血尿酸检测对痛风诊断的评价

目的:探讨痛风患者及其它疾病患者血清尿酸(UA)浓度的变化,为临床诊断提供依据。方法:用尿酸酶一过氧化物偶联法(URO-PAP)法分别对痛风、风湿性关节炎及溶血性贫血等患者128例,健康体检100例,进行血清UA测定。结果:痛风患者血清UA为(564.8±83.4)μmol/L,其它病患者UA为(330±44.1)μmol/L,健康体检者UA为(290±21.8)μmol/L。结论:在基层医院检验设备条件较落后的条件下,用尿酶法试剂盒测定UA可用于痛风的辅助诊断,动态检测痛风患者的疗效、预后及复发均有重要价值     

原发性痛风114例临床分析

目的 探讨原发性痛风的临床表现、诊断标准、治疗与转归以提高对该病的认识.方法 对114例原发性痛风进行回顾性分析.结果 114例首次发病于骨关节者107例,尿路结石7例;114原发性痛风患者,下肢关节受累89例（78.1%）,上肢关节受累47例（41.2%）;114例痛风患者均伴有不同程度的尿酸增高,男〉420 μmol/L,女〉350 μmol/L;经控制饮食、多饮水,急性期给予秋水仙碱治疗,间歇期给予别嘌醇治疗,疗效满意.结论 原发性痛风发病率明显升高,危害性加大,应引起临床医生的重视,同时患者应在临床医生的指导下合理应用痛风膳食并长期坚持服降尿酸药,有效地治疗原发性痛风.     

痛风患者肾结石发病情况及其影响因素的分析

目的分析和研究痛风患者肾结石发病情况及其影响因素。方法检测痛风患者和非痛风患者的血尿酸、尿尿酸、血肌酐、尿肌酐,对影响肾结石发病的因素进行分析。结果在70例痛风患者中出现肾结石25例（35．7％）。70例非痛风患者中出现肾结石11例（15．7％）;〈420μmol／L肾结石发病3例（25．0％）;420-500μmol／L肾结石发病6例（31．6％）;501-600μmol／L肾结石发病8例（38．1）;〉600μmol／L肾结石发病9例（90．0％）。结论痛风患者较容易发生肾结石,且肾结石的发生与患者的尿酸水平、尿量等有关系,对血糖还有血尿酸严格控制,可提高自身生活质量。     

次黄嘌呤与氧嗪酸钾不同剂量配伍制备高尿酸血症大鼠模型

目的确定次黄嘌呤与尿酸酶抑制剂氧嗪酸钾(OAPS)伍用制备高尿酸血症大鼠模型的合适剂量,为制备持续性高尿酸血症及痛风大鼠模型提供实验依据。方法给大鼠不同配伍剂量的次黄嘌呤(ig)与OAPS(sc)制备代谢性高尿酸血症大鼠模型,于造模后不同时间观察模型大鼠血清尿酸、尿素氮和肌酐水平。结果次黄嘌呤分别为125,250和500mg·kg-1,OAPS以25,50和100mg·kg-1与每个剂量的次黄嘌呤伍用造模。造模后3h血清尿酸和肌酐浓度均有所升高,造模后9h血清尿素氮浓度明显升高。在次黄嘌呤为500mg·kg-1,OAPS为100mg·kg-1时,造模后3,9和12h模型大鼠血清尿酸浓度分别为(781±167),(627±291)和(366±196)μmol·L-1,明显高于正常对照组(86±10),(75±16)和(80±15)μmol·L-1;造模后24h,血清尿素氮和肌酐水平〔(199±96)mg.L-1和(55±16)μmol·L-1〕均明显高于正常对照组〔(61±5)mg.L-1和(21±2)μmol·L-1〕。结论次黄嘌呤500mg·kg-1和OAPS100mg·kg-1伍用制备的代谢性高尿酸血症大鼠模型具有血清尿酸浓度高和维持时间长的特点。     

慢性心力衰竭患者血清尿酸水平的变化及其临床意义

目的探讨慢性心力衰竭患者血清尿酸浓度变化及其临床意义。方法测定100例心力衰竭患者治疗前后血清尿酸,分析尿酸水平与性别、年龄、病因、心功能分级、利尿剂的使用及肾功能关系。结果慢性心力衰竭患者血清尿酸浓度在不同病因和不同性别及年龄之间无明显差别,未用利尿剂和用利尿剂者尿酸、尿素氮、肌酐差别无统计学意义。但随心功能的恶化而升高,Ⅰ～Ⅱ、Ⅲ、Ⅳ级心力衰竭血尿酸浓度分别为285.5±34.6μmol/L,352.6±98.6μmol/L,612.2±114.5μmol/L。治疗前后尿酸浓度也有差别,即EF值≤0.4时治疗前后尿酸浓度分别为598.3±75.6μmol/L和448.5±65.7μmol/L(P<0.01);而EF值>0.4时治疗前后血尿酸浓度分别为382.6±56.8μmol/L和295.5±35.7μmol/L(P<0.05)。结论慢性心力衰竭患者血清尿酸浓度升高,与心力衰竭的严重程度相关,治疗后血尿酸浓度明显下降。     

尿酸肾病临床诊断的初步探讨

尿酸肾病常表现为高尿酸血症,除关节损伤表现为痛风关节炎外,尚可见肾脏受累的临床症状,亦称慢性高尿酸肾病(以下简称尿酸肾病)。本病较少见、症状多样、易误诊,现将治疗的六例报告如下:     

降尿酸的药需要终身服用吗?

正我曾经有过痛风,肾脏不太好,最近医师给我开了一盒降尿酸的药(非布司他),我需要长期吃吗?湘潭刘奶奶首先,吃降尿酸药的目的,就是把血尿酸水平降下去,防止痛风复发,阻止痛风对关节、肾脏等器官的伤害。一般的痛风病友需要把血尿酸降到360μmol/L以下,但如果有痛风石,或痛风发作很频繁,则需要更严格地把尿酸降到300μmol/L以下才行。把尿酸降到目标水平不算太难,难的是要长期把尿酸维持在     

中药外用内服治疗妊娠期肝内胆汁淤积症的疗效观察

目的 探讨妊娠期肝内胆汁淤积症的中药外洗内服治疗效果.方法 选取2014年9月至2015年9月本院收治的妊娠期肝内胆汁淤积孕妇共60例,随机分为治疗组和对照组,治疗组孕妇采用中药内服外洗方法治疗,而对照组孕妇给予思美泰针静脉注射.结果 治疗后治疗组孕妇血清谷草转氨酶[(28.32±6.95) U/L比(40.30±7.51)U/L]、血清谷丙转氨酶[(29.71±5.57) U/L比(45.78±7.80) U/L]、总胆汁酸[(0.99±0.20)μmol/L比(2.39±0.42)μmol/L]、血清胆红素[(15.25±3.93)μmol/L比(27.56±6.20)μmol/L]及直接胆红素[(5.90±1.30)μm01/L比(8.92±2.06)μmol/L]水平均明显低于对照组孕妇(P＜0.05);治疗后治疗组孕妇的瘙痒症状明显低于对照组孕妇低[(0.86±0.85)比(1.43±0.52)];治疗组发生早产(10.00％比30.00％)、剖宫产(23.30％比63.33％)、羊水污染(10.00％比33.33％)、胎儿 窘迫(6.67％比26.67％)、新生儿窒息(3.33％比20.00％)的情况均明显比对照组少(P＜0.05).结论 中药外洗内服治疗妊娠期肝内胆汁淤积症的疗效明显,能够有效地降低孕产妇的生化指标水平,改善妊娠结局,因此值得在临床上推广.     

血清尿酸水平与冠心病的关系

目的探讨血清尿酸水平与冠心病的关系。方法经冠状动脉造影确诊的冠心病患者(冠心病组)75例和非冠心病患者(对照组)52例,检测二组的血清尿酸水平及相关血脂、血糖等生化指标。结果冠心病组血清尿酸水平显著高于对照组(369±77)μmol/L与(343±70)μmol/L,P<0.01;相关分析显示血清尿酸与冠脉狭窄指数呈正相关(P<0.05)。多元Logistic回归分析显示冠心病的发病与血清尿酸有关。结论血清尿酸水平与冠心病密切相关,高尿酸血症是冠心病的独立危险因素之一。     

高血压病患者冠状动脉病变与血清尿酸水平的相关性

目的探讨高血压病患者血清尿酸水平与冠状动脉病变程度的相关性。方法对于经过冠状动脉造影的368例高血压病患者,测定血清尿酸及其它临床生化指标。根据冠状动脉造影结果分为冠心病组(n=240)和正常冠脉对照组(n=128)进行回顾性分析。结果冠心病组的血清尿酸水平(448.32± 115.12)μmol／L明显高于正常冠脉对照组(371.36±98.98)μmol／L(P＜0.001)；多因素逐步回归分析显示高血压病患者的冠状动脉狭窄程度与血清尿酸水平呈显著线性回归关系(P＜0.001)。结论高血压病患者的血清尿酸水平与冠状动脉狭窄程度密切相关。降低血清尿酸水平能否延缓或减轻冠脉病变程度,有待于进一步大规模前瞻性研究加以论证。     

The challenges of gout management in the elderly

Gout is common in the elderly and its management is frequently complicated by the presence of co-morbid conditions and medications prescribed for other conditions. The management of gout is 2-fold: (i) treatment of the acute attack to rapidly resolve the pain and inflammation; and (ii) long-term urate-lowering therapy (ULT) to prevent further gouty episodes. NSAIDs, colchicine, corticosteroids and more recently interleukin (IL)-1 inhibitors are effective treatments for acute gout. The choice of agent is determined by the patient's age, co-morbidities and concomitant medications. Renal impairment is of particular concern in the elderly and may preclude the use of NSAIDs and colchicine. The IL-1 inhibitors are rapidly effective but data in the elderly are limited. ULT aiming for a serum urate <0.36?mmol/L, or lower in severe tophaceous gout, is critical for the long-term management of gout. Urate lowering can be achieved by inhibiting the production of uric acid through xanthine oxidase inhibition (allopurinol, febuxostat), increasing uric acid excretion via the kidneys (uricosuric agents: probenecid, benzbromarone) or dissolving uric acid to the more water soluble allantoin (recombinant uricases: pegloticase, rasburicase). Allopurinol is the most commonly used ULT, but there is no consensus on dosing in renal impairment. Febuxostat is effective at lowering serum urate, but there are limited data in the elderly and patients with renal impairment. Furthermore, there are concerns about cardiovascular safety. Probenecid is ineffective in patients with renal impairment (creatinine clearance <60?mL/min) and the availability of benzbromarone is limited because of concerns about its hepatotoxicity. The recombinant uricases provide an exciting new therapeutic option, but there are limited data for their use in the elderly. These agents may be particularly useful in patients with a high urate burden (e.g. those with tophi); however, they may precipitate a severe flare of gout and this will require treatment in its own right. Careful consideration of the patient's concomitant medications is required as many drugs increase serum urate. Successful urate lowering will ultimately reduce gout flares and thereby improve patient quality of life.     

尿酸转运蛋白在原发性痛风中的研究进展

痛风是长期嘌呤代谢紊乱所导致的一种炎症性关节炎,具有一定的基因遗传性.基因突变所引起的功能缺失可导致原发性高尿酸血症与痛风,肾脏尿酸盐转运系统是原发性痛风相关基因研究的重点,维持尿酸盐的吸收和分泌平衡对血清尿酸水平的稳定起着决定性的的调节作用.该文对目前已发现的与原发性痛风发生、发展相关的尿酸转运蛋白作简要概述,以供临床合理诊治原发性痛风提供参考.     

PEG-uricase in the management of treatment-resistant gout and hyperuricemia

Hyperuricemia results from an imbalance between the rates of production and excretion of uric acid. Longstanding hyperuricemia can lead to gout, which is characterized by the deposition of monosodium urate monohydrate crystals in the joints and periarticular structures. Because such deposits are resolved very slowly by lowering plasma urate with available drugs or other measures, the symptoms of gout may become chronic. Persistent hyperuricemia may also increase the risk of renal and cardiovascular diseases. Unlike most mammals, humans lack the enzyme uricase (urate oxidase) that catalyzes the oxidation of uric acid to a more soluble product. This review describes the development of a poly(ethylene glycol) (PEG) conjugate of recombinant porcine-like uricase with which a substantial and persistent reduction of plasma urate concentrations has been demonstrated in a Phase 2 clinical trial. Two ongoing Phase 3 clinical trials include systematic assessments of gout symptoms, tophus resolution and quality of life, in addition to the primary endpoint of reduced plasma urate concentration.     

Gout in solid organ transplantation: a challenging clinical problem

Hyperuricaemia occurs in 5-84% and gout in 1.7-28% of recipients of solid organ transplants. Gout may be severe and crippling, and may hinder the improved quality of life gained through organ transplantation. Risk factors for gout in the general population include hyperuricaemia, obesity, weight gain, hypertension and diuretic use. In transplant recipients, therapy with ciclosporin (cyclosporin) is an additional risk factor.Hyperuricaemia is recognised as an independent risk factor for cardiovascular disease; however, whether anti-hyperuricaemic therapy reduces cardiovascular events remains to be determined.Dietary advice is important in the management of gout and patients should be educated to partake in a low-calorie diet with moderate carbohydrate restriction and increased proportional intake of protein and unsaturated fat. While gout is curable, its pharmacological management in transplant recipients is complicated by the risk of adverse effects and potentially severe interactions between immunosuppressive and hypouricaemic drugs. NSAIDs, colchicine and corticosteroids may be used to treat acute gouty attacks. NSAIDs have effects on renal haemodynamics, and must be used with caution and with close monitoring of renal function. Colchicine myotoxicty is of particular concern in transplant recipients with renal impairment or when used in combination with ciclosporin. Long-term urate-lowering therapy is required to promote dissolution of uric acid crystals, thereby preventing recurrent attacks of gout. Allopurinol should be used with caution because of its interaction with azathioprine, which results in bone marrow suppression. Substitution of mycophenylate mofetil for azathioprine avoids this interaction. Uricosuric agents, such as probenecid, are ineffective in patients with renal impairment. The exception is benzbromarone, which is effective in those with a creatinine clearance >25 mL/min. Benzbromarone is indicated in allopurinol-intolerant patients with renal failure, solid organ transplant or tophaceous/polyarticular gout. Monitoring for hepatotoxicty is essential for patients taking benzbromarone.Physicians should carefully consider therapeutic options for the management of hypertension and hyperlipidaemia, which are common in transplant recipients. While loop and thiazide diuretics increase serum urate, amlodipine and losartan have the same antihypertensive effect with the additional benefit of lowering serum urate. Atorvastatin, but not simvastatin, may lower uric acid, and while fenofibrate may reduce serum urate it has been associated with a decline in renal function.Gout in solid organ transplantation is an increasing and challenging clinical problem; it impacts adversely on patients' quality of life. Recognition and, if possible, alleviation of risk factors, prompt treatment of acute attacks and early introduction of hypouricaemic therapy with careful monitoring are the keys to successful management.     

Gout induced by intoxication of sodium bicarbonate in Korean native broilers

Gout is a metabolic disorder that results in hyperuricemia and the deposition of positively birefringent monosodium urate crystals in various parts of the body. Intoxication of sodium bicarbonate (SBC) for 35 days in Korean native broilers was investigated. Sixty birds, aged 2 weeks, divided into 5 groups were exposed to excess SBC: 2 g/L (group A), 7.5 g/L (group B), 20 g/L (group C), 40 g/L (group D). Toxicopathological examination of all exposed birds revealed the manifestation of visceral and articular gout in group C, while birds of group D showed acute kidney damage with manifestation of excessive visceral gout. Interestingly, few birds in group D also showed signs of rare condition of acute articular gout. Dose-dependent increments in erythrocytic count, hematocrit values, and hemoglobin levels of the exposed birds were observed. Hypernatremia, hyperuricemia, hypokalemia, and hypochloremia were common findings among exposed birds. Microscopic examination of birds that manifested visceral gout revealed significant urate deposit, tubular necrosis, and tophi formation in renal interstitium. These findings provide a pathophysiological link that SBC intoxication may support hyperuricemia, which is an independent risk factor for gout and other renal dysfunctions. Further study is required to delineate the effect of lowering uric acid on progression of gout and other renal diseases.     

Management of gout in older adults: barriers to optimal control

Gout, a common inflammatory arthritis, can be diagnosed with absolute certainty. Gout results from the body's reaction to urate crystals deposited in tissues, and this pathophysiology is well understood. If used appropriately, available therapies can be entirely effective in not only treating the symptoms of gout, but also in eliminating the excess urate from the body, thereby eradicating the disease. Because of these facts, management of patients with gout should be successful. However, management of gout is particularly challenging in the elderly, even though the principles of management are the same for all age groups. The purpose of this article is to review these principles and discuss them as they pertain to the elderly. The classic gout attack is acute in onset, extremely painful and associated with marked swelling, warmth, erythema and tenderness of a single joint. However, the diagnosis of gout may be challenging in the elderly because atypical presentations are more common in this group. Treatment of acute gout involves the use of NSAIDs, colchicine, corticosteroids or corticotropin (adrenocorticotropic hormone). Unfortunately, co-morbid conditions such as chronic kidney disease, peptic ulcer disease and congestive heart failure may make the use of these agents dangerous or contraindicated. Thus, it is important to try to treat an acute flare of gout at the earliest sign, because the sooner treatment is initiated, the faster the inflammation will resolve. Urate-lowering agents include allopurinol and uricosuric agents. These also must be used judiciously in the elderly. However, if used at the lowest dose that maintains the serum urate level below 5.0-6.0 mg/dL, the excess urate in the body will be eliminated, acute flares will no longer occur and tophi will resolve. Gout is often seen in association with hypertension, excessive alcohol consumption, obesity and hypertriglyceridaemia. These conditions and the medications used to treat them may contribute to the hyperuricaemia. Treating these conditions and using medications that do not promote hyperuricaemia will aid in the management of gout. Despite the challenges that often complicate the management of gout in the elderly, an understanding of the pathophysiology of the disease and both the indications and limitations of the medications used should allow successful treatment.     

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.     

Safety and tolerability of available drugs for hyperuricemia: a critical review and an update on recent developments

Hyperuricemia (HUA) is a metabolic disease caused by excessive production of serum uric acid (sUA) or decreased excretion of sUA in the body. HUA is an independent risk factor for chronic kidney disease, hypertension, cardiovascular and cerebrovascular diseases, and diabetes mellitus. Timely and effective treatment for reducing sUA plays a key role in reducing urate deposition, preventing gout attacks, and reducing kidney damage and the occurrence of other accompanying diseases. Four pharmacological methods can be used to treat HUA: decrease urate production, increase urate excretion, prevent urate formation, and catabolize urate. To provide a reference for clinical treatment and new medical research for HUA, the drugs and potential drugs for HUA were reviewed in the present work.     

Updates on the treatment of gout,including a review of updated treatment guidelines and use of small molecule therapies for difficult-to-treat gout and gout flares

Introduction: Gout is a rheumatologic condition associated with elevated serum uric acid levels and deposition of monosodium urate crystals in joints and soft tissues.

Areas covered: In this article, we describe the role of currently available drug therapies for managing acute gout flares and used in reducing serum urate levels. Further, we explore the role of novel small molecular therapies and biologic agents in the treatment of refractory or severe gout symptoms. A literature search of MEDLINE and MEDLINE In-Process & Other Non-Indexed Citations Databases (1996-June 2017) was conducted utilizing the key words ‘gout’, ‘interleukin-1 inhibitors’, ‘acute gout’, ‘gout treatment’, ‘urate lowering therapies’, ‘hyperuricemia’, ‘colchicine’, ‘pegloticase’, ‘lesinurad’, ‘xanthine oxidase’, ‘xanthine oxidase inhibitors’, ‘allopurinol’, ‘febuxostat’, ‘uricosurics’, ‘probenecid’, and ‘benzbromarone’. All published articles regarding therapeutic management of gout and hyperuricemia were evaluated. References of selected articles, data from poster presentations, and abstract publications were additionally reviewed.

Expert opinion: Numerous therapies are currently available to managing acute gout flares and for lowering serum urate levels; advances in the understanding of the pathophysiology of this disorder has led to the emergence of targeted therapies and novel biologic preparations currently in development which may improve the clinical management of severe or refractory cases of disease that fail to respond to traditional therapies.