Pyrophosphate arthropathy--recent clinical advances.
Pyrophosphate arthropathy--recent clinical advances.
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DOI：
10.1136/ard.42.suppl_1.38
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发表时间：
1983
影响因子：
27.4
通讯作者：
M. Doherty
中科院分区：
文献类型：
--
作者：
M. Doherty
现在距离McCarty等人已经20年了。在急性关节炎和放射性软骨钙化症患者的滑液中发现了焦磷酸二氢钙(CPPD)晶体。CPPD晶体随后在体内和体外都被证明是炎性的，它们在关节疾病中的因果作用，反映在术语“CPPD晶体诱导的滑膜炎”，很容易被接受。身体研究3后来确定慢性阻塞性肺疾病是膝关节软骨钙化的最常见(尽管不是唯一)原因，家族性关节软骨钙化病、5代谢性疾病、6和年龄7被认为是易感因素。然而，自从“假痛风综合征”被描述以来，焦磷酸盐关节病的情况越来越复杂。尤其明显的是：(A)与关节内CPPD晶体沉积相关的临床症状有很大的多样性，(B)CPPD晶体沉积，特别是在老年人，通常发生在没有炎症和关节损害的情况下。这两个观察结果都被纳入了McCarty的临床分类--焦磷酸钙沉淀症，其中有五种重叠的模式--“假性痛风”、“假性类风湿性关节炎”、“假性骨性关节炎”、“假性神经性关节”，以及无症状或“稀土”沉积。然而，在这种分类中固有的是一个无法解释的悖论，即在某些人中，CPPD晶体似乎会导致关节炎，正如关节疾病的特征性质和分布以及晶体的炎症属性所表明的那样，而在另一些人中，它们在明显没有关节疾病的情况下惯性沉积。由此引发的关于CPPD(和羟基磷灰石)晶体是主要致病颗粒、软骨损伤的附属物还是无辜旁观者的争论最近得到了审查，并在本期的其他地方得到了考虑。然而，似乎在大多数情况下，仅关节内CPPD晶体沉积不足以引起关节炎。这一点，再加上广泛的临床表现，意味着焦磷酸盐关节病的发病机制中存在多种因素的作用--这一点将贯穿整个讨论。这篇综述将主要局限于最近的临床研究，这些研究有助于我们理解与CPPD晶体沉积相关的关节炎。首先将考虑焦磷酸盐关节病的易感因素、临床范围和可能的治疗方法，然后将通过对最近提出的颗粒诱导关节疾病的‘放大环’假说的批判性检查来具体解决无症状软骨钙化病的问题。
It is now 20 years since McCarty et al. identified calcium pyrophosphate dihydrate (CPPD) crystals in synovial fluid from patients with acute arthritis and radiological chondrocalcinosis.' CPPD crystals were subsequently shown to be inflammatory both in vivo and in vitro2 and their causal role in joint disease, reflected by the term 'CPPD crystal-induced synovitis', was readily accepted. Cadaveric studies3 later established CPPD as the most common, though not exclusive, cause of cartilage calcification in the knee, and familial chondrocalcinosis articularis,5 metabolic disease,6 and aging7 became recognised as predisposing factors. Since description of'the pseudogout syndrome', however, an increasingly complex picture of pyrophosphate arthropathy has emerged. In particular it is apparent that: (a) there is great diversity in the clinical syndromes associated with intra-articular CPPD crystal deposition, and (b) CPPD crystal deposition, particularly in the elderly, commonly occurs in the absence of inflammation and joint damage. Both observations are incorporated in McCarty's clinical classification of 'calcium pyrophosphate deposition disease', in which five overlapping patterns are recognised-'pseudogout', 'pseudorheumatoid arthritis', 'pseudo-osteoarthritis', 'pseudoneuropathic joints', and asymptomatic or 'lanthanic' deposition.' Inherent in this classification, however, is the unexplained paradox that in some individuals CPPD crystals appear to cause arthritis, as suggested by the characteristic nature and distribution of joint disease and the phlogistic properties of the crystals, while in others they deposit inertly in the apparent absence of joint disease. The resultant debate as to whether CPPD (and hydroxyapatite) crystals are primary pathogenetic particles, epiphenomena to cartilage damage, or 'innocent bystanders' has been reviewed recently,' and is considered elsewhere in this issue. It would appear, however, that in most cases intra-articular CPPD crystal deposition alone is an insufficient cause for arthritis. This, together with the wide range of clinical expression, implies the operation of multiple factors in the pathogenesis of pyrophosphate arthropathy-a point that will recur throughout this discussion. This review will largely be confined to recent clinical studies that have contributed to our understanding of the arthritis associated with CPPD crystal deposition. The predisposing factors, clinical range, and possible methods of treatment of pyrophosphate arthropathy will be considered first, and then the question of asymptomatic chondrocalcinosis will specifically be addressed by critical examination of a recently proposed 'amplification loop' hypothesis for particle-induced joint disease."o