痛风患者肾脏结石与关节部位尿酸盐晶体沉积的相关性

目的:探讨痛风患者关节部位尿酸盐结晶沉积与肾脏结石形成的相关性。方法:回顾分析复旦大学附属中山医院门诊痛风患者(n=190)的肾脏超声检查结果及急性痛风性关节发作部位双源CT结果。采用卡方检验及Spearman相关分析明确双源CT上显示的尿酸盐结晶沉积部位、尿酸盐结晶大小与肾脏结石形成的关系。结果:肾脏超声显示无肾脏结石患者139例(73.2%),肾脏结石患者51例(26.8%)。双源CT检查部位分为双足、踝关节152例,双膝关节24例,双手、腕关节14例。其中,155例双源CT发现有尿酸盐结晶沉积,35例双源CT未见尿酸盐晶体沉积。以超声检查是否存在肾脏结石将患者分为肾脏结石组和无肾脏结石组。两组患者在尿酸盐沉积部位及体积上差异无统计学意义。结论:痛风患者肾脏结石的形成与关节尿酸盐沉积无明显相关性。     

痛风患者行外科治疗的护理

痛风是一种嘌呤代谢障碍性疾病,其特点为高尿酸血症.尿酸盐结晶沉积在关节周围、皮下或软骨下形成硬结,称为痛风石或痛风结节~([1]),因尿酸盐有抑菌作用,一般情况下很少发生继发感染~([2]).     

基于DECT分析高尿酸血症患者尿酸盐结晶的相关因素

目的:探讨高尿酸血症患者尿酸盐结晶的相关因素。方法:选择328例高尿酸血症患者作为研究对象,均行双侧足踝部DECT扫描,收集患者的临床资料、完善相关实验室检查,记录尿酸盐结晶分布情况,根据DECT检测有无尿酸盐结晶将所有研究对象分为两组,即无尿酸盐结晶的高尿酸血症组和有尿酸盐结晶的高尿酸血症组,分析两组尿酸盐结晶情况、一般人口统计学资料、生化指标以及发生尿酸盐结晶的风险因素。结果:328例高尿酸血症患者检出尿酸盐结晶者185例,215例伴发痛风。DECT检查发现有尿酸盐结晶组伴痛风发生率(93.0%)远高于无尿酸盐结晶组(30.1%),P<0.05。有尿酸盐结晶组患者BMI、高血压、高脂血症、伴发痛风率均高于无尿酸盐结晶组(P<0.05)。有尿酸盐结晶组的生化指标中SUA、TC及Scr水平均高于无尿酸盐结晶组(P<0.05),HDL-C水平低于无尿酸盐结晶组(P<0.05)。Logistics回归分析显示痛风、体重指数、高血压、高脂血症为高尿酸血症患者尿酸盐结晶的危险因素。结论:DECT可检测高尿酸血症患者尿酸盐结晶情况,提示临床对出现尿酸盐结晶的患者及早干预。对于肥胖、伴有高血压、高脂血症的高尿酸血症患者,需临床积极干预相关因素,有望使高尿酸血症患者止步于尿酸盐结晶形成之前。     

痛风结节破溃后的临床护理

痛风是一种嘌呤代谢障碍性疾病,其特点为高尿酸血症。尿酸盐结晶沉积在关节周围、皮下或软骨下形成硬结,称为痛风石或痛风结节。任何部位的痛风结节都有可能自行破溃,痛风石越大则破溃的可能性也越大,痛风石经皮破溃排出白色尿酸盐结晶,瘘管不易愈合,而且易发生细菌感染。再加上有些患者由于长期自服类固醇激素治疗,会出现继发性糖尿病,使痛风结节破溃后的皮肤愈合难度更大,给护理工作带来很大的挑战。我院近5年来接收18例痛风结节破溃的患者,经积极治疗和精心护理收到满意效果,现报告如下。     

浅谈痛风性关节炎的辩证治疗

痛风是一种嘌呤代谢紊乱的遗传性疾病，以血尿酸增高为特点，而痛风性关节炎是以尿酸盐沉积在关节囊、滑囊软骨、骨者及其他组织中，引起相应的病损及炎性反应。由于病人不合理膳食，如摄入过量蛋白质，因此，痛风患者明显增多，发病率逐年增高。     

双源CT双能量成像对痛风结晶诊断的临床应用价值

选取痛风患者38例为观察组,另选取同期非痛风患者25例为对照组,所有患者均接受双源CT双能量成像扫描,观察和对比两组患者的诊断结果。结果对照组患者未检测出尿酸盐沉积;观察组患者中,33例患者的双足踝关节检查出尿酸盐沉积,21例患者的双手腕检测出尿酸盐沉积,12例患者的双膝检测出尿酸盐沉积。在痛风患者的诊断过程中,采用双源CT双能量成像的诊断方式能够有效检测出尿酸盐沉积,且操作简单,可以作为痛风病的主要筛查手段,值得推广应用。     

章祖林治疗急性痛风性关节炎经验

<正>痛风是嘌呤代谢紊乱或尿酸排泄减少而致血尿酸水平升高,尿酸盐晶体沉积于组织或器官并引起组织损伤的一组临床综合征,主要表现为关节的红肿热痛,反复发作,后期常出现痛风石、间质性肾炎甚至关节畸形及功能障碍、尿酸性尿路结石等。西医治疗急性痛风性关节炎常采用多种药物联合运用,如给予秋水仙碱、非甾体抗炎药或糖皮质激素治疗,但易出现肝肾功能损伤、骨髓抑制、消化道不良反应、血糖升高、骨质疏松等副反应,患者耐受性低,     

痛风的诊治现状及进展

高尿酸血症是血尿酸水平增高。痛风是尿酸盐结晶在体内沉积引起组织损伤的一种代谢性疾病。随着各国经济的发展,全球的高尿酸血症及痛风的患病率呈上升趋势,因此相关研究日益增多,本文就近年来有关痛风的现状及进展作一综述。     

1例痛风伴腹部及四肢痛风结节化脓感染患者的护理

痛风是一种嘌呤代谢障碍性疾病，其特点为高尿酸血症。尿酸盐结晶沉积在关节周围、皮下或软骨下形成硬结．称为痛风石或痛风结节。因尿酸盐有抑制细菌作用，一般情况下很少发生继发感染。2004年5月我科收治1例罕见的痛风伴腹部及四肢痛风结节化脓感染的患，该患病种多、病情复杂，治疗难度大。经过78d的积极治疗和精心护理，皮肤破溃处全部愈合。报道如下。     

痛风病针灸治疗近况

痛风[1]是嘌呤代谢紊乱及/或尿酸排泄减少所引起的一种晶体性关节炎,临床表现为高尿酸血症和尿酸盐结晶沉积所致的特征性急性关节炎、痛风石形成、痛风性慢性关节炎,并可发生尿酸盐肾病、尿酸性尿路结石等,严重者可出现关节致残、肾功不全。其分为原发性和继发性两大类。原发性     

Gout: an update

Arthritis caused by gout (i.e., gouty arthritis) accounts for millions of outpatient visits annually, and the prevalence is increasing. Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is elevated serum uric acid levels (i.e., hyperuricemia). Asymptomatic hyperuricemia is common and usually does not progress to clinical gout. Acute gout most often presents as attacks of pain, erythema, and swelling of one or a few joints in the lower extremities. The diagnosis is confirmed if monosodium urate crystals are present in synovial fluid. First-line therapy for acute gout is nonsteroidal anti-inflammatory drugs or corticosteroids, depending on comorbidities; colchicine is second-line therapy. After the first gout attack, modifiable risk factors (e.g., high-purine diet, alcohol use, obesity, diuretic therapy) should be addressed. Urate-lowering therapy for gout is initiated after multiple attacks or after the development of tophi or urate nephrolithiasis. Allopurinol is the most common therapy for chronic gout. Uricosuric agents are alternative therapies in patients with preserved renal function and no history of nephrolithiasis. During urate-lowering therapy, the dose should be titrated upward until the serum uric acid level is less than 6 mg per dL (355 micromol per L). When initiating urate-lowering therapy, concurrent prophylactic therapy with low-dose colchicine for three to six months may reduce flare-ups.     

双能量CT对急性痛风结晶的评估及相关因素分析

目的:采用单源双能量CT(dual energy CT,DECT)处理技术测定痛风性关节炎患者急性发作时的尿酸盐结晶沉积量多少,评估其临床诊断价值,探讨尿酸盐结晶及相关影响因素.方法:选取2018年1月—2020年12月在高新区人民医院因急性痛风性关节炎住院的116例拟诊患者的病例资料并进行分析.所有患者均接受关节DE...     

Evaluation and Treatment of Gout as a Chronic Disease

Gout is a disease caused by deposition of monosodium urate crystals in tissues. One of the limitations for successful treatment of gout is to consider it as an intermittent disease rather than a chronic inflammatory disease which, if improperly treated, leads to chronic clinical manifestations. In addition, gout is linked to increased cardiovascular morbidity and mortality. Urate-lowering therapy comprises both nonpharmacologic and pharmacologic interventions, but most patients will need uratelowering drugs to achieve target therapeutic serum urate levels. Reaching target serum urate levels is associated with improvement in clinical outcomes, including a reduction of acute inflammation episodes, resolution of tophi, and improvement in health-related quality of life perception. A number of urate-lowering drugs are available but a number of patients fail to achieve or maintain therapeutic serum urate levels and go on to develop refractory chronic gout. For such patients, efforts have been made to develop new treatments (e.g., febuxostat or pegloticase). This review intends to increase the awareness of gout as a chronic deposition disease, and show that efforts should be made to properly control serum urate levels in order to achieve complete disappearance of urate crystal deposition.     

Diagnosis and management of gout

Gout is a disease resulting from the deposition of urate crystals caused by the overproduction or underexcretion of uric acid. The disease is often, but not always, associated with elevated serum uric acid levels. Clinical manifestations include acute and chronic arthritis, tophi, interstitial renal disease and uric acid nephrolithiasis. The diagnosis is based on the identification of uric acid crystals in joints, tissues or body fluids. Treatment goals include termination of the acute attack, prevention of recurrent attacks and prevention of complications associated with the deposition of urate crystals in tissues. Pharmacologic management remains the mainstay of treatment. Acute attacks may be terminated with the use of nonsteroidal anti-inflammatory agents, colchicine or intra-articular injections of corticosteroids. Probenecid, sulfinpyrazone and allopurinol can be used to prevent recurrent attacks. Obesity, alcohol intake and certain foods and medications can contribute to hyperuricemia. These potentially exacerbating factors should be identified and modified.     

Hyperuricemia and gout

Gout is a clinical syndrome encompassing a group of metabolic diseases that are all characterized by abnormal uric acid metabolism. In its fullest form, gout is defined by: an increase in the serum urate concentration; characteristic, recurrent, acute arthritic attacks, with monosodium urate monohydrate crystals demonstrable in synovial fluid leukocytes; tophi, usually in and around joints of the extremities, composed of monosodium urate monohydrate deposits; renal disease, often accompanied by hypertension with glomerular, tubular, interstitial, and vascular involvement; and uric acid nephrolithiasis. Any combination of these manifestations may occur, although tophi and urate nephropathy rarely antedate gouty arthritis.     

Self-Help Devices: Communication and Vocations

Increased understanding of the pathogenesis of acute gout has developed in the past few years. Investigators have indicated that an attack is precipitated by (1) deposition of sodium urate crystals, (2) development of an inflammatory reaction against these crystals, and (3) propagation of the inflammatory response by addition of more crystals to inflamed area.

The nature of the inborn metabolic errors of primary gout is still obscure. Studies point to a dual cause of the hyperuricemia. Until more evidence is accumulated, it seems useful to separate patients into two categories: those with overproduction and those with normal production of uric acid.     

Urolithiasis and nephropathy complicated with gout

Urolithiasis is a clinically important complication of gout. For effective prevention of this complication, it is necessary to comprehend the factors known to be important in its development. Our analysis of stones in gout patients revealed that the incidence of common calcium salt stones was over 60%, while that of uric acid stones was only about 30%. This implies that the disruption of uric acid metabolism promotes not only uric acid stones but also calcium salt stones. Twenty-four per cent of gout patients showed acidic urine throughout the day. Urinary management, which consists of hydration and alkalization of urine, is indispensable along with control of the serum urate level in the treatment of gout.     

How to Recognize and Treat Gout

The two unequivocal diagnostic criteria for gout are urate crystals in synovial fluid during an acute attack and subcutaneous or bony tophi. A serum uric acid level higher than 7.0 mg per 100 ml during acute joint pain also suggests gout. Colchicine is still a good agent for acute attacks, but phenylbutazone, indomethacin and ACTH also have a place. Probenecid alone or with colchicine is effective for long-term therapy.     

Assessment and management of gouty arthritis

Gout is a metabolic disorder of purine metabolism that leads to elevated serum concentrations of uric acid. When this happens, urate crystals may precipitate and accumulate in the joints and bursae. Gout is characterized by recurrent, painful attacks of arthritis, which is the major clinical complication of the disease. Early diagnosis and treatment of gout are important to prevent complications, and with early, sustained therapy, most patients can live without functional disability. If gout becomes chronic, individuals may experience severe limitations of activity. This article discusses the clinical manifestations, diagnosis and treatment of acute and chronic gout.