Pritzker K P
Mount Sinai Hospital, University of Toronto, Canada.
Curr Opin Rheumatol. 1994 Jul;6(4):442-7. doi: 10.1097/00002281-199407000-00016.
Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease continues to be of intense clinical and basic science interest. Follow-up of studies of hereditary CPPD crystal deposition indicate differences from the common sporadic disease. The results of a prospective study of CPPD crystal deposition arthropathy confirm that clinical symptoms appear to be independent of radiologic progression. Novel clinical presentations include association with pregnancy and simulation of meningitis. CPPD crystal deposition pathology in synovium ultrastructurally resembles that in cartilage. Factors such as the presence of ATP can induce experimental calcifications in tissue culture that resemble CPPD crystal deposition. Interleukin-8 and tyrosine phosphorylation of neutrophil protons can mediate CPPD crystal deposition-associated inflammation. The control of crystal function and dissolution recently has been the subject of many general reviews. The theory outlined in these papers is important for understanding CPPD crystal deposition and basic phosphate crystal formation and dissolution.
二水焦磷酸钙（CPPD）晶体沉积病一直是临床和基础科学研究的热点。对遗传性CPPD晶体沉积的研究随访表明，其与常见的散发性疾病存在差异。一项关于CPPD晶体沉积性关节病的前瞻性研究结果证实，临床症状似乎与放射学进展无关。新的临床表现包括与妊娠相关以及类似脑膜炎的症状。滑膜中CPPD晶体沉积的病理学在超微结构上类似于软骨中的情况。诸如ATP的存在等因素可在组织培养中诱导出类似于CPPD晶体沉积的实验性钙化。白细胞介素-8和中性粒素质子的酪氨酸磷酸化可介导与CPPD晶体沉积相关的炎症。晶体功能和溶解的控制最近已成为许多综述的主题。这些论文中概述的理论对于理解CPPD晶体沉积以及碱性磷酸盐晶体的形成和溶解非常重要。
