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手部、腕部及肘部痛风

Gout in the upper limb — what causes the attacks and lumps (tophi), how flares and high urate are treated, and when surgery is needed.

双手在多个指关节处出现慢性痛风石性痛风所致坚实结节(痛风石)的示意图。
慢性痛风可在指关节周围形成坚硬的结节,称为痛风石,这会限制手部的活动和功能。 Arthritis Research UK Primary Care Centre / Wikimedia Commons, CC BY 2.0

本页面由机器翻译,尚未经临床医生审核。英文版本为权威版本。

您的感受

痛风往往在夜间突然发作。某个关节(有时是拇指根部、指关节、手腕或肘尖)在短短几小时内变得剧烈疼痛。该部位看起来发热、发红且肿胀,触痛如此敏感,以至于即使床单的重量都令人难以忍受。这是一次急性发作,首次发作常发生在足部,但手部和手腕也是常见部位。

在两次发作之间,关节可能感觉完全正常,因此人们常常忽视首次发作。然而,经过数月乃至数年,痛风可能在皮肤下、指关节周围、指关节处或肘部上方留下坚硬的肿块。这些被称为痛风石。它们在皮肤下可能呈白垩色或白色,随着增大,会使手部僵硬、削弱握力,并使扣衬衫纽扣等精细动作变得困难。如果肿块压迫手腕处的神经,一些人还会注意到手指出现麻木或刺痛感。

实际发生了什么

痛风是一种全身性疾病,其症状表现在关节上。您的身体会产生一种名为尿酸(urate)的代谢废物。当血液中尿酸含量过高时,会形成微小且尖锐的结晶,沉积在关节内部及周围的软组织中,包括手部和腕部。

您的免疫系统将这些结晶视为入侵者并对其进行攻击,由此引发的反应即为您所感受到的突然且剧烈的炎症发作。如果高尿酸水平长期得不到控制,结晶会积聚成坚硬的沉积物(痛风石)。随着时间的推移,这些沉积物可能侵蚀骨骼、损伤肌腱,并偶尔压迫神经。关键在于,急性发作和肿块是同一问题的两个表现:体内尿酸过多。 控制尿酸水平,就能控制该疾病。

我们能做什么

治疗分为两个独立的部分,两者都至关重要。

控制急性发作。 急性发作期通过抗炎药物来缓解,通常使用抗炎药片(非甾体抗炎药,NSAID)、秋水仙碱或短期糖皮质激素。这些药物在早期使用时效果最佳,因此在下次发作前与医生商定一个计划是值得的。

长期降低尿酸水平。 这才是随时间推移真正治愈痛风的关键。每日服用一片药物,最常见的是别嘌醇,可逐渐将血液中的尿酸降至目标水平以下。只要维持在该水平足够长的时间,结晶会缓慢溶解,急性发作停止,痛风石缩小。饮食和生活方式的调整有帮助(减少啤酒和烈酒摄入,减少含糖饮料,保持健康体重,充分补水),但对大多数人来说,每日服用的药物才是主要作用。

手术仅在少数情况下需要,例如痛风石巨大且突破皮肤、干扰肌腱或压迫神经(例如导致腕管综合征症状)。即便如此,术后仍需继续服用降低尿酸的药物进行治疗。

预期情况

痛风是少数几种我们确实能够有效控制的关节炎之一。如果长期将尿酸水平维持在目标值以下,急性发作会变得罕见并最终停止,现有的痛风石也会逐渐消退。这是一个缓慢的过程:需要数月甚至数年,且降尿酸药物通常需要终身服用,因为停药会导致晶体重新形成。

等待的代价是真实存在的:手部痛风石堆积得越多,对手部功能限制就越大,因此尽早降低尿酸水平可以保护您的抓握能力和手部功能。坚持治疗的患者预后非常好。

何时就医

  • 首次出现发热、肿胀、疼痛的关节: 应尽快就医。关节感染与痛风的外观可能完全相同,且属于急症,因此必须加以鉴别。
  • 反复发作,或发作频率逐渐增加:这是开始降尿酸治疗的信号。
  • 关节周围出现肿块,或肿块破溃皮肤或渗出白色粉末状物质。
  • 手部出现麻木、刺痛或无力:可能是沉积物压迫神经,值得进行评估。

深入探讨

Advanced reading: the deeper science (optional)

本节内容超出了您做出自身治疗决策所需的范围。痛风值得额外阅读,因为它是少数几种具有真正治愈可能性的风湿病之一——同时也是治疗最不当的疾病之一,原因在于其治愈机制的作用时间尺度,在患者处于疼痛状态时往往显得不合时宜。

痛风的本质:尿酸盐结晶

关节液偏振光显微镜检查显示免疫细胞间存在针状单钠尿酸盐结晶。
偏振光下的尿酸钠结晶——被免疫细胞吞噬的针状结晶,从而诱发痛风发作。 Bobjgalindo, Wikimedia Commons, CC BY-SA 3.0

尿酸是身体分解称为嘌呤的物质(来自细胞和某些食物)时产生的正常代谢废物。当血液中尿酸盐水平持续偏高时,它会从溶液中析出,在关节内及周围形成微小的针状单钠尿酸盐(MSU)结晶。结晶在温度较低的部位更容易形成,这是大脚趾——人体最冷且最末端的关节——成为典型首发部位的重要原因之一。

在该关节处,这是一种真正具有破坏性的疾病,而不仅仅是引起疼痛的疾病。汇总5,478名患者的数据显示,第一跖趾关节的急性关节炎在痛风中高度普遍,对疼痛和功能障碍有显著的测量影响,并对关节本身的结构和功能产生可证实的影响 [1]。

炎性小体:为何发作如此突然且猛烈

当免疫吞噬细胞(巨噬细胞)吞噬MSU晶体时,发作便开始了。这些晶体触发了一个名为NLRP3炎性小体的内部警报复合物,该复合物激活了一种酶(caspase-1),从而释放出强效的炎症信使白细胞介素-1β(IL-1β)。IL-1β使关节内充满炎症,在数小时内引发急性发作所特有的快速、剧烈的发红、发热、肿胀和疼痛。随着反应消退,发作在数天内自行缓解。

这一机制解释了临床上重要的一点:发作是机体对晶体的免疫反应,而非晶体本身。平息发作与清除晶体是两个不同的问题,需要不同药物在不同时间尺度上进行干预。

决定一切的数值

长期治疗有一个可测量的目标:将血尿酸浓度降至晶体无法形成的水平以下,并维持在该水平。国际实践目标是将血尿酸控制在 0.36 mmol/L (6 mg/dL) 以下,若存在痛风石,则控制在 0.30 mmol/L (5 mg/dL) 以下,因为在这些水平下,现有晶体会溶解,而不仅仅是停止累积。

证据支持的是治疗至该目标值,而非开具固定剂量并寄希望于效果。在一项针对 183 人的随机对照试验中,每月递增别嘌醇剂量直至达到目标值,在 24个月 内显著降低了发生痛风发作的人群比例和平均痛风石大小,且耐受性良好 [2]。

这一原则同样适用于服务层面:一项英国随机试验显示,以患者教育和治疗至目标尿酸策略为核心的护士主导护理,在尿酸控制方面显著优于常规护理,且痛风发作更少,痛风石在 两年 时消退更明显 [3]。

由此得出两点结论:从未根据血液检测进行滴定调整的别嘌醇剂量算不上真正的治疗,而“我的痛风控制得很好”意味着一个数值,而非本月没有发作。

为何在最初几个月内被放弃

启动降尿酸治疗可能诱发发作。随着晶体溶解,其脱落的物质会引发炎症小体的反应,因此治愈初期的几个月可能比疾病表面看起来更为严重。这是患者停止治疗并认为其无效的最常见单一原因,而实际上,急性发作恰恰是治疗起效的证据。正因如此,治疗通常以低剂量起始,逐渐递增剂量,并在最初几个月内辅以抗炎预防治疗。

上肢外科医生关注的两件事

痛风并不局限于足部,在上肢,它可能模拟外科病理改变。已有文献报道,远端肱二头肌止点处的痛风性腱鞘炎可导致部分肌腱撕裂,其临床表现看似单纯的肱二头肌断裂,而患者的痛风病史最终被证实为病因 [4]。这种情况罕见,但唯有想到该诊断的医生才能做出此诊断。

更令人放心的是,一个常见的担忧并未得到证实。一项纳入 684,964 人的荟萃分析显示,痛风与骨折风险增加 无 关联,且早期处方的降尿酸药物对骨折风险既无不利影响也无有益影响 [5]。

参考文献

[1] Stewart S, Dalbeth N, Vandal AC, Rome K. 痛风中的第一跖趾关节:系统综述与荟萃分析。BMC Musculoskelet Disord. 2016;17(1). https://doi.org/10.1186/s12891-016-0919-9

[2] Stamp LK, Chapman PT, Barclay ML, Horne A, Frampton C, Tan P, et al. 一项关于通过增加别嘌醇剂量以达到目标血尿酸水平在痛风患者中的疗效和安全性的随机对照试验。Ann Rheum Dis. 2017;76(9):1522-8. https://doi.org/10.1136/annrheumdis-2016-210872

[3] Doherty M, Jenkins W, Richardson H, Sarmanova A, Abhishek A, Ashton D, et al. 由护士主导的护理(包括患者教育和参与以及治疗达标降尿酸策略)与常规护理相比,治疗痛风的疗效和成本效益:一项随机对照试验。Lancet. 2018;392(10156):1403-12. https://doi.org/10.1016/S0140-6736(18)32158-5

[4] Fairhurst RJ, Schwartz AM, Rozmaryn LM. 远端肱二头肌腱止点痛风性腱鞘炎并发部分肌腱断裂。Hand (N Y). 2016;12(1):NP1-NP5. https://doi.org/10.1177/1558944715627639

[5] Liu F, Dong J, Zhou D, Kang Q, Xiong F. 痛风与骨折风险无相关性:一项荟萃分析。J Orthop Surg Res. 2019;14(1). https://doi.org/10.1186/s13018-019-1317-4


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