个目的：及时控制痛风性关节炎的急性发作；长期治疗高尿酸血症，预防尿酸盐沉积及痛风急性复发，促进痛风石的吸收［4］。下面简述痛风的防治。1急性痛风性关节…     

原发性痛风的发病机制和治疗进展

<正>痛风是一组异质性疾病,其临床特点是高尿酸血症及尿酸盐结晶沉积所致的痛风性关节炎、痛风石及肾脏损害。在排除其他疾病的基础上,由先天遗传因素所致尿酸生成增加和(或)尿酸排泄减少所致的痛风,称为原发性痛风。国内外大量流行病学资料     

海军某驻岛部队官兵血尿酸检测结果分析

<正>近年来,随着生活水平的提高和饮食结构的改变,高尿酸血症和痛风的患病率越来越高。高尿酸血症是痛风的重要生化基础,高尿酸血症可能进展为痛风,引起反复发作的急性痛风性关节炎、慢性痛风性关节炎、痛风石、尿酸结石、尿酸性肾病等[1]。目前,在我国尤其沿海地区,高尿酸血症患病情况尤为严重,已严重影响公众健康和部队战斗力。海军驻岛部队地处沿海地区,其高尿酸血症防治工作逐渐受到部队各级领导重视,但高尿酸血症在驻岛部队的发病情况目前尚     

中西医结合治疗痛风46例

痛风是一组因嘌呤代谢紊乱所致的慢性代谢性疾病,主要临床特点为体内尿酸产生过多或肾脏排泄减少,引起血中尿酸升高形成高尿酸血症及反复发作的痛风性急性关节炎伴痛风石沉积,痛风性慢     

无症状高尿酸血症与急性痛风性关节炎超声特征比较

<正>痛风是一种代谢异常性疾病,普通人发病率为0.2%~0.35%[1]。该病是由于嘌呤代谢紊乱,尿酸生成过度或排泄不良,使血液中尿酸浓度增高。未发作痛风的高尿酸血症称为无症状高尿酸血症,其中5%~12%的无症状高尿酸血症发展为痛风。无症状高尿酸血症和急性痛风性关节炎均不宜进行关节滑液穿刺确诊,以至于一部分患者病情延误甚至误诊。本研究旨在分析痛风性关节炎不同时期的超声表现,为临床     

中西医结合治疗痛风29例分析

痛风性关节炎是由于"嘌呤"代谢紊乱引起高尿酸血症、尿酸盐在关节腔或软组织沉积而致关节红肿疼痛,活动受限,反复发作可使关节变形、功能障碍的一类疾病[1]。一旦发病,给患者带来很大的痛苦。该病急性发作期用西药     

高尿酸血症与痛风的临床治疗分析

目的探讨高尿酸血症与痛风的临床治疗。方法对40例高尿酸血症与痛风患者临床治疗方法资料进行分析。结果 40例高尿酸血症与痛风患者经治疗,治愈18例,好转18例,无效4例,总有效率90.0%。结论防止高尿酸血症尿酸盐沉积的控制;迅速停止急性关节炎的发作,防止尿酸结石的形成和对肾功能损害。     

痛风的治疗现状及预防原则

痛风以嘌呤代谢紊乱,尿酸排泄失常所致血尿酸增高,并伴有结缔组织内尿酸钠结晶沉着为特征的疾病。临床上表现为高尿酸血症、痛风性急性关节炎反复发作、痛风石沉积、特征性慢性关节炎和关节炎畸形,常累及肾脏引起慢性间质性肾炎和肾尿酸结石形成,并可出现关节致残及肾功能不全。急性痛风性关节炎是痛风最常见的首发症状。随着人们生活水平的提高及饮食结构的改变,     

痛风的药物治疗

<正>痛风(gout)是嘌呤代谢紊乱及(或)尿酸排泄减少,导致尿酸盐晶体沉积所引起的一种常见疾病。临床特点为高尿酸血症(hyperuricemia)、反复发作的急性特征性关节炎、痛风石(tophi)形成及痛风石性慢性关节炎,并发生慢性尿酸盐肾     

MicroRNA and long noncoding RNA involvement in gout and prospects for treatment

MicroRNAs (miRNAs) and long noncoding RNAs (lncRNAs) are both types of noncoding RNA. They have been demonstrated to be involved in the regulation of various human inflammatory diseases and can be used as biomarkers for disease diagnosis and prognosis, and even be developed into new drugs. Gout is an arthritic disease caused by the deposition of monosodium urate crystal (MSU) in the joints, which can lead to acute inflammation and damage adjacent tissue. Recent studies have shown that miRNAs and lncRNAs mediate the progress of gout. Based on the pathogenesis of gout, including hyperuricemia, MSU deposition, acute gouty arthritis and gouty bone erosion, this paper reviewed the role of miRNAs and lncRNAs in the processes and the possible therapeutic targets of miRNAs and lncRNAs in gout.     

Gouty Arthritis: A Review of Acute Management and Prevention

Gouty arthritis is one of the most common rheumatic diseases. The clinical burden of gouty arthritis has historically been well recognized; however, gout is often misdiagnosed and mismanaged. The prevalence of gout is rising and is likely attributed to several factors including increased incidence of comorbidities, lifestyle factors, and increased use of causative medications. With the increasing prevalence, there have been several innovations and evidence‐based updates related to the diagnosis and management of gout. Acute gouty arthritis should be treated with nonsteroidal antiinflammatory drugs (NSAIDs), colchicine, or corticosteroids, or a combination of two agents. Xanthine oxidase inhibitor therapy remains the consensus first‐line treatment option for the prevention of recurrent gout. Add‐on therapies that reduce serum urate concentration include traditional uricosuric agents and a novel uric acid reabsorption inhibitor. Prophylaxis of acute gout with NSAIDs, colchicine, or corticosteroids is universally recommended when initiating any urate‐lowering therapy in order to prevent acute gouty arthritis for a period of at least 6 months. In this review, we discuss the epidemiology and risk factors for gouty arthritis and evaluate diagnostic strategies and therapeutic regimens for the management of gout, including a new drug approval.     

Management of acute and chronic gouty arthritis: present state-of-the-art

There are three stages in the management of gout: (i) treating the acute attack; (ii) lowering excess stores of uric acid to prevent flares of gouty arthritis and to prevent tissue deposition of urate; and (iii) providing prophylaxis to prevent acute flares. It is important to distinguish between therapy to reduce acute inflammation in acute gout and therapy to manage hyperuricaemia in patients with chronic gouty arthritis.During the acute gouty attack nonpharmacological treatments such as topical ice and rest of the inflamed joint are useful. NSAIDs are the preferred treatment in acute gout. The most important determinant of therapeutic success is not which NSAID is chosen, but rather how soon NSAID therapy is initiated. Other treatments include oral and intravenous colchicine, intra-articular and systemic corticosteroids, and intramuscular corticotropin.Optimal treatment of chronic gout requires long-standing reduction in serum uric acid. The urate-lowering drugs used to treat chronic gout are the uricosuric drugs, the uricostatic drugs, which are xanthine oxidase inhibitors, and the uricolytic drugs. Xanthine oxidase inhibitors such as allopurinol, oxipurinol and febuxastat should be used as first-line treatment in patients with renal calculi, renal insufficiency, concomitant diuretic therapy and ciclosporin (cyclosporine) therapy, and urate overproduction. Uricosuric drugs include probenecid, benzbromarone, micronised fenofibrate and losartan. They are the urate-lowering drugs of choice in allopurinol-allergic patients and underexcretors with normal renal function and no history of urolithiasis. The use of recombinant urate oxidase in patients with chronic gout is limited by the need for parenteral administration, the potential antigenicity and production of anti-urate oxidase antibodies, and declining efficacy.The effectiveness of colchicine prophylaxis as an isolated therapy is still to be confirmed by placebo-controlled trials. Another issue is prophylaxis with NSAIDs. There are no comparative studies with colchicine.     

Overview of hyperuricaemia and gout

In most mammals purine degradation ultimately leads to the formation of allantoin. Humans lack the enzyme uricase, which catalyzes the conversion of uric acid to allantoin. The resulting higher level of uric acid has been hypothesized to play a role as an antioxidant. Hyperuricaemia is usually an asymptomatic condition which is hypothesized to play a role in cardiovascular disease and hypertension. Some hyperuricaemic individuals develop gout, an inflammatory arthritis caused by the deposition of monosodium urate crystals in joints. Over time, acute intermittent gouty arthritis can develop into a chronic condition with deposits of monosodium urate (MSU) crystals in joints and as tophi. The mechanisms by which MSU crystals lead to an acute inflammatory arthritis are under investigation and current knowledge is reviewed here. Treatment of gout includes management of acute flares with anti-inflammatory medications such as non-steroidal anti-inflammatory drugs or corticosteroids and long term management with urate-lowering therapy when indicated. Future directions in the treatment of gout, in part guided by a better understanding of pathophysiology, are discussed.     

中药复方治疗湿热型痛风性关节炎临床及作用机制研究进展

痛风性关节炎是嘌呤长期代谢障碍引起的一种临床常见疾病,湿热证是其主要证型。研究发现,中药复方对于湿热型痛风性关节炎具有较好的疗效,能有效地改善患者的炎症反应,降低血尿酸水平,并对肝肾功能影响较小。因此笔者就近5年来中药复方治疗湿热型痛风性关节炎的临床研究及相关作用机制进行综述,旨在为今后中药复方治疗湿热型痛风性关节炎提供指导及思路,并为临床治疗湿热型痛风性关节炎提供用方,提高对湿热型痛风性关节炎的防治率。     

四妙散加味治疗急性痛风性关节炎64例观察

目的:探讨四妙散加味治疗急性痛风性关节炎的临床疗效。方法:选取64例符合痛风性关节炎诊断标准的病例,运用四妙散加姜黄、赤芍等治疗,观察其治疗急性痛风性关节炎的临床疗效及血尿酸变化,并探讨其安全性。结果:四妙散加味治疗急性痛风性关节炎疗效确切,可降低尿酸,且安全性可靠。     

原发性痛风的诊治进展

原发性痛风是一种常见的代谢性疾病,随着饮食结构等生活方式的改变,发病率有逐年升高趋势。根据痛风的不同临床表现,可分为不同的疾病时期或阶段,而不同阶段痛风的治疗方法不同。痛风的治疗原则为控制急性痛风性关节炎、预防急性发作、纠正高尿酸血症、治疗慢性并发症。目前痛风的治疗仍存在一定的误区,需规范化。     

Pharmacologic inducers of the uric acid exporter ABCG2 as potential drugs for treatment of gouty arthritis

Uric acid is the end product of purine catabolism and its plasma levels are maintained below its maximum solubility in water(6–7 mg/dl).The plasma levels are tightly regulated as the balance between the rate of production and the rate of excretion,the latter occurring in urine(kidney),bile(liver)and feces(intestinal tract).Reabsorption in kidney is also an important component of this process.Both excretion and reabsorption are mediated by specific transporters.Disruption of the balance between production and excretion leads to hyperuricemia,which increases the risk of uric acid crystallization as monosodium urate with subsequent deposition of the crystals in joints causing gouty arthritis.Loss-of-function mutations in the transporters that mediate uric acid excretion are associated with gout.The ATP-Binding Cassette exporter ABCG2 is important in uric acid excretion at all three sites:kidney(urine),liver(bile),and intestine(feces).Mutations in this transporter cause gout and these mutations occur at significant prevalence in general population.However,mutations that are most prevalent result only in partial loss of transport function.Therefore,if the expression of these partially defective transporters could be induced,the increased number of the transporter molecules would compensate for the mutation-associated decrease in transport function and hence increase uric acid excretion.As such,pharmacologic agents with ability to induce the expression of ABCG2 represent potentially a novel class of drugs for treatment of gouty arthritis.     

药源性高尿酸血症的致病药物及防治对策

高尿酸血症是由嘌呤代谢紊乱所致的疾病,易诱发痛风从而引起急性痛风性关节炎反复发作、痛风石沉积及痛风石性慢性关节炎和关节畸形,还容易累及肾脏及心血管系统,严重影响患者的生活质量。药物是引起血尿酸升高的重要原因之一,本文对引起药源性高尿酸血症的常见药物进行综述,为临床用药安全提供参考,并简要介绍其防治对策。     

1例心力衰竭伴痛风发作患者的药物分析及文献回顾

摘 要 目的：探索心力衰竭伴利尿药诱发痛风性关节炎患者的合理用药原则。方法: 临床药师通过参与1例心力衰竭应用呋塞米诱发痛风性关节炎患者的诊疗和药物分析调整,充分考虑到患者疾病症状及可能诱导痛风发作的药物,建议停用相关药物,并调整治疗药物。结果: 临床药师考虑该患者自身特点,调整了合理治疗方案,医师采纳建议后,患者痛风症状缓解,心力衰竭得到控制,病情改善。结论:心力衰竭合并痛风史的患者应用利尿药,极易诱发痛风,建议小剂量使用对血尿酸水平影响相对较少的利尿药。临床药师通过参与临床治疗,发挥药师的专业优势,优化用药方案,可降低患者发生不良反应风险,促进患者安全合理用药。